The consequences of tubulo-interstitial changes for renal function in glomerulopathies. A morphometric and cytological analysis.
Morphometric investigation of the structures of the cortex in kidneys exhibiting various types of glomerulopathy revealed the following: 1. In various types of glomerulonephritis, diabetic glomerulosclerosis, and glomerular amyloidosis there are significant correlations between the severity of fibrosis of the renal cortical interstitium and tubular atrophy resulting from chronic interstitial inflammation, and the serum creatinine concentration, creatinine clearance, inulin clearance and PAH clearance. 2. As illustrated with the example of membranoproliferative glomerulonephritis type I, if glomerulopathy alone is present, there is no elevation of the serum creatinine concentration, even if the glomerular inflammatory changes are severe; neither are severe renal amyloidosis that is confined to the glomeruli and severe isolated diabetic glomerulosclerosis associated with elevation of the serum creatinine concentration. 3. There is a significant negative correlation between the severity of interstitial fibrosis resulting from chronic inflammation and the total number and cross-sectional area of the intertubular capillaries; i.e., the total cross-sectional area and number of capillaries per unit area decrease as the fibrosis of the cortical interstitium increases. 4. Cases of glomerulonephritis in which there is accompanying fibrosis of the renal cortical interstitium have a significantly worse long-term prognosis than those in which there is only severe glomerulitis. 5. Obliteration of the post-glomerular capillaries leads to an increase in the cross-sectional area of the glomerular capillary convolution, the morphological equivalent of an increase in intraglomerular pressure. 6. The cause of the disease of the renal cortical interstitium that may accompany the various types of glomerulonephritis is not known. It is considered possible, as a working hypothesis, that this inflammation represents a T-cell stimulated autoimmune process in which fibroblast proliferation occurs, leading to an increase in numbers of fibrocytes in the renal cortical interstitium and thus to increased production of collagen.
Bohle
A
A
Institute of Pathology, University of Tübingen, F.R.G.
Mackensen-Haen
S
S
von Gise
H
H
Grund
K E
KE
Wehrmann
M
M
Batz
C
C
Bogenschütz
O
O
Schmitt
H
H
Nagy
J
J
Müller
C
C
D003404:Creatinine / Q000097:blood*; D005355:Fibrosis; D005919:Glomerular Filtration Rate / Q000502:physiology; D005921:Glomerulonephritis / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007672:Kidney Cortex / Q000473:pathology*
D003404:Creatinine