Cephaloridine kidney damage

These drugs (e.g., cephaloridine) may be nephrotoxic causing proximal tubular necrosis. Cephaloridine is actively taken up from blood into proximal tubular cells by OAT 1. The drug therefore accumulates in the kidney. Metabolic activation via cytochrome P-450 may be involved. GSH is oxidized, and as NADPH is also depleted, the GSSG cannot be reduced back to GSH. As vitamin E-depleted animals are more susceptible, it has been suggested that lipid peroxidation may be involved. Damage to mitochondria also occurs. 

Most instance of drug-induced renal disease are probably due to direct toxicity. Even cephalosporins such as cephalothin or cephaloridin, which can produce immunological reactions, more frequently damage the kidney directly (Parker 1979 a). 

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