Sustained hypertension in children.

OBJECTIVE: To study the etiology and clinical profile of children with sustained hypertension. DESIGN: Retrospective hospital-based study. SETTING: Tertiary care, referral center. SUBJECTS: 246 children with sustained hypertension presenting between January 1983 and December 1996. RESULTS: The mean age at presentation was 8.2+/-3.9 yr; range 2 months-16 yr. There were 180 boys. An underlying cause for hypertension was identified in 242 (98.4%); 4 patients were considered to have essential hypertension. The chief causes included chronic glomerulonephritis (GN) in 121 (49.2%), obstructive uropathy in 39 (15.8%), reflux nephropathy in 30 (12.2%), thrombotic microangiopathy in 15 (6.1%) and renovascular disease in 14 (5.7%). Takayasu's disease was the most common cause of renovascular hypertension. Coarctation of aorta was the commonest cause of hypertension in infancy, being present in 53.3% of cases. In 198 subjects (80.5%) hypertension was detected as a feature of a known underlying disease. Thirty-five patients however, presented for the first time with complications of severe hypertension, including congestive cardiac failure in 21 and encephalopathy in 23. Thirteen patients presented with nonspecific symptoms and hypertension was detected on clinical examination. CONCLUSIONS: Most patients with sustained hypertension have an underlying etiology. A significant proportion of patients with renovascular and endocrine conditions may present, for the first time, with complications of hypertension.

Association of the ACE gene polymorphism with the progression of autosomal dominant polycystic kidney disease

Renin-angiotensin system is considered important in the genesis of hypertension and development of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD). The angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with susceptibility to the development of some renal diseases. We investigated the association of ACE gene polymorphism with the progression to hypertension and ESRD in 108 patients with ADPKD. The ACE I/D polymorphism was amplified with the flanking primers by polymerase chain reaction. In patients genotyped for ACE gene polymorphism, the frequencies of DD (15+ACU-), ID (51+ACU-) and II (34+ACU-) genotypes were similar to those of the general population. Of the 108 patients, 64 (59+ACU-) developed hypertension and 24 (22+ACU-) reached ESRD at the time of study. The prevalence of hypertension was not significantly different among the three genotypes. The mean renal survival time was 53-6 yr in II genotype, 5510 yr in ID genotype and 529 yr in DD genotype which was not significantly different among them. Cumulative renal survival was not significantly different either. There was no association of ACE gene polymorphism with the prevalence of hypertension and renal survival in ADPKD. We suggest that ACE I/D polymorphism is not an important modifying gene in the progression of ADPKD.

Association of the ACE gene polymorphism with the progression of autosomal dominant polycystic kidney disease

Renin-angiotensin system is considered important in the genesis of hypertension and development of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD). The angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with susceptibility to the development of some renal diseases. We investigated the association of ACE gene polymorphism with the progression to hypertension and ESRD in 108 patients with ADPKD. The ACE I/D polymorphism was amplified with the flanking primers by polymerase chain reaction. In patients genotyped for ACE gene polymorphism, the frequencies of DD (15+ACU-), ID (51+ACU-) and II (34+ACU-) genotypes were similar to those of the general population. Of the 108 patients, 64 (59+ACU-) developed hypertension and 24 (22+ACU-) reached ESRD at the time of study. The prevalence of hypertension was not significantly different among the three genotypes. The mean renal survival time was 53-6 yr in II genotype, 5510 yr in ID genotype and 529 yr in DD genotype which was not significantly different among them. Cumulative renal survival was not significantly different either. There was no association of ACE gene polymorphism with the prevalence of hypertension and renal survival in ADPKD. We suggest that ACE I/D polymorphism is not an important modifying gene in the progression of ADPKD.