This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (16)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Pathology & Laboratory Medicine  • Alert me on articles by topic  Social Bookmarking   What's this?

Shih-Hua Lin, MD; Yuh-Feng Lin, MD; Dung-Tsa Chen, PhD; Pauling Chu, MD, PhD; Chin-Wang Hsu, MD; Mitchell L. Halperin, MD

Arch Intern Med. 2004;164:1561-1566.

Background  Hypokalemia and paralysis may be due to a short-term shift of potassium into cells in hypokalemic periodic paralysis (HPP) or due to a large deficit of potassium in non-HPP. Failure to make a distinction between HPP and non-HPP may lead to improper management. Therefore, we evaluated the diagnostic value of spot urine tests in patients with hypokalemia and paralysis during 3 years.

Methods  Before therapy, the urine potassium concentration, potassium-creatinine ratio, and transtubular potassium concentration gradient were determined in a second voided urine sample.

Results  Forty-three patients with hypokalemia and paralysis were identified: 30 had HPP and 13 had non-HPP. There was no significant difference in the plasma potassium or bicarbonate concentrations and in the pH of arterial blood between the 2 groups. All but 2 patients in the non-HPP group had urine potassium concentration values less than 20 mmol/L. Although the potassium concentration was significantly lower in the HPP group, there was some overlap. In contrast, the transtubular potassium concentration gradient and potassium-creatinine ratio differentiated patients with HPP vs non-HPP. Although only a mean ± SD of 63 ± 36 mmol of potassium chloride was administered in the patients with HPP, rebound hyperkalemia (>5 mmol/L) occurred in 19 (63%) of these 30 patients.

Conclusions  Calculating the transtubular potassium concentration gradient and potassium-creatinine ratio provided a simple and reliable test to distinguish HPP from non-HPP. Minimal potassium chloride supplementation should be given to avoid rebound hyperkalemia in patients with HPP.

From the Division of Nephrology, Department of Medicine (Drs S. H. Lin, Y. F. Lin, and Chu), and Department of Emergency Medicine (Dr Chen), Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Biostatistics Unit, UAB Comprehensive Cancer Center, University of Alabama, Birmingham (Dr Hsu); and Renal Division, St Michael's Hospital, University of Toronto, Toronto, Ontario (Dr Halperin). The authors have no relevant financial interest in this article.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Hypokalaemia and dysmorphia, is there a link?
Burtey et al.
NDT Plus 2009;2:222-224.
ABSTRACT | FULL TEXT  

Recurring paralysis
Lin et al.
BMJ Case Reports 2009;2009:bcr0720080577-bcr0720080577.
ABSTRACT | FULL TEXT  

Hypokalaemia and subsequent hyperkalaemia in hospitalized patients
Crop et al.
Nephrol Dial Transplant 2007;22:3471-3477.
ABSTRACT | FULL TEXT  

Best practice in primary care pathology: review 9
Smellie et al.
J. Clin. Pathol. 2007;60:966-974.
ABSTRACT | FULL TEXT  

Hypokalemic paralysis due to Gitelman syndrome: A family study.
Ng et al.
Neurology 2006;67:1080-1082.
ABSTRACT | FULL TEXT  

Hypokalemic weakness in hyperaldosteronism: Activity-dependent conduction block
Krishnan et al.
Neurology 2005;65:1309-1312.
ABSTRACT | FULL TEXT  

Phenotype and Genotype Analysis in Chinese Patients with Gitelman's Syndrome
Lin et al.
J. Clin. Endocrinol. Metab. 2005;90:2500-2507.
ABSTRACT | FULL TEXT  

Thyrotoxic Periodic Paralysis
Lin
Mayo Clin Proc. 2005;80:99-105.
ABSTRACT