[A case report of aldosterone-producing adrenocortical adenoma complicated with chronic renal failure associated with nephrocalcinosis: review of APAs complicated with chronic renal failure].

H Sumitomo, N Yamashita, S Katayama
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引用次数: 3

Abstract

A 57-year-old man was admitted to our hospital because of dyspnea due to congestive heart failure caused by hypertensive heart disease in September, 1992. Twenty years ago, he was diagnosed to be hypertensive, and in 1980, he was diagnosed to at our hospital to have primary aldosteronism (PA) due to a right aldosterone-producing adrenocortical adenoma (APA). There were no hypertensive vascular complications at that time. He refused surgical removal, and anti-hypertensive drugs including spironolactone were administered. However, his drug compliance was very inaccurate. On this recent admission, left ventricular hypertrophy associated with impaired contractivity, hypertensive retinal change and mild protein uria were noted, but no hematuria was detected. His renal function was impaired (Ccr: 15.2ml/min). An abdominal CT scan showed a typical right APA, bilateral renal atrophy and fine granular calcification at renal medulla, even though he had no hypercalcemia and hypercalciuria. In addition, multiple cerebral infarction was demonstrated by a brain CT scan, along with coronary artery stenoses at the right coronary artery and left circumflex branch by coronary angiography and bilateral multiple renal artery stenoses by renal angiography. Right adrenalectomy and renal biopsy were performed. Histological examinations revealed a yellow tan-colored APA, many sclerotic glomerulus, and severely hyarinized renal arterioles. After adrenalectomy, blood pressure was not normalized but was controlled easily by hypotensive agents. Impaired renal function was not improved and deteriorated slightly but did not get worse there after. Since 1959, including ours, 22 cases of APAs complicated with chronic renal failure were reported in Japan. In conclusion, surgical removal should be recommended for APA, even if the patient's condition is complicated with chronic renal failure.

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【产生醛固酮的肾上腺皮质腺瘤合并慢性肾衰竭合并肾钙质沉着症1例:APAs合并慢性肾衰竭的文献回顾】。
1992年9月,一名57岁男性因高血压性心脏病致充血性心力衰竭呼吸困难入院。20年前,他被诊断为高血压,1980年,他在我院被诊断为原发性醛固酮增多症(PA),原因是右侧醛固酮产生肾上腺皮质腺瘤(APA)。当时无高血压血管并发症。他拒绝手术切除,并给予抗高血压药物,包括螺内酯。然而,他的服药依从性非常不准确。在最近入院的病人中,发现左心室肥厚伴收缩功能受损、高血压性视网膜改变和轻度蛋白尿,但未发现血尿。肾功能受损(Ccr: 15.2ml/min)。腹部CT扫描显示典型的右侧APA,双侧肾萎缩和肾髓质细颗粒钙化,尽管他没有高钙血症和高钙尿症。颅脑CT示多发脑梗死,冠状动脉造影示右冠状动脉及左旋支狭窄,肾造影示双侧多肾动脉狭窄。行右侧肾上腺切除术及肾活检。组织学检查显示黄褐色的APA,许多硬化肾小球和严重的肾小动脉透明化。肾上腺切除术后血压未恢复正常,但使用降压药可轻松控制血压。肾功能受损未见改善,有轻微恶化,但术后未见恶化。自1959年以来,日本共报告了22例APAs合并慢性肾功能衰竭的病例。综上所述,即使患者的病情合并慢性肾功能衰竭,也应建议APA手术切除。
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