Hypertension aggregates in families of kidney stone patients with high urinary excretion of uric acid

Citation
A. Tisler et al., Hypertension aggregates in families of kidney stone patients with high urinary excretion of uric acid, J HYPERTENS, 17(12), 1999, pp. 1853-1858
Citations number
39
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF HYPERTENSION
ISSN journal
02636352 → ACNP
Volume
17
Issue
12
Year of publication
1999
Part
2
Pages
1853 - 1858
Database
ISI
SICI code
0263-6352(199912)17:12<1853:HAIFOK>2.0.ZU;2-Q
Abstract
Objective To determine whether kidney stone disease (KSD) and hypertension (HTN) share a common familiar component that is determined by a specific ur inary biochemical abnormality. Design Familial aggregation study. Patients Two hundred and twelve KSD patients, aged 18-50 years, collected a 24-h urine sample to measure the urinary excretion of uric acid, calcium, oxalate, magnesium and citrate, and were interviewed about the occurrence o f HTN among first-degree relatives. Outcome Positive family history (FHx) of HTN defined as two or more relativ es with HTN, and HTN occurring in the fathers, mothers and siblings. Results Positive FHx of HTN was significantly associated with increasing ur inary excretion of uric acid (P = 0.03) but not with the excretion of the o ther substances. When the patients were divided into those with and without hyperuricosuria, the adjusted odds ratio (OR) for positive FHx of HTN in a hyperuricosuric KSD patient was 3.8 (95% CI, 1.22-11.66). Separate analysi s on the occurrence of HTN in the fathers, mothers and siblings of the prob ands indicated that hyperuricosuria is positively related to HTN occurring in the siblings of the patients (P < 0.001) but not in the fathers or in th e mothers. The adjusted OR for HTN occurring in siblings of hyperuricosuric patients compared with siblings of non-hyperuricosuric patients was 3.8 (2 .12-6.67). Conclusion Siblings of KSD patients with hyperuricosuria had a significantl y increased prevalence of HTN that could not be accounted for by age, famil y size, body-mass index and personal history of HTN of the probands, Additi onal studies need to be undertaken to determine whether this familial clust ering has a genetic or environmental origin. J Hypertens 1999, 17:1853-1858 (C) Lippincott Williams & Wilkins.