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Lead Nephrotoxicity Proximal Tubule — ESENeph MCQ

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ModerateAcute Kidney InjuryLead Nephrotoxicity Proximal TubuleESENeph

A 45-year-old man develops AKI after exposure to lead in an industrial accident. His blood lead level is 85 mcg/dL (very elevated). He has abdominal pain, anaemia with basophilic stippling, and gingival lead lines. What is the renal manifestation of acute lead toxicity?

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Correct answer: C — Acute proximal tubular dysfunction (Fanconi-like syndrome) – lead accumulates in proximal tubular cells causing mitochondrial dysfunction; chronic exposure leads to chronic tubulointerstitial nephritis with characteristic intranuclear inclusion bodies

Acute lead nephrotoxicity targets the proximal tubule, causing Fanconi-like syndrome (glycosuria, aminoaciduria, phosphaturia). Lead accumulates in proximal tubular cells, forming characteristic acid-fast intranuclear inclusion bodies on biopsy. Chronic lead exposure (occupational, environmental) causes progressive chronic tubulointerstitial nephritis ('lead nephropathy') with gout (lead impairs urate excretion), hypertension, and CKD. Treatment of acute lead toxicity includes chelation therapy (EDTA, DMSA/Succimer) and removing the exposure source. Blood lead levels guide chelation decisions.

Reference: Ekong et al 2006 – Lead Nephropathy; WHO – Lead Exposure Guidelines