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Low urinary citrate: an overview.

Miriam Zacchia¹, Patricia Preisig

¹Department of Nephrology, Second University of Naples, Naples, Italy. miriamzacchia@virgilio.it

Journal of Nephrology

|December 21, 2010

Summary

Hypocitraturia, or low urinary citrate, increases kidney stone risk. Acid-base balance significantly impacts citrate levels by affecting its reabsorption and metabolism in the kidneys.

Area of Science:

Nephrology
Biochemistry
Urology

Background:

Hypocitraturia is a significant risk factor for kidney stone formation.
Urinary citrate plays a crucial role in preventing calcium stone development by forming soluble calcium-citrate complexes.
Ingested citrate is rapidly metabolized, with plasma levels showing little variation, thus not significantly influencing urinary citrate excretion.

Purpose of the Study:

To elucidate the physiological mechanisms governing urinary citrate excretion.
To understand the role of acid-base status in regulating citrate transport and metabolism.
To identify key factors influencing hypocitraturia and calcium stone risk.

Main Methods:

The study focuses on the physiological regulation of urinary citrate excretion.

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Investigated the roles of NaDC1 cotransporter in citrate absorption and proximal tubule cell metabolism.

Examined the influence of acid-base status on citrate transport and enzymatic metabolism (ATP citrate lyase, m-aconitase).

Main Results:

Urinary citrate excretion is primarily determined by reabsorption from the glomerular filtrate and proximal tubule cell metabolism.
Acid-base status is the key physiological determinant, modulating NaDC1 activity and citrate-metabolizing enzymes.
Acid loads up-regulate both transport and metabolism, leading to hypocitraturia; alkaline loads primarily affect mitochondrial metabolism, increasing citrate excretion.

Conclusions:

Urinary citrate levels are tightly regulated by kidney function and acid-base balance.
Understanding these mechanisms is crucial for managing hypocitraturia and reducing kidney stone formation.
Targeting citrate transport and metabolism represents a potential therapeutic strategy for kidney stone prevention.