NSAIDs-induced renal diseases
| Diagnosis | Key Differentiator |
|---|---|
| AKI | Sudden ↑Cr, prerenal labs (FEurea <35%). |
| AIN | Fever/rash/eosinophilia, WBC casts, steroid response. |
| Chronic Interstitial | Slow CKD progression, small kidneys on imaging. |
| Papillary Necrosis | Gross hematuria, Flank pain, Sloughed papillae in urine, CT "ring sign". |
| Nephrotic Syndrome | Massive proteinuria, hypoalbuminemia, edema. |
1. Acute Kidney Injury (AKI)
- Mechanism: NSAIDs inhibit COX-1/COX-2, reducing vasodilatory prostaglandins (PGE₂, PGI₂), leading to afferent arteriolar vasoconstriction and decreased glomerular filtration rate (GFR).
- Types:
- Prerenal AKI: Reversible with hydration and NSAID discontinuation.
- Intrinsic AKI (e.g., acute tubular necrosis): Prolonged ischemia from severe vasoconstriction.
2. Acute Interstitial Nephritis (AIN)
- Mechanism: Immune-mediated hypersensitivity reaction, often with eosinophilic infiltration.
- Features: May present with fever, rash, eosinophilia, and AKI. Requires steroid therapy in severe cases.
3. Chronic Interstitial Nephritis
- Mechanism: Long-term NSAID use causes chronic inflammation and fibrosis.
- Outcome: Progressive chronic kidney disease (CKD) with tubular atrophy and interstitial scarring.
4. Renal Papillary Necrosis
- Mechanism: Chronic ischemia due to reduced medullary blood flow, exacerbated by long-term NSAID use.
- Features: Hematuria, flank pain, and sloughed papillae causing urinary obstruction.
5. Nephrotic Syndrome
- Types:
- Minimal Change Disease: Podocyte injury from NSAID-induced cytokine release.
- Membranous Nephropathy: Rare, immune-complex deposition.
- Presentation: Proteinuria (>3.5 g/day), hypoalbuminemia, edema.