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The Journal of Thoracic and Cardiovascular Surgery, Vol 79, 838-844, Copyright © 1980 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association


ARTICLES

Sequential pathophysiological changes characterizing the progression from renal dysfunction to acute renal failure following cardiac operation

M Hilberman, GC Derby, RJ Spencer and EB Stinson

Sequential pathophysiological data were analyzed from 14 patients who exhibited similar severe depression of cardiac and renal function within 24 hours of cardiac operation. Seven patients exhibited postoperative renal dysfunction (defined by a minimum postoperative clearance of inulin [Cin] between 20 ml/min/1.73 m2 and one-half normal) and seven progressed from renal dysfunction to acute renal failure (ARF) (Cin less than or equal to ml/min/1.73 m2). In ARF patients depression of cardiac function was profound and persistent from postoperative days 1 to 7. Urine flow remained greater than 1 ml/min, and serum creatinine rose progressively. The Cin declined progressively during the first postoperative week. The ratio or urinary to plasma osmolality fell, and the fractional excretion of sodium (FENa) and potassium (FEK) increased substantially. By contrast, in renal dysfunction patients definite hemodynamic improvement occurred and renal function remained stable. Increased FENa in renal dysfunction was associated with hemodynamic improvement, weight loss, and stable fractional potassium excretion. These data provide unique documentation of the indices of hemodynamic and renal function associated with the progression to postoperative ARF. The central role of sustained profound depression of cardiac function in this progression appears to be the primary factor in the lethality of postoperative ARF.


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