A young woman presented with arthralgia, a rash and dramatic haemoptysis, and renal involvement was indicated by proteinuria, haematuria and a rising serum creatinine. A systemic vasculitic disorder was suspected initially, but the diagnosis of Henoch-Schonlein purpura was established by the finding of mesangial IgA deposits on renal biopsy. Immunofluorescent study of renal biopsy material is vital to diagnosis where the clinical features of Henoch-Schonlein purpura and those of the systemic vasculitides with renal involvement prove to be indistinguishable.

The pharmacokinetics of the beta-blocking agents presently available render some subject to accumulation in renal or hepatic failure. Bisoprolol is one of the beta blockers possessing balanced clearance (both renal and hepatic clearance) which prevents such accumulation even in the case of complete failure of kidneys or liver. The single dose pharmacokinetics of bisoprolol were studied in patients with varying degrees of renal impairment and in healthy controls. Correlations were demonstrated between creatinine clearance and elimination half-life, mean residence time, area under the curve, total clearance and maximum concentration in those with renal dysfunction. The elimination half-life increased by a factor of 1.96 in those with severe renal dysfunction. Because of its balanced clearance, it is unlikely that accumulation of bisoprolol would occur beyond a factor of 2 on dosing to a steady state. The 48 hour plasma levels in the patients on dialysis were similar to those of the patients with severe renal dysfunction. This suggest that accumulation is unlikely, even in end stage renal failure. Bisoprolol may be used safely in patients with renal dysfunction. No adjustment of dose is necessary for those with mild to moderate dysfunction, but in severe or end stage renal failure the dose should not exceed 10 mg once daily.

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Serum oxalate is easily controlled in patients with chronic renal failure not yet on dialysis by dietary protein restriction but poorly controlled by both haemodialysis and continuous ambulatory peritoneal dialysis (CAPD). In the control of serum oxalate in chronic renal failure dietary protein restriction is effective in the pre-dialysis patient whereas both CAPD and haemodialysis are relatively inefficient in end-stage renal failure.

The inhibitory effect of omeprazole on gastric acid secretion was tested in a group of patients on haemodialysis for chronic renal failure. Single 30 mg doses almost totally inhibited basal acid output on both dialysis and non-dialysis days. Plateau acid output was reduced by a mean of 77% and 90% on non-dialysis and dialysis days respectively. The absorption and pharmacokinetic profile of omeprazole were not affected by dialysis. Omeprazole was not recoverable from dialysis fluid. It is concluded that omeprazole is a potent inhibitor of gastric acid secretion in patients with chronic renal failure, and its effect is not influenced by haemodialysis.