Cephaloridine - Adverse Effects - Toxicity

Toxicity

Cephaloridine can cause kidney damage in humans, since it is actively taken up from the blood by the proximal tubular cells via an organic anion transporter (OAT) in the basolateral membrane. Organic anions are secreted through the proximal tubular cells via unidirectional transcellular transport. The organic anions are taken up from the blood into the cells across the basolateral membrane and extruded across the brush border membrane into the tubular fluid. Cephaloridine is a substrate for OAT1 and thus can be transported into the proximal tubular cells, which form the renal cortex. The drugs, however, cannot move readily across the luminal membrane since it is a zwitterion. The cationic group (pyridinium ring) of the compound probably inhibits the efflux through the membrane. This results in an accumulation of cephaloridine in the renal cortex of the kidney, causing damage and necrosis of the S2 segment of the tubule. However, there are no adverse effects on renal function if serum levels of cephaloridine are maintained between 20 and 80 μg/ml.

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