Glomerular hyperfiltration after protein ingestion, during glucagon infusion, and in insulin-dependent diabetes is induced by a liver hormone: deficient production of this hormone in hepatic failure causes hepatorenal syndrome

Lancet. 1984 Jan 28;1(8370):195-7. doi: 10.1016/s0140-6736(84)92115-9.

Abstract

Glomerular hyperfiltration induced by various stimuli (protein ingestion, amino-acid infusion, glucagon infusion, diabetes mellitus) is postulated to be associated with increased secretion by the liver of a hormone that increases glomerular filtration rate. In severe liver failure deficient secretion of this hormone is presumed to cause or contribute to the development of the hepatorenal syndrome. There is evidence that increased hepatic uptake of aminoacids is a factor triggering secretion of this hormone. The hypothesis, which is based on earlier published studies in laboratory animals and in man, accords well with clinical observations. This hypothesis may explain how glomeruli respond to metabolic stimuli and raises the possibility of therapeutic intervention in the glomerular hyperfiltration of diabetes and chronic renal failure.

MeSH terms

  • Amino Acids / metabolism
  • Animals
  • Diabetes Mellitus, Type 1 / physiopathology*
  • Dietary Proteins / metabolism
  • Glomerular Filtration Rate* / drug effects
  • Glucagon / pharmacology
  • Glucuronates / metabolism*
  • Glucuronates / physiology
  • Hemodynamics
  • Humans
  • Kidney Failure, Chronic / etiology*
  • Kidney Glomerulus / blood supply
  • Liver / metabolism
  • Liver Diseases / etiology
  • Liver Diseases / physiopathology*
  • Models, Biological

Substances

  • Amino Acids
  • Dietary Proteins
  • Glucuronates
  • glomerulopressin
  • Glucagon