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Renal Drug Excretion: Tubular Secretion

Renal Drug Excretion: Tubular Secretion

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Related Experiment Video

Updated: May 14, 2025

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells

Published on: June 20, 2018

Updates on renal phosphate transport.

Carsten Alexande Wagner¹, Daniela Egli-Spichtig, Isabel Rubio-Aliaga

¹Institute of Physiology and Zurich Kidney Center, University of Zurich, Zurich, Switzerland.

Current Opinion in Nephrology and Hypertension

|May 13, 2025

Summary

This summary is machine-generated.

Kidneys regulate phosphate balance via NaPi transporters. Novel insights into their regulation, genetics, and potential as drug targets for hyperphosphatemia and kidney disease are discussed.

Keywords:

fibroblast growth factor 23 nephrolithiasis parathyroid hormone phosphate transporters

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Last Updated: May 14, 2025

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells

Published on: June 20, 2018

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry

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Published on: October 28, 2014

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Published on: June 27, 2015

Area of Science:

Nephrology
Molecular Biology
Genetics

Background:

Kidneys maintain systemic phosphate homeostasis through inorganic phosphate (Pi) reabsorption.
Proximal tubule cells express three key Na+-driven Pi cotransporters: NaPi-IIa (SLC34A1), NaPi-IIc (SLC34A3), and PiT-2 (SLC20A2).

Purpose of the Study:

To review novel aspects of renal phosphate transporter regulation, pharmacology, and genetics.
To explore the therapeutic potential of targeting these transporters.

Main Methods:

Review of current literature on renal phosphate transporters.
Analysis of genetic variants and their clinical manifestations.
Discussion of pharmacological interventions.

Main Results:

Renal NaPi transporters are regulated by hormones like PTH and FGF23, and potentially by IP6 kinases.
Inhibitors of NaPi transporters induce phosphaturia and may lower PTH and FGF23 in CKD models.
Loss-of-function mutations in SLC34 transporters are linked to nephrocalcinosis, rickets, and accelerated kidney function decline.

Conclusions:

Renal Pi transporters are dynamically regulated and represent potential therapeutic targets.
Targeting these transporters may offer new strategies for managing hyperphosphatemia.
Genetic variants in renal Pi transporters contribute to kidney stone formation and chronic kidney disease (CKD) risk.