Epithelial cell shedding in acute renal injury.
1. To address the postulate that sublethally injured tubular cells may be shed from renal epithelium while still viable, studies were undertaken in vivo in human 'acute tubular necrosis' and in rabbit models of renal tubular injury. 2. Substantial numbers of viable tubular cells were voided in the urine. When placed in culture, these cells gave rise to monolayers, confirming viability. The majority of intact cells demonstrated markers of proximal tubule. 3. In vitro studies of human renal proximal tubular cells exposed to hypoxia/anoxia showed rounding and retraction associated with disruption of actin microfilaments. Phalloidin stabilized the filaments and prevented the changes in cell shape indicative of altered adherence.
Racusen
L C
LC
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. LRACUSEN@PATHLAN.PATH.JHU.EDU
D000199:Actins / Q000378:metabolism; D058186:Acute Kidney Injury / Q000473:pathology*; D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects / Q000473:pathology*; D006801:Humans; D007511:Ischemia / Q000473:pathology*; D007668:Kidney / Q000098:blood supply*; D016030:Kidney Transplantation / Q000473:pathology; D007687:Kidney Tubules, Proximal / Q000473:pathology*; D010590:Phalloidine / Q000494:pharmacology; D011817:Rabbits
D000199:Actins; D010590:Phalloidine