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Gitelman's syndrome is a renal tubular disorder characterized by a sodium and chloride reabsorption defect in distal tubular cells that determines hypokalemia, metabolic alkalosis, hypomagnesemia, and low calcium excretion. The presence of choroidal calcifications was sought in five patients with Gitelman's syndrome by ophthalmic examination, fluorescein angiography, indocyanine green angiography, and ocular ultrasonography. Calcifications observed in the choroid of two patients were shown by ultrasonography in both patients. Ophthalmic and fluorangiographic examinations detected this alteration in one of the two subjects. Chondrocalcinosis was found in one patient with choroidal calcifications. These findings suggest that precipitation of calcium salts can occur in the choroidal tissue of patients with Gitelman's syndrome. Deposits appeared to be well seen by ultrasonography because of their depth in ocular tissues. Sclerochoroidal calcifications may be favored by the low calcium excretion, which is associated with normal intestinal calcium absorption in patients with Gitelman's syndrome.

The leukemias have long been associated, albeit rarely, with the development of renal failure and several metabolic perturbations. While renal insufficiency may result from a variety of mechanisms in the setting of leukemia, severe leukostasis with microvascular insufficiency and renal parenchymal infiltration by blast cells are rare and infrequently described etiologies. In addition, hypokalemia can occur from lysozyme-induced renal tubular injury with inappropriate kaliuresis. We present a case of acute myelomonocytic leukemia that was complicated by renal failure and severe hypokalemia and discuss the probable mechanisms.