Pathophysiology and prevention of acute renal failure associated with thoracoabdominal or abdominal aortic surgery D.Craig Miller, M.D., Bryan D. Myers, M.D. Journal of Vascular Surgery Volume 5, Issue 3, Pages 518-523 (March 1987) DOI: 10.1016/0741-5214(87)90086-3 Copyright © 1987 Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery Terms and Conditions
Fig. 1 Mechanisms of “filtration failure” and oligoanuria in canine postischemic acute renal failure. Tubular cell debris and shed brush border obstruct the proximal convoluted tubule, which results in sequestration of filtrate (panel 1). Tubular pressure (PT) then rises (panel 2), and the obstructed tubule is vented by transtubular back leak of filtrate across necrotic epithelium. Then afferent arteriolar vasoconstriction occurs (panel 3), which is mediated by a direct tubular-glomerular feedback mechanism and the renin-angiotensin system, which reduces glomerular capillary hydraulic pressure (PGC); this ultimately abolishes transcapillary ultrafiltration pressure (PUF), and glomerular filtration ceases. SFP = stop flow pressure, the imbalance between PGC and oncotic pressures (NGC). (Reprinted by permission of The New England Journal of Medicine, Myers BD, Moran SM. N Engl J Med 1986;314:97-105.) Journal of Vascular Surgery 1987 5, 518-523DOI: (10.1016/0741-5214(87)90086-3) Copyright © 1987 Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery Terms and Conditions
Fig. 2 Three typical patterns of acute renal failure (ARF) in humans, represented by creatinine clearance (CCREAT) and serum creatinine levels (SCREAT) in patients who did not undergo dialysis. Pattern A ARF (e.g., after brief suprarenal aortic cross-clamping) is characterized by a step decrement and ramp recovery of CCREAT, which is typical of abbreviated AFR. Pattern B ARF displays an exponential CCREAT decline accompanied by a linear increase in SCREAT out to day 12. Recovery (days 16 to 30) demonstrates a ramp increment in CCREAT and a sigmoidal decline in SCREAT. The most severe injury is manifested as pattern C (protracted) ARF. Successive linear decreases in CCREAT produce repetitive increases in SCREAT. Recovery of CCREAT occurs only after the first episode (linear increment, days 4 to 7). A persistent, refractory low cardiac output prevents recovery from the second insult. (Reprinted by permission of The New England Journal of Medicine, Myers BD, Moran SM. N Engl J Med 1986;314:97-105.) Journal of Vascular Surgery 1987 5, 518-523DOI: (10.1016/0741-5214(87)90086-3) Copyright © 1987 Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery Terms and Conditions