case study for renal failure

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Published: 10 January 2022

Chronic kidney disease and its health-related factors: a case-control study

Mousa Ghelichi-Ghojogh 1 ,
Mohammad Fararouei 2 ,
Mozhgan Seif 3 &
Maryam Pakfetrat 4

BMC Nephrology volume 23 , Article number: 24 ( 2022 ) Cite this article

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Chronic kidney disease (CKD) is a non-communicable disease that includes a range of different physiological disorders that are associated with abnormal renal function and progressive decline in glomerular filtration rate (GFR). This study aimed to investigate the associations of several behavioral and health-related factors with CKD in Iranian patients.

A hospital-based case-control study was conducted on 700 participants (350 cases and 350 controls). Logistic regression was applied to measure the association between the selected factors and CKD.

The mean age of cases and controls were 59.6 ± 12.4 and 58.9 ± 12.2 respectively ( p = 0.827). The results of multiple logistic regression suggested that many factors including low birth weight (OR yes/no = 4.07, 95%CI: 1.76–9.37, P = 0.001), history of diabetes (OR yes/no = 3.57, 95%CI: 2.36–5.40, P = 0.001), history of kidney diseases (OR yes/no = 3.35, 95%CI: 2.21–5.00, P = 0.001) and history of chemotherapy (OR yes/no = 2.18, 95%CI: 1.12–4.23, P = 0.02) are associated with the risk of CKD.

Conclusions

The present study covered a large number of potential risk/ preventive factors altogether. The results highlighted the importance of collaborative monitoring of kidney function among patients with the above conditions.

Peer Review reports

Chronic kidney disease (CKD) is a non-communicable disease that includes a range of different physiological disorders that are associated with an abnormal renal function and progressive decline in glomerular filtration rate (GFR) [ 1 , 2 , 3 ]. Chronic kidney disease includes five stages of kidney damage, from mild kidney dysfunction to complete failure [ 4 ]. Generally, a person with stage 3 or 4 of CKD is considered as having moderate to severe kidney damage. Stage 3 is broken up into two levels of kidney damage: 3A) a level of GFR between 45 to 59 ml/min/1.73 m 2 , and 3B) a level of GFR between 30 and 44 ml/min/1.73 m 2 . In addition, GFR for stage 4 is 15–29 ml/min/1.73 m 2 [ 4 , 5 ]. It is reported that both the prevalence and burden of CKD are increasing worldwide, especially in developing countries [ 6 ]. The worldwide prevalence of CKD (all stages) is estimated to be between 8 to 16%, a figure that may indicate millions of deaths annually [ 7 ]. According to a meta-analysis, the prevalence of stage 3 to 5 CKD in South Africa, Senegal, and Congo is about 7.6%. In China, Taiwan, and Mongolia the rate of CKD is about 10.06% and in Japan, South Korea, and Oceania the rate is about 11.73%. In Europe the prevalence of CKD is about 11.86% [ 8 ], and finally, about 14.44% in the United States and Canada. The prevalence of CKD is estimated to be about 11.68% among the Iranian adult population and about 2.9% of Iranian women and 1.3% of Iranian men are expected to develop CKD annually [ 9 ]. Patients with stages 3 or 4 CKD are at much higher risk of progressing to either end-stage renal disease (ESRD) or death even prior to the development of ESRD [ 10 , 11 ].

In general, a large number of risk factors including age, sex, family history of kidney disease, primary kidney disease, urinary tract infections, cardiovascular disease, diabetes mellitus, and nephrotoxins (non-steroidal anti-inflammatory drugs, antibiotics) are known as predisposing and initiating factors of CKD [ 12 , 13 , 14 ]. However, the existing studies are suffering from a small sample size of individuals with kidney disease, particularly those with ESRD [ 15 ].

Despite the fact that the prevalence of CKD in the world, including Iran, is increasing, the factors associated with CKD are explored very little. The present case-control study aimed to investigate the association of several behavioral and health-related factors with CKD in the Iranian population.

Materials and methods

In this study, participants were selected among individuals who were registered or were visiting Faghihi and Motahari hospitals (two largest referral centers in the South of Iran located in Shiraz (the capital of Fars province). Cases and controls were frequency-matched by sex and age. The GFR values were calculated using the CKD-EPI formula [ 16 , 17 ].

Data collection

An interview-administered questionnaire and the participant’s medical records were used to obtain the required data. The questionnaire and interview procedure were designed, evaluated, and revised by three experts via conducting a pilot study including 50 cases and 50 controls. The reliability of the questionnaire was measured using the test-retest method (Cronbach’s alpha was 0.75). The interview was conducted by a trained public health‌ nurse at the time of visiting the clinics.

Avoiding concurrent conditions that their association may interpreted as reverse causation; the questionnaire was designed to define factors preceding at least a year before experiencing CKD first symptoms. Accordingly participants reported their social and demographic characteristics (age, sex, marital status, educational level, place of residency), history of chronic diseases (diabetes, cardiovascular diseases, hypertension, kidney diseases, family history of kidney diseases, autoimmune diseases and thyroid diseases [ 18 ]). Also history of other conditions namely (smoking, urinary tract infection (UTI), surgery due to illness or accident, low birth weight, burns, kidney pain (flank pain), chemotherapy, taking drugs for weight loss or obesity, taking non-steroidal anti-inflammatory drugs, and taking antibiotic) before their current condition was started. Many researchers reported recalling birth weight to be reliable for research purposes [ 19 ]. Moreover, we asked the participants to report their birth weight as a categorical variable (< 2500 g or low, 2500- < 3500 g or normal, and > 3500 g or overweight). Medical records of the participants were used to confirm/complete the reported data. In the case of contradiction between the self-reported and recorded data, we used the recorded information for our study.

Verbal informed consent was obtained from patients because the majority of the participants were illiterate. The study protocol was reviewed and approved by the ethical committee of Shiraz University of Medical Sciences (approval number: 1399.865).

Sample size

The sample size was calculated to detect an association‌ between the history of using antibiotics (one of our main study variables) and CKD as small as OR = 1.5 [ 20 ]. With an alpha value of 0.05 (2-sided) and a power of 80%, the required sample size was estimated as large as n = 312 participants for each group.

Selection of cases

The selected clinics deliver medical care to patients from the southern part of the country. In this study, patients with CKD who were registered with the above centers from June to December 2020 were studied. A case was a patient with a GFR < 60 (ml/min/1.73 m 2 ) at least twice in 3 months. According to the latest version of the International Classification of Diseases (2010), Codes N18.3 and N18.4 are assigned to patients who have (GFR = 30–59 (ml/min/1.73 m 2 ) and GFR = 15–29 (ml/min/1.73 m 2 ) respectively [ 21 ]. In total, 350 patients who were diagnosed with CKD by a nephrologist during the study period.

Selection of the controls

We used hospital controls to avoid recall-bias. The control participants were selected from patients who were admitted to the general surgery (due to hernia, appendicitis, intestinal obstruction, hemorrhoids, and varicose veins), and orthopedic wards‌ from June to December 2020. Using the level of creatinine in the participants’ serum samples, GFR was calculated and the individuals with normal GFR (ml/min/1.73 m 2 ) GFR > 60) and those who reported no history of CKD were included ( n = 350).

Inclusion criteria

Patients were included if they were ≥ 20 years old and had a definitive diagnosis of CKD by a nephrologist.

Exclusion criteria

Participants were excluded if they were critically ill, had acute kidney injury, those undergone renal transplantation, and those with cognitive impairment.

Statistical analysis

The Chi-square test was used to measure the unadjusted associations between categorical variables and CKD. Multiple logistic regression was applied to measure the adjusted associations for the study variables and CKD. The backward variable selection strategy was used to include variables in the regression model. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. All p -values were two-sided and the results were considered statistically significant at p < 0.05. All analyses were conducted using Stata version 14.0 (Stata Corporation, College Station, TX, USA).

In total, 350 cases and 350 age and sex-matched controls were included in the analysis. The mean age of cases and controls were 59.6 ± 12.4 and 58.9 ± 12.2 respectively ( p = 0.83). Overall, 208 patients (59.4%) and 200 controls (57.1%) were male ( p = 0.54). Also, 149 patients (42.6%) and 133 controls (38.0%) were illiterate or had elementary education ( p = 0.001). Most cases (96.9%) and controls (95.7%) were married ( p = 0.42). The mean GFR for CKD and control groups were 38.6 ± 11.4 and 78.3 ± 10.2 (ml/min/1.73 m2) respectively.

Result of univariate analysis

Table 1 illustrates the unadjusted associations of demographic and health-related variables with CKD. Accordingly, significant (unadjusted) associations were found between the risk of CKD and several study variables including education, history of chronic diseases (diabetes, cardiovascular, hypertension, kidney diseases, autoimmune diseases, and hypothyroidism), family history of kidney diseases, smoking, UTI, surgery due to illness or accident, low birth weight, burns, kidney pain, chemotherapy, taking non-steroidal anti-inflammatory drugs, and taking antibiotics) ( P < 0.05 for all).

Results of multivariable analysis

Table 2 illustrates the adjusted associations between the study variables and the risk of CKD. Most noticeably, low birth weight (OR yes/no = 4.07, 95%CI: 1.76–9.37, P = 0.001), history of surgery (OR yes/no = 1.74, 95%CI: 1.18–2.54, P = 0.004), family history of kidney diseases (OR yes/no = 1.97, 95%CI: 1.20–3.23, P = 0.007), and history of chemotherapy (OR yes/no = 2.18, 95%CI: 1.12–4.23, P = 0.02) were significantly associated with a higher risk of CKD. On the other hand, education (OR college/illiterate or primary = 0.54, 95%CI: 0.31–0.92, P = 0.025) was found to be inversely associated with CKD.

The results of the present study suggested that several variables including, education, history of diabetes, history of hypertension, history of kidney diseases or a family history of kidney diseases, history of surgery due to illness or accident, low birth weight, history of chemotherapy, history of taking non-steroidal anti-inflammatory drugs, and history of taking antibiotics may affect the risk of CKD.

In our study, the level of education was inversely associated with the risk of CKD. This finding is in accordance with the results of a study conducted by K Lambert et.al, who suggested that illiteracy or elementary education may raise the risk of CKD [ 22 ]. The fact that education level is associated with health literacy, may partly explain our results that lower education and inadequate health literacy in individuals with CKD is associated with worse health outcomes including poorer control of biochemical parameters, higher risk of cardiovascular diseases (CVDs); a higher rate of hospitalization, and a higher rate of infections [ 23 ].

In the current study, the history of diabetes was associated with a higher risk of CKD. This finding is consistent with the results of other studies on the same subject [ 20 , 21 , 24 , 25 , 26 , 27 ]. It is not surprising that people with diabetes have an increased risk of CKD as diabetes is an important detrimental factor for kidney functioning as approximately, 40% of patients with diabetes develop CKD [ 27 ].

The other variable that was associated with an increased risk of CKD was a history of hypertension. Our result is consistent with the results of several other studies [ 20 , 24 , 25 , 28 ]. It is reported that hypertension is both a cause and effect of CKD and accelerates the progression of the CKD to ESRD [ 29 ].

After controlling for other variables, a significant association was observed between family history of kidney diseases and risk of CKD. Published studies suggested the same pattern [ 24 ]. Inherited kidney diseases (IKDs) are considered as the foremost reasons for the initiation of CKD and are accounted for about 10–15% of kidney replacement therapies (KRT) in adults [ 30 ].

The importance of the history of surgery due to illness or accident in this study is rarely investigated by other researchers who reported the effect of surgery in patients with acute kidney injury (AKI), and major abdominal and cardiac surgeries [ 31 , 32 ] on the risk of CKD. Also, AKI is associated with an increased risk of CKD with progression in various clinical settings [ 33 , 34 , 35 ]. In a study by Mizota et.al, although most AKI cases recovered completely within 7 days after major abdominal surgery, they were at higher risk of 1-year mortality and chronic kidney disease compared to those without AKI [ 31 ].

The present study also showed that low birth weight is a significant risk factor for CKD. This finding is consistent with the results of some other studies. However, the results of very few studies on the association between birth weight and risk of CKD are controversial as some suggested a significant association [ 19 , 36 , 37 ] whereas others suggested otherwise [ 36 ]. This may be explained by the relatively smaller size and volume of kidneys in LBW infants compared to infants that are normally grown [ 38 ]. This can lead to long-term complications in adolescence and adulthood including hypertension, decreased glomerular filtration, albuminuria, and cardiovascular diseases. Eventually, these long-term complications can also cause CKD [ 39 ].

Another important result of the current study is the association between chemotherapy for treating cancers and the risk of CKD. According to a study on chemotherapy for testicular cancer by Inai et al., 1 year after chemotherapy 23% of the patients showed CKD [ 40 ]. Another study suggested that the prevalence of stage 3 CKD among patients with cancer was 12, and < 1% of patients had stage 4 CKD [ 41 , 42 ]. Other studies have shown an even higher prevalence of CKD among cancer patients. For instance, only 38.6% of patients with breast cancer, 38.9% of patients with lung cancer, 38.3% of patients with prostate cancer, 27.5% of patients with gynecologic cancer, and 27.2% of patients with colorectal cancer had a GFR ≥90 (ml/min/1.73 m 2 ) at the time of therapy initiation [ 43 , 44 ]. The overall prevalence of CKD ranges from 12 to 25% across many cancer patients [ 45 , 46 , 47 ]. These results clearly demonstrate that, when patients with cancer develop acute or chronic kidney disease, outcomes are inferior, and the promise of curative therapeutic regimens is lessened.

In our study, the history of taking nephrotoxic agents (antibiotics or NSAIDs drugs) was associated with a higher risk of CKD. Our result is following the results reported by other studies [ 48 , 49 ]. Common agents that are associated with AKI include NSAIDs are different drugs including antibiotics, iodinated contrast media, and chemotherapeutic drugs [ 50 ].

Strengths and limitations of our study

Our study used a reasonably large sample size. In addition, a considerably large number of study variables was included in the study. With a very high participation rate, trained nurses conducted the interviews with the case and control participants in the same setting. However, histories of exposures are prone to recall error (bias), a common issue in the case-control studies. It is to be mentioned that the method of selecting controls (hospital controls) should have reduced the risk of recall bias when reporting the required information. In addition, we used the participants’ medical records to complete/ confirm the reported data. Although the design of the present study was not able to confirm a causal association between the associated variables and CKD, the potential importance and modifiable nature of the associated factors makes the results potentially valuable and easily applicable in the prevention of CKD.

Given that, chemotherapy is an important risk factor for CKD, we suggest the imperative for collaborative care between oncologists and nephrologists in the early diagnosis and treatment of kidney diseases in patients with cancer. Training clinicians and patients are important to reduce the risk of nephrotoxicity. Electronic medical records can simultaneously be used to monitor prescription practices, responsiveness to alerts and prompts, the incidence of CKD, and detecting barriers to the effective implementation of preventive measures [ 51 ]. Routine follow-up and management of diabetic patients is also important for the prevention of CKD. We suggest a tight collaboration between endocrinologists and nephrologists to take care of diabetic patients with kidney problems. In addition, surgeons in major operations should refer patients, especially patients with AKI, to a nephrologist for proper care related to their kidney function. Treatment of hypertension is among the most important interventions to slow down the progression of CKD [ 12 ]. Moreover, all patients with newly diagnosed hypertension should be screened for CKD. We suggest all patients with diabetes have their GFR and urine albumin-to-creatinine ratio (UACR) checked annually. Finally, the aging population and obesity cause the absolute numbers of people with diabetes and kidney diseases to raise significantly. This will require a more integrated approach between dialectologists/nephrologists and the primary care teams (55).

Availability of data and materials

The datasets generated and/or analyzed during the current study are not publicly available due to their being the intellectual property of Shiraz University of Medical Sciences but are available from the corresponding author on reasonable request.

Abbreviations

Chronic kidney disease

End-stage renal disease

Glomerular filtration rate

Renal replacement treatment

Urinary tract infection

Odds ratios

Confidence intervals

Hypertension

Acute kidney injury

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Acknowledgments

This paper is part of a thesis conducted by Mousa Ghelichi-Ghojogh, Ph.D. student of epidemiology, and a research project conducted at the Shiraz University of Medical sciences (99-01-04-22719). We would like to thank Dr. Bahram Shahryari and all nephrologists of Shiraz‌ University of medical sciences, interviewers, and CKD patients in Shiraz for their voluntary participation in the study and for providing data for the study.

Shiraz University of Medical Sciences financially supported this study. (Grant number: 99–01–04-22719).

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Mousa Ghelichi-Ghojogh

HIV/AIDS research center, School of Health, Shiraz University of Medical Sciences, P.O.Box: 71645-111, Shiraz, Iran

Mohammad Fararouei

Department of Epidemiology, School of Health, Shiraz University of Medical Sciences, Shiraz, Iran

Mozhgan Seif

Nephrologist, Shiraz Nephro-Urology Research Center, Department of Internal Medicine, Emergency Medicine Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

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Contributions

MGG: Conceptualization, Methodology, Statistical analysis, Investigation, and writing the draft of the manuscript. MP: were involved in methodology, writing the draft of the manuscript, and clinical consultation. MS: was involved in the methodology and statistical analysis. MF: was involved in conceptualization, methodology, supervision, writing, and reviewing the manuscript. The authors read and approved the final manuscript.

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Correspondence to Mohammad Fararouei .

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The study protocol was reviewed and approved by the ethical committee of Shiraz University of Medical Sciences (approval number: 1399.865). All methods were performed in accordance with the relevant guidelines and regulations of the Declaration of Helsinki. The participants were assured that their information is used for research purposes only. Because of the illiteracy of a considerable number of the patients, verbal informed consent was obtained from the participants. Using verbal informed consent was also granted by the ethical committee of Shiraz University of Medical Sciences.

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Ghelichi-Ghojogh, M., Fararouei, M., Seif, M. et al. Chronic kidney disease and its health-related factors: a case-control study. BMC Nephrol 23 , 24 (2022). https://doi.org/10.1186/s12882-021-02655-w

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Global case studies for chronic kidney disease/end-stage kidney disease care

Affiliations.

1 Kidney Research Center, Department of Nephrology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
2 Centre for Transplantation and Renal Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
3 Institute of Biomedical Ethics and the History of Medicine, University of Zurich, Zurich, Switzerland.
4 Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
5 Division of Nephrology, The University of Tokyo School of Medicine, Hongo, Japan.
6 State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
7 Servicio de Nefrologia, Hospital Civil de Guadalajara Fray Antonio Alcalde, University of Guadalajara Health Sciences Center, Hospital 278, Guadalajara, Jalisco, Mexico.
8 Almughtaribeen University, Khartoum, Sudan.
9 Department of Nephrology, Dalal Jamm Hospital, Cheikh Anta Diop University Teaching Hospital, Dakar, Senegal.
10 Dialysis Unit, CASMU-IAMPP, Montevideo, Uruguay.
11 Division of Nephrology, Department of Internal Medicine, Rajavithi Hospital, Bangkok, Thailand.
12 Department of Medicine, Chulalongkorn Hospital, Bangkok, Thailand.
13 Division of Nephrology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
14 Bhumirajanagarindra Kidney Institute, Bangkok, Thailand.
15 SEHA Dialysis Services, Abu Dhabi, United Arab Emirates.
16 Department of Nephrology and Clinical Research Centre, Hospital Serdang, Jalan Puchong, Kajang, Selangor, Malaysia.
17 Department of Nephrology, Barts Health NHS Trust, London, UK.
18 Centre for Nephrology, University College London, London, UK.
19 Malawi Ministry of Health, Queen Elizabeth Central Hospital, Blantyre, Malawi.
20 Parklands Kidney Centre, Nairobi, Kenya.
21 Department of Medicine, The Aga Khan University Hospital, Nairobi, Kenya.
22 Paediatric Intensive and Critical Unit, Red Cross War Memorial Children's Hospital, University of Cape Town, Cape Town, South Africa.
23 Division of Nephrology, College of Medicine, Seoul National University, Seoul, Korea.
24 School of Medicine and Dentistry, College of Health Sciences, University of Ghana, Legon, Accra, Ghana.
25 Department of Medicine, University of Calgary, Calgary, Alberta, Canada.
26 Pan American Health Organization/World Health Organization's Coordinating Centre in Prevention and Control of Chronic Kidney Disease, University of Calgary, Calgary, Alberta, Canada.
27 International Society of Nephrology, Brussels, Belgium.
PMID: 32149007
PMCID: PMC7031689
DOI: 10.1016/j.kisu.2019.11.010

The prevalence of chronic kidney disease and its risk factors is increasing worldwide, and the rapid rise in global need for end-stage kidney disease care is a major challenge for health systems, particularly in low- and middle-income countries. Countries are responding to the challenge of end-stage kidney disease in different ways, with variable provision of the components of a kidney care strategy, including effective prevention, detection, conservative care, kidney transplantation, and an appropriate mix of dialysis modalities. This collection of case studies is from 15 countries from around the world and offers valuable learning examples from a variety of contexts. The variability in approaches may be explained by country differences in burden of disease, available human or financial resources, income status, and cost structures. In addition, cultural considerations, political context, and competing interests from other stakeholders must be considered. Although the approaches taken have often varied substantially, a common theme is the potential benefits of multistakeholder engagement aimed at improving the availability and scope of integrated kidney care.

Keywords: chronic kidney disease; dialysis; end-stage kidney disease; transplantation.

PubMed Disclaimer

The second Global Kidney Health Summit outputs: developing a strategic plan to increase access to integrated end-stage kidney disease care worldwide. Harris DCH, Davies SJ, Finkelstein FO, Jha V. Harris DCH, et al. Kidney Int Suppl (2011). 2020 Mar;10(1):e1-e2. doi: 10.1016/j.kisu.2019.09.001. Epub 2020 Feb 19. Kidney Int Suppl (2011). 2020. PMID: 32154795 Free PMC article. No abstract available.

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Improving Outcomes for Patients with Chronic Kidney Disease

Norton, Jenna M. MPH; Newman, Eileen P. MS, RD; Romancito, Gayle RN; Mahooty, Stephanie DNP, MSN; Kuracina, Theresa MS, RD, CDE, LN; Narva, Andrew S. MD, FACP, FASN

Jenna M. Norton is the program manager of the National Kidney and Urologic Science Translation Program at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, MD. Andrew S. Narva is the director and Eileen P. Newman is the associate director of the National Kidney Disease Education Program in the Division of Kidney, Urologic, and Hematologic Diseases at the NIDDK. Gayle Romancito is a nurse at the Zuni Comprehensive Community Health Center, Indian Health Service, Zuni, NM. Stephanie Mahooty is an NP at Renal Medicine Associates and Desert Kidney Associates in Albuquerque, NM. Theresa Kuracina is a dietitian at the Albuquerque Indian Health Center, Indian Health Service, Albuquerque, NM. Authors Narva, Newman, and Norton are federal employees of the National Institutes of Health, and Romancito and Kuracina are federal employees of the Indian Health Service. Contact author: Andrew S. Narva, [email protected] . The authors and planners have disclosed no potential conflicts of interest, financial or otherwise.

Coping with chronic kidney disease (CKD) is challenging for many people, since symptoms often don't appear until the disease is advanced and the patient is close to requiring dialysis. This two-part article aims to provide nurses with the basic information necessary to assess and manage patients with CKD. Part 1, which appeared last month, offered an overview of the disease, described identification and etiology, and discussed ways to slow disease progression. Part 2 addresses disease complications and treatment for kidney failure.

The second installment of this two-part article on assessing and managing patients with chronic kidney disease addresses disease complications and treatment for kidney failure.

In Part 1 of this article, which appeared last month, we offered an overview of chronic kidney disease (CKD), described its identification and etiology, and discussed ways to slow disease progression. Here, in part 2, we address disease complications and treatment for kidney failure. As in part 1, the case study of Anna Lowry, a 49-year-old woman with CKD, will be used for illustration, offering nurses specific guidance in helping patients to better understand and manage their CKD. (This case is a composite based on the authors’ experience.)

COMPLICATIONS OF CKD

As kidney function declines, fewer functioning nephrons remain. The complications associated with CKD are complex, and may include anemia, hyperkalemia, hypoalbuminemia, metabolic acidosis, and abnormal mineral metabolism and bone disease. Laboratory work may show multiple metabolic abnormalities. Yet most people don't feel any different until their CKD is quite advanced. As noted in part 1, dietary choices can affect many of the metabolic abnormalities associated with CKD. Thus referral to a registered dietitian who is knowledgeable about CKD may help in managing complications.

There are many symptoms, signs, and laboratory values that must be tracked in patients with progressive CKD. The unique nature of the nurse–patient relationship may allow nurses to pick up on symptoms and signs that the primary care provider might have missed—particularly nonverbal behaviors and cues. It's essential for nurses to alert primary care providers to any subtle changes in a patient's condition, psychosocial issues, patient concerns, abnormal laboratory test results, or trends in laboratory values. (See Case Study: Metabolic Complications .)

Anemia. In the general population, a hemoglobin level of less than 13 g/dL in men and less than 12 g/dL in women indicates anemia. 1, 2 But the optimal target hemoglobin level for people with CKD is currently unknown.

Anemia may occur early in CKD and is generally due to inadequate synthesis of the hormone erythropoietin by the damaged kidneys. The prevalence of anemia increases as the glomerular filtration rate (GFR) declines, affecting nearly 50% of patients with an estimated GFR (eGFR) of less than 30 mL/min/1.73 m 2 . 3 Among patients with advanced CKD, there is evidence that the prevalence of anemia is higher in those with diabetes than in those without diabetes. 4

CKD-associated anemia is generally normochromic and normocytic. 5 That said, identifying and correcting other causes of anemia (such as iron deficiency) is necessary. 5 Assessing iron status in CKD requires a complete blood count and checking iron indices, including serum iron level and total iron-binding capacity (see Table 1 6-9 ). These two results are used to determine the transferrin saturation percentage, which reflects available iron. The serum ferritin level is used to assess stored iron. Optimal target levels of serum iron, total iron-binding capacity, and serum ferritin for people with CKD are unknown. Furthermore, they are affected by inflammation, 10 which is common in CKD, 11 making results more difficult to interpret. The absolute reticulocyte count may also be used to differentiate the cause of anemia or to monitor response to treatment. 8

Ruling out other causes of anemia, including vitamin-deficiency anemia, may also be important. Although megaloblastic anemia is not commonly seen with CKD, some people with diabetes who have taken metformin for years may be vitamin B 12 deficient. Metformin reportedly decreases absorption of this vitamin. 12 Both B 12 and folate levels may be lower than normal with metformin use. 13 Metformin is contraindicated in patients with an eGFR below 30 mL/min/1.73 m 2 . 14

Many other factors may contribute to inadequate iron stores in people with CKD. As their GFR declines, patients may lose interest in high-protein foods. Hepcidin, a hormone that plays a key role in controlling iron levels, regulating iron absorption from the gut, and mobilizing stored iron, accumulates in CKD, 15 and this may result in reduced serum iron levels. Inflammation may also play a significant role in reducing iron absorption. 5

Since iron deficiency is common in CKD, iron status and hemoglobin levels should be checked before the addition of any iron supplements to the regimen. 5 Supplemental iron is available in both oral and IV formulations. Absorption of oral iron supplements may be reduced by the intake of caffeinated beverages, supplemental calcium or calcium-containing antacids, and H 2 -receptor blockers or proton pump inhibitors. 16 Iron supplements may cause unwanted gastrointestinal effects such as heartburn or nausea. Beginning with half the recommended dosage and gradually increasing to the full dosage may help. 16 Patients may also have fewer adverse effects with a different preparation, or by taking iron with food, in divided doses, or along with stool softeners. 16 Injectable erythropoiesis-stimulating agents are used infrequently in treating CKD.

Hyperkalemia. Potassium excretion is regulated by the renin−angiotensin−aldosterone system (RAAS). Perturbations of this system may result in hyperkalemia. Potassium levels tend to increase as GFR declines. 17 Nearly half of patients with an eGFR less than 30 mL/min/1.73 m 2 have serum potassium levels of 4.5 mEq/L or greater. 3 RAAS antagonists may increase the risk of hyperkalemia. Potassium-sparing medications, dietary intake, and transcellular shifts may also affect serum potassium levels.

Several factors can cause potassium to shift between the intracellular and extracellular compartments. Insulin tends to move potassium into the cells; therefore, insulin deficiency can result in hyperkalemia. 18 Metabolic acidosis, characterized by an excess of hydrogen ions in the plasma, may drive potassium out of the cells, as hydrogen ions are buffered intracellularly. 18 As a result, treating both hyperglycemia and acidemia may lower serum potassium. 18 In some patients with CKD, treating acidosis may allow the continued use of RAAS antagonists. 19

Patients with hyperkalemia should be counseled to limit foods that are higher in dietary potassium and to read ingredient lists in order to avoid foods that contain potassium chloride. Beginning in July 2018, food manufacturers will be required to include potassium on the Nutrition Facts label. 20

Hypoalbuminemia occurs in CKD as a result of multiple factors. Both acute and chronic inflammation are associated with reduced albumin synthesis. 21 Loss of albumin in the urine in large quantities is associated with reduced serum albumin levels. Metabolic acidosis, 22 insulin resistance, 23 and a decrease in intake of high-protein foods 24 may also contribute to low serum albumin. One large study of patients on maintenance hemodialysis found that a serum albumin level of greater than 3.8 g/dL was associated with reduced mortality risk, with the lowest such risk seen at levels of 4.4 g/dL or greater. 25 Unfortunately, another study found that only 11% of new dialysis patients had serum albumin levels of 4 g/dL or greater. 26

Metabolic acidosis is usually defined as a serum bicarbonate level of less than 22 mEq/L. The prevalence of decreased serum bicarbonate increases as GFR declines. 27 Nearly a quarter of patients with an eGFR below 30 mL/min/1.73 m 2 have a serum bicarbonate level of 20.5 mEq/L or less. 3 Chronic metabolic acidosis is associated with accelerated muscle degradation, reduced albumin synthesis, exacerbation of metabolic bone disease, impaired glucose tolerance, increased inflammation, and accelerated CKD progression. 28 Animal protein is a source of acid load, while fresh fruits and vegetables are not. Serum bicarbonate levels may increase as dietary protein intake decreases. 29

Interventions to treat chronic metabolic acidosis include an adequate (but not excessive) intake of animal protein and a supplemental base, such as sodium bicarbonate. 28 It's important to note that one 650-mg tablet of sodium bicarbonate has 178 mg of sodium. Reemphasize dietary salt restriction when sodium bicarbonate is prescribed. Some patients may need an added diuretic to help remove the extra sodium. 28

Abnormal mineral metabolism and bone disease. Some CKD patients may have low levels of 25-hydroxyvitamin D, 30 which can trigger complications that affect bone strength and increase the risk of vascular calcification. 31, 32 Serum calcium levels also decrease as a result of low vitamin D levels. 33 Serum phosphorus levels may be within the normal range until CKD is advanced. 33

As eGFR declines, the prevalences of hypocalcemia and hyperphosphatemia increase. 3, 33 Over 19% of patients with an eGFR below 30 mL/min/1.73 m 2 have a serum calcium level of 8.9 mg/dL or less, and nearly 30% have a serum phosphorus level of 4.7 mg/dL or more. 3 The systemic disorders of mineral and bone metabolism associated with CKD are reflected in abnormalities in calcium, phosphorus, parathyroid hormone, and vitamin D metabolism. These derangements result in abnormalities in bone turnover, mineralization, volume, and linear growth or strength. 33 They may be associated with vascular or other soft tissue calcification. 34

Bone disease in people with CKD is complex, and interpreting laboratory test results is difficult. Although observational data support the correction of the metabolic abnormalities, there is limited high-quality evidence to support intervention. Phosphorus restriction may be implemented while trying to maintain adequate protein intake. 30 Phosphorus-binding medications are generally prescribed with meals in order to prevent phosphorus absorption. Low 25-hydroxyvitamin D levels may be treated with ergocalciferol or cholecalciferol, although further trials are needed to confirm the benefits. 31 Elevated parathyroid hormone levels may be managed with vitamin D and phosphorus restriction. 31 Most adults exceed the recommended dietary allowance of 700 mg/day for phosphorus. 35 According to 2011–2012 National Health and Nutrition Examination Survey (NHANES) data, the average phosphorus intake was 1,393 mg/day. 36

Depending on the food source, phosphorus absorption varies. Between 10% and 60% of phosphorus found naturally in protein-rich foods (such as meat, poultry, dairy, nuts, seeds, dried beans, and whole grains) is absorbed. 37 Between 80% and 100% of inorganic phosphorus, which is added to many packaged and processed foods, is absorbed. 37 For example, colas contain phosphoric acid. Sodium phosphates are often added to poultry and pork products to enhance flavor or preserve tenderness. Cereals fortified with calcium may contain calcium phosphate.

Patients should be counseled to check ingredient lists for words containing “phos”—such as phosphorus, sodium phosphate, or pyrophosphate—and to avoid foods that contain such ingredients. Because protein-rich foods tend to contain significant amounts of phosphorus, reducing consumption of such foods may also help in reducing phosphorus intake.

PREPARING FOR KIDNEY FAILURE

Coping with CKD and kidney failure is challenging for many people, since symptoms don't often appear until the disease is advanced and the patient is close to requiring dialysis. Many patients exert great effort in adhering to all treatment recommendations, yet still experience CKD progression. Furthermore, both the disease itself and treatment with dialysis are complicated matters. Patients may have difficulty understanding the implications of changes in their health status. It's not uncommon for patients to experience grief, fear, or depression.

Historically, the health care community has not done a good job in educating CKD patients. An analysis of 1994–1998 and 1999–2000 NHANES data showed that fewer than 20% of patients with both moderately decreased kidney function (an eGFR of 30 to 59 mL/min/1.73 m 2 ) and albuminuria (a urine albumin-to-creatinine ratio greater than 30 mg/g) had ever been told by a physician that they had “weak or failing kidneys.” 38 Such delayed awareness leaves many patients with little time to prepare for kidney failure, leaving them limited options when they face decisions about treatment. As one reflection of inadequate preparation, consider that in 2013 more than 80% of people started hemodialysis with a temporary vascular access (catheter). 39

Many nurses aren't comfortable discussing CKD or dialysis with patients, 40, 41 and may defer such discussions to the nephrologist. This is a missed opportunity, because it's both appropriate and helpful for nurses to initiate these conversations. A new provider may not know the patient well, whereas the nurse in the diabetes or hypertension clinic who has been involved in managing the patient's conditions will have established a trust that can make education more effective. Nurses can help patients to better understand CKD and begin accepting and coping with changes in their health status. (See Case Study: Preparing for Kidney Failure .)

TREATMENT CHOICES FOR KIDNEY FAILURE

There are four options for treating kidney failure. Three involve kidney replacement therapy, including kidney transplantation, peritoneal dialysis, or hemodialysis (either in a dialysis center or at home). The fourth option involves supportive care without transplantation or dialysis.

Transplantation. In general, a kidney transplant is associated with the best quality of life and survival (see Figure 1 42 ). To receive a kidney transplant, a patient must be healthy enough to endure a surgery that can last several hours; have access to a donated kidney, either through a living donor or by being on the waiting list for a deceased donor kidney; and be willing to take antirejection medications daily and to have routine follow-up appointments for the rest of her or his life. Although antirejection medications suppress the immune system, organ rejection remains a possibility. With a functioning transplant, dialysis is not needed, and a near-normal diet can be followed.

Kidney transplantation is a treatment, not a cure. The transplanted kidney will likely work very well for a time—according to recent data trends analyses, 92% of deceased donor and 97% of living donor kidneys continue to work at one year following transplantation, and 47% of deceased donor and 62% of living donor kidneys are still working 10 years later 39 —but eventually it is likely to fail. The outcome improves if the donor and the recipient are ABO blood-type compatible and a match for human leukocyte antigens. Pretransplantation evaluation can take several months and typically includes a comprehensive assessment to check for the presence of any conditions that might place the patient or the transplanted kidney at risk (such as severe coronary artery disease or cancer). Eligibility criteria vary from facility to facility, with some more willing to include patients with a higher body mass index.

Peritoneal dialysis may be a choice for a patient who has no contraindicating abdominal pathology (such as extensive abdominal surgery), wants to do in-home treatment, is willing to perform the treatment daily, and has room to store the necessary supplies. Patients using peritoneal dialysis usually don't require vascular access, but do require minor surgery for abdominal catheter placement.

In peritoneal dialysis, the peritoneal membrane is used as a semipermeable filter, replacing the kidneys. In a peritoneal dialysis exchange, a dialysis solution (the dialysate) flows through the catheter into the abdominal cavity, where it remains for a prescribed period of time known as the dwell time. Through the process of diffusion, waste products move down the concentration gradient from the blood in the peritoneal capillaries into the dialysate. The efficiency of this clearance is determined by the concentration gradient; the size of the solute; and the permeability of the peritoneal membrane, which can vary over time. The dialysate includes an osmotic agent that draws fluid into the peritoneal cavity, removing water and producing some additional clearance by bulk flow. At the end of the dwell time, the solution is drained out through the catheter. The continuous nature of peritoneal dialysis allows the patient to reach equilibrium, avoiding the up-and-down cycles of hemodialysis.

The dialysis prescription must be individualized for each patient. Generally, dextrose is used as the osmotic agent, with the concentration varying based on how much fluid must be removed. The higher the dextrose concentration, the more fluid will be removed—but more dextrose will also be absorbed, elevating blood sugar. Each dialysis exchange is generally two to three liters in volume. The dwell times and the number of exchanges per day vary depending on the patient and the characteristics of the peritoneal membrane.

There are several options for peritoneal dialysis. Continuous ambulatory peritoneal dialysis is performed manually four to five times during the day. Continuous cycling peritoneal dialysis involves the use of a cycler, a small appliance that performs the exchanges automatically. With the cycler, many patients can perform enough exchanges while asleep at night, such that they don't need additional exchanges during the day. Some patients need one or two additional manual exchanges during the day for adequate clearance. Most patients on peritoneal dialysis now use the cycler.

It's important for patients on peritoneal dialysis to restrict their potassium intake. (Such restriction may be greater for patients on hemodialysis.) Amino acids that are lost during the exchanges must be replaced, and the patient's dietary protein needs will be higher. Absorbed dextrose may cause the patient to gain weight. Because peritoneal dialysis is continuous, patients are never in a fasting state, and this has particular implications for those who have diabetes. Glucose levels may be harder to control, but insulin can be added to the dialysis solution. Some patients experience body-image concerns associated with the catheter, and may need psychological and emotional support.

Hemodialysis. In hemodialysis, patients are treated with a hemodialysis machine three or more times a week. A dialyzer serves as the filter, replacing the kidneys. The patient's blood is pumped from the body through tubing, passes through the dialyzer, and is returned to the body. Along the way, blood pressure monitors and airflow detectors ensure the patient's safety. (See Figure 2 .)

The blood enters at the top of the dialyzer and is forced through multiple hollow filaments, each about the size of a human hair. Each filament acts as a semipermeable membrane. As blood passes through the filaments, the dialysis solution flows around the outside of the filaments. It takes less than one second for blood to pass from the top of the dialyzer to the bottom; as it does, waste products diffuse into the dialysate and are carried off, and the blood returns to the body. Diffusion efficiency depends on the size of the solute. Protein-bound substances usually aren't removed; some amino acids, glucose, and water-soluble vitamins are removed. (See Figure 3 .)

In-center hemodialysis may be a choice for a patient who can travel to a dialysis center three times a week for scheduled treatments, prefers that trained staff handle the treatments, doesn't mind venipuncture, and is willing to follow a diet that includes numerous restrictions. Advantages of in-center hemodialysis include the availability of facilities nationwide and the presence of trained staff to do the work. If they so choose, patients can be relatively passive. The staff places the needles, monitors treatment, and maintains the equipment. As with many people with chronic illnesses, people with end-stage kidney disease may become socially isolated, and may enjoy the social setting of the dialysis center. Patients typically spend three to four hours three times a week with the same relatively small group of other patients and providers. Disadvantages include more stringent dietary restrictions, the loss of nutrients during hemodialysis, limited control over the procedure, and the burden of travel to and from the center. Furthermore, hemodialysis patients never reach equilibrium, experiencing instead either a gradual increase in waste products and fluids between treatments or a rapid decrease of these during treatment. These up-and-down cycles may fatigue patients.

Home hemodialysis may be a choice for a patient who wants to perform in-home treatments, has someone to help in doing so, can perform treatments three or more times per week, has room for the machine and supplies, and doesn't mind needlesticks and self-cannulation.

Home hemodialysis is becoming more popular. 39 It requires training and support. As with in-center hemodialysis, home hemodialysis can be done three times per week. But it also permits other options, including daily dialysis for two to three hours, five to six times per week, and nocturnal dialysis for six to eight hours, three or more nights per week. More frequent home dialysis appears to be associated with significant benefits to the patient. 43

Home hemodialysis has a different set of advantages and disadvantages. On the one hand, patients have more control over their schedules, travel isn't required, and the newer machines are smaller and easier to use than the older models were. The diet may be less restrictive, and phosphate binders may be less necessary or not needed. And if treatments are done more frequently, the ups and downs are less severe. On the other hand, home hemodialysis requires that a second person (often a partner or other family member) be present to assist, which may cause stress to the patient, the other person, or both. Either the patient or the person assisting has to insert the needles; and the machine and supplies require space. The patient might have to take time off from work in order to get the initial training, which may not be offered locally. Protein requirements are higher because of protein losses during treatment.

Vascular access . To perform hemodialysis, vascular access must be created. In dialysis, blood usually flows at a rate of about 400 mL/min. Withdrawing blood at that rapid rate from any native peripheral vein would collapse that vein. A blood vessel that can withstand that withdrawal rate without collapse is required.

With permanent vascular access, an artificial connection between an artery and a vein is created, such that some blood is diverted to the vein. This connection may be direct or indirect. An arteriovenous fistula establishes a direct connection, and is the preferred access method, as it's less likely to become infected or to clot (see Figure 4A ). Fistula maturation takes several weeks and involves dilation and thickening of the vein, which occurs as a result of increased blood flow. Once the fistula is mature, access to blood flow for dialysis occurs through a percutaneous needlestick. If a direct connection cannot be created because of small vessel size or another mechanical problem, then an arteriovenous graft is the second option. This connection is made indirectly, using a synthetic tube (see Figure 4B ).

Permanent vascular access is usually established in the nondominant arm. A large IV line (such as a peripherally inserted central catheter) placed in a peripheral vein can destroy that vein for future dialysis use. Patients with CKD should be counseled to protect the blood vessels in both arms by avoiding venipuncture or IV catheter placement above the wrist, if possible. When emergent dialysis must be performed, temporary vascular access may be established using a central vein, usually by placing a catheter in the internal jugular vein in the neck. However, this is only a temporary solution. Catheters are associated with inadequate dialysis, increased infection rates, increased clotting, and inflammation. 44

Supportive treatment without transplantation or dialysis. Opting for neither transplantation nor dialysis may be right for patients who feel that such treatments won't improve their health; feel they've done what they wanted to do in life; and, ideally, have family and friends who support their decision. Supportive treatment involves active medical management in which many complications can be treated. Medications for CKD are usually continued and can be adjusted. However, with supportive treatment there is no medical intervention aimed at replacing lost kidney function. Without clearance of uremic toxins, the patient will eventually become uremic.

It's essential to provide comfort and palliative care to these patients. Patients who choose supportive therapy need to understand that without kidney replacement therapy, they will eventually die from uremia; it's important that their family members understand this also. These facts must be presented in a manner that doesn't question the patient's decision, yet ensures that the decision is an informed one.

For additional information on caring for patients with CKD, visit the Web site of the National Kidney Disease Education Program ( http://bit.ly/2gaGy4w ).

For eight additional continuing nursing education activities on topics related to kidney disease, go to www.nursingcenter.com/ce .

chronic kidney disease; collaborative care; end-stage kidney failure; end-stage renal failure; interdisciplinary care; kidney disease

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Chronic Kidney Disease (CKD) Case Study (45 min)

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Mr. Stinson is a 52-year-old male with a history of HTN, DM Type II, CKD, and CHF. He presented to the Emergency Department (ED) complaining of severe itching, nausea, and vomiting. He appeared pale and is lethargic. He reported shortness of breath and the nurse notes crackles in his lungs. He has now been admitted to your unit.

What additional nursing assessments should be performed?

Full set of vital signs
Auscultate heart and lung sounds, as well as peripheral pulses
Assess skin turgor and edema
Assess the patient’s dialysis access site for functionality or bleeding

What diagnostic or lab tests would you expect the provider to order?

Complete metabolic panel (electrolytes, renal function, etc.
Complete blood count
Possibly an ABG to assess for acidosis
Possibly a BNP to assess volume overload and its effect on the heart

Upon further questioning, the patient reports he normally gets dialysis Monday, Wednesday, Friday, but that he skipped dialysis yesterday because he was “not feeling well”. He has +2 pitting edema in his legs. Vital signs are as follows:

HR 102 RR 24

BP 153/97 SpO 2 90%

The patient’s labs result and show the following:

BUN 62 mg/dL Na 134 mg/dL

Cr 3.9 mg/dL Ca 7.8 mg/dL

GFR 13 mL/min/m 2 Phos 5.0 mg/dL

K 6.3 mEq/L Mg 1.6 mg/dL

Gluc 224 mg/dL H/H 8.2 / 30%

pH 7.32 pCO 2 32 HCO 3 – 16

BNP 247 pg/mL

Interpret these lab results and explain their meaning.

The BUN/Cr and GFR indicate the patient is definitely in kidney failure as his glomerulus is not filtering the blood like it should and the waste products are building up
His electrolyte abnormalities (hyperkalemia, hyponatremia, hypocalcemia, hyperphosphatemia, and hypomagnesemia) are all indicative of kidney disease and acidosis. The kidneys would normally retain sodium and excrete potassium. In kidney failure, they do the opposite and potassium levels can get very high.
He is in metabolic acidosis, likely because his kidneys are not able to retain the bicarb buffer like they normally would – this also contributes to the hyperkalemia. As the body tries to balance the H+ ions, it kicks K+ out into the bloodstream.
His BNP is also elevated, indicating volume overload – this is probably caused both by the kidney failure and not getting dialysis and by the heart failure
He is anemic – chronic anemia is common in chronic kidney disease patients due to the lack of erythropoietin.

What is going on with Mr. Stinson physiologically?

Because of his CKD, Mr. Stinson requires dialysis to perform the normal functions of the kidneys, since his aren’t working. He likely felt sick because his potassium was elevated and because of the azotemia (toxins building up in his blood).
He missed dialysis and therefore he is now even more volume overloaded and azotemic
This will cause a risk to his heart and lungs because of the overload and the hyperkalemia

The nephrologist is consulted and determines that the patient needs hemodialysis. As soon as possible. The charge nurse of the dialysis unit is working to create a bed for him and will call back as soon as one is available, hopefully within the hour.

What do you, the nurse, need to consider and assess for Mr. Stinson PRIOR to sending him to dialysis?

ALWAYS hold antihypertensives before HD (obtain provider order)
Hold any medications that may be dialyzed off as they will not have their therapeutic benefit (confirm with pharmacist and obtain provider order)
May require potassium-lowering medications before dialysis if the wait is going to be too long – hyperkalemia can be deadly
Determine if any medications should be held prior to HD
Assess full set of vital signs
Obtain a weight, preferably on a standing scale
Assess heart and lung sounds, as well as skin/edema

Mr. Stinson goes to hemodialysis, where they are able to pull of 3 L of fluid. He tolerates the procedure well and returns to his room.

What would you need to assess for Mr. Stinson AFTER he returns from Dialysis?

Obtain a weight, preferable on a standing scale, to compare to the pre-HD weight. This helps determine how much fluid was pulled off (1 kg = 1 L)
Obtain a full set of vital sign
Re-draw a renal function panel as ordered to ensure electrolytes are not in a dangerous range (requires provider order)

What are some important patient education topics for Mr. Stinson before discharge?

Importance of hemodialysis – he likely didn’t feel well because he NEEDED dialysis.
Reasons to “skip” dialysis typically involve severe infections and fevers, in which case he should go the following day whenever possible or notify his nephrology team
Should also reinforce teaching regarding nutrition – foods to avoid (high in potassium) and when to take medications with or without food (especially Phos-Lo and Calcium supplements)

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Acute Renal Failure - Case Summary

In effect, the renal tubules are damaged and cannot fulfill their normal activities of tubular excretion, secretion, and reabsorption. Hypervolemia, the body's retention of water which in turn increases the blood volume, is one of the more serious effects, leading to increased blood pressure and cardiac overload. The exchange of potassium from intracellular fluid to the plasma poses the potential for disruption of the heart's conduction mechanism. Waste products such as urea and creatinine cannot be excreted. Hydrogen ion balances are disrupted leading to metabolic acidosis.

2. Symptoms of renal failure depend widely on the underlying cause(s). In this case, the disease was in its early stages. Edema (retention of fluid in tissues), oliguria (decreased urinary output), and increased blood pressure (due to increased fluid retention) were seen.

3. Diagnosis is based on the patient's history and key blood and chemistry values. BUN and Creatinine measure the waste products in the blood. Electrolyte values, bicarbonate, and pH measure the severity of the acidosis. Proteins, cells, and casts in the urine are indicative of renal damage.

4. Treatment options also vary with renal failure. In renal failure cases where toxin levels are extremely high in the blood, renal dialysis, either peritoneal or hemodialysis, must be performed to clear the bloodstream of the offending toxins as well as the build-up of waste products the kidneys have been unable to remove. Careful monitoring of the patient's blood electrolyte and water balance are the key to restoring the health of the renal failure patient. Diuretics may be used as indicated to reduce the blood volume and dilute the electrolyte values.

5. Prevention. Patients with underlying conditions such as diabetes mellitus may be more susceptible to the tubular necrosis described above. Care must be exercised when administering potential kidney toxins such as antibiotics, injectable x-ray contrast media, and other substances.

6. Prognosis of patients with renal failure vary. 50% will recover with some combination of treatments. Others will develop chronic renal insufficiency and will require long-term treatment. Others will ultimately develop what is called end-stage renal disease and die from such complications as heart failure.

7. The clinic physician, family physician, and nephrologist all worked together to diagnose and treat this patient. Nurses trained in treating kidney patients monitored vitals, administered I.V's and gave supportive therapy as needed. If the patient had required dialysis, technicians trained in dialysis would have performed the procedure. Medical Laboratory Technologists performed the blood and urine testing. This patient's medical records were vital to her diagnosis. Individuals trained in health information technology are responsible for accurately maintaining these records.

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Clinical pearls, case study: man with type 2 diabetes and stage 1 kidney disease on atkins-like diet.

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Deborah Thomas-Dobersen , Lynn Casey; Case Study: Man With Type 2 Diabetes and Stage 1 Kidney Disease on Atkins-Like Diet. Clin Diabetes 1 January 2005; 23 (1): 46–48. https://doi.org/10.2337/diaclin.23.1.46

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C.S. is a 45-year-old Hispanic man with a 10-year history of type 2 diabetes. He has a glycated hemoglobin of 7.0% and a blood pressure of 130/80 mmHg, treated with an angiotensin-converting enzyme inhibitor for the past 2 years. He has stable background retinopathy and is a nonsmoker. His BMI has been 30 (height 5′10″, weight 210 lb) for the past year. However,lately, he has put himself on the latest high-protein diet (i.e., the Atkins diet).

His weight has dropped by 10 lb, his fasting serum triglyceride level has fallen from 185 to 130 mg/dl, and his blood pressure has decreased to 120/78 mmHg. His LDL cholesterol has remained stable at 102 mg/dl on a statin. His serum creatinine is 0.9 mg/dl, and his 24-hour urine shows a significant increase in microalbumuria from 100 mg/24 hours last year to the current 200 mg/24 hours. He has stage 1 chronic kidney disease indicating kidney damage,with a normal glomerular filtration rate (GFR) of 98 ml/min/1.73 m 2 .

Would the weight reduction, blood pressure, and lipid-lowering accomplished by this high-protein, low-carbohydrate diet be an acceptable choice for a patient who is at significant risk of cardiovascular disease?

What are the recommendations of the American Heart Association (AHA), the National Kidney Foundation (NKF), the National Academy of Sciences, and the American Diabetes Association (ADA) regarding this type of diet for diabetes and/or weight loss?

What has research revealed about appropriate levels of macronutrients for patients such as C.S.?

It is likely that microalbuminuria is the start of a continuum progressing to macroalbuminuria and proteinuria. Microalbuminuria predicts renal disease in diabetes (both type 1 and type 2) and relates to premature mortality. Microalbuminuria is also a marker for pronounced diabetic vascular disease(endothelial dysfunction and chronic low-grade inflammation). Abnormal albuminuria is a major risk factor for cardiovascular complications,predicting increased cardiovascular morbidity and mortality. 1

Twenty to thirty percent of patients with type 2 diabetes develop evidence of nephropathy. Some patients already have microalbuminuria or overt nephropathy upon diagnosis. Without intervention, 20-40% of those with microalbuminuria progress to overt nephropathy. For those on the continuum from overt nephropathy to end-stage renal disease (ESRD), the greater risk of death from coronary artery disease (CAD) may intervene. 2

The average adult protein intake in the United States is 15-20% of total calories and has remained consistent from 1909 to the present. 3 Most Americans eat 50% more protein than they need. The Recommended Dietary Allowance (RDA) is 0.8 g of good quality protein per kilogram body weight per day for men and women. The high-protein Atkins and Zone diets recommend 125 g/day (36% kcal from protein) and 127 gm/day (34% kcal from protein),respectively. 4 The initial phases of the South Beach diet are similar, but no specific nutrient intake can be found in the diet's literature. In C.S., the Atkins diet would contribute 1.3 g protein/kg body weight and 36% of total daily calories from protein. Thus, high-protein diets promote a significantly abnormally high protein intake.

There is some evidence that a sustained high-protein diet can adversely affect renal function, especially in people with diabetes with or without mild renal insufficiency. In patients without renal insufficiency, a high-protein diet may act by acutely increasing the GFR and causing intraglomerular hypertension, which may cause progressive loss of renal function. In the Nurses Health Study, 1,624 female nurses between 30 and 55 years of age were followed for a period of > 11 years. The highest quartile of total protein intake, an average of 93 g/day, was significantly associated with a decline in GFR in women with mild renal insufficiency, thus worsening renal disease. 5 Previous studies had shown mixed results of high-protein diets on renal function but had limitations such as small patient numbers, limited follow-up, and a narrow range of protein intake.

Looking at this relationship from another angle, a meta-analysis recently showed that protein restriction retards the rate of decline in GFR, thus lessening kidney damage. The resulting decrease in kidney damage was small and not impressive. However, when studies looking at people with diabetes were combined, a total of 102 patients given a mean protein restriction of 0.7 g/kg/day versus a control group given 1 g/kg/day (a narrow range), showed a more impressive improvement in renal function independent of the original renal function over 22 months. 6 A crosssectional study of > 2,600 people with type 1 diabetes found that a protein intake > 20% of calories was associated with an increased urinary albumin excretion rate. Researchers concluded that people with diabetes should not exceed a protein intake of 20% of calories. 7 Any study in type 1 diabetes is applicable to type 2 diabetes as it relates to nephropathy. Therefore, there is evidence to recommend avoidance of high protein intakes in patients at risk for renal disease, i.e. all patients with type 1 or type 2 diabetes.

Nutrient analysis of high-protein diets is a concern. With some high-protein diets, such as Atkins, come carbohydrate restrictions. Yet high-carbohydrate foods, such as fruits, vegetables, and low-fat dairy products, provide potassium, magnesium, and calcium, which modestly reduce blood pressure. 8 Normal blood pressure is critically important in preventing CAD and microalbuminuria. With high-protein diets and carbohydrate restrictions come decreased-fiber diets. High-fiber diets have many beneficial effects,including weight loss and lower cardiovascular and cancer risks. With high-protein diets come higher intakes of saturated fats, which are potentially atherogenic. 9 In addition, experimental evidence indicates that a high-protein diet and the resultant increase in saturated fat intake may accelerate the progression of renal disease. Increased LDL cholesterol can stimulate mesangial hypertrophy and stimulate cytokine formation, which may ultimately cause tissue injury. In both type 1 and type 2 diabetes, hypercholesterolemia is a predictor of deteriorating kidney function. 10

The RDA for carbohydrate is set at 130 g carbohydrate/day for adults and children based on the average minimum amount of glucose utilized by the brain to ensure optimal brain function. 11 That pretty much omits Atkins (28-33 g/day) and the early phases of the South Beach diet. Recent AHA guidelines discourage high-protein diets for weight loss,citing potential increased risk for coronary heart disease and renal disease. 12 The most recent ADA technical review on nutrition states that high-protein diets are not recommended until further research establishes their safety. 3 Concerns include renal function and cardiovascular disease. The NKF states in its Kidney Disease Outcomes Quality Initiative guidelines for chronic kidney disease that there is no benefit from a protein intake higher than the RDA of 0.8 g/kg body weight and that this is a reasonable level to recommend for patients with chronic kidney disease in stages 1-3. 13 Thus, many respected nonprofit health care organizations discourage the use of high-protein, low-carbohydrate diets.

Literature reviews of research on the effect of high-protein,low-carbohydrate diets on obesity and lipid levels are not convincing. A review of the literature describing adult outpatient recipients of low-carbohydrate, high-protein diets compared a wide variety of study designs,carbohydrate levels, durations, and calorie levels. Only five studies evaluated low-carbohydrate, high-protein diets for > 90 days, and these were nonrandomized, uncontrolled studies. The three variables that most predicted weight loss were calorie level, duration of calorie restriction, and number of very obese participants in the study. Reduced carbohydrate content was not significantly associated with weight loss. 14

Another review concluded that populations at risk for renal disease, such as patients with diabetes, should avoid high-protein diets. The authors also caution that evidence suggested that protein intakes in excess of two to three times the RDA may have harmful effects on calcium homeostasis and possibly bone mass, 15 a problem for a population already predisposed to osteoporosis. In addition, a comparison of high-protein, low-carbohydrate diets versus a low-fat diet for weight loss shows them equally effective after 1 year in duration. 16 A recent small, randomized, clinical trial comparing a low-carbohydrate (< 30 g) to a conventional low-fat diet in severely obese patients, including individuals with diabetes, showed no significant difference in weight loss after 1 year, although weight loss was minimal (11 vs. 7 lb). Of interest was that the weight loss on the low-carbohydrate diet did not appear to be sustainable and that blood urea nitrogen levels increased more in the low-carbohydrate group. 17

Reduced energy intake is an important therapeutic objective for the patient in the case described above. Reduced energy intake would reduce his blood pressure and serum lipids as well as improve his glycemic control. Weight loss was effective in lowering his blood pressure and serum triglycerides, as one would expect. However, the macronutrient content of his diet may have exacerbated the microalbuminuria. Therefore, a patient such as C.S. would be illadvised to stay on the high-protein diet because of the potential risk to his kidney function as shown by his elevated microalbuminuria.

With guidance from a registered dietitian, C.S. started a 1,500-kcal,low-fat diet with a walking program of 2 miles/day, 6 days/week. He was very tired of the restrictive nature of the high-protein diet and welcomed a change. His urine microalbumin level fell to < 50 mg/24 hours.

Two important studies show strategies that work to yield long-term weight loss. In order to determine what strategies work for long-term weight loss,the National Weight Control Registry elicited and studied information from> 800 people who have been successful in this endeavor. Only half had lost weight through weight loss programs. The remainder had lost weight without medical intervention. Keys to success were an average calorie intake of ∼1,400 kcal/day, a low-fat diet (24% of kcal), and a high energy expenditure through exercise (2,800 kcal/week). 18 The Diabetes Prevention Program also documented that a low-fat diet, increased physical activity, and educational sessions with frequent follow-up allowed participants to lose 7% of their body weight and maintain a 5% weight loss for 3 years. 19

High protein intakes cause higher workloads for kidneys, whose function is to handle amino acid fragments during protein degradation and excrete nitrogen as urea.

There is no research documenting that a high-protein diet maintains weight reduction any better than a low-fat diet, which is safer and offers long-term results.

Safety and efficacy of high-protein, low-carbohydrate diets are a concern for patients with diabetes, regardless of documented kidney disease.

Additional Information

Concerns about the low-carbohydrate diet craze of 11 leading nonprofit consumer, nutrition, and public health organizations are discussed in a format appropriate for both health professionals and patients at the Partnership for Essential Nutrition website: www.essentialnutrition.org .

Deborah Thomas-Dobersen, RD, MS, CDE, is a diabetes educator at the Center for Diabetes and Endocrinology in Arvada, Colo. Lynn Casey, RD, CSR, is a renal dietitian at Renal Care Group, Inc., in Denver, Colo.

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J Nephropharmacol
v.4(1); 2015

Overview of management of acute renal failure and its evaluation; a case analysis

Chaudhary muhammad junaid nazar.

1 Department of Endocrinology, University of Buckingham, Royal Gwent Hospital, NHS Trust, Wales, UK

Faisal Bashir

2 Department of ENT, New City Teaching Hospital, Mohetarma Benazir Bhutto Shaheed Medical College, Mirpur Azad Kashmir, Pakistan

3 Department of Internal Medicine, Allma Iqbal Memorial Teaching Hospital Sialkot, Punjab, Pakistan

John Anderson

4 Division of Medical Education, Postgraduate Medicine Brighton and Sussex Medical School University of Brighton, Brighton, UK

The annual incidence is about 150 per million in the UK, but this figure is six times greater in the >80 years old group. Prerenal azotemia is considered as the most serious reason in community or hospital acquired acute renal failure (ARF). A 67-year-old middle age male was admitted to the hospital with a chief complaint of generalized weakness, volume depletion and dysuria. He has treated with metronidazole for diarrhoea caused by Clostridium difficile considered as the precipitating factor for the ARF. The patient has severe osteoarthritis and takes high dose non-steroidal anti-inflammatory drugs from the last two years. He also complains for obstructive sleep apnea (OSA) and obesity. He has controlled hypertension was on lisinopril to control blood pressure. ARF is quite common, occurring in 80 million populations. Urinary obstruction should be excluded (a cause in around 5-10 of cases) because this is readily reversible if it is diagnosed early. A renal US will be sufficient to identify obstruction in 95 of cases. Most cases of ARF are expected to pre renal failure/acute tubular necrosis (ATN) 70-80%. Risk factor for development for at ATN are old age, drugs (non-steroidal anti-inflammatory drugs, gentamicin), sepsis, and chronic kidney disease and must be considered.

Implication for health policy/practice/research/medical education:

Acute renal failure (ARF) is defined as the rapid decline in kidney function as manifested by a reduction in glomerular filtration rate. It is a more frequent problem observed in all hospital admission. The incidence of ARF increases with age; the annual incidence is about 150 per million in the UK, but this figure is six times greater in the >80 years old group. The overall mortality associated with the ARF is higher with hospital acquired ARF. Therefore, better understanding and early detection can help in better prognosis.

Introduction

Acute renal failure (ARF) is defined as the rapid decline in kidney function as manifested by a reduction in glomerular filtration rate (GFR). It is a more frequent problem observed in all hospital admission. The incidence of ARF increases with age; the annual incidence is about 150 per million in the UK, but this figure is six times greater in the >80 years old group ( 1 ). Pre renal azotemia is considered as the most serious reason in community or hospital acquired ARF. The overall mortality associated with the ARF is higher with hospital acquired ARF ( 2 ). The case study of ARF is discussed to develop a better understanding by studying the current research project. The discussion will be more focused on the pathophysiology and the new ways of treatment used in current practice.

Case presentation

A 67-year-old middle age male, was admitted to the hospital with a chief complaint of generalized weakness, volume depletion and dysuria. He has treated with metronidazole for diarrhea caused by clostridium difficile considered as the precipitating factor for the ARF. The patient has severe osteoarthritis and takes high dose non-steroidal anti-inflammatory drugs (NSAIDs) from the last 2 years. He also complains for obstructive sleep apnea (OSA) and obesity. He was using lisinopril to control his hypertension. He has five siblings with no significant medical history.

On physically examination, he was clinically volume depleted with a pulse rate of 100 beats per minute. He was dehydrated with dry mucous membranes and reduced skin turgor. His body temperature was 37.8 °C, BP; 105/55 mmHg lying, and 90/50 mmHg sitting. Jugular venous pluse not visible. He was in ARF with serum urea and creatinine of 79 mg/dl and 2.4 mg/dl respectively. He has hypokalemic alkalosis with a potassium level of the 1.4 mEq/l (3.5-5.0 mEq/l) and a bicarbonate level of the 41.1 mEq/l (22-28 mEq/l) He was also hyponatremic, sodium level of the 125 mEq/l (136-145 mEq/l) but his serum calcium level was within normal range.

Renal ultrasound showed the right kidney measuring 12.4 cm and left kidney measuring 12.1 cm, with no signs of the shadowing calculus or hydronephrosis. However, it showed the presence of the simple bilateral cyst. Urine dipstick results showed protein of +++ and no blood. A 24 h urine sample showed nephrotic range proteinuria with proteins of 6.48 g/24 h, but serum albumin level was normal at 3.6 g/dl. His hemoglobin was 13.3 g/dl. WBC=11.9×103/µ and platelet count was normal.

The history may point out to the cause of ARF (e.g. drugs, skin rash); assessment of the hemodynamic is crucial, and proper fluid resuscitation should be given. There are different sign and symptom including hypotension, hypovolemia and his dehydration state that give indication to the diagnosis. Fractional excretion of sodium (FENa) was calculated and its value was 0.77%. It is generally less than 1% in patients with acute glomerulonephritis, hepatorenal syndrome, and states of prerenal azotemia such as congestive heart failure or dehydration. This value gives confirmation of prerenal failure.

Renal ultrasound ruled-out urinary obstruction. The diagnostic specificity of FENa in differentiating prerenal azotemia from the interarenal cause of the ARF may also be influenced by the fact that the patients may actually be progressing from the prerenal azotemia state to established ARF. The drug history of the patients can also affect the values of FENa. Despite of these many limitations, FENa when it is considered as an important tool in the context of the other clinical scenario ( 3 ).

There is considerable interest in the potential utility of the different blood and urinary biomarker, which can be important for the diagnosis of ARF. Biochemically, serum creatinine and blood urea nitrogen (BUN) concentration are important diagnostic tool in the detection of ARF. An abrupt increase in serum creatinine concentration usually reflects a decrease in GFR and signals the occurrence of ARF. These two diagnostic tools are affected by the condition and have some limitations e.g. gender, muscle mass and the drugs so they are not fully reliable ( 4 ). Furthermore, serum creatinine concentration does not accurately influence GFR in the unsuspecting state of ARF. On the other hand, increased urea validity, gastrointestinal bleeding, protein intake, catabolic states, protein malnutrition and cirrhosis hit BUN values, which can lead to wrong diagnosis ( 4 ). Cystatin-C and alpha 1-microglobulin, are diverse tools on which research work is going on to find more reliable and efficient tool to diagnosis ARF early. Studies have shown cystatin-C to be an early and reliable marker of acute kidney injury (AKI) in patients in the ICU but it is not the validated as GFR indicator in ARF as compared to serum creatinine and still its requires further studies ( 5 ). Similarly, N-acetylglucosaminidase, KMI-1, neutrophil gelatinous associated lipocalin (NGAL) are under trial to find the fast and timely detection of ARF ( 5 ).

Urinary examination

Assessment of urine biochemistry is essential and inexpensive tool in the evaluation of AKI. The factors which need to be considered important are elaborated in Table 1 .


Urine sodium	40 mEq/l	20 mEq/l
Urine/Plasma osmolality	1.1/ 1	1.5/1
FENa	1%	1%
Urine/Plasma urea	7/1	10/1
Urine volume	Oliguric	1.5

FENa‏= Fractional sodium excretion; ATN= Acute tubular necrosis

Autoantibody profile

Antinuclear factor (ANF), anti-neutrophil cytoplasmic autoantibody (ANCA), anti-GBM, complement and urinary electrophoresis should be performed unless the cause of AKI is obvious, e.g. post myocardial infarction or renal obstruction.

Percutaneous renal biopsy

Renal biopsy is important diagnostic tool for those patients in whom prerenal and post renal ARF have been excluded. It helps further to rule out the cause of the intrinsic renal failure rests unclear e.g. vasculitis, glomerulonephritis, and interstitial nephritis.

Clinical follow up

On volume resuscitation, the patients became profoundly polyuric, with daily urine output of 7 to 10 liter. He needed large amounts of potassium and magnesium supplements, initially intravenous and later oral. The health of patient improved with correction of potassium and polyuria. Kidney function improved progressively, with creatinine level decreasing to 1.5 mg/dl during the course of 2 weeks. The proteinuria dramatically improved with the optimization of fluid level and electrolyte along with 24 h urine protein decreased to 0.73 g/24 h. The patient had good urine output with intravenous fistula and was in a positive fluid balance. However his mobility is much decreased due to malnutrition and weakness. The patients progressed a lot after treatment of six months and remain well with slight proteinuria but mild kidney function. His kidney serum creatinine was 1.6 mg/dl. His stool was clostridium difficile toxin positive. His diarrhea gradually improves over the next few days with metronidazole. Plasma renin and aldosterone concentration ambulant was grossly increased. On discussion with the multidisciplinary team he is unlikely to improve sufficiently to go back to his own house but require sheltered accommodation or even a residential home.

The first dispute to resolve is whether the renal failure is likely to be acute or chronic. Patient’s kidneys are on the small side and his creatinine was elevated on admission giving a GFR indicative of 20 ml/min/1.73 m. Although there may be chances of chronic kidney disease (CKD) in this case, the current history is acute reduction of urine output in the last 12 h and a precipitous increase in creatinine, in keeping with ARF. Therefore, this is likely to be an acute on chronic renal failure. There are many causes of ARF classified listed in Table 2 .

Reduced circulating volume (60%)	1. Blood loss, excess gastrointestinal losses, burns, low cardiac output, toxic or ischemic myocardial depression 2. Drug induced renal profusion angiotensin converting enzyme inhibitors, non- steroidal anti-inflammatory drugs) 3. Large vessels e.g. renovasculature disease), small vessel occlusion: disseminated intra-vasculature coagulation; hemolytic uremic syndrome (HUS)
Toxic ATN (5%)	Rhabdomyolysis with urinary myoglobin, Radio contrast nephropathy
Structure abnormality of renal vasculature (15%)	Large vessels e.g. renovascular diseases
Acute glomerulonephritis and vasculitis (15%)	ANCA –positive vacuities, Goodpasture syndrome
Interstitial nephritis (5%)
Myeloma/tubular cast nephropathy (5%)

ANCA= anti-neutrophil cytoplasmic autoantibody; ATN= acute tubular necrosis

But in this case the renal ultrasound shows no sign of the hydronephrosis, which might indicate obstruction. If obstruction is excluded then the most likely case is pre-renal failure. The prerenal failure will continue to the acute tubular necrosis (ATN) if left untreated. ATN occurs if there is nonstop hypovolemia, hypotension and exposure to nephrotoxic drugs or sepsis.

Pathophysiology of ATN

After an ischemic injury abuse there is forceful arterial vasoconstriction, facilitated by the release by the vasoconstriction (particularly endothelium and by the loss of intrinsic vasodilators (nitric oxide and prostaglandin I2 (PGI); this contributes to the loss of GFR and the restructuring of blood flow within the kidney. Hypoxic injury to the power–consuming cells of the proximal tubule and thick ascending limb of loop of henle occurs, then calcium and oxygen free radical mediated cell necrosis results in cell shedding from the tubular basement membrane, with the formation of the cast that block urine flow. Patients with suspected acute tubular necrosis are not routinely biopsied unless with further kidney pathology is suspected. A number of clinical features in this case are likely causes of ARF including his obvious dehydration and hypotension. Especially the patient was also using NSAIDs for long duration, which can be considered as an imperative factor in the causation of the AKI. NSAIDs (NSAIDs) are common cause of AKI used by the people either prescribed or bought over the counter ( 6 ). However, there is little evidence that NSAIDs own a role in the impairment of renal function of normal healthy person. However, in specific clinical setting such as atherosclerotic cardiovascular diseases in old age people, diuretic use, pre-existing chronic renal failure and NSAID using, AKI could be induced. Furthermore, study regarding NSAIDs, showed, this kind of AKI is reversible within 3-7 days when this drug is discontinued. Less frequently NSAIDs can cause acute tubular necrosis or even, more rarely papillary necrosis ( 7 ). There are many other drugs, which can be nephrotoxic and can play an important role in the pathogenesis of AKI such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) if used in combination can increased risk for post-operative renal dysfunction, possibly as a result of the intraoperative hypotensive episodes ( 7 ). Similarly, other drugs such as gentamicin or amphotericin can be nephrotoxic in order ( 7 ).

Management of acute renal failure

The mainstay of the management involves the increase of the fluid balance hemodynamic stabilization with the optimization of the cardiac output and blood pressure is considered as the most effective steps in the treatment of the acute renal failure. Initial fluid management is important intervention for the ARF patient and to prevent further injury e.g. hypotension and hypovolemia. Assessment of the volume level is challenging, especially patients in intensive care units ( 1 ). There are no specific guidelines for the increasing hemodynamic and fluid level for the renal function protection, but predetermine of data from the clinical setting associated with ARF can be informative. However to improve the assessment of volume status, international guidelines for the management of the sepsis from the surviving sepsis strategy recommended invasive monitoring with the measurement of central venous pressure and venous oxygen saturation (superior vena cava or mixed) based on the first goal-directed treatment approach can be helpful ( 8 ). However, there is debate about the optimal fluid to use for resuscitation in critically ill patients. The recent saline versus albumin fluid assessment safe trial of 6,997 patients found that fluid resuscitation with saline or albumin resulted in similar relative risk for death in critically ill patients ( 9 ) and avoidance of either hypovolemic or fluid overload. Blood pressure should be controlled, hemoglobin maintained above 9 g/dl and sepsis should be quickly and vigorously treated. In conclusion, a flexible fluid method as part of early goal directed therapy appears to be beneficial during the first 6 h. However, the potential risk of the fluid accumulation must be considered in the setting of ARF ( 10 ). Renal dose dopamine loop diuretics are often used in the acute tubular necrosis, although there is no evidence that they it can change the outcome of ARF in humans. Renal dose dopamine 0.5 to 3 mcg/kg/min given as specified vasodilator to increase blood flow and to avoid AKI increases urine output but does not disturb AKI outcome or mortality ( 11 ). Some cases of the ARF can be managed without dialysis, with the adoption of alert fluid balance and dietary restriction.

Key to ARF management is the devotion demanding nutritional support of the sicker patients, and the use of the continuous renal replacement (e.g. CVVH: continuous veno-venous hemofiltration), which are less likely to produce hemodynamic instability.

Other more specific treatments in ARF depend upon the causative form and include the following:

1. Specific immunosuppressive therapy and sometimes plasma exchange may be appropriate for some condition like goodpasture syndrome, ANCA positive vasculitis.
2. Obstruction: Bladder catheterization if there is urine outflow congestion, nephrostomy drainage for renal obstruction.
3. Other: e.g. steroids in acute interstitial nephritis (AIN), plasma exchange in hemolytic uremic syndrome (HUS) and Thrombotic thrombocytopenic purpura (TTP), chemotherapy in myeloma.

There are different drugs, which are used, in ARF listed in Table 3 along with level of evidence but still a lot of additional research going on to proof their effectiveness.


Loop diuretics	RCTs and meta-analysis	No effect
Atrial natriuretic peptide	RCTs	Possible beneficial on survival and kidney function
Dopamine	RCTs	No effect on mortality or kidney function
Norepinephrine	Prospective observational studies	Possible beneficial effect on kidney function
Fenoldopam	1. RCTs 2. One meta-analysis	1. No effect on mortality or kidney function 2. Beneficial effect on mortality and need for dialysis.
Insulin	Meta-analysis	Controversial effects
Mesenchymal stem cells	Animal models	Beneficial effect on kidney function
Erythropoietin	Animal models	Beneficial effect on kidney function

Randomized controlled trials

Emerging agents

There are numerous randomized trials ( Table 4 ) going on of different drugs such as calcium channel blockers, adenosine antagonist, multipotent stem cells and erythropoietin to check out their efficiency in the treatment of acute renal failure. Calcium channel blockers have shown some effects to alter the afferent arteriolar vasoconstriction induced by a variety of stimuli and also natriuretic result ( 9 ). In large multi-central randomized control trial to investigate the effectiveness of isradipine on renal function, incidence and severity of delayed graft rejection was done. It did not work and found no benefits ( 3 ). Similarly, small clinical studies assessing the role of the theophylline, an adenosine antagonist, in the prevention of the contrast nephropathy have shown some different effect ( 12 ). There is on going research project looking at the effects of erythropoietin (EPO) or placebo on the prevention of AKI in patients under going heart surgery or kidney transplantation. In the intensive care setting the study failed to show therapeutic renoprotective benefits of EPO however there were obvious flaws in the study the patients do not receive the medication on time and secondly extreme of EPO was used against the AKI patients but it did not alter the outcome ( 13 ).


Dopamine	RCT s	No effect on kidney function
Fenoldopamine	1.Small RCT 2.One meta analysis	1. No effect on kidney function 2. Beneficial effects on kidney
Loop of diuretics	RCTs and meta analysis	No effect on kidneys function
N-Acetlycestine	RCTs and meta analysis	Variable beneficial effects on kidney function
Statins	Animal mode	Beneficial effect on kidney
Calcium channel blocker	RCT in peri-transplant period	No effect on kidney function
Adenosine antagonist	RCTs	Controversial effect on kidney function
Multipotent stem cells	Animal models	Beneficial effects on kidney function
Erythropoietin	Animal models	Beneficial effects on Kidney
Small interfering RNA targeting p53	Animal models	Beneficial effects on kidney function

Prognosis and outcome of dialysis in ARF

The overall survival for patients with ARF remains relatively limited, 55-60% of the patients require dialysis treatment survive, but the numbers partly reflects the very poor outcome of the patients with who have ATN as a component of multiple organ failure (MOF) who are managed on the ICU. The registry data specified the lower risk of peritoneal dialysis as compared to hemodialysis during the first year of treatment ( 14 ). For example, only 10-20% for those with three or four organs failure will survive, yet 90 patients who have ARF in isolation survive. The survival speed fluctuates depending upon essential cause of end stage renal disease, age, and associated comorbidities e.g. cardiovascular diseases, diabetes and hypertension. One study performed by the Medicare in US shown HD is associated with increase chances of death among diabetic patients as compared with those patients without any co-morbidities ( 15 ). Indications for urgent dialysis in ARF was summarized in Table 5 .

Severe uremia	Uremic encephalopathy
Hyperkalemia	Potassium >6.5 mEq/l or lies, if ECG changes apparent
Severe acidosis
Uremic pericarditis
Pulmonary edema

The prognosis for the recovery of renal function varies according to the causative condition; renal recovery occurs <50% of cases with autoimmune vacuities. In survivor for ATN, renal function will return to the normal range in 60%, whereas 30% will be left with CKD and 10% will be dialysis–dependent.

ARF is quite common, occurring in 80 million populations. Urinary obstruction should be excluded (a cause in around 5-10 of cases) because this is readily reversible if it is diagnosed early. A renal US will be sufficient to identify obstruction in 95 of cases. Most cases of ARF are expected to pre-renal failure/ATN 70-80%. Risk factor for development for at ATN are old age, drugs (NSAIDs, ACEIs and gentamicin), sepsis, CKD. If obstruction has been excluded and there is nothing suggests a more unusual, renal cause of ARF, then ATN is the most likely diagnosis and patient should be treated with intravenous fluids to restore intravascular volume. The underlying cause of hypotension should be treated and any nephrotoxins must be removed. If blood pressure remains low following an adequate filling then the patients may require inotropic support, which will require an ITU bed. If intravenous rehydration restore intravascular volume and blood pressure but there is no improvement in oliguria, this is likely to be established acute tubular necrosis and the patient may require a period of renal support (hemodialysis or filtration) whilst tubular cells regenerate. This usually takes days to weeks but can take months. ARF in the elderly has a significant mortality, particularly if the patients require renal replacement therapy.

Authors’ contributions

CMJN and FB completed the article. SA and JA done critical appraisal.

Ethical considerations

Ethical issues (including plagiarism, misconduct, data fabrication, falsification, double publication or submission, redundancy) have been completely observed by the authors.

Conflicts of interests

There were no points of conflicts.

Funding/Support

Please cite this paper as: Nazar CMJ, Bashir F, Izhar S, Anderson J. Overview of management of acute renal failure and its evaluation; a case analysis. J Nephropharmacol 2015; 4(1): 17-22.

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