Contrast-induced nephrotoxicity in renal allograft recipients.

BACKGROUND: Intravenous administration of radiographic contrast agents is an important cause of acute renal failure, accounting for one third of the cases of hospital-acquired acute renal failure in patients with native kidneys. The safety of intravenous contrast has not been studied in renal allograft recipients since the availability of cyclosporine as a maintenance immunosuppressive therapy. As patients with renal transplantation may be at a higher risk of contrast-induced nephrotoxicity (CIN) due to concomitant use of cyclosporine and higher prevalence of diabetes and renal insufficiency, we retrospectively studied development of CIN in these patients.

PATIENTS AND METHODS: We identified 44 patients (1988 1997) with functioning renal allograft who underwent different intravenous or intraarterial contrast studies (ICS). Pre- and post-ICS renal function tests were done in 35 of these patients. The following were the various ICS done in these patients: coronary angiogram (6), CT scan with intravenous contrast ( 11), angiogram for evaluation of peripheral vascular disease (11), allograft angiogram with angioplasty (5), pulmonary angiogram (1) and intravenous pyelogram (1). The mean age of the patients was 42 +/- 2.1 years and the mean serum creatinine was 2.3 +/- 0.25 mg/dl (mean +/- SEM). Fourty percent of patients (14 of 35) had diabetes, and 25.7% (9 of 35) had chronic rejection. Ninety four percent (33 of 35) of the patients were taking cyclosporine at the time of ICS.

RESULTS: Nine patients had > or = 25% increase in serum creatinine from baseline after ICS. Two of these patients were excluded from the analysis as renal functions in these patients had deteriorated prior to ICS and renal failure was attributed to sepsis. Of the remaining 7 patients, 5 had diabetes and 2 had chronic rejection. Only 4 of these 7 patients with CIN received prophylaxis (I/V hydration) prior to ICS. The baseline serum creatinines were not different in patients who had no change in renal function to those who developed CIN (1.97 +/- 0.20 vs 1.54 +/- 0.17 mg/dl, p = 1.5, mean +/- SEM). More than 50% increase in baseline serum creatinine was seen in only 3 of these 7 patients, 2 of these patients had diabetes and third had chronic rejection and congestive heart failure. None of these patients received prophylaxis for CIN. Dialysis was not required in any patient. Three patients also had a > 25% decrease in baseline serum creatinine after ICS, and all of them had allograft angiography with angioplasty for renal artery stenosis.

CONCLUSION: In our retrospective study, the incidence of CIN in renal allograft recipients applying a broader classification of > or = 25% increase in baseline serum creatinine was 21.2% (7 of 33 patients). The incidence of CIN was lower 15.3% (4 of 26) in patients who received intravenous hydration compared to 42.8% (3 of 7) in patients who received no prophylaxis prior to ICS.