The infant (a girl aged 6 months) was admitted to the hospital because of oliguria and acute renal dysfunction. The laboratory examination results showed serious metabolic acidosis and increased blood urea nitrogen and serum creatinine levels. The patient continued to be anuric after 10 days of treatment with continuous renal replacement therapy (CRRT). she died a day later. The family history showed that the patient's sister died of acute renal failure 6 months after birth. The genomic sequencing results showed AGXT mutation in the patient and confirmed the diagnosis of primary hyperoxaluria type 1 (PH1). Her parents were heterozygous carriers. PH1 should be considered when the children have abnormal renal function or recurrent renal calculi or have a family history of these symptoms. AGXT gene analysis is an important method for PH1 diagnosis.
Acute Kidney Injury ; etiology ; Female ; Humans ; Hyperoxaluria, Primary ; complications ; Infant ; Mutation ; Oliguria ; etiology ; Transaminases ; genetics

Adolescent ; Adult ; Female ; Humans ; Hyperoxaluria, Primary ; diagnosis ; etiology ; Kidney Transplantation ; adverse effects ; Male ; Recurrence

OBJECTIVETo establish a rat model of low calcium diet related hyperoxaluria and explore its features.

METHODSBy means of randomized blocks design, totally 24 SD male rats were divided into low calcium diet group, medium calcium diet group, and high calcium diet group. Each group was sequentially fed on different calcium diets for 3 days. The urinary volume within 24 hours was recorded, the consistency of urinary oxalate by high-efficiency liquid chromatography, and the consistency of urine creatinine by automatic biochemical analyzer. The consistency was corrected to the output of urinary oxalate of rats in 24 hours, and the results were evaluated by repeated measurement of variance analysis and multivariate analysis of variance.

RESULTSThe output of urinary oxalate of rats in 24 hours varied with time (F=7.893, P0.05). The output of urinary oxalate of rats in 24 hours varied with group division (F=3.565, P<0.05). The output of urinary oxalate in 24 hours in three groups on the third day was significantly higher than that on the first day (P<0.05).

CONCLUSIONBy controlling the calcium intake, we successfully established the model of low calcium diet related hyperoxaluria in rat.

Animals ; Calcium Carbonate ; administration & dosage ; Diet ; Disease Models, Animal ; Hyperoxaluria ; etiology ; urine ; Male ; Rats ; Rats, Sprague-Dawley

No abstract available.
Bone Marrow/*metabolism/pathology ; Calcium Oxalate/chemistry/metabolism ; Humans ; Hyperoxaluria/*etiology ; Kidney Calculi/etiology ; Male ; Middle Aged ; Nephrectomy/*adverse effects ; Pancytopenia/*pathology ; Recurrence ; Renal Insufficiency/etiology ; Thyrotropin/blood