To the Editor:
We have read with great interest the article published by Cunha et al which was about association between urinary sodium/potassium ratio and blood pressure, structural and functional vascular functions. It is emphasized that higher values of urinary Na/K ratio are related to increased blood pressure and arterial stiffness values and worse endothelial functions.1
Non‐steroidal anti‐inflammatory drugs (NSAIDs) are the most common prescribed drugs worldwide. NSAIDs are used in the treatment of inflammatory diseases and pain syndromes. NSAIDs have several effects on kidney functions. They can cause acute kidney injury, renal papillary necrosis, interstitial nephritis, glomerulonephritis, and electrolyte imbalance. Cyclooxygenase (COX) enzymes act as primary role on tubular functions and inhibition of COX‐1 and COX‐2 leads changes on Na and K excretion.2 NSAIDs increase K levels by two main mechanisms. First of them is inhibiting the prostaglandin‐mediated renin secretion and downregulating angiotensin‐aldosterone system. The second mechanism is that NSAID related reduced glomerular filtration rate yields decreased K filtration.3 NSAIDs remove the inhibitory effects of prostaglandins on sodium reabsorbtion and cause Na and water retention. NSAIDs also exacerbate the thiazide diuretics‐related hyponatremia.2 NSAIDs inhibit aldosterone metabolism and cause increased endothelial injury, myocardial fibrosis, left ventricular remodeling, and Na retention.4
In conclusion, NSAIDs have several effects on both kidney functions and cardiovascular system. NSAIDs are the most common prescribed drugs. NSAID use affects urinary Na and K excretion, and it suppresses inflammation, so CRP levels might be influenced. Therefore, we think that it could be better if the status of NSAID use in the study population was evaluated.
REFERENCES
- 1. Cunha MR, Cunha AR, Marques BCAA, et al. Association of urinary sodium/potassium ratio with structural and functional vascular changes in non‐diabetic hypertensive patients. J Clin Hypertens (Greenwich). 2020;21(9):1360‐1369. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Rahman S, Malcoun A. Nonsteroidal Antiinflammatory Drugs, Cyclooxygenase‐2, and the Kidneys. Prim Care. 2014;41(4):803‐821. [DOI] [PubMed] [Google Scholar]
- 3. Campbell WB. Attenuation of angiotensin II‐ and III‐induced aldosterone release by prostaglandin synthesis inhibitors. J Clin Invest. 1979;64(6):1552. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. White W. Cardiovascular effects of the cyclooxygenase inhibitors. Hypertension. 2007;49:408‐418. [DOI] [PubMed] [Google Scholar]