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Abstract
Background and Aims
Uricase metabolizes uric acid into allantoin, a soluble compound that is easily excreted in the urine. Acute hyperuricemia is associated with endothelial injury and vasoconstriction, favoring acute renal failure. Preliminary studies show the protective role of lowering uric acid in cardiac patients.
Method
Pilot study conducted in patients with cardiorenal syndrome and hyperuricemia (>9 mg/dl). All received a single dose of rasburicase (0.20 mg/kg/day in the first 9 patients or a fixed dose of 6 mg in 14 patients) evaluating its effect on renal function and the need for renal replacement therapy.
Results
Twenty-three patients aged 68 ± 14 years were included, 14 men and 9 women, 87% hypertensive, 35% diabetic, 17% with liver disease, and 26% with cancer. Baseline: mean LVEF 40±14.1% (13-63), pro-BNP 19880±14000ng/l, basal Cr 1.55±0.58 mg/dl, uric acid 14.1±2.26, phosphorus 5 .3±1.6 mg/dl and CRP 7±8 mg/l. The evolution of renal function after treatment is shown in Table 1. In all patients, uric acid after rasburicase decreased to 0.5 mg/dl. There were no differences in renal function, RRT, and hospitalization between patients who received a dose of 0.20 mg/kg/day or 6 mg iv. Only 3 patients required RRT for 21±23 hours, with recovery from acute renal failure. Comparing the patients who required RRT versus those who did not, these presented higher baseline uric acid levels: 16.5±2.5 vs 13.7±1.1 mg/dl, P = .049, and there were no differences in LVEF. pro-BNP and previous renal function. One patient died during the hospital stay due to terminal CHF and sepsis, but having recovered kidney function.
Conclusion
Rasburicase administration may prevent established renal failure in patients with cardiorenal syndrome and hyperuricemia. Early treatment, avoiding very high levels of hyperuricemia, could be more effective in reducing the need for renal replacement therapy.