A retrospective study of the clinical records and biopsy specimens of all transplants performed between 1974 and 1987 was carried out. Recurrent glomerulonephritis was diagnosed only in those patients who had precise histological classification of their original disease. Of a total of 737 transplants performed in 633 recipients. 603 were from cadaveric and 134 from living related donors. Of 295 patients who were clinically classed as having chronic glomerulonephritis, histological confirmation was available in 156 (54%) as follows: membranoproliferative glomerulonephritis 34%, diffuse proliferative glomerulonephritis 27%, crescentic glomerulonephritis 13% IgA neuropathy 10%, focal sclerosing glomerulonephritis 10%, and membranous nephropathy 7%. There were 24 cases of recurrence in 23 recipients. Of these, 16 occurred in living-related and 8 in cadaveric grafts. Membranoproliferative glomerulonephritis recurred in 14 (8 type I and 6 type II), focal sclerosing glomerulonephritis in 5, IgA neuropathy in 3, crescentic glomerulonephritis in 1 and membranous nephropathy in 1. Graft failure occurred in 13 patients (54%) and was directly attributable to recurrent disease in 12. Membranoproliferative glomerulonephritis caused 8 graft losses, focal sclerosing glomerulonephritis 2, IgA 1 and crescentic glomerulonephritis 1. Recurrence caused graft loss in 50% of cases in which it occurred. The overall incidence of recurrence was 18%. In contrast to other series, a significantly higher incidence of recurrence was seen in our living-related group.

Four patients on continuous ambulatory peritoneal dialysis (CAPD) developed large, symptomatic pleural effusions after commencing peritoneal dialysis. Pleuroperitoneal fistula in each case was diagnosed by the presence of a high glucose content in pleural fluid, with a normal corresponding blood sugar, and was confirmed by isotope or contrast peritoneography. Two patients had their effusions drained percutaneously, and then underwent pleural sclerosis with intracavitary tetracycline. Two patients had a thoracotomy performed, of which no fistula was identified in one case, and the other patient underwent pleurectomy. All four patients successfully recommenced CAPD several weeks after therapy, without recurrence of effusions. We conclude that pleuroperitoneal connections associated with CAPD do not mandate cessation of peritoneal dialysis and conversion to maintenance haemodialysis. Definitive diagnosis requires aspiration of pleural effusions for glucose estimation. Contrast or isotopic peritoneography is helpful in localising the fistula, but in our experience did not alter management. Simple sclerotherapy is effective and avoids the need for a formal thoracotomy.

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1. Lisinopril and enalapril were administered as 2.5 mg single doses and as eight single daily 2.5 mg doses to separate groups of six patients with chronic renal failure. Patients were receiving regular haemodialysis. 2. In the absence of haemodialysis, the decline in plasma concentrations of lisinopril and enalaprilat was extremely slow and plasma concentrations were generally high. 3. Haemodialysis had large effects on plasma concentrations of lisinopril and enalaprilat. A 4 h period reduced plasma concentrations of both drugs by around one-half and often by significantly more than this. Even 1 or 2 h of haemodialysis had significant effects. 4. Haemodialysis plasma clearance was similar for both drugs with mean values of the order of 40 ml min-1. Clearance did not markedly differ when measured after 1, 2 or 4 h of haemodialysis or after single or multiple doses of lisinopril or enalapril. 5. The design of dosage regimens of both lisinopril and enalapril for patients with severe renal impairment or chronic renal failure should take into consideration the use and effects of haemodialysis.

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