A 6-year-old boy with steroid-sensitive minimal change disease presents with severe generalized edema. On day 3 of admission he develops sudden left flank pain, gross hematuria, and a fall in hemoglobin from 11 to 7 g/dL. Doppler ultrasound confirms left renal vein thrombosis. The single most important mechanism predisposing him to this complication is:

• A Loss of protein S leading to activated protein C resistance
• B Steroid-induced platelet hyperaggregability
• C Urinary loss of antithrombin III ✓
• D Hyperviscosity from polycythemia

Explanation

In nephrotic syndrome antithrombin III, a small plasma protein, is lost in urine, leaving free thrombin unopposed and creating the hypercoagulable state responsible for renal vein thrombosis, arterial thrombosis, and venous thromboembolism. Protein A and protein S are also lost, but antithrombin III depletion is the classic and dominant mechanism tested. Hyperviscosity contributes only marginally because these patients have hypoalbuminemia-driven hemoconcentration, not polycythemia.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.