Dialysis anaemia caused by subacute zinc toxicity.

Nine out of ten patients dialysed in a satellite dialysis unit became severely anaemic over a 2-month period. The onset of anaemia coincided with the installation of a new galvanised-iron water softener in the dialysate water-supply system. An activated carbon filter was installed and haemoglobin levels returned towards previous values. Two patients on home dialysis showed similar falls in haemoglobin after the installation of galvanised iron piping in their dialysate water-supply systems; these problems also resolved after carbon filtration of the dialysis water. It is suggested that elution of zinc from galvanised iron can cause anaemia in dialysis patients. Carbon filtration removes of 95-99% of the zinc eluted.

Membranous nephropathy long-term follow-up and association with neoplasia.

A ten years follow-up has been made on 66 patients with membranous glomerulonephritis. Eighty per cent of them showed nephrotic syndrome, one third elevated diastolic pressure and in 50% of the patients the GFR was reduced. Histopathologic stating and evolution were made as described by Ehrenreich histology with clinic and prognosis. Seven of 76 cases (11%) showed association with neoplasia; different pathogenetic hypothesis could be risen by this observation. The five year survival was 84% and the ten year survival about 50%. Increasing age and the presence of nephrotic syndrome mainly contribute to a poor prognosis.

Membranous nephropathy. Long-term follow-up and association with neoplasia.

Sixty-six patients of all ages whose renal biopsy appearances satisfied strict criteria for the histopathological diagnosis of membranous nephropathy were studied and followed for a mean of 5-4 years (range 1 to 20 years). From initial investigation seven patients were found to have associated neoplasia, and in two patients the condition followed treatment with a mercurial diuretic and gold. One patient was Australia antigen positive. Two patients developed renal vein thrombosis, but in both this appeared to follow not precede their nephrotic syndrome. In the remaining 56 patients there was no associated factor. During the follow-up period, approximately one-quarter of the patients (15) died, nine from renal failure; one-quarter (10) had a persistent nephrotic syndrome, another one-quarter (15) proteinuria of lesser degree. The final one-quarter (16) are now in complete remission. The prognosis of the 54 patients with an initial nephrotic syndrome was poorer than the 12 with lesser proteinuria and no oedema at onset; five of 11 children were in complete remission when last seen. All but one of the nine patients who developed terminal chronic renal failure 4 to 18 years from onset had an unremitting nephrotic syndrome, eight of the 10 currently alive with a persistent nephrotic syndrome have reduced renal function. Renal functional deterioration did not occur in the absence of proteinuria. There was only slight correspondence between the stage of biopsy appearance, glomerular filtration rate at time of biopsy, time of the biopsy from apparent onset, or status at last follow-up. Staging is therefore of limited prognostic value. Twenty-two patients were treated with corticosteroids for 2 to 36 months; we detected no short or long-term benefit when compared to patients not so treated.

Urinary excretion of C3 antigen in glomerulonephritis.

C3 and fibrin degradation products (F.D.P.) have been measured in early morning urine samples from 38 normal people and 123 patients with glomerulonephritis. Normal urine contained less than 0.3 mug of either antigen per ml. C3 and F.D.P. were both detected in the urine of many patients with glomerulonephritis. Levels above 1 mug/ml were exceptional in patients with "minimal change," and the highest excretion of both antigens occurred in mesangiocapillary glomerulonephritis, membranous nephropathy, and focal glomerulosclerosis.Both C3 and F.D.P. excretion showed considerable variation with time, with parellel fluctuations in the two antigens. These fluctuations did not depend on the total protein leakage and suggest that the complement and clotting sequence are closely related in these glomerular disorders.