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Background: The consequences of a supplemented very-lowprotein diet remain a matter of debate with regard to patient outcome before or after the onset of renal replacement therapy. Objective: We evaluated the long-term clinical outcome during maintenance dialysis and/or transplantation in patients who previously received a supplemented very-low-protein diet. Design: We assessed the outcome of 203 patients who received a supplemented very-low-protein diet for .3 mo (inclusion period: 1985–2000) and started dialysis after a mean diet duration of 33.1 mo (4–230 mo). Results: The survival rate in the whole cohort was 79% and 63% at 5 and 10 y, respectively. One hundred two patients continued with chronic dialysis during the entire follow-up, and 101 patients were grafted at least once. Patient outcomes were similar to those of the French Dialysis Registry patients for the dialysis group and similar to the 865 patients who were transplanted in Bordeaux during the same period for the transplant group. There was no correlation between death rate and duration of diet. Conclusions: The lack of correlation between death rate and duration of diet and the moderate mortality rate observed during the first 10 y of renal replacement therapy confirm that a supplemented very-low-protein diet has no detrimental effect on the outcome of patients with chronic kidney disease who receive renal replacement therapy. Am J Clin Nutr 2009;90:969–74.

Background Three-day food recall and normalized protein nitrogen appearance calculation from pre- and postdialysis plasma urea are the most commonly used techniques to assess nutritional intake, but a 7-day dietary recall is probably more accurate to approach dietary intake in clinical practice. Methods A total of 99 hemodialyzed patients from two units were analyzed in a 7-day dietary record with a large range of age and without having any signs of malnutrition. Dietary protein intake was estimated from the recall and calculated (normalized protein catabolic rate) from urea kinetic modeling. Calorie intake and quality and repartition of nutrients were estimated from diaries. Results Repartition of nutrients was close to that of a reference population except for a lower glucidic contribution (glucide 47%, lipid 36%, protein 16%). Normalized protein catabolic rate and dietary protein intake were well correlated (R2 = 0.4), but a large variability existed from day to day, according to age (older patients are less variable) and day of dialysis (long or short interval). Conclusion A large variation in alimentary intake exists from patient to patient and day to day. A 7-day evaluation of nutrient intake, dialysis adequacy, and nutritional parameters seems to be a good solution to guide dietetic counseling.

Background Thanks to advancements in immunosuppression, patients are living longer with kidney transplants, and nonimmunologic factors (particularly nutritional) have become a major source of morbidity and mortality after successful kidney transplantation (KTx). In this current study, we have prospectively assessed, in a cohort of kidney transplant recipients (KTR), the course of some nonimmunologic factors liable to hinder the long-term outcome of KTR. Methods Forty-four consecutive KTR with stable functioning grafts received dietary recommendations and were on the lowest effective dose of steroids. Biochemical nutritional markers, C-reactive protein, lipid profile, and body composition determined by dual-energy X-ray absorptiometry were studied over the first year, 2 years, and 5 years after KTx. Results No patients died during the follow-up. All patients but 2 were considered normotensive. Clinical diabetes developed in 3 patients. Visceral proteins stabilized at a normal range after the first year. Most of the patients normalized their inflammatory status. A significant improvement in lipid profile was observed. Female patients had a significant increase of weight (13.5%), mainly because of an increase in fat mass: 3.4 kg (19.4%) at 1 year and 5.6 kg (29.7%) at 2 years. In male patients, body composition remained stable and close to baseline values. The evolution of bone mass varied according to gender, total corticoid doses, and calcineurin inhibitors. Patients on low doses of steroids normalized their Z-score over the 5-year period. The increase in bone mass (paired t-test, P = .006) was only significant in patients treated with tacrolimus (analysis of variance for repeated measures, P Conclusions Simple measures and dietary intervention to prevent or correct nonimmunologic disorders should permit improvement of long-term morbidity and mortality of KTR without compromising the functional outcome of their transplant.

Leptin is a 16-kd protein that is thought to be a regulator of food intake and body weight. Many previous studies have reported elevated serum leptin levels in renal failure. In this study, we investigated the outcome of serum leptin and its relationship to body fat (BF), dietary intake, nutritional, and inflammatory markers after kidney transplantation (KTx). A total of 41 kidney transplant recipients were followed-up prospectively during 6 months posttransplantation. Serum leptin, albumin, transferrin, and C-reactive protein (CRP) were measured at KTx, 15 days, 3, and 6 months later. Dietary intake and BF were determined at KTx, 3, and 6 months later. A decrease in serum leptin was observed early at day 15 after KTx; this decrease was significant only in patients with BF/= 30% of body weight. The decrease was maintained at 3 and 6 months after KTx. In multivariate analysis, an independent impact of higher percentage BF at KTx on the decrease of serum leptin was observed. Serum leptin correlated positively with BF. Conversely, no correlation was found between changes of serum leptin and changes of dietary intake. Leptin correlated positively with CRP at KTx, but not after normalization of renal function. Changes of serum leptin levels were not correlated with those of serum albumin levels. In summary, hyperleptinemia at KTx is manifest in patients with a high percentage of BF. An early and maintained correction follows KTx. Serum leptin levels did not appear to affect alimentary intake at and after KTx.

Resume Le metabolisme proteique est affecte par l’insuffisance renale chronique, quel que soit le stade de celle-ci ou ses modalites de traitement substitutif, hemodialyse, dialyse peritoneale ou transplantation renale. Plus que l’insuffisance renale par elle-meme, ce sont les conditions qui lui sont associees, en premier lieu l’inflammation chronique, l’acidose metabolique et l’insulinoresistance peripherique qui entrainent des phenomenes responsables de catabolisme proteique. Les parametres nutritionnels proteiques sont frequemment affectes chez l’insuffisant renal, avec des consequences deleteres en termes de morbidite et mortalite. La correction de ces anomalies doit permettre le maintien d’un etat nutritionnel satisfaisant, et un meilleur devenir clinique des insuffisants renaux.

Background: It has been reported that patients on a very-low-protein diet (VLPD) maintain a satisfactory nutritional status because of a conserved adaptive metabolic response. However, only few studies have examined the course of nutritional status and body composition in the long term (2 years). Methods: Thirteen stable patients (8 men; age, 55 ± 12 years; glomerular filtration rate (GFR), 15 ± 5 mL/min) receiving a VLPD (0.3 g/kg/day protein) supplemented with amino acids and ketoanalogues (SVLPD) were studied for 2 years. A joint visit with a physician and a dietitian and routine blood and urine analyses were performed every month. Dual-energy x-ray absorptiometry (DEXA), which was used to assess modification of body composition, and GFR (urinary 51 Cr-EDTA) and urinary urea and creatinine excretion, which were used to assess nutritional status and compliance to the diet, were assessed every 3 months. Results: GFR, albumin, and prealbumin levels remained stable. Urea urinary excretion decreased at 3 months and then slightly increased at 2 years, but the calculated protein intake remained low at 0.38 ± 0.1 g/kg/day. Energy intake remained close to 30 kcal/kg/day. No significant change was observed for total fat mass or percent fat mass. After an initial decrease, lean body mass stabilized at 6 months and then increased significantly from 6 to 24 months ( P = .02, paired t -test); the mean increase during this period was of 2 kg, that is, 4.6%. Urinary creatinine excretion showed the same profile. Total bone mass, lumbar or hip site bone mass, and Z-score significantly decreased from T0 to 1 and 2 years ( P Conclusion: This study confirms that a supplemented VLPD is nutritionally safe for a long period, but attention must be paid to bone mass.

Nutrition in hemodialysis patients previously on a supplemented very low protein diet.BackgroundNutritional safety of protein-restricted diets in patients with chronic renal failure is controversial. In the present study, we have assessed the evolution of nutritional status after initiation of hemodialysis in patients previously treated by a supplemented very low protein diet (SVLPD).MethodsNutritional data were prospectively collected during the first year of hemodialysis from 15 consecutive patients treated with a SVLPD (0.3 g protein/kg/day supplemented with essential amino acids, calcium, iron, and vitamins) and compared to 15 age- and gender-matched end-stage renal disease (ESRD) patients previously on a less-restricted diet (0.90 ± 0.21 g protein/kg/day) who started hemodialysis during the same period. Dual-energy x-ray absorptiometry (DEXA) was used to assess body composition at 0, 6, and 12 months. Hemodialysis prescriptions, biologic data and 3-day food records were collected every 3 months.ResultsProtein intake was higher than 1.2 g/kg/day in both groups as soon as 3 months after the start of hemodialysis. Albumin and prealbumin increased significantly during the first 6 months in all patients. Body mass index (BMI) increased in all patients (+0.97 ± 1.31 kg/m2; P < 0.001) reflecting a gain in fat mass in the overall population (+2.36 ± 2.94 kg/m2; P < 0.001) while lean body mass remained stable overall.ConclusionOnce on hemodialysis, SVLPD patients rapidly increased protein intake. Nutritional status improved in all patients, with a gain in fat mass in all, and a gain in lean body mass in SVLPD men only. These data indicate that treatment with a SVLPD prior to hemodialysis initiation is nutritionally safe.

Resume Introduction. – La gemcitabine est un analogue nucleosidique utilise dans les tumeurs solides depuis 1987. Sa toxicite principale est hematologique. Elle peut aussi etre responsable dˈinsuffisance renale aigue par microangiopathie thrombotique. Nous rapportons un nouveau cas et suggerons une possibilite de depistage precoce. Exegese. – Un patient âge de 71 ans traite au long cours par gemcitabine pour un adenocarcinome pancreatique metastatique a presente plusieurs poussees dˈhemolyse a bas bruit precedant un syndrome hemolytique et uremique avec insuffisance renale aigue qui a necessite une seance dˈhemodialyse. Lˈenquete etiologique etait negative et la responsabilite de la gemcitabine a ete etablie. La gemcitabine est une nouvelle cause de microangiopathie thrombotique. Cette toxicite est cumulative, survient preferentiellement sur un rein fragilise et le diagnostic est souvent retarde. Le traitement doit etre interrompu definitivement. Conclusion. – La surveillance de la reticulocytose, de lˈhaptoglobine serique et du sediment urinaire pourrait permettre un depistage precoce de cet effet indesirable meconnu et sous-declare.

We have previously shown that a ketoacid-supplemented very-low-protein diet (KSVLPD), which has been proposed to slow down the rate of progression of chronic renal failure (CRF), improves tissue insulin sensitivity and decreases hyperinsulinemia in predialytic uremic patients. However, this diet may interfere with nutritional status. The aim of this study was to study basal energy expenditure (EE) and EE after an oral glucose load in patients with CRF before and during a KSVLPD (0.3 cal x kg wt(-1) x d(-1) supplemented with aminoacid and ketoanalogs) using oral glucose loading in combination with indirect calorimetry. We also monitored body weight and analyzed body composition by dual-energy x-ray (DEXA) during KSVLPD. In the third month of KSVLPD, no significant change in total body weight was observed, but DEXA showed a decrease in lean tissue mass (LTM; 46.2 +/- 3.6 kg before v 44 +/- 3.4 kg in the third month; P.01) and an increase in body fat mass (20.1 +/- 2.4 kg before v 21.3 +/- 2.4 kg on KSVLPD; P.05). Postabsorptive plasma glucose level was significantly lower, and glucose oxidation and energy expenditure per LTM were significantly increased (EE, 20 +/- 0.8 cal x kg LTM(-1) x min(-1) before diet v 21.9 +/- 1.1 cal x kg LTM(-1) x min(-1) after 3 months on KSVLPD; P.01). Plasma glucose and serum insulin levels were significantly lower after glucose loading, and glucose oxidation increased. EE values were significantly higher after the oral glucose load, and cumulative EE after oral load increased from 20.7 +/- 0.7 cal x kg LTM(-1) x min(-1) before the diet to 22.9 +/- 1.1 cal x kg LTM(-1) x min(-1) in the third month of KSVLPD; P.001). Glucose oxidation was higher and cumulative glucose storage was decreased after diet (29.6 +/- 4.2 g v 20.9 +/- 3.4 g on KSVLPD; P.01). We conclude that KSVLPD increases EE in the postabsorptive state and after an oral glucose load with an adaptation of lean tissue mass in the third month of the diet. Therefore, during KSVLPD, strict monitoring of dietetic management is necessary to maintain energy requirements at high levels appropriate to the new EE.

Chronic renal failure (CRF) is often accompanied by hyperleptinemia caused by deficient renal metabolism of leptin and possibly increased leptin production, which in turn may result from the hyperinsulinemia and increased proinflammatory cytokine levels in patients with CRF. The hyperinsulinemia and insulin resistance observed in patients with CRF improve on supplemented very low protein diets (SVLPDs). The goal of our study is to determine whether the correction of hyperinsulinemia and insulin resistance in patients with CRF by SVLPDs is accompanied by improvement in hyperleptinemia. Thirteen patients were studied before and 1 year after following SVLPDs providing 0.3 g/kg/d of protein, supplemented with amino acids and ketoanalogues. After 1 year, patients showed markedly less hyperinsulinemia (7.4 +/- 1.6 versus 13.8 +/- 2 microU/mL at the start of diet; P: = 0.05) and insulin resistance, whereas serum leptin levels remained unchanged (16.1 +/- 4.7 versus 19.1 +/- 7.4 ng/mL at start of the study; P: = not significant). The initial correlation between serum leptin level and percentage of body fat persisted during follow-up. No correlation was found between insulin and leptin levels or between the variation of these two parameters during the study. Our study shows that the correction of hyperinsulinemia and insulin resistance in patients with CRF by SVLPDs is not accompanied by improvement in hyperleptinemia, which consequently does not appear to result from changes in carbohydrate metabolism.

Reduced parathyroid functional mass after successful kidney transplantation.BackgroundChronic uremia is responsible for secondary hyperparathyroidism (HPT II). Parathyroid secretion usually tends to normalize after kidney transplantation (KT), but the parameters of the reversibility of HPT II remain poorly defined, particularly the intrinsic mechanisms underlying the improvement of parathyroid function.MethodsThe kinetic functional parameters of the ionized calcium (iCa)/parathormone (PTH) relationship curve were studied in 11 patients with mild to moderate HPT II one and six months after successful KT. Hypercalcemia and hypocalcemia were induced, respectively, by CaCl2 and Na2-ethylenediaminetetraacetic acid (Na2-EDTA) infusions.ResultsThe mean glomerular filtration rate remained stable during follow-up. Basal PTH decreased from 195 ± 54 pg/ml before KT to 70 ± 12 pg/ml six months later (P < 0.005). During the tests, mean PTH levels decreased significantly between the two measured times for all iCa levels, indicating an improved parathyroid function. An analysis of the kinetic parameters of the curves showed significant decreases of the mean maximal and minimal PTH levels, respectively, from 340 ± 91 to 220 ± 30 pg/ml (P = 0.03) and from 25 ± 6 to 15 ± 5 pg/ml (P = 0.005). On the other hand, no change was noted in the parathyroid-cell calcium-sensitivity parameters (slope, set point) assessed using two different approaches, either the entire curve or the limited calcium-mediated suppression curve.ConclusionImprovement of the parathyroid function between the first and sixth months post-KT seems mainly attributable to a reduction of the parathyroid functional mass.

Resume Une denutrition proteino-calorique n'est pas exceptionnelle a un stade evolue de l'IRC, elle conditionnera la morbidite et la mortalite des premiers mois du traitement dialytique. La diminution de l'apport energetico-protidique qui accompagne la progression de l'IRC est en rapport avec la retention de molecules anorexigenes et constitue le principal facteur de denutrition auquel s'associent l'acidose metabolique, facteur d'hypercatabolisme, et des anomalies portant sur le metabolisme des principaux nutriments. L'apport proteique et energetique doit etre regulierement surveille, la persistance de troubles nutritionnels malgre le suivi medical et dietetique doit faire commencer sans tarder le traitement dialytique.

A low-protein, low-phosphorus diet (LPD) has been shown to improve insulin sensitivity in uremic patients; however, this improvement has not been studied at low physiologic concentrations of plasma insulin, and the metabolic pathways concerned with this improvement have not been located. We used the glucose clamp technique at a low (0.25 mU kg -1 . min -1 ) level of hyperinsulinemia associated with the infusion of D[6,6- 2 H 2 ] glucose to assess the insulin sensitivity of endogenous glucose production (EGP). Eight nondialyzed uremic patients were studied before and after 3 mo on an LPD providing 0.3 g/kg protein, 5-7 mg P/kg, and 146 kJ/kg (67% of energy as carbohydrates and 30% as lipids) per day, supplemented with ketoanalog amino acids. Postabsorptive plasma glucose and insulin declined after 3 mo of the diet (plasma glucose: 5.0 ± 0.1 mmol/L before compared with 4.7 ± 0.1 mmol/L after the LPD, P < 0.05; plasma insulin: 82.4 ± 20.7 pmol/L before compared with 48.8 ± 6.0 pmol/L after, P < 0.05). Postabsorptive glucose turnover rates did not change with the diet (2.06 ± 0.14 mg. kg -1 . min -1 before compared with 2.11 ± 0.17 mg. kg -1 . min -1 after LPD; NS). The insulin metabolic clearance rate was enhanced after the diet, so a lower level of hyperinsulinemia was obtained during the clamp (168.8 ± 28.1 pmol/L before compared with 115.2 ± 14.7 pmoVL after; P < 0.05). However, EGP was more easily inhibited after the diet (0.90 ± 0.31 mg. kg -1 . min -1 before compared with 0.30 ± 0.17 mg.kg -1 .min -1 after; P < 0.05), providing evidence of an improved insulin sensitivity of this parameter. This beneficial influence takes place at a physiologic level of hyperinsulinemia, and it probably plays an important role in the better glucose tolerance that has been reported in uremic patients on an LPD. An abnormal insulin sensitivity of EGP may participate in the disturbances of glucose metabolism in chronic renal failure.

Low protein diet in uremia: Effects on glucose metabolism and energy production rate. Low-protein diets (LPD) increase insulin-mediated glucose disposal in chronic renal failure (CRF), but the fate of the better utilized glucose and the effect on energy production rate are unknown. Using a two-step (1 and 5mU · kg−1 · min−1) euglycemic hyperinsulinemic clamp combined with indirect calorimetry, we studied the effects of a LPD (0.3g · kg−1 · day−1, supplemented with essential amino acids and ketoanalogs) in six patients suffering from chronic renal failure. After three months of diet, no significant change was observed concerning glomerular filtration rate, body wt, or arterial pH. In the postabsorptive state, plasma glucose and insulin levels were significantly lower, and energy production rose from 15.72 ± 0.48 to 17.16 ± 0.67Cal · kg−1 · min−1 (P < 0.05). Insulin-stimulated glucose oxidation (2.36 ± 0.29 vs. 3.37 ± 0.35mg · kg−1 · min−1; P < 0.05 at first clamp step) and nonoxidative disposal (P < 0.05 at both clamp steps) increased after LPD. This confirms that LPD ameliorates insulin sensitivity in CRF, even for low plasma insulin concentrations. Since energy production rate is increased by LPD, the caloric intake should be increased when protein intake is restricted.

Increased peroxidation of lipids in red blood cells (RBC) in patients with advanced chronic renal failure (CRF) reflects increased generation of reactive oxygen species (ROS), which may contribute to the metabolic damage induced by CRF and to its progression. We have evaluated parameters indicative of lipoperoxidation (LPO) of RBC at baseline in patients with CRF compared to controls, and the effects of a very low protein diet supplemented with amino and keto acids and vitamins A, C, E (VLPD) over a 6-month period. The presence of peroxidation damage in CRF patients before the administration VLPD was demonstrated by elevated levels of free malondialdehyde (MDA) (p.0003) and decreased levels of polyunsaturated fatty acids (PUFA), particularly C20:4 (p.001), C22:4 (p.0001) and C22:5 (p.0001) when compared to controls. Similarly, RBC vitamin E content was significantly decreased (p.0001) while enzymatic activities were unalterated. VLPD reduced erythrocyte LPO as suggested by (a) decreased levels of free and total RBC MDA (p.003 and p.03, respectively), (b) increased levels of PUFA, particularly C22:4 and C22:5 (p.003 and p.03, respectively), and (c) increased levels of vitamins A and E (p.001 and p.04, respectively) as compared to prediet results. Antioxidant enzyme activities were not modified. These results suggest that VLPD has a protective role against LPO of erythrocytes in patients with CRF.

R'esume Quarante cas de purpura rhumatoide de l'adulte (21 femmes, 19 hommes, d'âge moyen: 39 ans) sont etudies, issus d'un service de nephrologie (28 cas) et de medecine interne ( 12 cas). Les signes cutanes sont quasi constants (39 cas), sans particularite clinique ou histologique par rapport a ceux de l'enfant. Les manifestations digestives (23 cas) sont essentiellement des douleurs abdominales et des troubles du transit, les hemorragies restant rares. Elles sont, dans cette serie comme dans la litterature, moins graves que chez l'enfant. L'atteinte articulaire (22 cas)evolue parallelement au purpura et guerit sans sequelle. Le pronostic de l'affection est finalement le fait de l'atteinte renale, objectivee chez 33 de nos patients (82.5 %). Cette frequence elevee s'explique probablement par l'importance du recrutement nephrologique. Dans un tiers des cas elle est decouverte tardivement (jusqu'a 24 mois) ce qui souligne la necessite d'un suivi prolonge de ces patients. Comme chez l'enfant, l'hematurie et la proteinurie sont quasi constantes. La biopsie renale montre dans 58 % des cas une glomerulonephrite proliferative segmentaire et focale, avec depots mesangiaux d'igA 16 fois sur 21. En dehors du repos toujours preconise, le traitement est constitue par la corticotherapie seule dix fois, les corticoides et les immunosuppresseurs huit fois, l'association corticoides-immunosuppresseurs-plasmaphereses deux fois, la dapsone une fois. L'evolution de la nephropathie est connue chez 26 patients suivis en moyenne 37 mois: 11 guerissent completement, sept gardent des anomalies du sediment urinaire sans insuffisance renale, et huit developpent une insuffisance renale chronique terminale en 3 mois a 13 ans. Les facteurs de mauvais pronostic, dans notre serie, sont l'insuffisance renale initiale, l'HTA, et le jeune âge. Cette evolution pejorative peut s'expliquer par l'importance du recrutement nephrologique. Elle contraste avec le caractere aigu de l'affection chez l'enfant.

Hemodialysis with complement-activating membranes, such as cuprophane, induces neutropenia and expression of the granulocyte adhesion receptor Mac-1 (CD11b/CD18), while hemodialysis with noncomplement-activating membranes does not. Increased expression of CD11b by neutrophils may mediate cuprophane-induced leukopenia. However, the rebound granulocytosis that follows leukopenia is not fully understood. Ten patients on regular hemodialysis were included in a cross-over study. Hemodialysis was performed for 2 weeks with cuprophane and 2 weeks with polyamide, a high-flux noncomplement-activating membrane. At the end of each period, the following parameters were determined during a hemodialysis session: C5a concentration by enzyme immunoassay and the neutrophil expression of CD11b, LFA-1 (CD11a/CD18), and the antigen recognized by MoF11 (MoF11 Ag), a monoclonal antibody that recognizes activated neutrophils, by immunofluorescence flow cytometry. Hemodialysis with cuprophane induced an increase in C5a concentration and in the expression of CD11b and MoF11 Ag, which were maximal after 15 minutes of hemodialysis, at the nadir of neutropenia. CD11 b expression was maintained throughout hemodialysis, despite the reversal of neutropenia. Conversely, after peak expression, C5a and MoF11 Ag decreased as the neutrophil count increased to baseline values. Polyamide hemodialysis did not induce variations in C5a concentration, nor in CD11 b and MoF11 Ag expression. CD11a/CD18 expression remained stable during hemodialysis with both membrane types. Neutrophil activation, as determined by MoF11 Ag expression, was correlated with the evolution of neutrophil count and C5a concentration during cuprophane hemodialysis, while CD11 b expression was not correlated with neutrophil count throughout dialysis. A decrease in neutrophil activation could explain in part the detachment of neutrophils previously bound to endothelium and, therefore, the reversal of neutropenia. Hemodialysis with polyamide did not induce variations in either C5a levels, neutrophil count, or neutrophil membrane expression of CD11b and MoF11 Ag.

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.

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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.

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.