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OBJECTIVE: Assess the efficiency of estradiol programming in In Vitro Fertilization (IVF) with antagonists by comparing with classical long luteal agonist protocol. PATIENTS AND METHODS: It is a prospective randomized study, comparing 426 cycles in the arm estradiol antagonist with 412 cycles in the arm long agonist. Estradiol 4 mg/day begins on the 25th day of the previous cycle and continues during the menses until the first day of the stimulation which is from Thursday to Sunday whatever the beginning of the menses. The luteal protocol use Decapeptyl 0,1mg which begins on the 20th day of the previous cycle. RESULTS: Our two populations are similar. No pick-up has been done on Sunday. We have got significantly less oocytes and embryos in estradiol-antagonist (6,8+/-5,3 vs 7,6+/-5,7) and (3,7+/-3,2 vs 4,1+/-3,6) respectively. The ongoing pregnancy rate is comparable in the two groups: 28,6 % for estradiol antagonist 27,9 % for agonist for the whole population and 37 % vs 34,8 % respectively when at least one top embryo was transferred. DISCUSSION AND CONCLUSION: Programming antagonist cycles with estradiol allows the organization of the center; it is easy to implement and seems to give results as good as a long agonist protocol.

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Phosphorus (Pi) retention linked to chronic renal failure (CRF) favors secondary hyperparathyroidism (HPT). Reduction of Pi and protein intake has been shown to prevent the development of HPT in CRF. The aim of the present study was to assess in patients with advanced CRF the long-term effects on phosphate and calcium metabolism of a low-Pi (5-7 mg/kg/day), low-protein (0.4 g/kg/day) diet providing 300 mg/day calcium (Ca) and supplemented with amino acids and ketoacids, Ca carbonate (400-800 mg/day) and vitamin D2 (1,000 IU/day). Twenty-nine patients with advanced CRF (glomerular filtration rate (GFR) 13.7 +/- 4.5 ml/min) were selected for the study, on the basis of a follow-up of a least 2 years and a satisfactory compliance to the prescribed diet. At the start of the study, biological evidence of HPT was present with increased plasma PTH concentration (144 +/- 95 pg/ml), increased plasma Pi (1.57 +/- 0.33 mmol/l), an increase in alkaline phosphatase activity and plasma osteocalcin concentration. Plasma PTH concentration was positively correlated with plasma Pi and inversely with plasma Ca concentrations and GFR. Pi and protein restriction induced a significant correction of HPT within 3 months after starting the diet. After 2 years of diet, despite the diminution of GFR (11.1 +/- 3.7 ml/min, p < 0.0001), plasma PTH was still lower than at the start of the diet (88 +/- 57 pg/ml, p < 0.01), as was plasma Pi (1.32 +/- 0.24 mmol/l, p < 0.001), total plasma Ca being higher (p < 0.01). Plasma PTH levels were correlated only to plasma Ca concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

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Several reports emphasize the adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) on renal function. We have observed over the last 10 years seven cases of acute renal failure (ARF) due to immune interstitial nephritis in children. A recommended oral or rectal dose of niflumic acid was prescribed for ear-nose-throat disorders. Length of exposure was 1-5 days. Clinical symptoms (oedema, oliguria or anuria) appeared between 3 and 6 days. Three patients had previously received the drug. Hypersensitivity signs (fever, skin rash, eosinophilia, and/or increased IgE) were present in all cases, leukocyturia in five cases, and haematuria in six cases. Renal biopsy showed interstitial lesions with lymphocyte, eosinophil, and plasma cell infiltrates without tubular cell necrosis. Glomeruli were normal on light-microscopy, except in one patient. Electron-microscopy showed extensive podocyte fusion in two patients, who had clinical and laboratory evidence of nephrotic syndrome (NS). ARF rapidly disappeared after NSAID withdrawal, except in two patients whose renal failure was irreversible despite methylprednisolone bolus. ARF is very rare in children treated with niflumic acid. When ARF occurs, different pathophysiological mechanisms are involved but the most common is immunological.

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Leucocytic Na+ K+ pump activity was assessed in 20 patients with advanced renal failure. Na+ K(+)-ATPase activity was reduced when compared with the values obtained from normal subjects (101.8 +/- 48.6 versus 165.13 +/- 8.9 microM of Pi hr-1.g-1; P less than 0.001) and the mean 86Rb uptake by U 937 cells was depressed by 38% after the addition of patients' sera. Subsequently, patients were put on a diet providing 0.3 g protein/kg body weight daily and supplemented with ketoacids. After three months of dietary treatment Na+ K(+)-ATPase activity increased to 142 +/- 48.3 (P less than 0.01) and reached normal values at the sixth month (162.8 +/- 54.70 microM of Pi hr-1.g-1; P less than 0.001) whereas 86Rb uptake increased by 23 percent when compared to initial values. These data suggest that among the different mechanisms which have been advanced to explain the defects in the Na+ pump observed in uremic patients, circulating inhibitors deriving from alimentary protein intake may affect cation transport.

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The pregnancy rate per transfer does not appear to be increased if the embryos are placed in the Fallopian tube rather than using in-vitro fertilization or inserting the gametes into the tubule ampulla. Consequently, the indications are specific to particular cases.

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Tissue insulin sensitivity was measured by the glucose clamp technique in 8 uremic insulin-dependent diabetic patients before and after 3 months on a low-protein diet (LPD) providing daily 35 kcal/kg body weight, 60% of the caloric supply being obtained from carbohydrates. An improvement in tissue insulin sensitivity was observed for each steady state of the clamp and daily insulin requirements decreased significantly from 38.3 +/- 3.2 to 28.2 +/- 2.5 units (p less than 0.01) in spite of an increased carbohydrate intake. It is suggested that LPD lowers the production and accumulation of uremic toxins interfering with insulin sensitivity.

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Effects of a low protein (0.3 g/kg/day) diet on glucose tolerance and tissue insulin sensitivity were studied in 25 non-diabetic and eight insulin-dependent diabetic uremic patients before and three months after dietary treatment. Carbohydrates accounted for 65% of the caloric intake in the first group and 57% in the second. In the first group, a 50 g oral glucose tolerance test showed that after three months blood glucose was significantly reduced at T60 (P less than 0.05) and serum insulin at T0, T30 (P less than 0.05) and T60 (P less than 0.02). Ten patients of the first group underwent an euglycemic, hyperinsulinemic clamp study; the tissue sensitivity to insulin index of all three clamp periods improved (P less than 0.01 for the first and second, P less than 0.02 for the third). Five patients in the second group underwent a euglycemic clamp study; glucose metabolism increased with each clamp period. Concomitantly, their daily insulin requirements decreased from 37.2 +/- 3.1 to 24.8 +/- 2.7 U/day (P less than 0.05). This conspicuous improvement observed in both groups might be related to a decrease in uremic toxin(s) derived from protein intake. Beneficial results on atherosclerosis and cardiovascular pathology may occur from the reduction of hyperinsulinism.

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Seven years after a cadaver kidney transplantation a 33-year-old man presented with a monoclonal gammopathy secondarily complicated by AL amyloidosis mainly expressed as a sicca syndrome, gammopathy that ultimately developed into multiple myeloma. The mechanisms responsible for the occurrence of monoclonal gammopathy in renal transplant recipients are discussed.

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We report a case of Castleman's disease of multifocal plasma-cell type revealed by a severe general weakness, associated to a nephrotic syndrome with renal failure. The characteristic aspects of lymphoid hyperplasia with hyalinization of follicles and interfollicular vascular proliferation were observed in mesenteric lymph nodes, the spleen was involved by an infarcted localisation of Castleman's disease. The glomerular lesions were consistent with a proliferative mesangial glomerulonephritis. The removal of the spleen and of the mesenteric nodes involved by the disease, associated with a steroid course was curative. The nephrotic syndrome appears to be etiologically related to the presence of the Castleman's tumor. The removal of the tumor relieves the proteinuria and the renal failure as in other cases reported in the literature.

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