GLOMERULAR EPITHELIAL-CELL CHANGES IN EARLY POST-ISCHEMIC ACUTE-RENAL-FAILURE IN RABBITS AND MAN
- 1 January 1981
- journal article
- research article
- Vol. 103 (2) , 163-173
Abstract
Spreading and flattening of glomerular podocyte cell bodies and major processes and an apparent lack of foot processes were observed by scanning electron microscopy in a reversible pedicle-clamping model of acute renal failure in ADH-treated rabbits and in biopsy specimens taken 1 h after transplantation from patients who later showed clinical signs of acute tubular necrosis. Glomerular changes were quantified by morphometry in normal rabbit kidneys (group A), rabbit kidneys obtained 2 h after 1 h of left pedicle clamping and right nephrectomy (group B), kidneys similar to Group B except that the animals were treated with an agent that reliably lessens the eventual severity of renal failure (clonidine, 30 .mu.g/kg given i.v. 1/2 h before unclamping) (group C), 1 h posttransplantation biopsy specimens from human kidneys that functioned well after transplantation (recipient serum creatinine < 2.5 mg/dl on Day 3) (group D), and 1 h posttransplant biopsy specimens from kidneys that later manifested posttransplantation ischemic acute renal failure (recipient serum creatinine .gtoreq. 2.5 mg/dl on Day 3) (group E). The fraction of glomerular capillary surface covered only by podocyte processes smaller than 1 .mu. (and not by cell bodies and wider processes) was 0.65 .+-. 0.02 (SEM) in A; 0.48 .+-. 0.03 in B; 0.64 .+-. 0.03 in C; 0.57 .+-. 0.01 in D; and 0.38 .+-. 0.04 in E (A vs. B, P < 0.01; B vs. C, P < 0.02; D vs. E, P < 0.01). In Groups D and E there was a significant negative correlation between the fraction of glomerular capillary surface covered only by podocyte processes < 1 .mu. in width and serum creatinine on the third posttransplantation day (r = -0.86, P < 0.01 by the Spearman rank test). Apparently, podocyte changes are seen by scanning electron microscopy early in clinical and experimental postischemic acute renal failure and are more pronounced in groups that eventually develop more severe renal failure. It is unclear whether these changes reflect a decrease in glomerular hydraulic permeability or an increase in glomerular permeability to protein.This publication has 36 references indexed in Scilit:
- Glomerular Endothelial Cells in Uranyl Nitrate-induced Acute Renal Failure in RatsJournal of Clinical Investigation, 1980
- Pathogenic mechanisms in early norepinephrine-induced acute renal failure: Functional and histological correlates of protectionKidney International, 1978
- Acute effects of antiglomerular basement membrane antibody on the process of glomerular filtration in the rat.Journal of Clinical Investigation, 1976
- Prediction of kidney viability before transplantationBritish Journal of Surgery, 1975
- Glomerular Epithelium: Structural Alterations Induced by PolycationsScience, 1975
- Pathophysiology of a nephrotoxic model of acute renal failureKidney International, 1975
- Determinants of glomerular filtration in experimental glomerulonephritis in the rat.Journal of Clinical Investigation, 1975
- Medullary plasma flow and intravascular leukocyte accumulation in acute renal failureKidney International, 1974
- Micropuncture studies of proximal tubule albumin concentrations in normal and nephrotic ratsJournal of Clinical Investigation, 1971
- Differentiation of glomerular, tubular, and normal proteinuria: determinations of urinary excretion of β2-microglobulin, albumin, and total proteinJournal of Clinical Investigation, 1969