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Rosa Maria Scuteri, MD, Paraguay 2342, 8A, 1121 Buenos Aires (Argentina) Dear Sir, Tumoral calcifications are an infrequent finding in hemodialysis patients. In reference to the paper published by Zins et al. [1], we report upon a hypothyroid female patient aged 51 years who developed this kind of metastatic calcification after 7 years of maintenance hemodialysis in a unit with water treatment including reverse osmosis. She was the only case who developed this complication among 971 patients followed up between 1974 and 1992. She was started on hemodialysis in 1980. Arterial hypertension and hypothyroidism were reported in her clinical history. She was never compliant respective to thyroid hormone replacement and phosphorous chela-tors (aluminum hydroxide and calcium carbonate), thus she received vitamin D supplements, irregularly. A transiliac bone biopsy was performed in 1984 and osteitis fibrosa cystica was informed from a decalcified specimen. Nonparathyroid enlargement was shown by ultrasonographic scan. In 1987, roentgeno-graphic features of ectopic calcifications sized 20 × 20 cm were observed in the adductor muscles (fig. 1) and periarticular zones bilaterally, as well as a compressive fracture of Dll and a periarticular calcification of the shoulders. Computed tomography revealed intrapulmonary and mitral valve calcium deposits as visceral calcifications. Disseminated vascular calcifications had previously been detected. The patient refused a second bone biopsy which was suggested in order to investigate aluminum bone disease. A septic complication caused her death in 1988. Visceral and nonvisceral metastatic calcifications represent different etiological mechanisms and rarely coincide [2]. Nonvisceral calcifications are related to: (a) hyperphosphatemia and (b) increased calcium-phosphate product. Instead, visceral calcifications are associated to other factors such as tissue distrophy [3]. In our patient, laboratory data revealed the following (table 1): persistent hyperphosphatemia, alkaline phosphatase progressive elevation without hepatic disease, and increased PTH levels without echographic confirmation of an enlarged gland [4].