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Chronic kidney disease (CKD) confers a high burden of uremic symptoms that may be underrecognized, underdiagnosed, and undertreated. Unpleasant symptoms, such as CKD-associated pruritus and emotional/psychological distress, often occur within symptom clusters, and treating 1 symptom may potentially alleviate other symptoms in that cluster. The Living Well with Kidney Disease and Effective Symptom Management Consensus Conference convened health experts and leaders of kidney advocacy groups and kidney networks worldwide to discuss the effects of unpleasant symptoms related to CKD on the health and well-being of those affected, and to consider strategies for optimal symptom management. Optimizing symptom management is a cornerstone of conservative and preservative management which aim to prevent or delay dialysis initiation. In persons with kidney dysfunction requiring dialysis (KDRD), incremental transition to dialysis and home dialysis modalities offer personalized approaches. KDRD is proposed as the preferred term given the negative connotations of “failure” as a kidney descriptor, and the success stories in CKD journeys. Engaging persons with CKD to identify and prioritize their personal values and individual needs must be central to ensure their active participation in CKD management, including KDRD. Person-centered communication and care are required to ensure diversity, equity, and inclusion; education/awareness that considers the health literacy of persons with CKD; and shared decision-making among the person with CKD, care partners, and providers. By putting the needs of people with CKD, including effective symptom management, at the center of their treatment, CKD can be optimally treated in a way that aligns with their goals.

This comprehensive book examines the complex interplay between endocrine and kidney disorders, and how this inter-relationship impacts patients with chronic kidney disease. Authored by experts in areas of endocrinology and nephrology, chapters cover a variety of topics, including diabetes, metabolic syndrome, thyroid dysfunction, gonadal disorders, dyslipidemia, mineral bone disorders, obesity, and pituitary disorders. These comorbidities are thoroughly examined and provide the clinician, researcher, and trainee with a greater understanding of the impact of endocrine disorders on kidney disease patients, the ability to identify persistent gaps in knowledge for future investigation, and move closer towards the goal of improving the health and survival of the chronic kidney disease population.

This comprehensive book examines the complex interplay between endocrine and kidney disorders, and how this inter-relationship impacts patients with chronic kidney disease. Authored by experts in areas of endocrinology and nephrology, chapters cover a variety of topics, including diabetes, metabolic syndrome, thyroid dysfunction, gonadal disorders, dyslipidemia, mineral bone disorders, obesity, and pituitary disorders. These comorbidities are thoroughly examined and provide the clinician, researcher, and trainee with a greater understanding of the impact of endocrine disorders on kidney disease patients, the ability to identify persistent gaps in knowledge for future investigation, and move closer towards the goal of improving the health and survival of the chronic kidney disease population.

More than 720,000 patients with end-stage renal disease in the United States require life-sustaining dialysis treatment. In this population of typically older patients with a high morbidity burden, hospitalization is frequent at a rate of about twice per patient-year. Aside from frequent hospitalizations, which is a major source of death risk, overall mortality in dialysis patients is higher than other comparable populations, including Medicare patients with cancer. Thus, understanding patient- and facility-level risk factors that jointly contribute to longitudinal hospitalizations and mortality is of interest. Towards this objective, we propose a novel methodology to jointly model hospitalization, a binary longitudinal outcome, and survival, based on multilevel data from the United States Renal Data System (USRDS), with repeated observations over time nested in patients and patients nested in dialysis facilities. In our approach, the outcomes are modeled through a common set of multilevel random effects. In order to accommodate the USRDS data structure, we depart from the literature on joint modeling of longitudinal and survival data by including multilevel random effects and multilevel covariates, at both the patient and facility levels. An approximate Expectation-Maximization algorithm is developed for estimation and inference where fully exponential Laplace approximations are utilized to address computational challenges.

More than 720,000 patients with end-stage renal disease in the United States require life-sustaining dialysis treatment. In this population of typically older patients with a high morbidity burden, hospitalization is frequent at a rate of about twice per patient-year. Aside from frequent hospitalizations, which is a major source of death risk, overall mortality in dialysis patients is higher than other comparable populations, including Medicare patients with cancer. Thus, understanding patient- and facility-level risk factors that jointly contribute to longitudinal hospitalizations and mortality is of interest. Towards this objective, we propose a novel methodology to jointly model hospitalization, a binary longitudinal outcome, and survival, based on multilevel data from the United States Renal Data System (USRDS), with repeated observations over time nested in patients and patients nested in dialysis facilities. In our approach, the outcomes are modeled through a common set of multilevel random effects. In order to accommodate the USRDS data structure, we depart from the literature on joint modeling of longitudinal and survival data by including multilevel random effects and multilevel covariates, at both the patient and facility levels. An approximate Expectation-Maximization algorithm is developed for estimation and inference where fully exponential Laplace approximations are utilized to address computational challenges.

Chronic hyponatremia may contribute to decreased bone density. We studied 341,003 men and women who underwent DXA testing and observed that individuals with chronic hyponatremia (sodium < 135 mEq/L) had an 11% greater likelihood of having osteoporosis. There was a dose-dependent effect with lower sodium and stronger association with osteoporosis.IntroductionChronic hyponatremia has been associated with both neurologic deficits and increased risk of gait abnormalities leading to falls and resultant bone fractures. Whether chronic hyponatremia contributes to decreased bone density is uncertain. We evaluated whether chronic, mild hyponatremia based on serial sodium measurements was associated with increased risk of osteoporosis within a large, ethnically diverse population.MethodsThis is a retrospective cohort study between January 1, 1998 and December 31, 2014 within Kaiser Permanente Southern California, an integrated healthcare delivery system. Men and women were aged ≥ 55 years with ≥ 2 serum sodium measurements prior to dual-energy X-ray absorptiometry (DXA) testing. Time-weighted (TW) mean sodium values were calculated by using the proportion of time (weight) elapsed between sodium measurements and defined as < 135 mEq/L. Osteoporosis defined as any T-score value ≤ - 2.5 of lumbar spine, femoral neck, or hip.ResultsAmong 341,003 individuals with 3,330,903 sodium measurements, 11,539 (3.4%) had chronic hyponatremia and 151,505 (44.4%) had osteoporosis. Chronic hyponatremic individuals had an osteoporosis RR (95% CI) of 1.11 (1.09, 1.13) compared to those with normonatremia. A TW mean sodium increase of 3 mEq/L was associated with a lower risk of osteoporosis [adjusted RR (95% CI) 0.95 (0.93, 0.96)]. A similar association was observed when the arithmetic mean sodium value was used for comparison.ConclusionsWe observed a modest increase in risk for osteoporosis in people with chronic hyponatremia. There was also a graded association between

Chronic hyponatremia may contribute to decreased bone density. We studied 341,003 men and women who underwent DXA testing and observed that individuals with chronic hyponatremia (sodium < 135 mEq/L) had an 11% greater likelihood of having osteoporosis. There was a dose-dependent effect with lower sodium and stronger association with osteoporosis.IntroductionChronic hyponatremia has been associated with both neurologic deficits and increased risk of gait abnormalities leading to falls and resultant bone fractures. Whether chronic hyponatremia contributes to decreased bone density is uncertain. We evaluated whether chronic, mild hyponatremia based on serial sodium measurements was associated with increased risk of osteoporosis within a large, ethnically diverse population.MethodsThis is a retrospective cohort study between January 1, 1998 and December 31, 2014 within Kaiser Permanente Southern California, an integrated healthcare delivery system. Men and women were aged ≥ 55 years with ≥ 2 serum sodium measurements prior to dual-energy X-ray absorptiometry (DXA) testing. Time-weighted (TW) mean sodium values were calculated by using the proportion of time (weight) elapsed between sodium measurements and defined as < 135 mEq/L. Osteoporosis defined as any T-score value ≤ - 2.5 of lumbar spine, femoral neck, or hip.ResultsAmong 341,003 individuals with 3,330,903 sodium measurements, 11,539 (3.4%) had chronic hyponatremia and 151,505 (44.4%) had osteoporosis. Chronic hyponatremic individuals had an osteoporosis RR (95% CI) of 1.11 (1.09, 1.13) compared to those with normonatremia. A TW mean sodium increase of 3 mEq/L was associated with a lower risk of osteoporosis [adjusted RR (95% CI) 0.95 (0.93, 0.96)]. A similar association was observed when the arithmetic mean sodium value was used for comparison.ConclusionsWe observed a modest increase in risk for osteoporosis in people with chronic hyponatremia. There was also a graded association between

© Springer-Verlag Berlin Heidelberg 2014. Muscle wasting is a common complication afflicting maintenance hemodialysis (HD) patients, and it is associated with decreased muscle function, exercise performance, physical function, and quality of life. Meanwhile, numerous epidemiologic studies have consistently shown that greater muscle mass (ascertained by body anthropometry surrogates, body composition tests such as dual x-ray absorptiometry, and/or serum creatinine in patients with little to no residual kidney function) is associated with increased survival in this population. The pathophysiology of muscle wasting in HD patients is complex and may be caused by poor dietary intake, catabolic effects of dialysis therapy, hormonal alterations (e.g., decreased levels or resistance to anabolic hormones, increased levels of catabolic hormones), inflammation, metabolic acidosis, and concurrent comorbidities. Muscle disuse resulting from low physical activity is an important yet under-appreciated risk factor for muscle wasting. Intra-dialytic resistance exercise training has been suggested as a potential strategy to correct and/or prevent this complication in HD patients, but prior studies examining this exercise modality as an anabolic intervention have shown mixed results. In a recently published 12-week randomized controlled trial of a novel intra-dialytic progressive resistance exercise training (PRET) program vs. control therapy conducted in HD and non-HD patients, PRET resulted in increased muscle volume and strength in both groups. At this time, further study is needed to determine if anabolic improvements imparted by resistance exercise translates into improved physical function and quality of life, decreased hospitalization and mortality risk, and greater cost-effectiveness in HD patients.

© Springer-Verlag Berlin Heidelberg 2014. Muscle wasting is a common complication afflicting maintenance hemodialysis (HD) patients, and it is associated with decreased muscle function, exercise performance, physical function, and quality of life. Meanwhile, numerous epidemiologic studies have consistently shown that greater muscle mass (ascertained by body anthropometry surrogates, body composition tests such as dual x-ray absorptiometry, and/or serum creatinine in patients with little to no residual kidney function) is associated with increased survival in this population. The pathophysiology of muscle wasting in HD patients is complex and may be caused by poor dietary intake, catabolic effects of dialysis therapy, hormonal alterations (e.g., decreased levels or resistance to anabolic hormones, increased levels of catabolic hormones), inflammation, metabolic acidosis, and concurrent comorbidities. Muscle disuse resulting from low physical activity is an important yet under-appreciated risk factor for muscle wasting. Intra-dialytic resistance exercise training has been suggested as a potential strategy to correct and/or prevent this complication in HD patients, but prior studies examining this exercise modality as an anabolic intervention have shown mixed results. In a recently published 12-week randomized controlled trial of a novel intra-dialytic progressive resistance exercise training (PRET) program vs. control therapy conducted in HD and non-HD patients, PRET resulted in increased muscle volume and strength in both groups. At this time, further study is needed to determine if anabolic improvements imparted by resistance exercise translates into improved physical function and quality of life, decreased hospitalization and mortality risk, and greater cost-effectiveness in HD patients.

© Springer-Verlag Berlin Heidelberg 2014. Muscle wasting is a common complication afflicting maintenance hemodialysis (HD) patients, and it is associated with decreased muscle function, exercise performance, physical function, and quality of life. Meanwhile, numerous epidemiologic studies have consistently shown that greater muscle mass (ascertained by body anthropometry surrogates, body composition tests such as dual x-ray absorptiometry, and/or serum creatinine in patients with little to no residual kidney function) is associated with increased survival in this population. The pathophysiology of muscle wasting in HD patients is complex and may be caused by poor dietary intake, catabolic effects of dialysis therapy, hormonal alterations (e.g., decreased levels or resistance to anabolic hormones, increased levels of catabolic hormones), inflammation, metabolic acidosis, and concurrent comorbidities. Muscle disuse resulting from low physical activity is an important yet under-appreciated risk factor for muscle wasting. Intra-dialytic resistance exercise training has been suggested as a potential strategy to correct and/or prevent this complication in HD patients, but prior studies examining this exercise modality as an anabolic intervention have shown mixed results. In a recently published 12-week randomized controlled trial of a novel intra-dialytic progressive resistance exercise training (PRET) program vs. control therapy conducted in HD and non-HD patients, PRET resulted in increased muscle volume and strength in both groups. At this time, further study is needed to determine if anabolic improvements imparted by resistance exercise translates into improved physical function and quality of life, decreased hospitalization and mortality risk, and greater cost-effectiveness in HD patients.

© Springer-Verlag Berlin Heidelberg 2014. Muscle wasting is a common complication afflicting maintenance hemodialysis (HD) patients, and it is associated with decreased muscle function, exercise performance, physical function, and quality of life. Meanwhile, numerous epidemiologic studies have consistently shown that greater muscle mass (ascertained by body anthropometry surrogates, body composition tests such as dual x-ray absorptiometry, and/or serum creatinine in patients with little to no residual kidney function) is associated with increased survival in this population. The pathophysiology of muscle wasting in HD patients is complex and may be caused by poor dietary intake, catabolic effects of dialysis therapy, hormonal alterations (e.g., decreased levels or resistance to anabolic hormones, increased levels of catabolic hormones), inflammation, metabolic acidosis, and concurrent comorbidities. Muscle disuse resulting from low physical activity is an important yet under-appreciated risk factor for muscle wasting. Intra-dialytic resistance exercise training has been suggested as a potential strategy to correct and/or prevent this complication in HD patients, but prior studies examining this exercise modality as an anabolic intervention have shown mixed results. In a recently published 12-week randomized controlled trial of a novel intra-dialytic progressive resistance exercise training (PRET) program vs. control therapy conducted in HD and non-HD patients, PRET resulted in increased muscle volume and strength in both groups. At this time, further study is needed to determine if anabolic improvements imparted by resistance exercise translates into improved physical function and quality of life, decreased hospitalization and mortality risk, and greater cost-effectiveness in HD patients.

Background In the general population, low serum magnesium levels are associated with poor outcomes and death. While limited data suggest that low baseline magnesium levels may be associated with higher mortality in hemodialysis (HD) patients, the impact of changes in magnesium levels over time is unknown. Study Design We examined the association of time-varying serum magnesium levels with all-cause mortality using multivariable time-varying survival models adjusted for clinical characteristics and other time-varying laboratory measures. Setting & Participants 9,359 maintenance HD patients treated in a large dialysis organization between 2007 and 2011. Predictor Time-varying serum magnesium levels across 5 magnesium increments (<1.8, 1.8-<2.0, 2.0-<2.2, 2.2-<2.4, and ≥2.4 mg/dL). Outcome All-cause mortality. Results 2,636 individuals died over 5 years. Time-varying serum magnesium levels < 2.0 mg/dL were associated with higher mortality after adjustment for demographics and comorbid conditions, including hypertension, diabetes, and malignancies (reference: magnesium, 2.2-<2.4 mg/dL): adjusted HRs for serum magnesium level < 1.8 and 1.8 to <2.0 mg/dL were 1.39 (95% CI, 1.23-1.58; P < 0.001) and 1.20 (95% CI, 1.06-1.36; P = 0.004), respectively. Some associations were attenuated to the null after incremental adjustment for laboratory test results, particularly serum albumin. However, among patients with serum albumin measurements, low albumin level (<3.5 g/dL) and magnesium level < 2.0 mg/dL were associated with an additional death risk (adjusted HR, 1.17; 95% CI, 1.05-1.31; P = 0.004), whereas patients with high serum albumin levels (≥3.5 g/dL) exhibited low death risk (adjusted HRs of 0.53 and 0.53 [P ≤ 0.001] for magnesium < 2.0 and ≥2.0 mg/dL, respectively; reference: albumin < 3.5 g/dL and magnesium ≥ 2.0 mg/dL). Limitations Causality cannot be determined, and residual confounding cannot be excluded given the observationa

A significant number of dietary restrictions are imposed traditionally and uniformly on maintenance dialysis patients, whereas there is very little data to support their benefits. Recent studies indicate that dietary restrictions of phosphorus may lead to worse survival and poorer nutritional status. Restricting dietary potassium may deprive dialysis patients of heart-healthy diets and lead to intake of more atherogenic diets. There is little data about the survival benefits of dietary sodium restriction, and limiting fluid intake may inherently lead to lower protein and calorie consumption, when in fact dialysis patients often need higher protein intake to prevent and correct protein-energy wasting. Restricting dietary carbohydrates in diabetic dialysis patients may not be beneficial in those with burnt-out diabetes. Dietary fat including omega-3 fatty acids may be important caloric sources and should not be restricted. Data to justify other dietary restrictions related to calcium, vitamins, and trace elements are scarce and often contradictory. The restriction of eating during hemodialysis treatment is likely another incorrect practice that may worsen hemodialysis induced hypoglycemia and nutritional derangements. We suggest careful relaxation of most dietary restrictions and adoption of a more balanced and individualized approach, thereby easing some of these overzealous restrictions that have not been proven to offer major advantages to patients and their outcomes and which may in fact worsen patients' quality of life and satisfaction. This manuscript critically reviews the current paradigms and practices of recommended dietary regimens in dialysis patients including those related to dietary protein, carbohydrate, fat, phosphorus, potassium, sodium, and calcium, and discusses the feasibility and implications of adherence to ardent dietary restrictions and future research.

© 2015 National Kidney Foundation, Inc. Background: In the general population, low serum magnesium levels are associated with poor outcomes and death. While limited data suggest that low baseline magnesium levels may be associated with higher mortality in hemodialysis (HD) patients, the impact of changes in magnesium levels over time is unknown. Study Design: We examined the association of time-varying serum magnesium levels with all-cause mortality using multivariable time-varying survival models adjusted for clinical characteristics and other time-varying laboratory measures. Setting & Participants: 9,359 maintenance HD patients treated in a large dialysis organization between 2007 and 2011. Predictor: Time-varying serum magnesium levels across 5 magnesium increments (<1.8, 1.8-<2.0, 2.0-<2.2, 2.2-<2.4, and ≥2.4. mg/dL). Outcome: All-cause mortality. Results: 2,636 individuals died over 5 years. Time-varying serum magnesium levels < 2.0. mg/dL were associated with higher mortality after adjustment for demographics and comorbid conditions, including hypertension, diabetes, and malignancies (reference: magnesium, 2.2-<2.4. mg/dL): adjusted HRs for serum magnesium level < 1.8 and 1.8 to <2.0. mg/dL were 1.39 (95% CI, 1.23-1.58; . P . <. 0.001) and 1.20 (95% CI, 1.06-1.36; . P =0.004), respectively. Some associations were attenuated to the null after incremental adjustment for laboratory test results, particularly serum albumin. However, among patients with serum albumin measurements, low albumin level (<3.5. g/dL) and magnesium level < 2.0. mg/dL were associated with an additional death risk (adjusted HR, 1.17; 95% CI, 1.05-1.31; . P =0.004), whereas patients with high serum albumin levels (≥3.5. g/dL) exhibited low death risk (adjusted HRs of 0.53 and 0.53 [. P . ≤. 0.001] for magnesium < 2.0 and ≥2.0. mg/dL, respectively; reference: albumin < 3.5. g/dL and magnesium ≥ 2.0. mg/dL). Limitations: Causality cannot be determine

© 2015 Springer Science+Business Media Dordrecht Background: Protein–energy wasting (PEW) is a common condition in patients with chronic kidney disease (CKD) including dialysis and kidney transplant recipients (TX) and frequently assessed with malnutrition–inflammation score (MIS). We hypothesized that (1) the MIS and PEW parameters are correlated with kidney function and (2) the MIS and PEW parameters are more severe in TX than in non-dialysis (ND) CKD patients with similar eGFR. Methods: In this study, we matched 203 ND-CKD and 203 TX patients from two independently assembled cohorts of patients based on estimated glomerular filtration rate (eGFR) and compared various PEW parameters between the two groups using unadjusted and case-mix adjusted linear regression and conditional logistic regression analysis models. Results: In the combined cohort (n = 406) of patients, the mean ± SD age was 57 ± 12 years; included 55 % men and 35 % diabetics; and demonstrated a mean ± SD baseline eGFR of 29 ± 11 ml/min/1.73 m2. The eGFR correlated positively with serum albumin (ρ = 0.26, p < 0.001) and negatively (ρ = −0.33, p < 0.001) with MIS. ND-CKD and TX patients had similar MIS, PEW parameters such as waist circumference, serum CRP, albumin, and leptin levels. After case-mix adjustment, TX status was associated with higher waist circumference (standardized coefficient: 0.187, p < 0.001), lower BMI (standardized coefficient: −0.204, p < 0.001), and lower SGA score (standardized coefficient: 0.156, p = 0.006). Conclusions: We found associations between lower eGFR and various PEW measures in both the ND-CKD and TX populations. Additionally, we did not observe significant differences in the burden of PEW parameters between the CKD and TX populations.

Background In the general population, low serum magnesium levels are associated with poor outcomes and death. While limited data suggest that low baseline magnesium levels may be associated with higher mortality in hemodialysis (HD) patients, the impact of changes in magnesium levels over time is unknown. Study Design We examined the association of time-varying serum magnesium levels with all-cause mortality using multivariable time-varying survival models adjusted for clinical characteristics and other time-varying laboratory measures. Setting & Participants 9,359 maintenance HD patients treated in a large dialysis organization between 2007 and 2011. Predictor Time-varying serum magnesium levels across 5 magnesium increments (<1.8, 1.8-<2.0, 2.0-<2.2, 2.2-<2.4, and ≥2.4 mg/dL). Outcome All-cause mortality. Results 2,636 individuals died over 5 years. Time-varying serum magnesium levels < 2.0 mg/dL were associated with higher mortality after adjustment for demographics and comorbid conditions, including hypertension, diabetes, and malignancies (reference: magnesium, 2.2-<2.4 mg/dL): adjusted HRs for serum magnesium level < 1.8 and 1.8 to <2.0 mg/dL were 1.39 (95% CI, 1.23-1.58; P < 0.001) and 1.20 (95% CI, 1.06-1.36; P = 0.004), respectively. Some associations were attenuated to the null after incremental adjustment for laboratory test results, particularly serum albumin. However, among patients with serum albumin measurements, low albumin level (<3.5 g/dL) and magnesium level < 2.0 mg/dL were associated with an additional death risk (adjusted HR, 1.17; 95% CI, 1.05-1.31; P = 0.004), whereas patients with high serum albumin levels (≥3.5 g/dL) exhibited low death risk (adjusted HRs of 0.53 and 0.53 [P ≤ 0.001] for magnesium < 2.0 and ≥2.0 mg/dL, respectively; reference: albumin < 3.5 g/dL and magnesium ≥ 2.0 mg/dL). Limitations Causality cannot be determined, and residual confounding cannot be excluded given the observationa

© 2015 National Kidney Foundation, Inc. Background: In the general population, low serum magnesium levels are associated with poor outcomes and death. While limited data suggest that low baseline magnesium levels may be associated with higher mortality in hemodialysis (HD) patients, the impact of changes in magnesium levels over time is unknown. Study Design: We examined the association of time-varying serum magnesium levels with all-cause mortality using multivariable time-varying survival models adjusted for clinical characteristics and other time-varying laboratory measures. Setting & Participants: 9,359 maintenance HD patients treated in a large dialysis organization between 2007 and 2011. Predictor: Time-varying serum magnesium levels across 5 magnesium increments (<1.8, 1.8-<2.0, 2.0-<2.2, 2.2-<2.4, and ≥2.4. mg/dL). Outcome: All-cause mortality. Results: 2,636 individuals died over 5 years. Time-varying serum magnesium levels < 2.0. mg/dL were associated with higher mortality after adjustment for demographics and comorbid conditions, including hypertension, diabetes, and malignancies (reference: magnesium, 2.2-<2.4. mg/dL): adjusted HRs for serum magnesium level < 1.8 and 1.8 to <2.0. mg/dL were 1.39 (95% CI, 1.23-1.58; . P . <. 0.001) and 1.20 (95% CI, 1.06-1.36; . P =0.004), respectively. Some associations were attenuated to the null after incremental adjustment for laboratory test results, particularly serum albumin. However, among patients with serum albumin measurements, low albumin level (<3.5. g/dL) and magnesium level < 2.0. mg/dL were associated with an additional death risk (adjusted HR, 1.17; 95% CI, 1.05-1.31; . P =0.004), whereas patients with high serum albumin levels (≥3.5. g/dL) exhibited low death risk (adjusted HRs of 0.53 and 0.53 [. P . ≤. 0.001] for magnesium < 2.0 and ≥2.0. mg/dL, respectively; reference: albumin < 3.5. g/dL and magnesium ≥ 2.0. mg/dL). Limitations: Causality cannot be determine

A significant number of dietary restrictions are imposed traditionally and uniformly on maintenance dialysis patients, whereas there is very little data to support their benefits. Recent studies indicate that dietary restrictions of phosphorus may lead to worse survival and poorer nutritional status. Restricting dietary potassium may deprive dialysis patients of heart-healthy diets and lead to intake of more atherogenic diets. There is little data about the survival benefits of dietary sodium restriction, and limiting fluid intake may inherently lead to lower protein and calorie consumption, when in fact dialysis patients often need higher protein intake to prevent and correct protein-energy wasting. Restricting dietary carbohydrates in diabetic dialysis patients may not be beneficial in those with burnt-out diabetes. Dietary fat including omega-3 fatty acids may be important caloric sources and should not be restricted. Data to justify other dietary restrictions related to calcium, vitamins, and trace elements are scarce and often contradictory. The restriction of eating during hemodialysis treatment is likely another incorrect practice that may worsen hemodialysis induced hypoglycemia and nutritional derangements. We suggest careful relaxation of most dietary restrictions and adoption of a more balanced and individualized approach, thereby easing some of these overzealous restrictions that have not been proven to offer major advantages to patients and their outcomes and which may in fact worsen patients' quality of life and satisfaction. This manuscript critically reviews the current paradigms and practices of recommended dietary regimens in dialysis patients including those related to dietary protein, carbohydrate, fat, phosphorus, potassium, sodium, and calcium, and discusses the feasibility and implications of adherence to ardent dietary restrictions and future research.

Protein-energy wasting (PEW), a condition of decreased body protein and fat mass, is highly prevalent in patients with chronic kidney disease (CKD) and a potent predictor of mortality in this population. In adults with CKD, PEW has typically been defined on the basis of (1) deranged biochemical parameters, (2) reduced body mass, (3) reduced muscle mass, and (4) decreased dietary protein intake. Emerging data suggest that PEW may also commonly afflict children with CKD and have a negative impact on growth and development (“uremic failure to thrive”), yet it remains comparatively understudied and less well characterized in these patients. Given the challenges of applying adult-defined PEW criteria to the pediatric population, the authors of a recent study entitled “Protein energy wasting in children with chronic kidney disease” [Abraham et al. (2014) Pediatr Nephrol 29:1231–1238] have sought to develop a scoring system and three alterative definitions for this condition using a combination of biochemical markers, clinical measurements, and subjective reporting in children in the CKiD cohort: (1) minimal PEW definition (≥2 adult-defined PEW criteria); (2) standard PEW definition (≥3 adult-defined PEW criteria); (3) modified PEW definition (≥3 adult-defined PEW criteria, plus short stature or poor growth). These authors observed that meeting the modified PEW definition was associated with a significantly increased risk of hospitalization in unadjusted analyses, i.e., a 2.2-fold higher risk, and trended towards increased risk in multivariable adjusted analyses, i.e., 2.0-fold higher risk. At the present time, future studies validating these findings and developing further refined definitions and/or scoring systems for the detection and management of PEW in children and uremic failure to thrive are urgently needed.

The incidence of early stage renal cell carcinoma (RCC) is increasing and observational studies have shown equivalent oncological outcomes of partial versus radical nephrectomy for stage I tumours. Population studies suggest that compared with radical nephrectomy, partial nephrectomy is associated with decreased mortality and a lower rate of postoperative decline in kidney function. However, rates of chronic kidney disease (CKD) in patients who have undergone nephrectomy might be higher than in the general population. The risks of new-onset or accelerated CKD and worsened survival after nephrectomy might be linked, as kidney insufficiency is a risk factor for cardiovascular disease and mortality. Nephron-sparing approaches have, therefore, been proposed as the standard of care for patients with type 1a tumours and as a viable option for those with type 1b tumours. However, prospective data on the incidence of de novo and accelerated CKD after cancer nephrectomy is lacking, and the only randomized trial to date was closed prematurely. Intrinsic abnormalities in non-neoplastic kidney parenchyma and comorbid conditions (including diabetes mellitus and hypertension) might increase the risks of CKD and RCC. More research is needed to better understand the risk of CKD post-nephrectomy, to develop and validate predictive scores for risk-stratification, and to optimize patient management.

Protein-energy wasting (PEW), a condition of decreased body protein and fat mass, is highly prevalent in patients with chronic kidney disease (CKD) and a potent predictor of mortality in this population. In adults with CKD, PEW has typically been defined on the basis of (1) deranged biochemical parameters, (2) reduced body mass, (3) reduced muscle mass, and (4) decreased dietary protein intake. Emerging data suggest that PEW may also commonly afflict children with CKD and have a negative impact on growth and development (“uremic failure to thrive”), yet it remains comparatively understudied and less well characterized in these patients. Given the challenges of applying adult-defined PEW criteria to the pediatric population, the authors of a recent study entitled “Protein energy wasting in children with chronic kidney disease” [Abraham et al. (2014) Pediatr Nephrol 29:1231–1238] have sought to develop a scoring system and three alterative definitions for this condition using a combination of biochemical markers, clinical measurements, and subjective reporting in children in the CKiD cohort: (1) minimal PEW definition (≥2 adult-defined PEW criteria); (2) standard PEW definition (≥3 adult-defined PEW criteria); (3) modified PEW definition (≥3 adult-defined PEW criteria, plus short stature or poor growth). These authors observed that meeting the modified PEW definition was associated with a significantly increased risk of hospitalization in unadjusted analyses, i.e., a 2.2-fold higher risk, and trended towards increased risk in multivariable adjusted analyses, i.e., 2.0-fold higher risk. At the present time, future studies validating these findings and developing further refined definitions and/or scoring systems for the detection and management of PEW in children and uremic failure to thrive are urgently needed.

The incidence of early stage renal cell carcinoma (RCC) is increasing and observational studies have shown equivalent oncological outcomes of partial versus radical nephrectomy for stage I tumours. Population studies suggest that compared with radical nephrectomy, partial nephrectomy is associated with decreased mortality and a lower rate of postoperative decline in kidney function. However, rates of chronic kidney disease (CKD) in patients who have undergone nephrectomy might be higher than in the general population. The risks of new-onset or accelerated CKD and worsened survival after nephrectomy might be linked, as kidney insufficiency is a risk factor for cardiovascular disease and mortality. Nephron-sparing approaches have, therefore, been proposed as the standard of care for patients with type 1a tumours and as a viable option for those with type 1b tumours. However, prospective data on the incidence of de novo and accelerated CKD after cancer nephrectomy is lacking, and the only randomized trial to date was closed prematurely. Intrinsic abnormalities in non-neoplastic kidney parenchyma and comorbid conditions (including diabetes mellitus and hypertension) might increase the risks of CKD and RCC. More research is needed to better understand the risk of CKD post-nephrectomy, to develop and validate predictive scores for risk-stratification, and to optimize patient management.