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Nonselective non steroidal anti inflammatory drugs (ns NSAIDS) are known to have important kidney adverse effects such as acute kidney injury, electrolyte imbalance, acute and chronic interstitial nephritis, acute papillary necrosis, nephrotic syndrome, increased risk of renal cancer. We describe a case of a young male patient presenting with severe nephrotic syndrome after naproxen intake.
We report a case of 33 year old male patient who was diagnosed with plantar fasciitis and was prescribed naproxen 500 mg twice daily for 6 weeks. After 4 weeks, he presented at the emergency room for increased swelling of lower limbs, scrotal swelling, fatigue and dry cough. His past history was irrelevant and he had no family history of hypertension, diabetes or kidney disease.
Physical examination showed pitting oedema of lower limbs up to mid abdomen and manifest scrotal oedema. Heart, chest and abdominal examination were normal. No purpuric rash or joint inflammation were noticed.
Lab work demonstrated severe hypoalbuminemia of 10 g/L and heavy albuminuria of 15.06 g/24 h. Kidney function was normal with eGFR of 114 ml/min. Urinary sediment showed microscopic hematuria, hyaline and granular casts with no RBCs cast. AST and ALT were slightly elevated with normal bilirubin. Immunological profile including ANA, ENA, ANCA, Anti GBM, RF, IgA, C3 and C4 was normal. PPE showed no monoclonal peak. Serology of HBV, HCV, HIV was negative. Lipid profile demonstrated high LDL cholesterol. Renal ultrasound revealed normal kidneys.
Renal biopsy light microscopy showed normal glomeruli with slight tubulointerstitial fibrosis without any signs of inflammation. Immunofluorescence didn't denote any immunoglobulin or complement deposits. Electron microscopy revealed severe effacement of foot processes, a picture compatible with Minimal Change Disease (MCD).
The patient was treated with prednisone 1 mg/kg/day for 8 weeks together with supportive treatment including furosemide, ramipril and rosuvastatin. Prednisone was gradually tapered by 5 mg/week till stopped. Proteinuria disappeared 2 weeks after starting treatment and complete remission was obtained.
4 weeks after prednisone was stopped, the patient presented with reccurrence of nephrotic syndrome. The course of the initial therapy was given with slower tapering of prednisone. Proteinuria disappeared with no relapse.
Although kidney toxicity of NSAIDs is well known, we should be aware that it may rarely present with severe nephrotic syndrome secondary to MCD which may be relapsing even after stopping the offending drug.