Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy

Noel M. Delos Santos, Bettina H. Ault, Ali G. Gharavi, Stephen B. Kritchevsky, Michael W. Quasney, Elizabeth C. Jackson, Kimberly A. Fisher, Susan Y. Woodford, Bonnie L. Mitchell, Lillian W. Gaber, Kristopher Arheart, Robert J. Wyatt

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Angiotensin-converting enzyme (ACE) I/D polymorphism has been implicated as a genetic marker for progression of glomerular disease. Studies of ACE genotypes in adults with IgA nephropathy (IgAN) have yielded conflicting results. We performed ACE genotyping on 79 patients with IgAN diagnosed prior to age 18 years who had either progressed to end-stage renal disease (ESRD) or are now more than 5 years post biopsy. Mean follow-up was 14.8 years for those with normal renal function. Forty-three (54.4%) subjects had normal renal function and a normal urinalysis at last evaluation. Sixteen (20%) progressed to ESRD and 1 has chronic renal insufficiency. Kaplan-Meier survival curves for progression to ESRD did not differ significantly for the ACE DD, ID, and II genotype groups (P=0.095, log-rank test). By univariate analysis, presence of hypertension and degree of proteinuria at diagnosis, and unfavorable histology but not ACE genotype, was significantly associated with progression to ESRD. In the Cox proportional hazards model that included grade of proteinuria, the ACE D allele was a significant independent predictor of outcome with a hazard ratio of 2.37 (P=0.031). Our data, while inconclusive, suggest that the ACE D allele may associate with poor outcome in pediatric IgAN.

Original languageEnglish
Pages (from-to)496-502
Number of pages7
JournalPediatric Nephrology
Volume17
Issue number7
DOIs
StatePublished - Dec 1 2002
Externally publishedYes

Fingerprint

Peptidyl-Dipeptidase A
Immunoglobulin A
Genotype
Pediatrics
Chronic Kidney Failure
Proteinuria
Alleles
Kidney
Urinalysis
Kaplan-Meier Estimate
Chronic Renal Insufficiency
Genetic Markers
Proportional Hazards Models
Disease Progression
Histology
Hypertension
Biopsy

Keywords

  • Angiotensin-converting enzyme genotype
  • End-stage renal disease
  • IgA nephropathy
  • Proportional hazards models
  • Survival analysis

ASJC Scopus subject areas

  • Nephrology
  • Pediatrics, Perinatology, and Child Health

Cite this

Delos Santos, N. M., Ault, B. H., Gharavi, A. G., Kritchevsky, S. B., Quasney, M. W., Jackson, E. C., ... Wyatt, R. J. (2002). Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy. Pediatric Nephrology, 17(7), 496-502. https://doi.org/10.1007/s00467-002-0916-0

Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy. / Delos Santos, Noel M.; Ault, Bettina H.; Gharavi, Ali G.; Kritchevsky, Stephen B.; Quasney, Michael W.; Jackson, Elizabeth C.; Fisher, Kimberly A.; Woodford, Susan Y.; Mitchell, Bonnie L.; Gaber, Lillian W.; Arheart, Kristopher; Wyatt, Robert J.

In: Pediatric Nephrology, Vol. 17, No. 7, 01.12.2002, p. 496-502.

Research output: Contribution to journalArticle

Delos Santos, NM, Ault, BH, Gharavi, AG, Kritchevsky, SB, Quasney, MW, Jackson, EC, Fisher, KA, Woodford, SY, Mitchell, BL, Gaber, LW, Arheart, K & Wyatt, RJ 2002, 'Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy', Pediatric Nephrology, vol. 17, no. 7, pp. 496-502. https://doi.org/10.1007/s00467-002-0916-0
Delos Santos NM, Ault BH, Gharavi AG, Kritchevsky SB, Quasney MW, Jackson EC et al. Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy. Pediatric Nephrology. 2002 Dec 1;17(7):496-502. https://doi.org/10.1007/s00467-002-0916-0
Delos Santos, Noel M. ; Ault, Bettina H. ; Gharavi, Ali G. ; Kritchevsky, Stephen B. ; Quasney, Michael W. ; Jackson, Elizabeth C. ; Fisher, Kimberly A. ; Woodford, Susan Y. ; Mitchell, Bonnie L. ; Gaber, Lillian W. ; Arheart, Kristopher ; Wyatt, Robert J. / Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy. In: Pediatric Nephrology. 2002 ; Vol. 17, No. 7. pp. 496-502.
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