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Sulphadimethoxine is metabolized in humans by N1-glucuronidation and by N4-acetylation. Sulphadimethoxine-N1-glucuronide can be measured by the direct high-performance liquid chromatographic analysis and without enzymic deglucuronidation. The N1-glucuronide can be measured by an isocratic as well as by a gradient mobile phase. The group contribution of the N1-glucuronide moiety to the capacity factor is a reduction of 0.24 in the isocratic system and 0.55 in the gradient system. N4-Acetylation increases the capacity factor by a factor 1.4 in the isocratic system and by 1.06 in the gradient system.

Cefradine and co-trimoxazole pharmacokinetics were studied in a patient with peritonitis that complicated continuous ambulatory peritoneal dialysis (CAPD). Concentrations in the plasma reached after oral administration of 500 mg cefradine four times daily and 400/80 mg co-trimoxazole four times daily were for cefradine 100 micrograms/ml, for trimethoprim 15 micrograms/ml, and for sulfamethoxazole 100 micrograms/ml, respectively. In the dialysate concentrations were reached of 35-70 micrograms/ml cefradine, 2-5 micrograms/ml trimethoprim and 8-17 micrograms/ml sulfamethoxazole. The values for sulfamethoxazole are regarded too low to be clinically effective. Half-lives, protein binding values and CAPD clearances are presented. Low CAPD clearances were obtained during the night and high values during the day. The dosage yielded too high plasma trimethoprim concentrations, while sulfamethoxazole dialysate concentrations were too low. It seems questionable therefore whether co-trimoxazole can be used orally for the treatment of CAPD peritonitis.

High doses of co-trimoxazole in a patient with Pneumocystis carinii and impaired kidney function (creatinine clearance 10 ml/min) resulted in a declining renal clearance of the drug but did not affect the average creatinine clearance. The renal clearance of sulfamethoxazole and its metabolites 5-hydroxy-, N4-acetyl-, N4-acetyl-5-hydroxysulfamethoxazole decreased 80%, while the renal clearance of trimethoprim decreased 60%. The renal clearance of all compounds was evidently dependent on urine flow. The observed phenomena may be explained by the assumption that crystalluria occurred, obstructing kidney tubules. The crystalluria effect can be reversed by cessation of the drug or by lowering its dosage.

Absence of kidney function results in high steady-state plasma concentrations of the theophylline metabolites. The CAPD clearance of theophylline and its metabolites is correlated with the CAPD clearance of creatinine. N-demethylation of theophylline results in a higher CAPD clearance of these metabolites than that of the parent drug. The relatively low protein binding values of theophylline and its metabolites can be explained by the low albumin concentration.