Weil's disease (icterohaemorrhagiae leptospirosis) is diagnosed by the microscopic agglutination test (MAT). What is the mechanism of renal injury in severe leptospirosis?
- A Direct tubular toxicity by leptospiral glycolipoprotein and LPS causing acute tubular necrosis with proximal tubular dysfunction (Fanconi syndrome pattern) ✓
- B Immune complex deposition in glomeruli causing nephritic syndrome
- C Hemoglobin pigment nephropathy from intravascular hemolysis
- D Thrombotic microangiopathy from platelet-activating factor
Explanation
Leptospiral outer membrane lipopolysaccharide (LPS) and glycolipoprotein toxins directly damage renal tubular epithelium, particularly proximal tubules, causing non-oliguric acute tubular necrosis. A characteristic feature is disproportionately preserved urine output (non-oliguric renal failure) and hypokalemia from tubular potassium wasting. This contrasts with other causes of ARF. The mechanism involves direct cytotoxicity and local inflammatory infiltrate in the renal interstitium (interstitial nephritis), not primarily immune complex deposition or hemoglobin pigment nephropathy.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.