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Upper extremity deep venous thromboembolism has become increasingly common due to the use of subclavian venous access. However, forearm deep venous thrombosis is rare. We report a case of chronic pulmonary thromboembolism originating from left forearm deep venous thrombosis. A 66-year-old woman was admitted to our hospital because of dyspnea, which had worsened over the previous 2 months. Echocardiography showed severe right ventricular enlargement and pulmonary hypertension. Perfusion lung scintigraphy revealed multisegmental perfusion defects. No likely factors responsible for hypercoagulability were found. The patient had a history of left radial fracture and had been treated with external fixation. Venography of the upper and lower extremities revealed total occlusion of the deep veins of the left forearm with collateral vessels, but no evidence of other upper or lower extremity venous thrombosis.

A 65-year-old man had been followed by a family doctor for the treatment of hypertension and chronic hepatitis (type C) for about 20 years. Although he was pointed out to have impaired glucose tolerance and primary aldosteronism in 1995, he refused an adrenal tumor operation. He was admitted to our hospital on December, 1997 for further evaluation of general malaise, pitting edema of the legs, and positive urinary protein. A diagnosis of nephrotic syndrome was made on admission and a renal biopsy was performed. Histological findings indicated that he was at the early phase of diabetic nephropathy and hypertensive renal sclerosis. It is commonly believed that diabetic nephropathy develops after ten years of diabetic history and under poor control conditions. The diabetic history of this patient was only several years and the disease was under good control. In contrast to blood glucose, hypertension was not well-controlled with any antihypertensive drug, because he had a primary aldosteronism. Unfortunately, he could not take a spironolactone because of side effects. After removal of his adrenal tumor, his blood pressure was normalized gradually, and concomitantly his urinary protein was reduced and plasma protein and albumin were restored. Hypokalemia also disappeared. These findings suggest that uncontrolled hypertension may have accelerated the condition of diabetic nephropathy. The data indicates that the control of hypertension is important for inhibiting the progression of diabetic nephropathy.