Correlation between endogenous creatinine clearance and relative interstitial volume of the renal cortex in patients with diffuse membranous glomerulonephritis having a normal serum creatinine concentration
Riemenschneider, T.; Mackensen-Haen, S.; Christ, H.; Bohle, A.
Laboratory Investigation; a Journal of Technical Methods and Pathology 43(2): 145-149
1980
ISSN/ISBN: 0023-6837 PMID: 7401629 Document Number: 161447
Correlations between structural and functional changes in kidneys were investigated on 72 biopsy cylinders from patients with diffuse membranous glomerulonephritis having normal serum creatinine concentrations. The relative interstitial volume of the renal cortex was measured by point-counting on periodic acid-Schiff-stained sections. The glomerular changes of stages I, II and III were examined on semithin and ultrathin sections and graded according to the classification of Ehrenreich and Churg. A significant correlation between increasing relative interstitial volume and decreasing endogenous creatinine clearance was established. A negative relationship between age of patients and creatinine clearance and a positive correlation for age and interstitial volume was found. There was no difference for the mean clearance values related to the glomerular changes in stages I-III. Severe diffuse transformation of the glomerular basement membrane did not affect the glomerular filtration rate. A moderately increased interstitial volume had a pronounced negative effect on creatinine clearance. With increasing age, the creatinine excretion diminishes mainly as a result of an enlarged interstitial volume. The augmented interstitial volume due to the accumulation of collagenous fibers may be a result of deposition of immunocomplexes with following sclerosing inflammation, persistent edema with subsequent organization or the aging process itself. The interstitial fibrosis could influence the glomerular filtration rate in 2 pathophysiologic ways: by narrowing the lumina of postglomerular vessel network and the concomitant slowing of glomerular blood flow; by damaging interstitial and tubular tissue, impairing Na reabsorbation and altering tubuloglomerular feedback mechanism.