The Case for Cautious Consumption: NSAIDs in Chronic Kidney Disease

Sriram Sriperumbuduri; Swapnil Hiremath


Curr Opin Nephrol Hypertens. 2019;28(2):163-170. 

In This Article

NSAIDs and Hypertension

Sodium and water retention with consequent edema and hypertension have been reported with all NSAIDs. Decreased synthesis of vasodilatory prostacyclins may also play a role in increasing blood pressure (BP). However, this effect does not occur in all individuals consuming NSAIDs in a predictable dose dependent manner as the mechanism might suggest. Amongst individuals without preexisting hypertension studied in the Nurses Health Study, there was a small increase in subsequent hypertension diagnosis only in those taking more than an average daily dose of 400 mg of ibuprofen, though there was residual confounding.[7] No such effect was seen in the Physicians Health Study, after adjusting for covariates.[8] Amongst individuals with preexisting hypertension, meta analysis from randomized trials report an increase in SBP overall of about 3–5 mmHg, however this was mostly seen with indomethacin, and not ibuprofen.[9,10] Lastly, empiric data supports the use of calcium channel blockers over renin–angiotensin system (RAS) blockade or diuretics for management of hypertension in this setting.[11,12]