Differential renal function during angiotensin converting enzyme inhibition in renovascular hypertension.

Abstract

Renal function was measured sequentially in 32 patients with proven renovascular hypertension who were treated with the oral angiotensin converting enzyme inhibitor captopril. Renal function was assessed by serial measurement of serum creatinine. Six patients showed acute rises in serum creatinine concentration compatible with acute renal failure. Acute renal failure was confined to those patients with stenosis to a solitary kidney (transplant or native, occurring in 3 of 8 patients) or bilateral renal artery stenosis (occurring in 3 of 13 patients). No rise in serum creatinine concentration was observed in 11 patients with unilateral renal artery stenosis during long-term angiotensin converting enzyme inhibitor therapy. Acute renal failure during angiotensin converting enzyme inhibitor therapy was not related to the degree of blood pressure fall or the plasma angiotensin II level. Eleven patients with renovascular hypertension were followed prospectively with estimation of renal function by 99mTc-diethylenetriaminepentaacetic acid (DTPA) clearance (determined by computer analysis of scintillation camera renography). In six patients with unilateral renal artery stenosis, total 99mTc-DTPA clearance and serum creatinine level remained constant following angiotensin converting enzyme inhibitor therapy, while in five patients with bilateral renal artery stenosis 99mTc-DTPA clearance fell from 40 +/- 9 to 27 +/- 5 ml/min (p less than 0.05). Split renal function studies revealed that 99mTc-DTPA clearance fell in most kidneys with stenosed arteries during angiotensin converting enzyme inhibition, including the stenosed kidney from patients with unilateral renal artery stenosis (16 stenosed kidneys studied; change in Tc-DTPA clearance, -7.5 +/- 2.7 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of Renin-Angiotensin System Blockade in Atherosclerotic Renal Artery Stenosis and Renovascular Hypertension

“…44 Multiple series suggest that acute deterioration in renal function is mainly confined to cases in which the entire renal mass is subject to renovascular obstruction. 42,[45][46][47][48][49] In such cases, angiotensin blockade can be considered a form of "medical nephrectomy." Additional risk factors for acute renal failure in this setting include severe congestive heart failure, use of high-dose loop diuretics, volume contraction, and poor baseline renal function.…”

Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

“…[23] The association of accelerated renal failure in CKD patients concurrently receiving ACE inhibitors, ARBs, or a combination of both is well reported and acknowledged in the medical literature. [24][25][26][27][28][29][30][31][32][33][34][35][36][37] Precipitating risk factors reported include initiation of RAAS blockade, volume depletion, hypotension and cardiovascular hemodynamic instability, the presence of hemodynamically significant renal artery stenosis, use or abuse of NSAIDs or cox II inhibitors with or without concurrent administration of diuretics, the presence of severe illness or infections following a dose increase or switch between an ACE inhibitor and an ARB, and exacerbation of heart failure. [24][25][26][27][28][29][30][31][32][33][34][35][36][37] Against this backdrop, and cognizant of anecdotal observations made by the first author about ten years ago in a practice in Baltimore, Maryland, we hypothesized that susceptible CKD patients with normal renal arteries on conventional angiography, including MRA, but who have microvascular arteriolar narrowing in the renal circulation, mimicking large vessel renal artery stenosis, could experience worsening azotemia after long periods of time (>3 months), on stable doses of RAAS blockade, even without precipitating risk factors.…”

Pathogenesis of Renovascular Hypertension: Challenges and Controversies

“…However, there is concern with the often-seen deleterious effects on renal function of the stenotic kidney caused by these anti-hypertensive agents. With already compromised blood flow, concern about increased damage to the ischemic kidney must be weighed with the benefits to the contralateral kidney (Jackson et al, 1986). With substanstial arterial obstruction, simply reducing perfusion pressure can reduce post-stenotic blood flow beyond that required for metabolic demands in the kidney.…”