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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Angiotensin I level and sporadic hypokalemic periodic paralysis.

A patient with secondary (sporadic type) hypokalemic periodic paralysis with relative hypertension had reninism with a high concentration of plasma angiotensin I (ANG-I) but no hyperaldosteronism or high angiotensin II value. Angiotensin-converting enzyme (ACE) activity was usually normal. Results of other hormonal analyses were also normal. However, the glomerular filtration rate and filtration fraction of the kidneys were greatly elevated. Despite severe hypokalemia, the patient's potassium clearance was high. No evidence of distinct hyperplasia of the juxtaglomerular cells was obtained. These results suggest that decreased affinity of ACE to the substrate ANG-I (so-called ACE dysfunction syndrome) produced the reninism and high concentration of plasma ANG-I, and that the latter induced an increase in the glomerular filtration rate of the kidneys with sequential occurrence of secondary hypokalemic periodic paralysis.[1]


  1. Angiotensin I level and sporadic hypokalemic periodic paralysis. Umeki, S., Ohga, R., Ono, S., Yasuda, T., Morimoto, K., Terao, A. Arch. Intern. Med. (1986) [Pubmed]
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