Determinants of the renal response to ACE inhibition in patients with congestive heart failure The objective of the present study was to determine whether pretreatment neurohormonal and renal hemodynamic parameters predict the change in renal function with the administration of quinapril, a new angiotensin-converting enzyme (ACE) inhibitor. Twenty patients with New York Heart Association (NYHA) class Ill and IV heart failure were evaluated. Following pretreatment determination of renal function and plasma neurohormones, patients were treated daily with 10 mg of quinapril. Measurements of glomerular filtration rate (GFR) and renal plasma flow (RPF) were repeated after 7 weeks to assess changes in function (AGFR and ARPF). Mean GFR increased from 49 t 6 to 56 * 7 mllmin11.73 m2 (p = O.lO), but decreased in five patients. Mean RPF increased from 235 F 23 to 252 i 23 mllmin11.73 m2 (p = 0.08), but decreased in five patients. There was no relation between AGFR and baseline determinations of GFR, RPF, plasma renin activity, plasma angiotensin II, or serum Na. Only a high filtration fraction (GFRIRPF) predicted a decreased GFR (r = 0.61, p < 0.005). In contrast, no baseline renal hemodynamic parameter correlated with ARPF. We conclude that poor renal function does not increase the risk of renal deterioration with quinapril. However, dependence of renal function upon the renin-angiotensin system may be predicted by a high filtration fraction. (AM HEART J 1992;124:131.) Stephen S. Gottlieb. MD, Shawn Robinson, MD, Matthew R. Weir, MD, Michael L. Fisher, MD, and Catherine M. Krichten, RN, MS. Ba2tinore. Md. Some actions of angiotensin-converting enzyme (ACE) inhibitors lead to functional renal impair- ment, while others help sustain kidney perfusion and filt.ration. l For example, angiotensin II-induced glom- erular efferent arteriolar constriction works to main- tain glomerular perfusion pressure, and prevention of this action with an ACE inhibitor may decrease the glomerular filtration rate (GFR). Yet the systemic vasodilatory actions of ACE inhibition, with conse- quent increased renal plasma flow (RPF), should re- sult in the opposite effect. In patients with congestive heart failure, the net renal response to these con- flicting effects of inhibition of the renin-angiotensin system is inconsistent.‘*” ‘I’he pathophysiologic factors that place certain patients at increased risk of renal function deterio- ration with ACE inhibitors are disputed. It is possi- From the Divisions IJ! (‘ard~ology and Uephrology, Department ofMedicine, Ii ?iversity of Maryland +hwl of Medicine. Received furor publication Ike 5, 199!; accepted Jan. 20, 1992. Reprint requests: Stephqen 5. Gottlieh, MD, Division ot Cardiology, The I’niversit v of Maryland School r)fMedicine .22 South Greene St., Baltimore. Sli) 11201. 4’1’37370 ble that individuals with the most intense activation of the systemic renin-angiotensin system are depen- dent upon angiotensin II for maintenance of glomer- ular perfusion pressure. However, these patients may also be the ones most likely to experience increased renal plasma flow with ACE inhibitors. With recent investigations indicating that the extent of stimula- tion of the renin-angiotensin system within a tissue may not be reflected by plasma neurohormone con- centrations, indices of intrarenal renin-angiotensin system activation may be better predictors of change in renal funct.ion caused by ACE inhibition than markers of systemic activation. For example, it has been suggested that poor pretreatment kidney func- tion indicates compromised renal perfusion and may identify patients with heart failure with increased dependence of renal function upon intrarenal neuro- hormones. Such patients would presumably exhibit increased sensitivity to ACE inhibition. Identification of patients with heart failure at greatest risk of renal deterioration with converting enzyme inhibition is clinically important. In addi- tion, characterization of these patients should pro- vide an insight as to the systemic and intrarenal neu- 131