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Making a Dent in Dent Disease.

Katherine E Shipman¹, Ora A Weisz¹

¹Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.

Function (Oxford, England)

|October 5, 2020

Summary

Dent disease, a rare kidney disorder, stems from ClC-5 mutations. This review explores how ClC-5 transporter dysfunction causes kidney tubule damage and proteinuria.

Area of Science:

Nephrology
Molecular Biology
Cell Biology

Background:

Dent disease (DD) is a rare inherited kidney disorder linked to mutations in the chloride/proton exchanger ClC-5.
ClC-5 plays a crucial role in endosomal ion homeostasis within kidney proximal tubule cells.
The precise mechanisms by which ClC-5 dysfunction leads to megalin and cubilin receptor trafficking defects and subsequent proteinuria remain unclear.

Approach:

This review synthesizes current knowledge on ClC-5 function in kidney proximal tubules.
It critically evaluates existing literature regarding the link between ClC-5 and endosomal receptor trafficking.
New testable models are proposed to explain the pathogenesis of tubular proteinuria in Dent disease.

Key Points:

Loss of ClC-5 function disrupts endosomal pH and ion balance.

Keywords:

Dent disease cubilin endocytosis megalin recycling tubular proteinuria

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Impaired trafficking of megalin and cubilin receptors is a key consequence of ClC-5 deficiency.

This receptor trafficking defect is strongly implicated in the low molecular weight proteinuria characteristic of Dent disease.

Conclusions:

Further research is needed to fully elucidate the molecular pathways connecting ClC-5 to receptor-mediated endocytosis in proximal tubules.
Understanding these pathways is critical for developing targeted therapies for Dent disease.
New models provide a framework for future experimental investigations into DD pathogenesis.