Wulf G G, Jahns-Streubel G, Strutz F, Basenau D, Hüfner M, Buske C, Wörmann B, Hiddemann W
Department of Internal Medicine, Georg-August-Universität, Göttingen, Germany.
Ann Hematol. 1996 Sep;73(3):139-41. doi: 10.1007/s002770050215.
Hypokalemia due to renal potassium loss has frequently been observed in patients with acute myeloid leukemia (AML). The pathogenic mechanism for this hyperkaluresis is unclear. In this report we describe a patient with AML FAB M4, in whom the clinical course, the electrolyte disturbances, the serum aldosterone levels, and the diffuse hyperplasia of the adrenal cortex documented a typical case of marked secondary hyperaldosteronism. On analysis of the leukemic cells of this patient compared with normal bone marrow cells, a significant increase of renin-like activity in the cytosol of the blast cells was noted. Activation of the renin-angiotensin-aldosterone system by paraneoplastic production of renin-like activity in AML blast cells might contribute to the hypokalemia often observed in patients with acute myeloid leukemia.
急性髓系白血病（AML）患者中，因肾失钾导致的低钾血症屡见不鲜。这种高钾尿症的致病机制尚不清楚。在本报告中，我们描述了一名AML FAB M4患者，其临床病程、电解质紊乱、血清醛固酮水平以及肾上腺皮质弥漫性增生记录了一例典型的显著继发性醛固酮增多症病例。通过对该患者白血病细胞与正常骨髓细胞进行分析，发现原始细胞胞质中的肾素样活性显著增加。AML原始细胞中副肿瘤性产生的肾素样活性激活肾素 - 血管紧张素 - 醛固酮系统，可能是急性髓系白血病患者常出现低钾血症的原因。
