Objective: To analyze the clinical symptoms and treatment process of a cases of type 1 Dent disease in children with Bartter syndrome

so as to enhance clinical awareness of the disease. Methods: Retrospective analysis was conducted by collecting clinical data from a patient diagnosed with type 1 Dent disease complicated with Bartter syndrome through clinical characteristics and genetic testing. The clinical characteristics and treatment process were summarized

and relevant literature was reviewed. Results: The child initially presented with Bartter syndrome (persistent hypokalemia

elevated plasma renin and aldosterone levels

normal blood pressure). Significant increases were observed in quantitative urine protein

predominantly low-molecular-weight proteins (LMWP)

and elevated levels of α1 and β2 microglobulin (MG). Genetic analysis revealed a heterozygous mutation in the CLCN5 gene c. 1265-c. 1266 insA. The child exhibited normal renal function at the initial stage

with no abnormalities detected in the urinary system on ultrasound examination. Initially

dietary adjustments (such as low oxalate

low sodium and low calcium) and oral potassium supplementation

along with benazepril at 0. 25 mg/ (kg·d)

were implemented. However

after one month of treatment

the child experienced acute kidney injury

and subsequent administration of methylprednisolone and blood purification led to improvement in renal function. Conclusion: The clinical phenotype of Dent disease is complex and requires timely improvement of genetic testing for co-diagnosis. Dent patients with Bartter syndrome are prone to develop renal failure

and renal function should be evaluated in a timely manner and followed up regularly for a long period of time.