Heavy metals pose a significant health hazard, especially with occupational exposure, among which lead is one of the common ones. Acute manifestations include headache, paraesthesias, gastrointestinal symptoms, encephalopathy and seizures, whereas chronic toxicity may lead to cognitive decline and neuropathy. However, the coexistence of renal involvement along with neuropathy and encephalopathy is rare.

A 38-years old male, battery factory worker, presented with insidious onset progressive bilateral grip weakness since 1.5 years, associated with episodic memory loss, seizures, and constitutional symptoms in the form of loss of appetite and weight loss. Examination showed pure motor neuropathy, finger drop and wasting of small muscles of hand. Blood investigations showed microcytic hypochromic anemia, elevated ESR, deranged renal function with peripheral smear showing basophilic stippling. Neuroimaging showed symmetric T2/FLAIR hyperintensities in basal ganglia, thalami, and periventricular white matter. Nerve conduction studies showed pure motor axonal polyneuropathy. Hence, a diagnosis of chronic lead toxicity was considered, and toxicology screening showed elevated serum lead levels. In view of multisystemic manifestations and elevated inflammatory markers, autoimmune and paraneoplastic workup was performed, which showed CASPR2 antibody positivity, raising the suspicion of autoimmune phenomenon. He was treated with chelators (Dimercaprol and EDTA) and steroids for the possible autoimmunity, and was monitored with serial serum and urinary lead levels. He improved symptomatically, with improvement in renal functions and resolution of MRI changes.

This case highlights the rare presentation of coexisting neuropathy, nephropathy and encephalopathy in chronic lead poisoning, and the importance of occupational history in routine practice. Associated CASPR2 antibody positivity in this case shows a possible novel lead associated autoimmune phenomenon.