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Diets high in plant-based foods are commonly recommended for people with CKD. One putative advantage of these diets is reduced intestinal phosphate absorption. This effect has been ascribed to phytic acid (myoinositol hexaphosphoric acid) and its anion, phytate, that are present in many plant foods, particularly in the seeds, nuts, grains, and fruits of plants. This article reviews the structure and many actions of phytate with particular reference to its potential effects on people with CKD. Phytate binds avidly to and can reduce gastrointestinal absorption of the phosphate anion and many macrominerals and trace elements including iron, zinc, calcium, and magnesium. This has led some opinion leaders to label phytate as an anti-nutrient. The human intestine lacks phytase; hence, phytate is essentially not degraded in the small intestine. A small amount of phytate is absorbed from the small intestine, although phytate bound to phosphate is poorly absorbed. Clinical trials in maintenance hemodialysis patients indicate that intravenously administered phytate may decrease hydroxyapatite formation, vascular calcification, and calciphylaxis. Orally administered phytate or in vitrostudies indicate that phytate may also reduce osteoporosis, urinary calcium calculi formation, and dental plaque formation. Phytate seems to have anti-inflammatory and antioxidant effects, at least partly because of its ability to chelate iron. Other potential therapeutic roles for phytate, not definitively established, include suppression of cancer formation, reduction in cognitive decline that occurs with aging, and amelioration of certain neurodegenerative diseases and several gastrointestinal and metabolic disorders. These latter potential benefits of phytate are supported by cell or animal research or observational studies in humans. Many of the above disorders are particularly common in patients with CKD. Definitive clinical trials to identify potential therapeutic benefits of phytate in patients with CKD are clearly warranted.

This paper summarizes the biochemistry, metabolism, and dietary needs of vitamins in patients with chronic kidney disease (CKD) and kidney transplant recipients. Evidence indicates that the dietary intake, in vivo synthesis, urinary excretion or metabolism of different vitamins may be substantially altered in kidney failure. There are discrepancies in vitamin status assessment depending on whether the assay is functional or measuring the blood vitamin level. Whether vitamin supplements should be routinely prescribed for patients with CKD is controversial. Because low dietary intake and compounds that interfere with vitamin activity are not uncommon in patients with CKD, and water-soluble vitamin supplements appear safe and not costly, the authors recommend that supplements of the water-soluble vitamins should be routinely offered to these individuals. More research is needed to assess vitamin nutrition and function and to determine the daily vitamin needs for all patients with CKD.

A recently published nomenclature by a “Kidney Disease Improving Global Outcomes” (KDIGO) Consensus Conference suggested that the word “kidney” should be used in medical writings instead of “renal” or “nephro” when referring to kidney disease and kidney health. Whereas the decade-old move to use “kidney” more frequently should be supported when communicating with the public-at-large, such as the World Kidney Day, or in English speaking countries in communications with patients, care-partners, and non-medical persons, our point of view is that “renal” or “nephro" should not be removed from scientific and technical writings. Instead, the terms can coexist and be used in their relevant contexts. Cardiologists use “heart” and “cardio” as appropriate such as “heart failure” and “cardiac care units” and have not replaced “cardiovascular” with “heartvessel”, for instance. Likewise, in nephrology, we consider that “chronic kidney disease” and “continuous renal replacement therapy” should coexist. We suggest that in scientific writings and technical communications, the words “renal” and “nephro" and their derivatives are more appropriate and should be freely used without any pressure by medical journals to compel patients, care-partners, healthcare providers, researchers and other stakeholders to change their selected words and terminologies. We call to embrace the terms “kidney”, “renal” and “nephro” as they are used in different contexts and ask that scientific and medical journals not impose terminology restrictions for kidney disease and kidney health. The choice should be at the discretion of the authors, in the different contexts including in scientific journals.

Serum albumin is a marker of malnutrition and inflammation and has been demonstrated as a strong predictor of mortality in chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients. Yet, whether serum albumin levels in late-stage CKD are associated with adverse outcomes after the transition to ESRD is unknown. We hypothesize that lower levels and a decline in serum albumin in late-stage CKD are associated with higher risk of mortality and hospitalization rates 1 year after transition to ESRD.

Protein-energy wasting (PEW), which essentially refers to decreased body protein mass and fuel (energy) reserves, is common in advanced chronic kidney disease (CKD) patients and end-stage kidney disease patients undergoing chronic dialysis. The term PEW is used rather than protein-energy malnutrition because many causes of PEW in CKD and end-stage kidney disease patients does not involve reduced nutrient intake (e.g., catabolic illness, oxidants, biologicals lost in urine and dialysate, acidemia). The prevalence of PEW in CKD increases as glomerular filtration rate declines and is highest in chronic dialysis patients. PEW in CKD is important because it is associated with substantially increased morbidity and mortality and reduced quality of life. Many signs of PEW can be improved with nutritional therapy. It is not known whether amelioration or eradication of PEW by treatment of underlying illnesses, nutritional therapy, and/or other measures will reduce morbidity and mortality or improve quality of life. Clinical trials are indicated to answer these questions.

Summary:Chronic kidney disease (CKD) is a global public health burden. Dialysis is not only costly but may not be readily available in developing countries. Even in highly developed nations, many patients may prefer to defer or avoid dialysis. Thus, alternative options to dialysis therapy or to complement dialysis are needed urgently and are important objectives in CKD management that could have huge clinical and economic implications globally. The role of nutritional therapy as a strategy to slow CKD progression and uremia was discussed as early as the late 19th and early 20th century, but was only seriously explored in the 1970s. There is a revival of interest recently owing to encouraging data as well as the increase of precision medicine with an emphasis on a personalized approach to CKD management. Although part of the explanation for the inconclusive data may relate to variations in study design and dietary prescription, diversity in genetic make-up, variations in the non-nutritional management of CKD, intra-individual variations in responses to dietary and nondietary treatment, psychosocial factors, and dietary compliance issues, these all may contribute to the heterogeneous data and responses. This brings in the evolving concept of precision medicine, in which disease management should be tailored and individualized according not only to clinical manifestations but also to the genetic make-up and biologic responses to therapy, which may vary depending on genetic composition. Precision nutrition management also should take into account patient demographics, social, psychological, education, and compliance factors, which all may influence the therapeutic needs and responses to the nutritional therapy prescribed. In this review, we provide a novel concept of precision medicine in nutritional management in end-stage kidney disease with a transition to dialysis and propose how this may be the way forward for nutritional therapy in the CKD population.

Few studies have investigated the changes in weight that may occur over time among adults with the progression of chronic kidney disease (CKD). Whether such weight changes are independently associated with death after the onset of end-stage renal disease has also not been rigorously examined.

Anorexia and malnutrition are associated with poor outcomes in children with chronic kidney disease (CKD).

Poor nutritional status and protein-energy wasting are common among maintenance dialysis patients and associated with unfavorable outcomes. Providing foods, meal trays, snack boxes, and/or oral nutritional supplements during hemodialysis can improve nutritional status and might also reduce inflammation, enhance health-related quality of life, boost patient satisfaction, and improve survival. Potential challenges include postprandial hypotension and other hemodynamic instabilities, aspiration risk, gastrointestinal symptoms, hygiene issues, staff burden, reduced solute removal, and increased costs. Differing in-center nutrition policies exist within organizations and countries around the world. Recent studies have demonstrated clinical benefits and highlight the need to work toward clear guidelines. Meals or supplements during hemodialysis may be an effective strategy to improve nutritional status with limited reports of complications in real-world scenarios. Whereas larger multicenter randomized trials are needed, meals and supplements during hemodialysis should be considered as a part of the standard-of-care practice for patients without contraindications.

Diaphoresis therapy to remove water and solutes for the treatment of advanced chronic kidney disease (CKD) and chronic dialysis patients is an inadequately characterized treatment that was first reported over 50 years ago. Intensive diaphoresis, induced by heat treatment with saunas (dry heat) or hot baths (wet heat), can substantially increase cutaneous losses of water, urea, sodium, potassium, chloride, lactate, and possibly other solutes. How effectively diaphoresis therapy might remove many uremic toxins is not known. Diaphoresis therapy is not sufficiently effective to replace dialysis treatments, but theoretically it might be used to delay the start of chronic dialysis, supplement infrequent dialysis therapy, or augment chronic dialysis treatment perhaps especially for dialysis patients with excessive salt and water intake. Diaphoresis might be helpful for managing edema resistant states. Because it is inexpensive, diaphoresis may be particularly valuable in lower income countries where some patients may need to pay for dialysis. Diaphoresis might enhance some aspects of dietary treatment. The short-term and long-term effectiveness, safety, and patient acceptance of diaphoretic therapy need to be more carefully investigated.

The nutritional adequacy of both animal-based and plant-based low protein diets (LPDs) and moderate protein diets that are recommended for patients with chronic kidney disease have not been well examined. We therefore analyzed the nutrient content of three representative LPDs and moderate protein diets (lacto-ovo vegetarian, omnivorous, and vegan) containing foods that are likely to be prescribed for nondialyzed chronic kidney disease or chronic dialysis patients in the United States to determine the nutritional adequacy at different levels of protein intake.

Studies suggest that maintenance hemodialysis (MHD) patients report dietary energy intakes (EIs) that are lower than what is actually ingested. Data supporting this conclusion have several important limitations. The present study introduces a novel approach of assessing underreporting of EI in MHD patients.

Maintenance hemodialysis (MHD) patients display reduced daily physical activity (DPA) and physical performance (PP). Previous studies did not differentiate the effects of kidney failure and MHD treatments from comorbidities as causes for reduced DPA and PP. In relatively healthy MHD patients and normal adults, we evaluated DPA and PP and examined relationships between DPA and PP and possible associations between anxiety or depression and DPA and PP. DPA, 6-minute walk distance (6-MWD), sit-to-stand (STS), and stair-climbing tests were measured in 72 MHD patients (40% diabetics) with limited comorbidities and 39 normal adults of similar age and gender mix. Anxiety and depression were measured by the Beck anxiety and depression inventories. DPA, time-averaged over 7 days, and all 3 PP tests were impaired in MHD patients, to about 60% to 70% of normal values (P < .0001 for each measurement). MHD patients spent more time sleeping or physically inactive (P < .0001) and less time in ≥moderate activity (P < .0001). Adjusted DPA correlated with 6-MWD but not STS or stair-climbing. Anxiety and depression were identified in 43% and 33% of MHD patients and 2.5% and 5.1% of normals (P < .0001 for each comparison). Most of the impairment in DPA and PP tests were also observed in MHD patients without anxiety or depression. However, MHD patients with both anxiety and depression generally had the most impaired DPA and PP. In MHD patients, higher adjusted anxiety scores were correlated with impaired 6-MWD and STS, whereas adjusted average DPA was negatively correlated with depression (r = −0.33, P = .006) but not anxiety. DPA on the hemodialysis day (P = .01), day after dialysis (P = .03), and day 2 after dialysis (P = .03) each correlated negatively with degree of depression but not with anxiety. MHD patients displayed negative-adjusted correlations between anxiety and 6-MWD (P = .03) and STS (P = .04). In relatively healthy MHD patients, DPA and PP are substantially impaired and correlated with each other, even in patients without evidence for anxiety or depression. Anxiety and depression are common in MHD patients and are associated with further impairment in DPA and PP.

Maintenance hemodialysis (MHD) patients have a high prevalence of anxiety and depression and decreased daily physical activity (DPA) and exercise capacity. Because affective disorders may affect DPA and physical performance, we investigated possible relationships between anxiety or depression and DPA and physical performance in relatively healthy MHD patients.

Recent studies show a survival advantage with kidney transplant in elderly patients compared with those on dialysis therapy.

Anxiety and depression affect the quality of life of maintenance dialysis (MD) patients. There is little information concerning the extent to which the experience of individual hemodialysis treatments engenders anxiety in this patient population. This preliminary study examined the prevalence and severity of anxiety and depression in MD patients and the incidence of anxiety related to dialysis treatment.

In maintenance hemodialysis (HD) patients, overweight and obesity are associated with survival advantages. Given the greater survival of maintenance HD patients who are minorities, we hypothesized that increased body mass index (BMI) is associated more strongly with lower mortality in blacks and Hispanics relative to non-Hispanic whites.

Serum albumin level predicts mortality in dialysis patients and is used to assess their health status and the quality of delivered care. Whether the threshold level of serum albumin at which mortality risk increases in peritoneal dialysis (PD) patients is the same as for hemodialysis (HD) patients has not been studied.

Patients with chronic kidney disease (CKD) often experience a decline in their nutrient intake starting at early stages of CKD. This reduction in intake can affect both energy-producing nutrients, such as carbohydrates, proteins, and fats, as well as vitamins, minerals, and trace elements. Knowledge of the burden and bioactivity of vitamins and their effect on the health of the patients with CKD is very incomplete. However, without sufficient data, the use of nutritional supplements to prevent inadequate intake may result in either excessive or insufficient intake of micronutrients for people with CKD. The purpose of this article is to briefly summarize the current knowledge regarding vitamin requirements for people with stages 3, 4, or 5 CKD who are not receiving dialysis.

Mortality in long-term hemodialysis patients is high, mostly attributed to cardiovascular events, and may be related to chronic inflammation. We hypothesized that the anti-inflammatory benefits of higher dietary intake of omega-3 compared with omega-6 polyunsaturated fatty acids may modulate the inflammatory processes and decrease death risk.

Observational studies indicate greater survival in African American and Hispanic maintenance hemodialysis patients compared with their non-Hispanic white counterparts, although African Americans have shorter life expectancy than whites in the general population. We hypothesized that this apparent survival advantage is due to a more favorable nutritional/inflammatory profile in minority hemodialysis patients.

Periodic assessment of dietary intake across a given dialysis population may help to improve the clinical outcomes related to nutrients such as dietary protein, phosphorus, or potassium. Although dietary recalls and food records are used to assess dietary intake at individual level and over shorter periods, food frequency questionnaires (FFQ) are used to rank subjects of a given population according to their nutrient intake over longer periods.

Overweightness and obesity are associated with many hemodynamic, structural, and histopathologic alterations in the kidney and with metabolic and biochemical changes that predispose to these abnormalities. Consequent to these disorders, these individuals are more likely to develop chronic kidney disease and end-stage renal failure. Overweight and obese people are more prone to develop albuminuria and, for at least some types of kidney disease, a greater amount of albuminuria and more rapid progression of renal failure. These individuals are more likely to develop diabetes mellitus and hypertension. Diabetic nephropathy, hypertensive nephrosclerosis, focal and segmental glomerulosclerosis, renal cell carcinoma, and urate and calcium oxalate urolithiasis are the more common kidney and urological diseases reported in obese people. Preliminary data indicate that many of the clinical and nephropathologic manifestations associated with obesity can be reversed or ameliorated with reductions in body fat induced by dietary energy restriction or surgical procedures that reduce intake and gastrointestinal absorption of calories.

Low serum parathyroid hormone (PTH) has been implicated as a primary biochemical marker of adynamic bone disease in individuals with chronic kidney disease (CKD) who undergo maintenance hemodialysis (MHD) treatment. We hypothesized that the malnutrition-inflammation complex is associated with low PTH levels in these patients and confounds the PTH-survival association.

Metabolic acidosis is an important cause of protein-energy wasting, commonly observed in chronic kidney disease (CKD). This wasting is, in part, a result of the imbalance between protein degradation and synthesis induced by metabolic acidosis. The increase in protein degradation seen with metabolic acidosis is largely secondary to increased activities of the adenosine triphosphate–dependent, ubiquitin-proteasome system and branched-chain ketoacid dehydrogenase. Studies consistently have shown increased protein degradation with lower serum bicarbonate levels and/or arterial pH; however, the evidence for the anti-anabolic effects of metabolic acidosis is less consistent. In contrast to these metabolic studies, many cross-sectional studies have shown a direct relationship between the severity of metabolic acidosis and the adequacy of nutritional status in CKD patients. Moreover, lower serum bicarbonate levels have been associated with better survival in some epidemiologic studies of patients undergoing maintenance hemodialysis. It is likely that these relationships are confounded by the direct association of dietary protein intakes with metabolic acidosis—controlling the survival data for measures of dietary protein intakes, malnutrition, and inflammation shows a rather steep increase in the risk of death with lower serum bicarbonate levels. Two randomized controlled studies have shown that correction of metabolic acidosis is associated with reduction in risk for hospitalization in chronic peritoneal dialysis patients; the studies in maintenance hemodialysis patients have been small and inconsistent. For now, metabolic studies and data from clinical trials lend support to the recommendations made by the Nutrition Workgroup of the Kidney Disease Outcomes Quality Initiative to maintain serum bicarbonate levels of 22 mEq/L or greater in all CKD patients. Limited data suggest that a higher serum bicarbonate level (around 24 mEq/L) may be even more beneficial, particularly in chronic peritoneal dialysis patients.

Protein-energy wasting (PEW), defined as reduced somatic and/or circulating body protein mass, decreased fat mass, and usually reduced protein and energy intake, has a prevalence that is variously estimated to be 18% to 75% in maintenance hemodialysis and chronic peritoneal dialysis patients. PEW is associated with increased morbidity and mortality and often is preventable or treatable. Thus, it has been argued that maintenance hemodialysis and chronic peritoneal dialysis patients should be monitored routinely for PEW and treated for this condition, when it occurs. A trend toward PEW can emerge in early stage 3 chronic kidney disease with an increasing risk toward the development and worsening of PEW as chronic kidney disease progresses. A main cause of PEW is inflammation, which may occur with or without clinically evident illness and can be associated with the most severe forms of PEW. Another major cause of PEW is decreased nutrient intake relative to the patient's nutritional needs, and may be caused by anorexia, which may be engendered by uremic toxicity, emotional depression, medications, or inflammatory disorders. Nonanorexic causes of reduced nutrient intake include inadequate finances to purchase or prepare foods; medical or surgical illnesses that impair the person's ability to ingest, digest, assimilate, or process the nutrients; impaired cognitive function; other mental or physical disabilities; and loss of dentures. Losses of nutrients during dialysis treatments or in urine (eg, the nephrotic syndrome), acidemia, and hormonal disorders can contribute to the development of PEW. Early initiation and adequate doses of renal replacement therapy, rapid treatment of reversible inflammatory processes, ensuring an adequate nutrient intake, and prevention of acidemia may be used to prevent and treat PEW.

Malnutrition is a powerful predictor of mortality in chronic kidney disease (CKD). However, its etiology is unclear. We hypothesized that the adipocyte-derived proteins leptin and adiponectin, inflammation (as measured by C-reactive protein, CRP), and insulin resistance (as measured by homeostasis model assessment, HOMA), implicated in the malnutrition-inflammation complex syndrome commonly seen in maintenance dialysis patients, would be associated with the loss of muscle mass in earlier stages of CKD. Arm muscle area was used as an indicator of muscle mass.

Background Recommended dietary protein allowances for chronic peritoneal dialysis (PD) patients are approximately 60% higher than the dietary protein allowances for healthy adults. The relative contribution of dialysate protein and amino acid losses to these high protein requirements or total nitrogen losses is uncertain.Methods Following a peritoneal equilibration test, two 24-hour dialysate collections (24–1 and 24–2) were performed in 9 stable patients undergoing automated PD [4 males, 3 diabetics, age 43 ± 5 years (mean ± SEM), dialysis vintage 42 ± 6 months, dialysate-to-plasma ratio of creatinine 0.61 ± 0.04]. Dialysate effluent from nighttime cycling was collected separately from the daytime dwells.Results The measured 24-hour protein losses were 9.4 ± 0.6 (24-31) and 10.8 ± 0.8 (24-32) g/day. Even though day dwells accounted for 27% of daily dialysate volume, they accounted for 40% of daily protein and amino acid losses. The frequency of nighttime cycling and duration of dwell were significant predictors of peritoneal protein losses. Dialysate protein and amino acid losses constituted 24% ± 2% and 3.1% ± 0.3% of dialysate nitrogen and 14% ± 1% and 1.7% ± 0.1% of dietary nitrogen intake respectively.Conclusions Treatment with automated PD is associated with somewhat higher 24-hour dialysate protein losses compared to previous reports among continuous ambulatory PD patients. Dialysate protein and amino acid losses constitute a small, albeit significant, proportion of total nitrogen appearance and thus may contribute to the increased dietary protein requirements of chronic PD patients.

Muscle mass and muscle mRNA levels for certain growth factors are reduced in maintenance hemodialysis (MHD) patients. This study tested the hypothesis that in MHD patients endurance exercise training (EET) increases mRNA levels for insulin-like growth factors and reduces myostatin mRNA.

This study was performed to assess the mRNA levels in skeletal muscle of maintenance hemodialysis (MHD) patients. Fifty-one sedentary MHD patients and 21 sedentary normal adults of similar age, gender distribution, and racial/ethnic mix as the patients were examined. The subjects had needle muscle biopsy to measure mRNA levels. They were assessed in right vastus lateralis muscle for insulinlike growth factor I (IGF-IEa and IGF-IEc), IGF-II, the IGF-I receptor, the IGF-II receptor, and myostatin. mRNA was measured by real-time polymerase chain reaction amplification of reverse transcribed cDNA. The results showed that in the MHD patients, as compared with the normal control patients, skeletal muscle mRNA levels for IGF-IEa, IGF-II, and the IGF-I receptor were significantly reduced, whereas mRNA for IGF-IEc, IGF-II receptor, and myostatin were not different than normal. We conclude that sedentary MHD patients show reductions in mRNA levels in the right vastus lateralis muscle for certain growth factor proteins, notably IGF-IEa, IGF-II, and the IGF-I receptor. These abnormalities may contribute to the sarcopenia and impaired endurance capacity, strength, and physical performance that occur in MHD patients.

Background:The long-term effect of a low-protein diet on the progression of chronic kidney disease is unknown. We evaluated effects of protein restriction on kidney failure and all-cause mortality during extended follow-up of the Modification of Diet in Renal Disease Study. Methods:Study A was a randomized controlled trial from 1989 to 1993 of 585 patients with predominantly nondiabetic kidney disease and a moderate decrease in glomerular filtration rate (25 to 55 mL/min/1.73 m2[0.42 to 0.92 mL/s/1.73 m2]) assigned to a low- versus usual-protein diet (0.58 versus 1.3 g/kg/d). We used registries to ascertain the development of kidney failure (initiation of dialysis therapy or transplantation) or a composite of kidney failure and all-cause mortality through December 31, 2000. We used Cox regression models and intention-to-treat principles to compute hazard ratios for the low- versus usual-protein diet, adjusted for baseline glomerular filtration rate and other factors previously associated with the rate of decrease in glomerular filtration rate. We estimated hazard ratios for the entire follow-up period and then, in time-dependent analyses, separately for 2 consecutive 6-year periods of follow-up. Results:Kidney failure and the composite outcome occurred in 327 (56%) and 380 patients (65%), respectively. After adjustment for baseline factors, hazard ratios were 0.89 (95% confidence interval [CI], 0.71 to 1.12) and 0.88 (95% CI, 0.71 to 1.08), respectively. Adjusted hazard ratios for both outcomes were lower during the first 6 years (0.68; 95% CI, 0.51 to 0.93 and 0.66; 95% CI, 0.50 to 0.87, respectively) than afterward (1.27; 95% CI, 0.90 to 1.80 and 1.29; 95% CI, 0.94 to 1.78; interaction P= 0.008 and 0.002, respectively). Limitations include lack of data for dietary intake and clinical conditions after conclusion of the trial. Conclusion:The efficacy of a 2- to 3-year intervention of dietary protein restriction on progression of nondiabetic kidney disease remains inconclusive. Future studies should include a longer duration of intervention and follow-up.

Background:Decreased dietary protein intake may be associated with increased mortality risk in individuals with kidney failure undergoing maintenance hemodialysis (MHD). We hypothesized that longitudinal changes in dietary protein intake have independent associations with survival in MHD patients. Methods:The relation between urea kinetic–based normalized protein nitrogen appearance (nPNA) and all-cause and cardiovascular mortality was examined in a 2-year (July 2001 to June 2003) cohort of 53,933 MHD patients from virtually all DaVita dialysis clinics in the United States, using both conventional and time-dependent (repeated-measure) Cox models to estimate death hazard ratios for quarterly averaged nPNA categories controlled for case-mix, comorbidity, dialysis dose (Kt/V), and available markers of malnutrition-inflammation complex syndrome (MICS). Results:The best survival was associated with nPNA between 1.0 and 1.4 g/kg/d, whereas nPNA less than 0.8 or greater than 1.4 g/kg/d was associated with greater mortality in almost all models. Adjustment for MICS mitigated the associations substantially. A decrease in protein intake during the first 6 months in patients with an nPNA in the 0.8- to 1.2-g/kg/d range was associated incrementally with greater death risks in the subsequent 18 months, whereas an increase in nPNA tended to correlate with reduced death risk. Conclusion:Low daily protein intake or decrease in its magnitude over time is associated with increased risk for death in MHD patients. Whether the association between time-varying protein intake and survival is causal or a consequence of anorexia secondary to MICS or other factors needs to be explored further in interventional trials.

Serum free carnitine is decreased and serum acylcarnitines are increased in maintenance hemodialysis (MHD) patients, and the causes for these abnormalities are not known. This study examined the role of renal failure in the occurrence of low serum carnitine and increased acylcarnitines in patients with advanced chronic kidney disease (CKD) by assessing the relationship between these compounds and renal function in normal individuals and patients with CKD. If these compounds decrease as glomerular filtration rate (GFR) decreases, this suggests that decreased intake or impaired synthesis in kidneys explain the low serum values. If serum compounds increase as GFR decreases, this suggests that impaired excretion may predispose to these values.