A highly sensitive thin layer chromatographic assay was used to establish distinct anomalies in hepatic and renal prophyrin synthesis associated with chronic renal failure. Urinary and plasma coproporphyrin disappeared but plasma uroporphyrin (isomer III) levels rose. Patients on maintenance hemodialysis showed elevated red cell protoporphyrin and decreased total stool porphyrins whilst the raised plasma uroporphyrin did not pass into the dialysate, even in 2 cases of overt symptomatic porphyria. These results indicate that urinary coproporphyrin is of renal and not hepatic origin and that azotemia may reduce the activity of the enzyme uroporphyrinogen decarboxylase.

The cation content of the erythrocyte was studied in 36 patients with chronic renal failure. A normal or high erythrocyte potassium was found. Erythrocyte sodium values showed a wide range, from very high to very low, and the rate constant for Na efflux was found to be higher than normal. The interpretation of these findings is discussed. It is suggested that the high erythrocyte K content may reflect abnormal total body K, may be explained on the basis of a young red cell population or may be related to abnormal function of the erythrocyte cation pump. It is probable that the development of these changes in chronic renal failure depends on many factors.

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