ArticlePediatric research2020
Clinical features, genetic background, and outcome in infants with urinary tract infection and type IV renal tubular acidosis.
Article in Pediatric research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Transient secondary pseudo-hypoaldosteronism in infants with urinary tract infections: systematic literature review.European journal of pediatrics · 2024Pooled it
- Renal pseudohypoaldosteronism type 1-an adult case series including a novel gene variant.Endocrine · 2025Article
- Underestimated reason of hyperkalemia in diabetic patients: type IV renal tubular acidosis- mini review.Frontiers in clinical diabetes and healthcare · 2025Review
- Pseudo-hypoaldosteronism secondary to infantile urinary tract infections: role of ultrasound.Italian journal of pediatrics · 2022Article
- Aldosterone signaling defect in young infants: single-center report and review.BMC endocrine disorders · 2021Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundType IV renal tubular acidosis (RTA) is a severe complication of urinary tract infection (UTI) in infants. A detailed clinical and molecular analysis is still lacking.
methodsInfants with UTI who exhibited features of type IV RTA were prospectively enrolled. Clinical, laboratory, and image characteristics and sequencing of genes responsible for phenotype were determined with follow-up.
resultsThe study cohort included 12 infants (9 males, age 1-8 months). All exhibited typical type IV RTA such as hyperkalemia with low transtubular potassium gradient, hyperchloremic metabolic acidosis with positive urine anion gap, hypovolemic hyponatremia with renal salt wasting, and high plasma renin and aldosterone levels. Seven had hyperkalemia-related arrhythmia and two of them developed life-threatening ventricular tachycardia. With prompt therapy, all clinical and biochemical abnormalities resolved within 1 week. Five had normal urinary tract anatomy, and three of them carried genetic variants on NR3C2. Three variants, c.1645T>G (S549A), c.538G>A (V180I), and c.1-2C>G, on NR3C2 were identified in four patients. During follow-up, none of them had recurrent type IV RTA, but four developed renal scaring.
conclusionsGenetic mutation on NR3C2 may contribute to the development of type IV RTA as a complication of UTI in infants without identifiable risk factors, such as urinary tract anomalies.
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