Glomerular filtration rate measured by (51)Cr-EDTA clearance: Evaluation of captopril-induced changes in hypertensive patients with and without renal artery stenosis.

INTRODUCTION

Renal artery stenosis can lead to renovascular hypertension; however, the detection of stenosis alone does not guarantee the presence of renovascular hypertension. Renovascular hypertension depends on activation of the renin-angiotensin system, which can be detected by functional tests such as captopril renal scintigraphy. A method that allows direct measurement of the baseline and post-captopril glomerular filtration rate using chromium-51 labeled ethylenediamine tetraacetic acid ((51)Cr-EDTA) could add valuable information to the investigation of hypertensive patients with renal artery stenosis. The purposes of this study were to create a protocol to measure the baseline and post-captopril glomerular filtration rate using (51)Cr-EDTA, and to verify whether changes in the glomerular filtration rate permit differentiation between hypertensive patients with and without renal artery stenosis.

METHODS

This prospective study included 41 consecutive patients with poorly controlled severe hypertension. All patients had undergone a radiological investigation of renal artery stenosis within the month prior to their inclusion. The patients were divided into two groups: patients with (n=21) and without renal artery stenosis, (n=20). In vitro glomerular filtration rate analysis ((51)Cr-EDTA) and (99m)Tc-DMSA scintigraphy were performed before and after captopril administration in all patients.

RESULTS

The mean baseline glomerular filtration rate was 48.6+/-21.8 ml/kg/1.73 m(2) in the group wuth renal artery stenosis, which was significantly lower than the GFR of 65.1+/-28.7 ml/kg/1.73m(2) in the group without renal artery stenosis (p=0.04). Captopril induced a significant reduction of the glomerular filtration rate in the group with renal artery stenosis (to 32.6+/-14.8 ml/ kg/1.73m(2), p=0.001) and an insignificant change in the group without RAS (to 62.2+/-23.6 ml/kg/1.73m(2), p=0.68). Scintigraphy with technetium-99m dimercapto-succinic acid (DMSA) did not show significant differences in differential renal function from baseline to post-captopril images in either group.

CONCLUSIONS

Captopril induced a decrease in the GFR that could be quantitatively measured with (51)Cr-EDTA. The reduction is more pronounced in hypertensive patients with RAS.