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.