Dent disease is a rare kidney disorder characterized by excess protein in the urine (proteinuria) caused by mutation of the chloride/proton exchanger ClC-5. People with Dent disease often develop chronic kidney disease that progresses to end-stage kidney disease. A new review, published ahead of print in Function, explores how loss of ClC-5 function impairs receptors in the renal proximal tubule to cause proteinuria. The review’s authors have performed a literature review addressing relevant questions and have identified additional questions that remain unanswered.
“Progress deciphering the pathogenesis of [Dent disease] will likely inform our understanding of other conditions that result in [low molecular weight] proteinuria and may suggest global therapeutic targets to modulate [proximal tubule] endocytic capacity,” the authors wrote.
Read the full review, “Making a dent in Dent disease,” published ahead of print in Function. Contact the APS Communications Office or call 301.634.7314 to schedule an interview with a member of the research team.
