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Resume L'insuffisance renale chronique est associee a differentes anomalies du systeme immunitaire impliquant a la fois l'immunite specifique et non specifique. Par ailleurs, les patients insuffisants renaux chroniques presentent frequemment des troubles nutritionnels, soit a type de malnutrition proteinoenergetique, soit des carences plus specifiques, telles que des deficits en oligo-elements. Les travaux consacres a l'effet de la correction des troubles nutritionnels sur l'immunite des insuffisants renaux chroniques sont rapportes. Ils montrent qu'une part des anomalies attribuees a l'uremie sont potentiellement reversibles apres correction des anomalies metaboliques secondaires aux carences nutritionnelles. Une meilleure prise en charge nutritionnelle devrait conduire a une diminution de la morbidite associee a l'insuffisance renale chronique, que les patients soient dialyses ou non.

Ketodiet, physiological calcium intake and native vitamin D improve renal osteodystrophy. The effects of a very low-protein diet (VLPD) supplemented with amino acids and ketoanalogues (KA) and with 1g of calcium carbonate and 1000IU of vitamin D2, were studied in 17 patients with advanced renal failure (GFR ≤ 20ml/min) over a period of one year. The protein intake was 0.3g protein/kg body wt/day. Daily phosphorus and calcium intake were respectively 1,500mg and 300mg. Sequential bone densitometry was performed and bone histomorphometry after double tetracyclin labeling was evaluated, before and after one year of diet. Calcium and phosphate metabolism parameters were monitored every two months. In spite of a significant decrease of GFR, phosphorus, parathyroid hormone (1-84) and osteocalcin plasma levels decreased significantly, while low plasma bicarbonate normalized, and calcitriol and calcium levels remained respectively low and normal. Before the diet, histological study disclosed four cases of mixed osteopathy: osteomalacia associated with osteitis fibrosa (OM/OF), nine pure osteitis fibrosa (OF) and four with normal bone remodeling (NB). After one year of diet, the OM component of OM/OF disappeared, as evidenced by a normalization of the mineral apposition rate and osteoid thickness. In the patients presenting pure OF, a significant decrease in osteoblastic and osteoclastic surfaces, in the number of osteoclasts, and in the bone formation rate (BFR) were found. Vertebral mineral density measured by quantitative computerized tomodensitometry did not change significantly. In conclusion, this study not only confirms the benefical effects of VLPD + KA + calcium on uremic hyperparathyroid bone disease in advanced renal failure assessed using static bone histomorphometry, but also shows a correction of histodynamic bone parameters. These results were achieved without pharmacological doses of vitamin D. Furthermore it suggests that: (1) the suppression of hyperparathyroidism appears largely due to the decrease in plasma phosphate, the correction of acidosis and the increase in 25 OH vitamin D plasma levels, independently of significant permanent changes in plasma concentrations of calcium and calcitriol; and (2) this diet also corrects the osteomalacic component, in spite of the absence of a significant increase in plasma concentration of calcium and calcitriol, probably because of the correction of metabolic acidosis, since the increases in mineral apposition rate and in plasma bicarbonate levels were correlated.

Enteral nutrition (EN) by means of oral nutritional supplements (ONS) and tube feeding (TF) offers the possibility of increasing or ensuring nutrient intake in cases where normal food intake is inadequate. These guidelines are intended to give evidence-based recommendations for the use of ONS and TF in nephrology patients. They were developed by an interdisciplinary expert group in accordance with officially accepted standards and are based on all relevant publications since 1985. They were discussed and accepted in a consensus conference. Because of the nutritional impact of renal diseases, EN is widely used in nephrology practice. Patients with acute renal failure (ARF) and critical illness are characterized by a highly catabolic state and need depurative techniques inducing massive nutrient loss. EN by TF is the preferred route for nutritional support in these patients. EN by means of ONS is the preferred way of refeeding for depleted conservatively treated chronic renal failure patients and dialysis patients. Undernutrition is an independent factor of survival in dialysis patients. ONS was shown to improve nutritional status in this setting. An increase in survival has been recently reported when nutritional status was improved by ONS.

ANCA; immune complex-mediated glom- At admission, she presented with bilateral pretibialerulonephritis; infectious diseases; shunt nephritis oedema and a pattern of anaemia. Her temperaturewas normal. Blood pressure was 150/80 mmHg.Clinical examination showed no neurologic, cardiac,pulmonary or cutaneous abnormalities. Laboratory

Insulin resistance is characterized by a lesser biological response to a standard level of insulin. Currently the most popular method used to quantify insulin resistance is the homeostasis model of assessment of insulin resistance (HOMA-IR). A state of insulin resistance is present from the early stages of chronic renal failure (CRF). Defects in glucose utilization observed during CRF concern both nonoxidative metabolism (storage in the form of glycogen) and oxidative metabolism. Resistance to the action of insulin during the CRF concerns traditionally peripheral tissues, particularly skeletal muscle. The mechanisms are multiple: retention of nitrogenous waste, metabolic acidosis, hypovitaminosis D or inflammation. The insulin resistance is associated with a disturbance of endothelial function and is involved in increased vascular risk and aggravates muscle metabolic disorders. Recent studies demonstrated a link between insulin resistance and progression of renal failure. Physical activity is known to improve insulin resistance status, the correction of metabolic abnormalities and attempts to reduce the inflammatory syndrome are potential targets of treatment. Thiazolidinedione have recently shown their interest, but in CRF the balance between risk and benefit remains to be evaluated.

Dietary manipulation, including protein, phosphorus, and sodium restriction, when coupled with the vegetarian nature of the renal diet and ketoacid supplementation can potentially exert a cardiovascular protective effect in chronic renal failure patients by acting on both traditional and nontraditional cardiovascular risk factors. Blood pressure control may be favored by the reduction of sodium intake and by the vegetarian nature of the diet, which is very important also for lowering serum cholesterol and improving plasma lipid profile. The low protein and phosphorus intake has a crucial role for reducing proteinuria and preventing and reversing hyperphosphatemia and secondary hyperparathyroidism, which are major causes of the vascular calcifications, cardiac damage, and mortality risk of uremic patients. The reduction of nitrogenous waste products and lowering of serum PTH levels may also help ameliorate insulin sensitivity and metabolic control in diabetic patients, as well as increase the responsiveness to erythropoietin therapy, thus allowing greater control of anemia. Protein-restricted diets may have also anti-inflammatory and anti-oxidant properties. Thus, putting aside the still debatable effects on the progression of renal disease and the more admitted effects on uremic signs and symptoms, it is possible that a proper nutritional treatment early in the course of renal disease may be useful also to reduce the cardiovascular risk in the renal patient. However, conclusive data cannot yet be drawn because quality studies are lacking in this field; future studies should be planned to assess the effect of renal diets on hard outcomes, as cardiovascular events or mortality.

The number of individuals with diabetes is rapidly growing worldwide, and in most countries, diabetic nephropathy has become the most important cause of ESRD. Although excessive protein intake may negatively influence the progression of renal disease, diabetics are rather reluctant to restrict their protein intake. However, in diabetic patients with renal failure, dietary protein restriction seems to have a beneficial effect on the course of the nephropathy without untoward effect on nutritional status. Moreover, the reduction in protein intake improves insulin sensitivity and has beneficial influences on different steps of carbohydrate metabolism. Dietary protein restriction should be considered as a safe therapy and deserves to be associated with the most important aspects of the medical management i.e. glycemic control and blood pressure control.

La prevalence actuelle de ľinsuffisance renale chronique (IRC) est estimee a 3,5 % de la population en France, celle de ľIRC teminale (IRCT) a un pour mille habitants, et celle des hemodialyses a environ cinq pour dix mille. Malgre les progres de la technique, ďhemodialyse et de ľensemble du traitement de ľIRCT, la mortalite annuelle des patients hemodialyses reste voisine de 10% a 15 % en France (1). La denutrition est apparue actuellement comme un element determinant du pronostic (1, 2, 3, 4). Ainsi, la National Kidney Foundation (NKF) aux Etats-Unis (5,6) et ľEuropean Society of Parenteral and Enteral Nutrition (ESPEN) (7, 8) ont elabore des recommandations concernant ľevaluation et le traitement de la denutrition de ľIRC.

For many years patients with chronic kidney disease have been advised to control the protein content of their diet. This advice has been given on the basis of a number of reported metabolic effects of lowering protein intake, such as lowering serum urea nitrogen levels, improving phosphocalcic metabolism and insulin resistance and, more recently, ameliorating proteinuria (independent of antiproteinuric medications). The effects on the progression of kidney disease, although spectacular in experimental studies, have been less convincing in humans. It is possible that flawed design of clinical trials is responsible for this discrepancy. In this Review, we comment on experimental findings that indicate that limiting protein intake protects the kidney and ameliorates uremic symptoms, outline how the body adapts to a reduction in protein intake, and describe the metabolic benefits to the patient. We then review the evidence from randomized controlled trials and meta-analyses that pertains to the effects of low-protein diets in adults with chronic kidney disease.

Reduction of proteinuria is associated with a slower progression of renal failure. We questioned whether the change in proteinuria in response to a supplemented very low protein diet (SVLPD), which is known to reduce proteinuria, could function as a marker of the potential renoprotective effect of an SVLPD.In the 220 consecutive patients of our previously published cohort, the glomerular filtration rate (GFR) was assessed every 3 months using the (51)Cr-EDTA method. Seventy-eight patients (mean age 52 +/- 17 years, body mass index 23 +/- 3 kg/m(2), GFR 15 +/- 6 mL/min) exhibited a proteinuria more than 1 g per day at the start of the regimen. Mean protein intake assessed by urinary nitrogen appearance was 0.42 +/- 0.24 g/kg per day at 4 months. The median follow-up was 24 months.Proteinuria decreased significantly after patients were treated with an SVLPD. The maximum mean percent reduction was attained at 3 months (47% +/- 27%), was not influenced by the levels of baseline proteinuria, and was similar in patients receiving or not receiving angiotensin-converting enzyme inhibition at the start of the study. The percent reduction and the residual proteinuria at 3 months predicted the rate of the later GFR decline. GFR decline was significantly lower in patients whose reduction in proteinuria at 3 months was higher than 50% (0.42 +/- 0.37 mL/min/mo vs. 0.10 +/- 0.15 mL/min/mo and 1.0 +/- 0.6 mL/min/mo vs. 0.15 +/- 0.19 mL/min/mo, P.001 in patients with proteinuria higher or lesser than 3 g/d at start, respectively).These results do not differ from those reported with therapies antagonizing angiotensin II formation and/or activity aiming at reducing proteinuria in chronic renal diseases.

International audience; Objective: Determine the mechanism of glucose intolerance in chronically uremic subjects. Design: Comparison of doubly labeled oral glucose tolerance tests. Subjects: Seven nondialyzed chronically uremic subjects (creatinine, 420 ± 104 μmol/L) and 7 healthy subjects, matched for age and body mass index. Intervention: Plasma glucose was labeled by an infusion of dideuterated glucose started 120 minutes before ingestion of 1 g/kg of naturally 13C-enriched corn starch glucose. Glucose levels and oxidation were monitored for 330 minutes after glucose ingestion. Results: Uremic subjects had normal fasting plasma glucose levels and impaired glucose tolerance with high plasma insulin (P < .001 versus controls). Glucose tolerance was impaired because of an increased total rate of appearance of glucose (cumulated on 330 minutes: uremic, 1,231 ± 42 mg/kg/330 min, controls, 1,031 ± 64; P < .05). Peripheral glucose uptake was increased (P < .05) because of an increased nonoxidative disposal (P = .051). Conclusions: Although peripheral glucose uptake resisted the stimulatory effect of the high insulin levels, glucose tolerance was impaired through splanchnic metabolic disturbances: reduced splanchnic glucose uptake and increased endogenous glucose production. The respective contribution of these abnormalities remains to be determined.

Previous series have dealt with nutritional status after kidney transplantation. However, few studies have described the outcome of body composition after kidney transplantation.A total of 44 cadaver kidney transplant recipients (28 men and 16 women) were followed prospectively during the first post-transplant year. Biochemical nutritional markers, dietary records, anthropometric measurements, and body composition were assessed at kidney transplantation and 3, 6, and 12 months later.By the end of the first year, serum albumin level was not significantly different from initial values. Prealbumin and retinol binding protein decreased from 42.3 +/- 10.2 mg/dL to 30.4 +/- 6.3 mg/dL and from 1.96 +/- 0.61 g/dL to 0.65 +/- 0.2 g/dL (P0.0001). Separating patients by gender showed that dietary caloric and protein intake increased in women only. At the end of the follow-up period, mean weight change was +5.4 kg in women (P = 0.009) and -0.9 kg in men (not significant). Body composition analyses showed that in women total fat and lean masses increased (+2.1 kg, P = 0.05, and +2.4 kg, P = 0.006), whereas in men total fat mass decreased (-1.4 kg, P = 0.04), and total lean mass tended to increase (+0.5 kg, not significant). Percentage change in total bone mass was +1.4% in women (not significant) and -2.1% in men (P = 0.05). In multivariate analyses, an independent impact of female gender on weight gain was observed, although increased fat mass was related only to energy intake. Increased total lean mass was related to low steroid doses and the absence of acute rejection and delayed graft function. Bone loss was related to male gender and high steroid doses.Changes in body composition during the first year after kidney transplantation are modulated by gender, energy intake, steroid doses, the occurrence of acute rejection, and delayed graft function.

In patients with chronic renal failure (CRF), the reduction of dietary protein intake may correct uremic symptoms, slow the rate of progression of renal failure, and delay the onset on dialysis. Concerns have been made on the nutritional consequences of protein-restricted diets. Over 15 years, 239 patients were treated with a very-low-protein diet providing 0.3 g vegetable protein/kg/day supplemented (SLPD) with essential amino acids and keto analogs. Many adverse consequences of uremia were corrected by this regimen, such as metabolic acidosis, secondary hyperparathyroidism, resistance to insulin, decreased Na + -K + -ATPase activity. A joint physician-dietitian monitoring contributed to the maintenance or obtention of a satisfactory nutritional status, even in patients at risk, diabetics, patients with the nephrotic syndrome and with renal allograft chronic rejection. The outcome of these patients when treated by hemodialysis or transplantation was favorable, their nutritional status being preserved. Results from the present study and results of other studies show that SLPD can be used in patients with advanced CRF without adverse effects in carefully selected and monitored patients.

International audience; Nutritional factors and dialysis adequacy are associated with outcome in hemodialyzed patients, but their relative contribution remains controversial, particularly when dialysis adequacy complies with current recommendations (Kt/V >1.2). Survival, clinical, and nutritional data from a cohort of prevalent 1,610 patients treated by hemodialysis in 20 centers in France have been collected over a 2.5-year period, from January 1996 to July 1998. Data including age, sex, cause of end-stage renal disease (ESRD), clinical outcome, time on dialysis, body mass index (BMI), blood levels of midweek predialysis albumin, prealbumin, and bicarbonate were analyzed. Normalized protein catabolic rate (nPCR), dialysis adequacy parameters, and estimation of lean body mass (LBM) from creatinine generation were computed from pre- and postdialysis urea and creatinine levels. The characteristics of the patients were as follows: age 59.6 +/- 16.5 years, 58.8% males, 11% of diabetics, time on dialysis 63.2 +/- 64.5 m. Weekly dialysis time was 12.18 +/- 1.78 hrs, Kt/V 1.34 +/- 0.34, nPCR 1.10 +/- 0.35 g/kg body weight/day. Albumin concentration was 39.4 +/- 5.3 g/L, prealbumin was 0.33 +/- 0.09 g/L, BMI was 23.0 +/- 4.5 kg/m(2). Overall survival was 89.7% +/- 0.8% and 78.4% +/- 1.1% after 1 and 2 years. In the Cox proportional hazard model, survival was significantly influenced by age, the presence of diabetes, and by concentrations of albumin and prealbumin, but not by other variables, including Kt/V and urea reduction ratio. These results indicate that nutritional protein concentrations were predictive of dialysis outcome, whereas variables reflecting actual body composition and dialysis dose were not. Furthermore, in this well-dialyzed population, dialysis adequacy had no influence on survival. In conclusion, when adequacy targets are met in hemodialyzed patients, survival is mainly dependent on age and nutritional status. Efforts should be focused on the most efficient ways to maintain nutritional status in these patients.

The second part of the report deals with the nutritional therapy of 1) patients with chronic renal failure on haemodialytic treatment or peritoneal dialysis, 2) patients with nephrotic syndrome, 3) patients with acute renal failure and 4) kidney transplanted patients. Each of these situations is unique as to the aetiology of malnutrition and nutritional treatment. Haemodialytic treatment or peritoneal dialysis are in themselves additional catabolic stimuli. Preventing protein-energy malnutrition in hemodialysis patients is important because of its prognostic relevance. Peritoneal dialysis patients pose a special problem because the energy intake can be in excess, while the nitrogen balance is often negative, and they are at risk of developing a kwashiorkor-like syndrome. The nutritional risk of patients with acute renal failure and the diAculty in nourishing them adequately is outlined. Specific recommendations are given for the pre-transplant, early posttransplant and late post-transplant phases.

Protein-restricted diets are prescribed in patients with chronic renal failure (CRF) to alleviate uremic symptoms and to slow the progression of CRF. The potential deleterious effects of protein restriction on nutritional status and clinical outcome of patients with CRF have raised concern. In this study, data were collected from 1985 to 1998 on 239 consecutive patients (age 50.2 +/- 15.6 yr) with advanced CRF (GFR 13.1 +/- 4.8 ml/min) to whom a supplemented very low protein diet (SVLPD) providing 0.3 g protein, 35 kcal, and 5 to 7 mg of inorganic phosphorus per kg per day was administered for a mean duration of 29.6 +/- 25.1 mo. The diet was supplemented with essential amino acids and ketoanalogs, calcium carbonate, iron, and multivitamins. During SVLPD, protein intake decreased from 0.85 +/- 0.23 to 0.43 +/- 0.11 g/kg per d, and body mass index and serum albumin concentration remained unchanged overall. Fourteen patients died during SVLPD; death was unrelated to nutritional parameters. Hemodialysis was initiated after SVLPD in 165 patients at a mean GFR of 5.8 +/-1.5 ml/min. During an average of 54 mo on hemodialysis, mortality was low (2.4% after 1 yr) and correlated to age only, not to nutritional parameters observed at the end of SVLPD. Similar results were obtained in 66 transplanted patients (12 were not dialyzed before transplantation). SVLPD can be safely used in patients with CRF without adverse effects on the clinical and nutritional status of the patients. Due to the preservation of nutritional status and the correction of uremic symptoms, the initiation of dialysis was deferred in these patients. The outcome of patients on renal replacement therapy is not affected by prior treatment with SVLPD during the predialysis phase of CRF.

One year of a very low protein diet (VLPD) can reverse secondary hyperparathyroidism in uremic patients. We studied bone histology, bone mineral density (BMD), and dynamic parathyroid function (calcium/PTH curves) in 16 nondialyzed patients with advanced renal failure who had been receiving a VLPD for a mean of 5 yr (mean protein intake, 0.34 +/- 0.12 mg/kg x day; mean phosphorus intake, 8.2 +/- 2.1 mg/kg x day) and daily supplementation with essential amino acids and their ketoanalogs (1000 IU vitamin D2 and 1-2 g calcium carbonate). Three patients exhibited a high bone formation rate (BFR), 7 patients had normal bone remodeling, and 6 patients had a low BFR, including 2 with osteomalacia and 4 with adynamic bone disease without aluminum overload. A longer diet duration and lower caloric intake were associated with low BFR. More than half of the patients exhibited moderate or severe osteoporosis at the appendicular skeleton. The t score of femur BMD explained 65% of the BFR variance. Patients with a low BFR had a dynamic parathyroid function similar to that of patients with a normal BFR, except they had a lower capacity to buffer a calcium load, whereas patients with a high BFR had a higher basal PTH/maximum PTH and a steeper calcium/PTH curve slope; the calcium set-point was identical in the three groups.

Cardiovascular morbidity and mortality in hemodialyzed patients are increased due to the frequently abnormal lipid metabolism. It has been reported that this abnormal lipid metabolism could be partially corrected by some highly permeable membranes, such as polysulfone or cellulose triacetate. We investigated the influence of 4 months of dialysis with a polyamide membrane upon the course of lipid parameters in 6 patients presenting a hypertriglyceridemia2 mmol/l while on bicarbonate dialysis with a cellulose membrane. Lipid parameters improved after 4 months of hemodialysis with a polyamide membrane. Serum triglyceride and cholesterol levels decreased, while HDL cholesterol and HDL levels rose significantly (p0.05). Apolipoprotein B decreased significantly (p0.05). Following heparin administration, lipoprotein lipase activity improved (p0.02), associated with a decrease apolipoprotein C3 (p0.05). The fractional clearance rate of triglycerides rose significantly (p0.01). The use of highly permeable polyamide membranes results in a significant improvement in lipid disturbances of dialysis patients due to an increased lipoprotein lipase activity, induced perhaps by the removal of circulating inhibitors such as apolipoprotein C3.

In eight patients remaining acidotic after more than 1 year of bicarbonate haemodialysis, we studied the effect of correcting the chronic metabolic acidosis using acetate-free biofiltration for 4 months on the course of secondary hyperparathyroidism. An AN69 capillary membrane was employed with a bicarbonate infusion rate initially set at 1.8 l/h in all patients and then adjusted in each one to obtain a predialysis bicarbonate of ≥23 mmol/l. Standard blood chemistry parameters were determined every 2 weeks. Measurements of PTH, calcifediol and calcitriol, as well as calcium-PTH curves were determined at the beginning and end of the study. While acetate-free biofiltration appears to be an adequate technique for the correction of chronic metabolic acidosis when bicarbonate dialysis fails, this study indicates that it does not influence secondary hyperparathyroidism in haemodialysed patients. The level of intact PTH did not vary significantly and the calcium-PTH curves at 0 and 4 months were superimposable with no significant differences in the set point and the slope of the curves.

A significant percentage of dialysed patients have inadequate protein intake. One strategy for treating the protein malnutrition in peritoneal dialysis patients is to replace glucose in the dialysis solution by amino acids. A new peritoneal dialysis solution containing 1.1% amino acids in a formulation optimized for renal patients and with a lactate concentration of 40 mmol/l has been evaluated. Fifteen CAPD patients completed a non-randomized prospective 3-month study. Each patient received 2 litres of the optimised 1.1% amino acid solution for the second exchange of the day with a dwell time of 5-6 h. Indicators of efficacy were serum albumin and transferrin. After 3 months of intraperitoneal amino acids, serum albumin levels significantly increased from 32.7 +/- 2.3 to 35.1 +/- 2.2 g/l (mean +/- SD; P < 0.01). This occurred in parallel with a significant increase in transferrin levels from 2.21 +/- 0.26 to 2.39 +/- 0.27 g/l (P < 0.05). As expected, urea rose from 23.7 +/- 6.8 to 29.9 +/- 9.4 mmol/l. Interestingly bicarbonate did not change (25.5 +/- 4.2 versus 25.2 +/- 3.3 mmol/l). These results suggest that the optimized formulation is effective in improving nutritional parameters in CAPD patients while avoiding unwanted side-effects such as acidosis.

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Authors' response to “The two best reasons NOT to focus on protein restriction in chronic kidney disease”

The authors report retrospectively 38 cases of Schonlein-Henoch purpura (20 males, 18 females; median age, 26 years). Skin (37/38) and joint (21/38) manifestations are similar to those seen in children. Gastro intestinal (22/38) manifestations are less complicated. Long term outcome of the disease depends on kidney's involvement (32/38) and is severe: chronic renal failure in 31%.

A study of heart lesions has been conducted in 38 patients with systemic sclerosis using echocardiography, doppler and colour doppler. Abnormalities were found in 66% patients. Valvulopathies (mainly mitral regurgitation) were the most frequent lesions (45%). The presence of anti-SCL70 antibody was correlated to right cavities dilatation. Pulmonary hypertension was found in 6 patients.

The association of minimal change nephropathy and chronic lymphocytic leukemia is exceptional. We report two cases with this association, with reversible renal failure in one.

A 12 year-old patient presents a systemic lupus erythematosus with thrombotic micro-angiopathy. Corticosteroids, cyclophosphamide and plasmapheresis are not efficient. Under prostacyclin the hematologic disorders disappear.

Chemiluminescence (CL) emission from leukocytes was studied in 20 uremic patients after ingestion of opsonized zymosan. CL production was impaired when compared with control groups. Six months after a low-protein, low-phosphorus diet supplemented with essential amino acids and ketoanalogues (SD) was started, a significant improvement in CL production was observed. SD may be expected to decrease the susceptibility of uremic patients to bacterial infections.

Ten patients with advanced renal failure (glomerular filtration rate 25 mL/min) were treated with a low phosphorus and low protein diet supplemented with ketoacid analogues. Before starting the diet and four months afterwards, a 50 g oral glucose tolerance test with a three step euglycemic insulin clamp was carried out. A dose-response curve of total body insulin sensitivity was plotted. By the fourth month, glucose tolerance had improved with significantly lower T0, T30, and T60 insulin levels. These results are attributed to the improvement in insulin action as demonstrated by the clamp technique. The dose-response curve had a distinctly higher plateau after dietary treatment, and the tissue sensitivity index to insulin ( M I ratio) was significantly improved. It is suggested that treatment of uremic patients with a low protein diet may reduce levels of a putative insulin inhibitor.