Tolerance of the Human Kidney to Isolated Controlled Ischemia

Abstract

Tolerance of the human kidney to ischemia is controversial. Here, we prospectively studied the renal response to clamp ischemia and reperfusion in humans, including changes in putative biomarkers of AKI. We performed renal biopsies before, during, and after surgically induced renal clamp ischemia in 40 patients undergoing partial nephrectomy. Ischemia duration was .30 minutes in 82.5% of patients. There was a mild, transient increase in serum creatinine, but serum cystatin C remained stable. Renal functional changes did not correlate with ischemia duration. Renal structural changes were much less severe than observed in animal models that used similar durations of ischemia. Other biomarkers were only mildly elevated and did not correlate with renal function or ischemia duration. In summary, these data suggest that human kidneys can safely tolerate 30-60 minutes of controlled clamp ischemia with only mild structural changes and no acute functional loss.

Atherosclerotic renal artery stenosis is associated with elevated cell cycle arrest markers related to reduced renal blood flow and postcontrast hypoxia

“…Temporary ischemic changes in mitochondria were evident by electron microscopy with minor tubular injury that began to recover after reflow [40]. These data are consistent with our observations that major tissue hypoxia in the human kidney after 24 h may not result in sustained tissue injury, unlike that observed in experimental models.…”

“…Remarkably, a recent study of human subjects with total renal artery clamp occlusion for periods between 30 and 60 min during surgery reported minimal kidney injury as determined by levels of creatinine, plasma biomarkers or tissue biopsy [40]. Temporary ischemic changes in mitochondria were evident by electron microscopy with minor tubular injury that began to recover after reflow [40].…”

Renal Hemodynamics in AKI

“…However, studies in large mammals, including humans, suggest that global renal hypoperfusion cannot be invoked as the sole etiology of AKI. [2][3][4][5] The causative contribution of renal blood flow (RBF) to kidney dysfunction is particularly puzzling in sepsis, and there is widespread disagreement as to whether RBF is reduced, normal, or even increased. 2,3,[6][7][8] In the few large animal and clinical studies, the patterns of RBF in AKI and its relation with systemic hemodynamics are highly variable.…”

Risk factors of long-term postoperative renal function after partial nephrectomy in a solitary kidney

“…The results demonstrated that differential block methods and block time durations were not associated with acute renal function damage, and there were no significant correlations between block time and postoperative renal function. In addition, this study reported surprisingly that the human kidney can tolerate an ischemia time as long as 30 to 60 min [13]. However, all patients in the study had a normal, contralateral kidney.…”