lisinopril and Renal-Artery-Obstruction

Acute renal failure is a well recognized complication from the use of angiotensin-converting enzyme inhibitors in patients with severe bilateral renovascular disease. A 54-year-old woman presented with acute pulmonary edema with intractable hypertension and a history of lower limb claudication. The addition of lisinopril to her antihypertensive regimen resulted, within 48 h, in the development of acute renal failure that remitted with cessation of the drug. She was found to have a heavily calcified occlusion of her aortic arch and another occlusion of the aorta below the renal arteries. Angiography and Doppler ultrasonography showed normal renal arteries. This is the first reported case of angiotensin-converting enzyme inhibitor-induced renal failure occurring in a patient with atherosclerotic occlusion of the aorta. The literature on suprarenal aortic occlusion is reviewed to determine the manner of presentation, prevalent risk factors and physical findings that typify this unique clinical entity.

Topics: Acute Kidney Injury; Adult; Aged; Angiography; Angiotensin-Converting Enzyme Inhibitors; Aortic Valve Stenosis; Arteriosclerosis; Female; Humans; Lisinopril; Male; Middle Aged; Renal Artery; Renal Artery Obstruction; Risk Factors; Ultrasonography, Doppler

Topics: Angioplasty; Antihypertensive Agents; Atherosclerosis; Blood Pressure Monitoring, Ambulatory; Diagnosis, Differential; Drug Resistance; Female; Fibromuscular Dysplasia; Humans; Hypertension, Renovascular; Lisinopril; Middle Aged; Patient Care Management; Renal Artery; Renal Artery Obstruction; Risk Reduction Behavior; Stents

The angiotensin II subtype 1 receptor (AT(1)R) has been linked to the development and progression of renovascular hypertension. In this study we applied a pig model of renovascular hypertension to investigate the AT(1)R in vivo with positron-emission tomography (PET) and in vitro with quantitative autoradiography. AT(1)R PET measurements were performed with the radioligand [(11)C]KR31173 in 11 control pigs and in 13 pigs with hemodynamically significant renal artery stenosis; 4 were treated with lisinopril for 2 weeks before PET imaging. The radioligand impulse response function was calculated by deconvolution analysis of the renal time-activity curves. Radioligand binding was quantified by the 80-minute retention of the impulse response function. Median values and interquartile ranges were used to illustrate group statistics. Radioligand retention was significantly increased (P=0.044) in hypoperfused kidneys of untreated (0.225; range: 0.150 to 0.373) and lisinopril-treated (0.237; range:0.224 to 0.272) animals compared with controls (0.142; range:0.096 to 0.156). Increased binding of [(11)C]KR31173 documented by PET in vivo was confirmed by in vitro autoradiography. Both in vivo and in vitro binding measurements showed that the effect of renal artery stenosis on the AT(1)R was not abolished by lisinopril treatment. These studies provide insight into kidney biology as the first in vivo/in vitro experimental evidence about AT(1)R regulation in response to reduced perfusion of the kidney. The findings support the concept of introducing AT(1)R PET as a diagnostic biomarker of renovascular disease.

Topics: Animals; Antihypertensive Agents; Autoradiography; Carbon Radioisotopes; Imidazoles; Kidney; Lisinopril; Magnetic Resonance Angiography; Positron-Emission Tomography; Receptor, Angiotensin, Type 1; Renal Artery Obstruction; Swine; Tetrazoles