There is experimental evidence to suggest that hypercholesterolaemia may play a pathogenetic role in progressive glomerular injury. We investigated the effect of cholesterol-lowering therapy on the progression of diabetic nephropathy in 34 patients with non-insulin-dependent diabetes mellitus. Patients were randomly assigned in a single-blind fashion to treatment with either lovastatin, an HMG CoA reductase inhibitor (n = 16; mean dose 30.0 +/- 12.6 mg/day) or placebo (n = 18) for 2 years. Renal function was assessed by serially measuring the serum creatinine, glomerular filtration rate (using Cr51-EDTA), and 24-h urinary protein excretion. Lovastatin treatment was associated with significant reductions in total cholesterol (p < 0.001), LDL-cholesterol (p < 0.001) and apo B (p < 0.01), the reductions at 24 months being 26, 30 and 18%, respectively. Beneficial effects on serum triglyceride, HDL-cholesterol and apo A1 levels were also observed. Lp(a) showed no significant change in both groups. Glomerular filtration rate deteriorated significantly in the placebo group after 24 months (p < 0.025) but showed no significant change in the lovastatin-treated patients. The increase in serum creatinine was statistically significant (p < 0.02) in placebo-treated patients at 12 and 24 months, and in the lovastatin group after 24 months. Twenty-four hour urinary protein excretion increased in both groups (p < 0.05). Lovastatin treatment was not associated with significant elevations in liver or muscle enzymes. We conclude that effective normalisation of hypercholesterolaemia may retard the progression of diabetic nephropathy.

A retrospective single-center cohort study was conducted on 35 patients with diffuse proliferative (WHO type IV) and/or membranous (type V) lupus nephritis (22 with type IV, 6 with type V, and 7 with type IV plus V) who had been treated with a sequential regimen comprising prednisolone and cyclophosphamide during active disease, followed by low-dose prednisolone and azathioprine maintenance. The follow-up period was 33.2 ± 4.5 months. At presentation, 32 (91.4%) patients were nephrotic, and an abnormal serum cre-atinine level was noted in 14 (48.3%) patients with type IV changes. Cyclophosphamide was given for 26.8 ± 2.8 weeks. 33 (94.3%) patients achieved complete or partial renal remissions: 77.3 and 22.7% of the type IV patients, 16.7 and 66.6% of the type V patients, and 14.3 and 71.4% of the type IV plus V patients, respectively (p < 0.0001 for type IV versus type V and for type IV versus type IV plus V). The duration of therapy before renal remissions and normalization of C3 were attained was similar among the three groups of patients. Disease relapse occurred in 4 (18.2%) of 22 type IV patients and in 1 of the 5 type V patients in remission. Mortality was not observed, and none of the patients had an increase in serum creatinine level to double the baseline value. Adverse effects related to therapy included: hair loss (42.9%), transient amenorrhea (53.6%), leukopenia (11.4%), febrile episodes (14.3%), and herpes zoster (28.6%). We conclude that sequential use of prednisolone and cyclophosphamide followed by low-dose prednisolone and azathioprine can achieve favorable therapeutic results in the majority of patients with diffuse proliferative and/or membranous lupus nephritis, without excessive toxici-ties.

Twenty-one episodes of fungal peritonitis occurred over 35 months among 290 patients on CAPD, accounting for 6.3% of all peritonitis episodes. Patients with more frequent bacterial peritonitis were at higher risk of developing fungal peritonitis, and 28.6% of cases followed antimicrobial therapy. Candida species accounted for 85.7% of cases. Oral fluconazole was used as initial therapy in all patients, which was followed by catheter removal if peritonitis failed to improve. The cure rate with fluconazole therapy alone without catheter removal was 9.5%. Fluconazole plus catheter removal, the latter necessitated in 85.7% of cases, resulted in a cure rate of 66.7%. The remaining 3 (14.3%) patients responded to intravenous amphotericin given as salvage therapy. Disease-related mortality was 14.3%. Reinsertion of dialysis catheter was attempted in 15 patients and CAPD was successfully resumed in 13 (86.7%). We conclude that oral fluconazole can be safely used as initial therapy in patients with fungal peritonitis complicating CAPD. Although catheter removal was necessary in the majority of patients, this sequential approach resulted in a relatively low prevalence of peritoneal adhesions and subsequent CAPD failure.

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The characteristics of 5 patients who developed tuberculous peritonitis while receiving long-term peritoneal dialysis (PD) are presented. There were 2 males and 3 females. 3 patients were on intermittent and 2 were on continuous ambulatory peritoneal dialysis when tuberculous peritonitis was first diagnosed. None of the patients had recently received immunosuppression therapy or were diabetics. The clinical presentations were similar to other forms of peritonitis complicating PD except for a more insidious onset. As extraperitoneal involvement and peritoneal lymphocytosis were rarely present, the diagnosis was mainly dependent on the direct demonstration of Mycobacterium tuberculosis with smear (1 patient) and culture (4 patients). In 1 patient with a pleuroperitoneal communication, the diagnosis was made by pleural biopsy and a positive response to antituberculous therapy. All patients responded to treatment with a combination of three antituberculous drugs which included streptomycin, isoniazid, rifampicin and pyrazinamide. Two patients were transferred to hemodialysis. In 3 patients, peritoneal dialysis was continued. Peritoneal clearance and ultrafiltration capacity were unchanged for up to 16 months after treatment in 2 patients who continued peritoneal dialysis but was reduced by 30 and 50%, respectively, in the remaining patient. Only 1 patient died, but her death was not directly related to tuberculous peritonitis. It was concluded that with a high index of suspicion and early institution of treatment, tuberculous peritonitis complicating PD can be successfully treated with low mortality and without compromising the dialysis capacity of the peritoneal membrane.

Three hundred and thirty-nine dialysis patients from two centres (278 patients on continuous ambulatory peritoneal dialysis (CAPD) and 61 on maintenance haemodialysis (HD) were tested for antibody against hepatitis C virus (anti-HCV) using first-generation enzyme immunoassay kits (Ortho Diagnostics). Anti-HCV was detected in five (1.8%) CAPD patients and ten (16.4%) HD patients (P less than 0.00001). Anti-HCV was confirmed to be positive in three (1.1%) CAPD patients and eight (13.2%) HD patients using neutralisation enzyme immunoassay kits (Abbott Laboratories). The marked difference in prevalence of anti-HCV among CAPD and HD patients was related to a significantly greater transfusion requirement of the HD patients. All the anti-HCV positive patients had been transfused. The risk of HCV infection was significantly increased in those who had received more than five units of blood. Four (26.7%) anti-HCV positive patients had one or more episodes of elevated serum alanine aminotransferase (ALT) values.

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