Rarefaction of peritubular capillaries following ischemic acute renal failure: a potential factor predisposing to progressive nephropathy.
OBJECTIVE
Long-term renal complications of acute renal failure have generally not been expected in patients that recover from acute renal failure. However, as the incidence of acute renal failure is rising, the incidence of long-term complications is likely to increase. As a corollary to ischemic acute renal failure, ischemic injury in the setting of transplant is a leading cause of delayed graft function. Unlike acute renal failure in native kidneys, delayed graft function is highly predictive of chronic nephropathy and organ failure. It is generally well accepted that acute reversible injuries mediated by ischemia render grafts susceptible toward future demise. The nature of the susceptibility that is conveyed to grafts following ischemic injury is not well understood.


RESULTS
Evidence from animal models suggests that acute injury results in microvascular damage and vessel loss in the kidney, which, as opposed to tubular damage, is largely persistent. In addition, various studies of biopsies of renal transplants suggest that ischemia imposes an early and sustained loss in peritubular capillaries in the transplanted graft. The loss of peritubular capillaries has been associated with nephropathies of diverse etiologies and may represent a single, common pathway towards progressive damage.


CONCLUSIONS
It is hypothesized that rarefaction of peritubular capillaries represents a critical event, following ischemic injury, that permanently alters renal function and predisposes patients to the development of chronic renal insufficiency. Factors that affect vascular reactivity or the structural dynamics of the kidney vascular system following injury may represent future treatment modalities following renal injury.
Basile
David P
DP
Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA. dbasile@mcw.edu
D058186:Acute Kidney Injury / Q000150:complications / Q000175:diagnosis / Q000473:pathology*; D000818:Animals; D002196:Capillaries / Q000473:pathology*; D018450:Disease Progression; D005355:Fibrosis / Q000473:pathology; D006801:Humans; D006977:Hypertension, Renal / Q000503:physiopathology; D007511:Ischemia / Q000473:pathology*; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000503:physiopathology; D012038:Regeneration; D012079:Renal Circulation