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Paraneoplastic hypokalemia in acute myeloid leukemia: a case of renin activity in AML blast cells
Authors:G. G. Wulf  G. Jahns-Streubel  F. Strutz  D. Basenau  M. Hüfner  C. Buske  B. Wörmann  W. Hiddemann
Affiliation:Department of Internal Medicine, Georg-August-Universit?t, Robert-Koch-Strasse 40, D-37075 G?ttingen, Germany, DE
Department of Pathology, Georg-August-Universit?t, G?ttingen, Germany, DE
Abstract: 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. Received: 19 March 1996 / Accepted: 30 April 1996
Keywords:  Acute myeloid leukemia  Hypokalemia  Renin  Aldosteronism
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