In this study 43 patients with idiopathic nephrotic syndrome were randomly distributed into 2 age- and sex-matched groups. The first group was given fluvastatin while the second was used as control. The cases in the 2 groups were evaluated clinically, biochemically (creatinine clearance, albumin, 24-hour proteinuria, and lipogram), neurologically, and histopathologically (examination of renal biopsies obtained basally and after 1 year of treatment with fluvastatin). In the fluvastatin-treated group but not in the control group, we observed a significant reduction in cholesterol, low-density lipoprotein, and triglyceride. Clinical and laboratory assessment showed satisfactory tolerance of the drug by the patients. Proteinuria, serum albumin and creatinine clearance values were significantly better in the statin-treated patients. There was no difference in glomerular sclerosis between the 2 groups while interstitial fibrosis and renal fat deposits were less in the statin-treated group. The reduction in renal fat deposits in the statin-treated group was highly significant, while that of interstitial fibrosis was not. We conclude that: (1) statin can be safely and effectively used in the treatment of dyslipidemia in patients with persistent idiopathic nephrotic syndrome; (2) control of dyslipidemia in nephrotic patients is associated with better control of proteinuria and creatinine clearance; (3) statin treatment may cause regression of renal fat deposits in patients with nephrotic syndrome, and (4) longer term studies are still required to study further possible beneficial effects on renal histology and disease progression.

In an attempt to study the impact of HCV viremia on renal transplant clinical course and outcome, we prospectively followed 133 HBsAg-negative end stage renal disease (ESRD) patients, in whom HCV-RNA-PCR results were available, from the pre- to post-transplant period. Eighty (60%) ESRD patients tested PCR-positive, of these, 12 (15%) were anti-HCV negative by second generation ELISA. The viremic patients had a longer time on dialysis (p < 0.001), received more blood units (p < 0.001) and had a higher frequency of pre-transplantation liver disease (p < 0.001). Further, 41% of PCR-positive patients gave a history of antischistosomal treatment compared with 23% of PCR-negative ones (p = 0.048). Recipients with and without HCV viremia were followed for a mean of 31.8 ± 5.8 (range 6–42) months and 29.8 ± 9 (range 6–41) months respectively, p = 0.14. While the prevalence of HCV viremia increased from 60 to 64% at the last follow-up, the anti-HCV seroprevalence decreased from 63 to 61%. PCR-positive patients had higher rates of both acute (p = 0.005) and chronic (p < 0.001) liver disease after transplantation compared with PCR-negative patients. However, none of our HCV RNA positive recipients developed a fulminant liver disease or hepatic failure until the last follow-up. Stepwise logistic regression analysis identified pre-transplant liver disease (Odds ratio = 2.4; p = 0.07) and a cumulative corticosteroid dose in excess of 15 g at the last follow-up (Odds ratio = 3; p = 0.03) as independent predictors of post-transplant hepatic dysfunction in PCR-positive patients. Azathioprine was discontinued due to hepatic dysfunction in a significantly (p = 0.005) higher proportion of viremic patients compared with the non-viremic ones. There were no significant differences between PCR-positive and -negative patients in terms of frequencies and individual causes of graft and patient losses. Our results demonstrate that HCV infection is extremely prevalent in Egyptian hemodialysis patients and is responsible for most hepatic dysfunctions after transplantation. Although HCV viremia did not negatively affect graft or patient outcome until 31 months post-transplantation, the authors would recommend that a viremic patient should have a liver biopsy before transplantation and be immunosuppressed with caution post-transplantation. A longer follow-up may be required to exclude increased rates of HCV-induced hepatic mortalities.

In children with minimal change nephrotic syndrome (MCNS), the steroid dependent group constitutes an especially difficult case for management. Patients in this group are prone to serious steroid side effects. Additionally, alkylating agents commonly fail to maintain remission and expose patients to more side effects. Therapy with the immunostimulant drug levamisole may therefore be another option in the attempt to maintain remission with minimal side effects. We prospectively treated 20 of our steroid dependent primary MCNS patients with levamisole. All patients were children, with an age range of 3-15 years; 16 were boys and 4 were girls. Remission was firstly induced by steroids, then levamisole was added in a dose of 2.5 mg/kg body weight on alternate days for 6 months. During this period we attempted to withdraw steroids completely and maintain patients on levamisole alone. We followed up our patients for the occurrence of relapse and side effects during this period and for a further 6 months after stopping levamisole. In 11 out of 20 children (55%), we successfully stopped steroids for more than 2 weeks. At the end of the 6-month treatment period (i.e. after 4 months of steroid discontinuation), ten patients (50%) were maintaining remission on levamisole alone. At the end of the 12-month study period (i.e. after 6 months of levamisole discontinuation), five patients (25%) were still in remission without any treatment for the previous 6 months. No significant side effects were reported during levamisole therapy. None of the patients developed neutropenia, but the leukocyte count showed a significant reduction in those who responded to levamisole treatment. We concluded that levamisole therapy for 6 months is a safe and perhaps effective therapy in a subset of children with steroid dependent MCNS to enable an otherwise infeasible withdrawal of steroids. This may be worth a trial before other types of more hazardous adjunctive therapies are considered.

In this study 240 patients with active Schistosoma mansoni infection with no symptoms suggestive of glomerular disease were subjected to investigation. All were evaluated clinically and their urine was examined for proteinuria. Out of the 240 patients 48 (20%) had proteinuria as detected by the dipstick test. All these patients were found to be free of any secondary cause other than schistosomiasis which could explain their proteinuria. Out of these 48 patients, 15 agreed to be subjected to kidney biopsy. When examined by light microscopy and immunofluorescent microscopy, kidney biopsies showed positive findings in 8 cases. These were mainly focal mesangial proliferation and immunofluorescent deposits which were mainly IgM and C3. We have concluded that early kidney lesions could be detected in 20% of this particular group of patients.

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