Literature DB >> 7354777

Responses to hydrochlorothiazide and acetazolamide in patients with calcium stones. Evidence suggesting a defect in renal tubular function.

R A Sutton, V R Walker.   

Abstract

Urinary excretion of sodium, calcium, and magnesium has been measured after single oral doses of hydrochlorothiazide (100 mg) and acetazolamide (500 mg) in unselected patients with calcareous renal stone formation and in normal control subjects. With hydrochlorothiazide, 36 stone formers had significantly greater increments in sodium (P less than 0.01), calcium (P less than 0.05), and magnesium (P less than 0.05) excretion than 20 normal subjects. With acetazolamide, 13 stone formers had a smaller increment in sodium excretion (P less than 0.05) than 10 normal subjects. The abnormal responses to both diuretics were most marked in the patients with hypercalciuria during fasting. These data suggest that the tubular handling of sodium, magnesium, and calcium may be abnormal in patients with calcareous renal stones and are consistent with the presence of a defect in proximal-tubular reabsorption of fluid and electrolytes that may be partly offset by increased reabsorption in the distal nephron.

Entities:  

Mesh:

Substances:

Year:  1980        PMID: 7354777     DOI: 10.1056/NEJM198003273021302

Source DB:  PubMed          Journal:  N Engl J Med        ISSN: 0028-4793            Impact factor:   91.245


  21 in total

Review 1.  Environmental factors in the pathophysiology of recurrent idiopathic calcium urolithiasis (RCU), with emphasis on nutrition.

Authors:  P O Schwille; U Herrmann
Journal:  Urol Res       Date:  1992

2.  Oral calcium loading test and response to diuretics in normal Taiwanese school children.

Authors:  Y H Chen; A J Lee; C S Lin; C H Chen; R W Chesney; F B Stapleton; S Roy
Journal:  Pediatr Nephrol       Date:  1996-04       Impact factor: 3.714

3.  Hyperresponsiveness of vitamin D receptor gene expression to 1,25-dihydroxyvitamin D3. A new characteristic of genetic hypercalciuric stone-forming rats.

Authors:  J Yao; P Kathpalia; D A Bushinsky; M J Favus
Journal:  J Clin Invest       Date:  1998-05-15       Impact factor: 14.808

Review 4.  Diuretics. Clinical pharmacology and therapeutic use (Part II).

Authors:  A Lant
Journal:  Drugs       Date:  1985-02       Impact factor: 9.546

5.  Bone alterations in children with idiopathic hypercalciuria at the time of diagnosis.

Authors:  Maria-Goretti Moreira Guimarães Penido; Eleonora Moreira Lima; Viviane Santuari Parizotto Marino; Ana-Luiza Fialho Tupinambá; Anderson França; Marcelo Ferraz Oliveira Souto
Journal:  Pediatr Nephrol       Date:  2002-12-19       Impact factor: 3.714

Review 6.  New insights into the pathogenesis of idiopathic hypercalciuria.

Authors:  Elaine M Worcester; Fredric L Coe
Journal:  Semin Nephrol       Date:  2008-03       Impact factor: 5.299

7.  Mechanism of hypercalciuria in genetic hypercalciuric rats. Inherited defect in intestinal calcium transport.

Authors:  D A Bushinsky; M J Favus
Journal:  J Clin Invest       Date:  1988-11       Impact factor: 14.808

8.  Comparison of reduction in microalbuminuria by enalapril and hydrochlorothiazide in normotensive patients with insulin dependent diabetes.

Authors:  M Hallab; Y Gallois; G Chatellier; V Rohmer; P Fressinaud; M Marre
Journal:  BMJ       Date:  1993-01-16

9.  Pathophysiology of spontaneous hypercalciuria in laboratory rats. Role of deranged vitamin D metabolism.

Authors:  K Lau; D Thomas; C Langman; B Eby
Journal:  J Clin Invest       Date:  1985-08       Impact factor: 14.808

10.  Tubular mechanism for the spontaneous hypercalciuria in laboratory rat.

Authors:  K Lau; B K Eby
Journal:  J Clin Invest       Date:  1982-10       Impact factor: 14.808

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.