Focal segmental glomerular sclerosis in two patients with Addison's disease: any more than fortuitous development of glomerular disease?

Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison's disease. We report the clinical and biological conditions of 2 patients with Addison's disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison's disease.

Plasmapheresis induced recovery from renal failure in mesangiocapillary glomerulonephritis of acute onset.

Plasmapheresis (PE) was used in the treatment of three patients with biopsy proven mesangiocapillary glomerulonephritis (MCGN) of acute onset and renal failure. The percent of glomeruli with extracapillary proliferation varied from 40 to 90 per cent. Following PE, there were reductions in serum creatinine of 66 per cent, 61 per cent and 82 per cent in patients, one, two and three respectively. Plasmapheresis proved effective in a second episode of renal failure in patient three. After the completion of PE, renal function has remained stable in all patients for periods ranging from two to 12 months. However, haematuria and heavy proteinuria persist in every case. PE appears to facilitate recovery from renal failure in MCGN of acute onset, possibly by removing circulating mediators of acute inflammatory glomerular damage.