Does renin-angiotensin aldosterone system blockade exacerbate contrast-induced nephropathy in patients with chronic kidney disease? A prospective 50-month Mayo Clinic study

Macaulay A C Onuigbo, Nnonyelum T C Onuigbo
Renal Failure 2008, 30 (1): 67-72
Contrast induced nephropathy, a leading cause of new-onset renal failure in U.S. hospitals, may be accelerated by concurrent RAAS blockade in CKD patients. Current literature is inconclusive. Between September 2002 and February 2005, we prospectively enrolled all CKD patients on RAAS blockade who developed contrast-induced nephropathy. RAAS blockade was discontinued, standard nephrology care applied, and eGFR by MDRD was monitored. Seven patients (M:F, 3:4; age, 72.3 years) were enrolled. Mean duration of RAAS blockade at enrollment was 25.8 months. Baseline vs. enrollment eGFR was 45.5 +/- 17 vs. 16.6 +/- 6.8 mL/min/1.73 m(2), p = 0.009. Three of the seven patients (43%) required dialysis, one temporarily. Two older patients (mean age, 81.5 vs. 68.6 years, p = 0.017) progressed to ESRD. eGFR in five non-ESRD patients increased from 18.5 +/- 7.1 to 41.0 +/- 27.1 mL/min/1.73 m(2) after 29.4 months. Baseline eGFR was lower in the two patients who developed ESRD (29.5 vs. 51.2 mL/min/1.73 m(2)). Two patients exhibited very steep serum creatinine trajectories, indicative of rapid loss of eGFR. New onset proteinuria was observed. We have demonstrated very bad renal outcomes with three of seven (43%) patients requiring dialysis, with two (29%) progressing to ESRD. In two patients, loss of eGFR was clearly accelerated. These findings support the view that concurrent RAAS blockade, particularly in older CKD patients, exacerbates contrast-induced nephropathy. Also, lower baseline eGFR predicted worse renal outcomes. We support the recommendation to withhold RAAS blockade, 48 hours before contrast exposure, to improve renal outcomes.

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