Evidence against a role for prostaglandins in sustaining renal hyperfiltration in type 1 diabetes mellitus.
The acute effect of inhibition of prostaglandin synthesis with indomethacin 50 mg by mouth on renal haemodynamics has been examined in 8 male Type 1 diabetic patients with elevated glomerular filtration rate who were free of diabetic complications. Renal plasma flow and glomerular filtration rate were measured by constant infusion of para-amino hippurate and polyfructosan, the patients being studied at normoglycaemia. Urinary excretion of prostaglandin E2 fell from 885 +/- 160 to 345 +/- 115 pg min-1, and excretion of 6-keto-prostaglandin F1 alpha fell from 489 +/- 77 to 283 +/- 50 pg min-1. There was no change in renal plasma flow or glomerular filtration rate following indomethacin. The results do not support the hypothesis that increased renal prostaglandin synthesis is a cause of hyperfiltration in diabetes mellitus.
Jenkins
D A
DA
Department of Medicine, Royal Infirmary of Edinburgh, UK.
Craig
K
K
Collier
A
A
Watson
M L
ML
Clarke
B F
BF
D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000328:Adult; D000419:Albuminuria; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D015232:Dinoprostone / Q000652:urine; D005919:Glomerular Filtration Rate; D006801:Humans; D007213:Indomethacin; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D012079:Renal Circulation; D012964:Sodium / Q000652:urine
D001786:Blood Glucose; D011453:Prostaglandins; D015121:6-Ketoprostaglandin F1 alpha; D012964:Sodium; D015232:Dinoprostone; D007213:Indomethacin