Porphyria cutanea tarda (PCT) is a vesiculobullous skin disorder characterized by a defect in heme biosynthesis. Reduced activity of the hepatic enzyme uroporphyrinogen decarboxylase (URO‐D) results in accumulation of photosensitive porphyrins; this ultimately leads to the skin fragility and blistering that is characteristic of this disease. The majority of cases of PCT are associated with acquired deficiencies of the enzyme URO‐D, secondary to hepatic injury precipitated by medications or infections. Less commonly, PCT has been documented in patients with end‐stage renal disease. The pathogenesis of PCT in long‐term hemodialysis (HD) has been attributed to many factors, but the following mechanisms have been implicated: (i) decreased hepatic URO‐D activity due to suppressive effects of iron and other hepatotoxins and (ii) poor porphyrin clearance by renal replacement therapies. We report a case of PCT that developed in a patient on maintenance HD for 4 years. He had a history of hepatitis C and evidence of iron overload. However, as the patient was anemic, therapeutic phlebotomy was problematic and therefore erythrocyte‐stimulating agents were maximized to mobilize iron stores and allow phlebotomy. With this treatment, the patient’s skin lesions improved in conjunction with decreasing ferritin levels.