[1] Cephaloridine was briefly popular because it tolerated intramuscularly and attained higher and more sustained levels in blood than cephalothin.

Because it is also poorly absorbed after oral administration the use of this drug for humans declined rapidly, especially since the second generation of cephalosporins was introduced in the 1970s.

[1] Today, it is more commonly used in veterinary practice to treat mild to severe bacterial infections caused by penicillin resistant and penicillin sensitive Staphylococcus aureus, Escherichia coli, Streptococcus pyogenes, Streptococcus pneumoniae, Bacillus subtilis, Klebsiella, Clostridium diphtheriae, Salmonella and Shigella.

This antibiotic stands in sharp contrast to various other cephalosporins and to the structurally related penicillins in undergoing little or no net secretion by the mammalian kidney.

Cephaloridine is, however, highly cytotoxic to the proximal renal tubule, the segment of the nephron responsible for the secretion of organic anions, including para-am-minohippurate (PAH), as well as the various penicillin and cephalosporin antibiotics.

The cytotoxicity of cephaloridine is completely prevented by probenecid and several other inhibitors of organic anion transport, including the nearly nontoxic cephalothin.

After cooling, diluting with water, and adjusting the pH with mineral acid, cephaloridine thiocyanate salt precipitates.

Cephaloridine is distributed well into the liver, stomach wall, lung and spleen and is also found in fresh wounds one hour after injection.

However, the drug is poorly penetrated into the cerebrospinal fluid and is found in a much smaller amount in the cerebral cortex.

[7] 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.

[9][10] 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.

In case of chronic kidney failure dietary management also includes erythropoietin agonists (since anaemia is associated with chronic kidney failure), phosphate binders (in case of hyperphosphatemia), calcium supplements, Vitamin D supplements and sodium bicarbonate (to correct the acid-base disturbance).