[Pathogenesis of the toxic and allergic nephrotic syndrome. Metabolic studies on kidney-cortex slices and on glomeruli].

The in vitro metabolism of isolated rat glomeruli in Daunomycin-nephrosis (DMS) and neophrotoxic nephritis (ANS) was determined in order to investigate questions about the nephrotic syndrome. Glomeruli of rats with Daunomycin-nephrosis influenced metabolic steps as follows: 1. Oxydative decarboxydation of pyruvate and probably also of alpha-ketoglutarate is decreased. This disturbance might be located in the formation of acetyl-and/or succinyl-CoA. 2. Incubation with pyruvate and alpha-ketoglutarat resulted in reduced oxygen uptake, and resynthesis of ATP. 3. Incorporation of thimidin into glomerular DNS is inhibited in the beginning stage of Daunomycin-nephrosis; while incorporation of amino acids into glomerular protein is not, beta-oxydation of fatty acids is at least until entrance into the TCA cycle undisturbed. In contrast, glomeruli of rats with nephrotoxic nephritis utilised more oxygen and the stationary concentration of ATP within the glomeruli was elevated. The pathway of the nephrotic syndrome is not exactly known. Metabolic and morphologic studies with glomeruli of the immunologically and the toxically induced nephrotic syndrome showed different biochemical and histological disorders for the same clinical symptoms. As the beginning of nephrotic syndrome very different lesions in the glomerulus have to be expected, which result in a greater permeability of basal membranes.