Zur Morphologie und Pathogenese der diabetischen Glomerulosklerose

Abstract

The diabetic glomerulosclerosis as a consequence of the abnormal metabolic state is characterized by an uniform thickening of the glomerular basement membrane (GBM) and an augmentation of the mesangial matrix. Both alterations begin already few years after the onset of the diabetes and are observed in all glomeruli to the same extent (=diffuse type). Later on, nodular deposits of glycoproteins are additionally found in the mesangium (=nodular type). Only these nodules are morphologically specific for the diabetic disorder. In association with both the diffuse and the nodular glomerulosclerosis, insudation of plasma can be seen in the afferent and efferent vessels and the glomerular capillary loops. The mechanism of the increase in the amount of GBM-material is not known, since contradictory data have been reported with regards to both the chemical composition and metabolism of the GBM in human and experimental diabetes. Some postulate that the abnormal deposition of GBM-mateiral is due to an excessive synthesis (anabolic disorder), others argue that a further decrease in the normally slow breakdown and disposal (catabolic disorder) might be responsible. This review presents the different pathogenetic concepts of the glomerulosclerosis and attemps to explain the possible causes for the current discrepancies.

The effect of alloxan, and alloxan‐induced diabetes on the kidney

“…Similarly, little is known of the mechanisms responsible for the increase in amount of glomerular basementmembrane material. The latter has been attributed to abnormal deposition due to excessive synthesis of glomerular basementmembrane material as well as faulty disposal (Romen, 1980). The functional relationships between capillary endothelium and glomerular basement membrane are imper-fectly defined.…”