Captopril for prevention of contrast-induced nephropathy in diabetic patients: a randomised study.

ABSTRACT

Contrast-induced nephrotoxicity is an important cause of hospital-acquired acute renal insufficiency. Different modalities have been used to prevent contrast induced-nephrotoxicity namely saline infusion, mannitol, furosemide, calcium channel blockers, atrial natriuretic factor and dopamine infusion with variable success. The possible role of medullary ischaemia mediated by renin angiotensin system in genesis of contrast-induced nephrotoxicity prompted us to investigate the role of captopril (a sulfhydryl group containing angiotensin-converting enzyme inhibitor) in its prevention. Seventy-one patients of diabetes mellitus undergoing coronary angiography were included in the study. Patients randomised to receive captopril, received the drug in a dose of 25 mg thrice a day for three days, starting one hour prior to angiography while the patients in the control group underwent angiography in a routine manner without receiving captopril. Following angiography, patients in the control group developed a significant increase in serum creatinine and blood urea nitrogen levels, as compared to those who received captopril. Contrast-induced nephrotoxicity (i.e. a rise of 0.5 mg/dL in serum creatinine) developed in 29 percent of the control group. Administration of captopril reduced the risk of development of contrast-induced nephrotoxicity by 79 percent. Glomerular filtration rate as measured by Tc DTPA renal scanning prior to and 24-72 hours following angiography demonstrated a mean fall of 9.6 ml/min in the control group while those in the captopril group had a mean increase of 13 ml/min in glomerular filtration rate. We conclude that abnormalities of renal perfusion possibly mediated by renin angiotensin system are responsible for development of contrast-induced nephrotoxicity. Administration of the angiotensin-converting enzyme inhibitor, captopril, offers protection against development of contrast-induced nephrotoxicity.