Urinary prostaglandins and kallikrein in the course of acute renal failure

Abstract

To examine the role of prostaglandins and the kallikrein system in the recovery from acute renal failure, we studied the sequential changes in urinary prostaglandins and kallikrein after the onset of oliguria. The six patients studied had acute tubular necrosis of the vasomotor type. Urinary PGE 2, PGF 2α, the PGF 2α-main urinary metabolite, 6-keto-PGF 1α, and TXB 2 were all measured by radioimmunoassay. Urinary kallikrein was assayed by means of hydrolytic activity using a chromogenic tripeptide substrate. Following onset of diuresis, urinary PGE 2 excretion was increased to normal, parallel to the increase in urine volume. In contrast, the ratio of urinary PGF 2α/PGE 2 peaked at the onset of diuresis, indicating a relative increase in PGF 2α, production at this time. Prior to this peak, urinary kallikrein concentrations reached the highest levels, suggesting a close connection with renal prostaglandin metabolism. On the other hand, changes in PGF 2α-MUM, 6-keto-PGF 1α and TXB 2 were not found. These results indicate that there may be an interlocking acute alteration of the kallikrein-prostaglandin system occurring immediately before the resolution of oliguria, although the role of the acute shift to PGF 2α production observed needs further study.