Dynamics of glomerular ultrafiltration following open-heart surgery

Abstract

To elucidate how individual determinants might lower the rate of glomerular ultrafiltration (GFR) in some patients following cardiac surgery, we performed hemodynamic measurements and clearances of inulin (as a measure of GFR), PAH (as a measure of effective renal plasma flow [ERPF]), and dextran-40. Two groups of 17 patients each were distinguished by the presence or absence of prerenal azotemia. Glomerular hypofiltration (GFR=21±2 vs. 76±6 ml/min/1.73m2, P<0.001) in the former was accompanied by depressed left ventricular function, arterial pressure, and ERPF (152±26 vs. 317±32 ml/min/1.73 m2, P<0.001). To determine if factors beside ERPF play a role in lowering GFR, we calculated the efferent oncotic pressure (π(e)). Failure of GFR to change over a 24-hour period despite increases in ERPF suggested that both patient groups were at filtration pressure disequilibrium (FPD). This condition permits calculation of a unique glomerular ultrafiltration coefficient (Kf). Over a range of pressures for transcapillary hydraulic pressure (ΔP), such that 3≤ (Δ-P-π(e)) ≤ 10 mm Hg (to simulate FPD), Kf was less than 0.08 ml·sec-1·mm Hg-1·1.73 m-2 in azotemic, but exceeded this value in nonazotemic patients. Although a selective reduction of Kf is predicted to lower the fractional clearance of dextrans, these were significantly elevated in azotemic relative to nonazotemic patients (molecular radii 30-40 Å). A theoretical analysis of the latter data suggests that over the foregoing range of FPD, a 15 to 30% decline in Δ̄P̄ combined with a 30 to 0% reduction of Kf from values in nonazotemic patients best explains the experimental findings in azotemic patients.