Regression of diabetic glomerular changes following islet transplantation. a study of rats with streptozotocin diabetes
Kösters, W.
Fortschritte der Medizin 97(17): 825-829
1979
ISSN/ISBN: 0015-8178 PMID: 155638 Document Number: 145962
The precise etiology and pathogenesis of diabetic glomerulosclerosis still remain obscure. The aim of the present study was 1. to evaluate the morphologic and functional alterations of mesangial cells in long term diabetic rats and 2. to study the effect of islet transplantation on these lesions. Diabetes was induced in inbred Lewis rats with streptozotocin (65 mg per kg). 7 month later glomeruli of diabetic rats showed hyaline nodular deposits, exsudative lesions and glomerular aneurysms. The thickening of the mesangium measured by point counting method was statistically significant compared with age matched controls. Large quantities of IgG, beta 1c and fibrinogen in a predominantly mesangial pattern could be demonstrated by fluorescence microscopy. After injection of aggregated immunoglobulin the uptake of IgG by the mesangial cells was delayed in the diabetics compared with normal controls. Islet transplantation resulted in a marked reduction of the light microscopic and immunohistological glomerular lesions and restored the phagocytic capacity of the mesangial cells almost completely. From these results it is concluded, that the fundamental defect in diabetic glomerulosclerosis is a metabolically induced functional defect of the mesangial cells.