The inhibition of prostaglandin synthesis by NSAIDs has specific effects on the kidneys. These effects range from mild changes in fluid and electrolyte homeostasis to acute renal insufficiency. NSAIDs promote sodium and water retention by attenuating prostaglandin-mediated inhibition of chloride reabsorption. NSAIDs may lead to hyperkalemia either by increased potassium reabsorption secondary to decreased sodium concentration at the distal tubule or by decreased secretion of renin. There is at least one report in the literature of cardiac arrest secondary to NSAID-induced hyperkalemia. 8
Prostaglandins have a vasodilatory effect on the renal vasculature. The most important of these renal vasodilatory prostaglandins are PGI 2 and PGE2.
Prostaglandin-mediated vasodilatation is probably of little importance in euvolemic patients with normally functioning kidneys. However, prostaglandins appear to attenuate the vasoconstricting affects of the renin-angiotensin system and sympathetic nervous system during times of stress, during periods of decreased intravascular volume (sepsis, hemorrhage, and diuretic therapy),9 and in disease states that predispose patients to sodium retention (congestive heart failure, cirrhosis, and nephrotic syndrome).9 The lack of these vasodilatory prostaglandins, due to COX inhibition by NSAIDs, may put stressed kidneys at risk for azotemia and renal insufficiency. The aforementioned comorbid states are speculated to contribute to the risk of NSAID-mediated renal insufficiency.
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