Pathogenesis of sodium and water retention in high-output and low-output cardiac failure, nephrotic syndrome, cirrhosis, and pregnancy (2)

N Engl J Med. 1988 Oct 27;319(17):1127-34. doi: 10.1056/NEJM198810273191705.


This article has analyzed the pathogenesis of sodium and water retention in several circumstances. The initiator of retention has been proposed to be either a fall in cardiac output (e.g., low-output cardiac failure and vasoconstrictor hypovolemic nephrotic syndrome) or peripheral arterial vasodilatation (e.g., high-output cardiac failure, cirrhosis, arteriovenous fistula, and pregnancy). In the only state discussed, in which the kidney is diseased and not merely responding to extrarenal reflexes--i.e., nephrotic syndrome--intrarenal mechanisms may predominate and lead to expansion of the arterial vascular tree and suppression of the renin-angiotensin-aldosterone system (i.e., hypervolemic nephrotic syndrome). Otherwise, when kidneys are healthy, either a fall in cardiac output or peripheral arterial vasodilatation may diminish arterial vascular filling and thereby initiate a series of hemodynamic and hormonal events that result in renal sodium and water retention (Fig. 7). Finally, the approach presented in this article should be considered to be a vantage point from which to evaluate states of sodium and water retention, but not to be an exclusive position.

Publication types

  • Review

MeSH terms

  • Animals
  • Body Water / metabolism*
  • Cardiac Output
  • Female
  • Heart Failure / metabolism*
  • Humans
  • Liver Cirrhosis / metabolism
  • Nephrotic Syndrome / metabolism*
  • Pregnancy
  • Pregnancy Complications / metabolism
  • Sodium / metabolism*


  • Sodium