Background: Free radical damage in conjunction with antioxidant deficiency has been observed in patients with chronic renal failure. In this larger study, we report whether treatment with antioxidant coenzyme Q10 can decrease progression or reverse chronic renal dysfunction and delay the need for dialysis. Design: A randomized, double-blind, placebo-controlled trial of coenzyme Q10 vs. placebo for a period of 12 weeks. Subjects and Methods: All patients with proven chronic renal failure with a history of declining renal function for at least the last 12 weeks were stratified into haemodialysis or no dialysis and blindly randomly divided into coenzyme Q10 (n~48) and control (n~49) subgroups with the help of computer-generated numbers. Results: Both coenzyme Q groups showed a significant decline in serum creatinine, blood urea nitrogen and a significant increase in creatinine clearance and urine output compared with the placebo groups on dialysis and no dialysis over the 12 weeks of the trial, whereas the baseline values of these characteristics showed no significant difference between the concerned subgroups. The frequency of dialysis and the proportion of subjects taking dialysis were not significantly different at entry to the study. However, after 12 weeks, the number of subjects taking dialysis was significantly less in the antioxidant subgroup than the placebo subgroup (12 vs. 24; pv0.02). Plasma levels of thiobarbituric acid reactive substances, diene conjugates and malondialdehyde, indicators of oxidative damage, showed a significant reduction whereas antioxidant vitamins E and C and beta-carotene showed a significant increase in the antioxidant subgroups compared with the control groups. After 12 weeks of follow-up, all patients were alive. Conclusions: Treatment with coenzyme Q10 reduces serum creatinine and blood urea nitrogen and increases creatinine clearance and urine output in patients with chronic renal failure. This treatment also decreases the need for dialysis in patients on chronic dialysis. Approximately one-fifth of the patients showed no response to treatment.

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We conclude that immunological factors, as well as non-immunological factors such as CrCl, SCr and dyslipidaemia, play important roles in the pathogenesis of graft rejection and renal graft dysfunction.

Recent data regarding the clinical and histopathologic spectrum of crescentic glomerulonephritis (CSGN) among the Indian adult population is unknown. Our aim is to study the clinicopathological features and outcome of CSGN. It is a retrospective observational study from a tertiary care hospital in India over 3.5 years. Biopsy-proven cases of CSGN (i.e., >50% crescents in glomeruli) were included in the study. Cases with insufficient data were excluded. There were 34 cases of CSGN, accounting for an incidence of 5.5% among kidney biopsies. The mean age was 32.2 ± 16.09 years, with male to female ratio of 12:22. Clinical presentations of CSGN include rapidly progressive glomerulonephritis in 23 (67.7%), chronic renal failure (CRF) in seven (20.5%), nephrotic syndrome in two (5.8%) and acute nephritic syndrome in two (5.8%) patients. The immunological profile of CSGN showed MPO-ANCA in nine (26.4%), PR3-ANCA in one (2.9%), both PR3 and MPO-ANCA in one (2.9%), anti-GBM antibody in five (14.7%) and lupus nephritis in six (17.6%) patients. All the three antibodies were present in one patient. The percentage of glomeruli showing crescents were 100% in nine (26.4%) and ≥80% in seven (20.5%) patients. Type of crescents seen were cellular in 11 (32.3%) and fibrocellular in 22 (64.7%) patients and fibrous in one (2.9%) patient. Interstitial fibrosis was found in seven (20.5%) patients. Dialysis dependency was seen in 11 (32.3%) patients. After 3 months of follow-up, mortality was seen in three (8.8%), remission in eight (23.5%), CRF in 15 (44.1%) and ESRD in five (14.7%) patients. CSGN carries a poor prognosis. The disorder may have an insidious onset and a slowly progressive course. ANCA, anti-GBM-antibody and anti-dsDNA can coexist in CSGN.