Electrolyte and Acid-Base Disturbances Associated with Non-Steroidal Anti-Inflammatory Drugs.
- Author:
Sejoong KIM
1
;
Kwon Wook JOO
Author Information
- Publication Type:Review
- Keywords: Edema; Hyponatremia; Renal tubular acidosis; Non-steroidal anti-inflammatory agents; Acute renal failure
- MeSH: Acidosis, Renal Tubular; Acute Kidney Injury; Anti-Inflammatory Agents, Non-Steroidal; Antihypertensive Agents; Arrhythmias, Cardiac; Cardiac Output, Low; Edema; Heart Failure; Humans; Hyperkalemia; Hyponatremia; Perfusion; Sodium; Water; Weight Gain
- From:Electrolytes & Blood Pressure 2007;5(2):116-125
- CountryRepublic of Korea
- Language:English
- Abstract: Inhibition of renal prostaglandin synthesis by non-steroidal anti-inflammatory drugs (NSAIDs) causes various electrolyte and acid-base disturbances including sodium retention (edema, hypertension), hyponatremia, hyperkalemia, and decreased renal function. Decreased sodium excretion can result in weight gain, peripheral edema, attenuation of the effects of antihypertensive agents, and rarely aggravation of congestive heart failure. Although rare, NSAIDs can cause hyponatremia by reducing renal free water clearance. Hyperkalemia could occur to a degree sufficient to cause cardiac arrhythmias. Renal function can decline sufficiently enough to cause acute renal failure. NSAIDs associated electrolyte and acid-base disturbances are not uncommon in some clinical situations. Adverse renal effects of NSAIDs are generally associated with prostaglandin dependent states such as volume-contracted states, low cardiac output, or other conditions that tend to compromise renal perfusion. All NSAIDs seem to share these adverse effects. In view of many NSAIDs users' susceptibility to renal adverse effects due to their underlying disease or condition, physicians should be cautious in prescribing NSAIDs to susceptible patients.
