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Renal involvement is an unusual complication of human visceral leishmaniasis (VL). The kidney lesions are characterized more by interstitial damage than glomerular or vascular damage. This case represents a 20 years-old man admitted with pancytopenia, purpura, acute renal failure, and nephrotic syndrome associated with heavy proteinuria. The diagnosis of VL was made on bone marrow smear cytology where Leishmania amastigotes were found. The renal biopsy revealed a segmental necrotising glomerulonephritis with 70% crescents. Treatment with liposomal amphotericine B alone has been ineffective on the course of renal failure, however, partial recovery was obtained after the administration of high dose corticosteroids. We present the various clinical, biological, and histological aspects of this case, from the south of France. It gave us the opportunity to discuss these unusual manifestations of immunomediated necrotising skin and renal lesions.

Chronic inflammation is very common in patients on maintenance dialysis. It is associated with an increase of many cytokines (especially: IL-1, IL-6 and TNF alpha). This inflammation leads to hormonal dysregulation (leptin, adiponectin, insulin). Increase in cytokines is associated with a high cardio-vascular morbi-mortality for general population as well as for uremic patients. Many metabolic abnormalities are due to chronic inflammation: protein catabolism, anorexia and many others. Among them, the "metabolic" syndrome includes adiposis, dyslipemia, insulinoresistance and high blood pressure very often present in chronic uremic patients. It is still unknown whether anti-inflammatory treatments would improve inflammation consequences in dialysis.

Since recent years, a number of systematic reviews have been published in the renal field. These publications will be used to develop the concept of evidence based nephrology. The design and quality of renal systematic reviews relies on technical skills and efficient trials search. The reasons for discrepancies that are sometimes reported between systematic reviews and controlled clinical trials are now better understood and may be partly explained by inadequate trial recovery and publication biases. The applicability of evidence findings is not always an easy task on patients level. The example of the low protein diet in chronic renal failure highlights such caveats. However, producing high level systematic reviews in the renal field may be of great help to clarify the use of controversial treatments and to design new studies in the renal field.

Despite numerous progresses, including extracorporeal epuration, acute renal failure (ARF) remains associated with a high level of mortality and morbidity, particularly in intensive care unit. Experimental research on different acute renal failure models has clearly shown that growth factors and particularly Insulin-like Growth Factor I (IGF-I) can reduce renal injury, improve renal recovery and even reduce mortality. IGF-I, that is locally produced in injured renal tubules, promotes the proliferation and differentiation of new tubular cells. Moreover, IGF-I carriers (IGFBPs) and IGF-I receptor are altered in ARF and modify the growth factor bioactivity. To date, only two clinical trials studied IGF-I treatment in the ARF condition. Other studies are required to demonstrate a role for IGF-I in treating or preventing acute renal failure.

The adult protein turn-over daily affects 250 grammes, which is equivalent to four times the average daily protein intake. Regulation of synthesis and catabolism appears to occur by independent ways. These systems are altered during the nephrotic syndrome and ultimately lead to a loss of total body nitrogen and a risk for malnutrition. Indeed, during the nephrotic syndrome, muscle protein synthesis is further impaired as the urinary protein losses increase. This may suggest that anabolic compounds are lost in the urine of such patients. A moderate protein restriction (0.8 g/kg BW/day) allows a reduction in proteinuria, as well as pharmacological agents (ACE inhibitors) and should therefore slow the progressive renal insult.

We report the renal and metabolic effects of a 40 day administration of recombinant human growth hormone in a 31 years old diabetic and GH-deficient patient who underwent a kidney and pancreas transplantation. The data show an increase in glomerular filtration rate, tubular reabsorption of phosphate, and plasma hemoglobin level. Anabolism is suggested from a decrease in serum urea nitrogen and an increase in muscle mass (increase in plasma creatinine). These positive effects might be partly explained by an overcome of endogenous growth hormone resistance when administering pharmacological doses of recombinant growth hormone.

Accurate methods of measuring glomerular filtration rate are usually considered as expansive and time consuming. Therefore, alternative methods (creatinine clearance, either calculated or measured, reciprocal plasma creatinine, slopes of creatinine vs time) have frequently been used to assess the rate of progression of renal failure and predict the time of dialysis. The present review underlines the limitations of such techniques frequently underestimated in recent trials intending to evaluate the potential benefit of protein restriction. It delimitates the restrictive conditions in which such methods could be used for clinical but not research purposes.