title: Reversible compensatory hypertrophy in rat kidneys: morphometric characterization.
abstract: Functional renal compensatory hypertrophy (RCH) in the uninephrectomized rat is completely reversible by transplantation in Brown Norway (BN) rats, while anatomic RCH is not. To determine the nephron element(s) responsible for persistent anatomic RCH, we performed morphometric analysis on perfusion fixed rat kidneys following renal function studies. In this model the function of renal transplants is not different from contralateral and unmanipulated control kidneys, and there is no histological evidence of rejection. Rats uninephrectomized for three or six weeks had larger glomeruli than controls, and after transplantation of a previously hypertrophied kidney into a rat with a normal or a solitary hypertrophied kidney, glomerular size returned to control levels. Increased glomerular capillary volume (CVCP) in kidneys with RCH was due to increased capillary length (LCP; 13.1 +/- 1.0 mm cf. 10.3 +/- 0.9, P < 0.01) without increase in capillary radius (RCP; 3.26 +/- 0.33 microM cf. 3.28 +/- 0.24). In contrast, return of CVCP to control levels in kidneys undergoing regression was associated with persistently elevated LCP (13.0 +2- 2.9 mm; native previously hypertrophied kidney; 12.2 +/- 0.9; transplanted previously hypertrophied kidney vs. 10.3 +/- 0.9, P < 0.01) and decreased RCP (2.79 +/- 0.10 microM and 2.73 +/- 0.09, cf 3.28 +/- 0.24, P < 0.01). RCH was associated with proportional increases in glomerular, tubular, and vascular-interstitial volumes while only elevated tubular volume persisted during regression. Altered glomerular capillary dimensions and increased tubular volumes acquired during renal RCH induced by unilateral nephrectomy persisted during complete functional regression.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pathology, Rush Medical College, Chicago, Illinois.
authors.forename: M M
authors.initials: MM
authors.lastname: Schwartz
authors.forename: M
authors.initials: M
authors.lastname: Churchill
authors.forename: A
authors.initials: A
authors.lastname: Bidani
authors.forename: P C
authors.initials: PC
authors.lastname: Churchill
mesh_terms: D000818:Animals; D002196:Capillaries / Q000473:pathology; D006984:Hypertrophy; D007668:Kidney / Q000098:blood supply / Q000473:pathology*; D007672:Kidney Cortex / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D009392:Nephrectomy; D051381:Rats; D011914:Rats, Inbred BN