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1: Ann Hematol. 1996 Sep;73(3):139-41.Click here to read Links
Comment in:
Ann Hematol. 1997 Jul-Aug;75(1-2):69-70.
Ann Hematol. 1997 May;74(5):251-2.

Paraneoplastic hypokalemia in acute myeloid leukemia: a case of renin activity in AML blast cells.

Wulf GG, Jahns-Streubel G, Strutz F, Basenau D, Hüfner M, Buske C, Wörmann B, Hiddemann W.

Department of Internal Medicine, Georg-August-Universität, Göttingen, Germany.

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.

PMID: 8841102 [PubMed - indexed for MEDLINE]

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