In vitro chemotaxis of neutrophils was evaluated in rabbits with acute renal failure induced by cephaloridine. Reduction in generation of chemotactic factors was proportional to the degree of azotemia in uremic serum. This defect appears to be mediated by an inhibitor, possibly urea, which blocks the formation of chemotactic factors in serum. In contrast to the defect in serum, uremic neutrophils retained full capacity to respond to a chemotactic stimulus. These results may help to explain the reduced local inflammatory response and increased incidence of bacterial infections in renal failure.