How NSAIDS cause renal failure?

Non-steroidal anti-inflammatory drugs (NSAIDs) can cause renal failure through several mechanisms:

1. Inhibition of prostaglandin synthesis: NSAIDs inhibit the enzyme cyclooxygenase (COX), which is responsible for the synthesis of prostaglandins. Prostaglandins play a crucial role in maintaining renal blood flow and glomerular filtration rate (GFR). By inhibiting prostaglandin synthesis, NSAIDs can reduce renal blood flow and GFR, leading to kidney damage and renal failure.

2. Sodium and water retention: NSAIDs can cause sodium and water retention by inhibiting the production of natriuretic hormones, such as prostaglandin E2. This can lead to fluid overload and increased pressure within the kidneys, which can damage the delicate structures of the nephrons and impair kidney function.

3. Direct tubular toxicity: Some NSAIDs, particularly in high doses or with prolonged use, can directly damage the renal tubules, the functional units of the kidneys responsible for filtering waste products and regulating electrolyte balance. This direct tubular toxicity can lead to acute kidney injury and renal failure.

4. Interstitial nephritis: NSAIDs can cause interstitial nephritis, an inflammation of the tissues between the tubules in the kidneys. This inflammation can disrupt the normal functioning of the nephrons and lead to renal failure.

5. Exacerbation of underlying kidney disease: In individuals with pre-existing kidney disease, NSAIDs can worsen the underlying condition and accelerate the progression of renal failure.

It's important to use NSAIDs cautiously, especially in individuals with kidney disease, the elderly, and those taking other medications that can affect kidney function. Regular monitoring of kidney function is recommended when using NSAIDs long-term or in high doses. If signs of renal failure, such as decreased urine output, swelling, or unexplained weight gain, occur, it's crucial to stop NSAID use and consult a healthcare professional promptly.