| Literature DB >> 34669168 |
Shigo Ikeyama1, Shoichiro Kanda2,3,4, Shinichi Sakamoto5, Akiko Sakoda6, Kenichiro Miura7, Ryu Yoneda1, Ayumi Nogi1, Shohei Ariji1, Mai Shimoda1, Mayumi Ono1, Sachiko Kanda1, Seiichiro Yokoyama1, Kan Takahashi1, Yoshiki Yokoyama1, Motoshi Hattori7.
Abstract
Cystinuria is an autosomal recessive disorder characterized by a decrease in the reabsorption of cystine and dibasic amino acids (lysine, ornithine, and arginine) in the renal proximal tubule. It presents with recurrent urolithiasis. Cystinuria accounts for 6-8% of all pediatric urolithiasis. The age of onset is typically 10-30 years. Here, we report a case of early-onset cystinuria. A 4-month-old girl presented with hematuria. We noticed multiple renal calculi in ultrasonography and abdominal computerized tomography scans. The diagnosis was cystinuria with urinary calculus analysis and urinary amino acid analysis. The patient was treated with urine alkalinization and cystine chelating drugs. Gene analysis showed a P482L heterozygous mutation from her mother, and an A70V heterozygous mutation from her father, in the SLC7A9 gene. This gene encodes a putative subunit of the neutral and basic amino acid transport protein, BAT1. Although cystinuria is an autosomal recessive disease, there have been previous reports of P482L heterozygous mutations greatly suppressing cystine reabsorption and causing cystinuria symptoms. Therefore, the highly influential P482L mutation of the SLC7A9 gene may have contributed to the onset of this autosomal recessive disease at an extremely young age.Entities:
Keywords: BAT1; Cystinuria; SLC7A9; Urolithiasis
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Year: 2021 PMID: 34669168 PMCID: PMC9061909 DOI: 10.1007/s13730-021-00655-1
Source DB: PubMed Journal: CEN Case Rep ISSN: 2192-4449