In a retrospective study of the effect of treatment in biopsy-proved idiopathic membranous nephropathy, 91 adults and 12 children were followed for periods up to 29 years after clinical onset (mean, 6.5 years). Forty-four were treated with corticosteroids, 15 with corticosteroids and immunosuppressants; 44 had no treatment and served as a control group. Clinical cure and improvement were significantly greater in the treated than in the nontreated group (P less than 0.01). The recurrence rate, occurrence of renal failure and probability of death were significantly greater in the nontreated group, although some of these patients eventually showed improvement. Prognosis was better in patients who responded to therapy. These data strongly suggest that steroid therapy is beneficial in patients with membranous nephropathy.
Renal biopsy specimens of 16 adult patients with nephrotic syndrome and focal glomerular sclerosis were examined by light and electron microscopy. Particular attention was paid to alterations of podocytes. Except for loss of foot processes, five patients had no podocyte changes, five had mild changes and six had severe changes. Of the last group (group III), four patients were heroin addicts, the fifth had infectious mononucleosis and the sixth, an apparent idiopathic disease; five patients were males, 16 to 25 yr old. Podocyte changes consisted of cytoplasmic degeneration, detachment of epithelial cells from basement membranes, with filling of resulting space by cell debris and new membranes. Underlying capillaries were often collapsed. Repeat biopsies in three patients in group III revealed progression of lesions, paralleling rapid clinical deterioration. It is concluded that some cases of focal glomerular sclerosis are associated with severe damage to podocytes which may be caused by drugs, infection or unknown factors and may contribute to the development and progression of the glomerular lesions.
Thirty-one specimens of tissue were obtained from 15 renal allografts 3-96 months after transplantation and studied by light, electron and in some cases also by immunofluorescence microscopy. All patients had a degree of renal insufficiency and almost all had proteinuria and moderate hypertension; nephrotic syndrome was present in one and hematuria in two. On histological examination one patient showed cellular proliferation suggestive of glomerulonephritis (recurrent or de novo) and another patient had numerous crescents. The most frequent glomerular lesion was widening of the lamina rara interna with subendothelial accumulation of finely granular material, formation of new subendothelial basement membrane and deposition of microfibrils and fine filaments. The mesangial changes were mainly those of mesangiolysis and mesangial sclerosis with deposition of mesangial matrix and microfibrils, but little cellular proliferation. Fragmented red blood cells were seen in nearly half of the patients. In another seven patients the lesion resembled focal segmental glomerulosclerosis. This combination of changes termed transplant glomerulopathy leads to diffuse glomerular sclerosis. Arterial intimal thickening and occasionally also thrombosis produced ischaemic changes in the kidney and in the glomeruli and contributed significantly to the process of transplant rejection.
The report describes 22 cases of lupus nephritis (20 diffuse and 2 mesangial) showing frequent tubuloreticular inclusions (TRI) in the glomerular and peritubular capillary endothelial cells as well as cylindric confronting cisternae (CCC) mainly in interstitial infiltrating cells. Ten other cases of lupus nephritis that were actively treated or were in the sclerosing stage and did not show CCC were also studied. The presence of cytoplasmic inclusions correlated with various clinical and histologic parameters. Cytoplasmic inclusions, especially CCC, are associated with clinically active, minimally treated renal disease of recent onset and histologically with active diffuse glomerular and acute interstitial lupus nephritis with many immune deposits.
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