title: The role of the interstitium of the renal cortex in renal disease.
abstract: Morphometrical investigations (point-counting method) showed that in different inflammatory (endocapillary -- acute -- GN, mesangioproliferative GN, membranoproliferative GN) glomerulonephritides and in non-inflammatory glomerular diseases (perireticular amyloidosis), there are statistically significant correlation between serum creatine concentrations at the time of biopsy and the enlargement of the cortical interstitium by fibrosis. Similar results were obtained in investigating different grades of benign nephrosclerosis with transition into secondary malignant nephrosclerosis conditioned by hypertension and in chronic diffuse sclerosing interstitial nephritides of different etiologies. As hypothesis, we assume that a narrowing of the postglomerular vessel network by interstitial fibrosis take place. This could lead to an increase resistance of the renal cortical blood flow. In spite of an elevated effective filtration pressure, the slowing of the glomerular blood flow may lead to the reduction of GRF and to an increase of the serum creatinine concentration. Additionally, in the case of interstitial fibrosis the tubules look atrophied. This could be the consequence of the reduced GFR as a sign of inactivity. On the other hand, tubular atrophy could result from malnutrition in the case of interstitial fibrosis. The resorptive capacity of these atrophied-looking tubules could be lowered and the GFR could be diminished by the so-called Thurau mechanism.
mesh_terms: D000686:Amyloidosis / Q000473:pathology; D002908:Chronic Disease; D003238:Connective Tissue / Q000473:pathology; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000473:pathology; D006801:Humans; D007672:Kidney Cortex / Q000473:pathology*; D007674:Kidney Diseases / Q000473:pathology*; D007678:Kidney Glomerulus / Q000473:pathology; D009395:Nephritis, Interstitial / Q000473:pathology; D009400:Nephrosclerosis / Q000473:pathology