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Metabolic reactions in the body produce nonvolatile acids, such as sulfuric acid, which generate an acid load of approximately 1 mEq of H+ per kilogram of body weight daily. Excreting H+ in the urine is essential to balance this acid load.
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Urine formation is an essential function of the human body. It plays a critical role in maintaining homeostasis by regulating the volume and composition of body fluids. The kidneys, the primary organs involved in this process, filter blood to remove waste products and excess substances, ultimately producing urine.
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Related Experiment Video

Updated: Sep 15, 2025

Measuring Oral Fatty Acid Thresholds, Fat Perception, Fatty Food Liking, and Papillae Density in Humans
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Acute Effect of High Fat Intake on Urinary Acidification Parameters.

Alireza Zomorodian1, Xilong Li2, John Poindexter1

  • 1Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

Kidney International Reports
|July 18, 2025
PubMed
Summary
This summary is machine-generated.

Uric acid stone formers have a chronic defect in ammonium excretion, unlike controls who show reduced excretion after a fat load. Dietary fat restriction may not be enough to manage their acidic urine.

Keywords:
acid-basefree fatty acidmetabolic syndromeuric acidurolithiasis

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Area of Science:

  • Nephrology
  • Metabolic Disorders
  • Urology

Background:

  • Uric acid nephrolithiasis is increasingly prevalent, linked to obesity and acidic urine pH (UpH).
  • Acidic UpH stems partly from reduced ammonia (NH3) buffering of H+.
  • Renal ammoniagenesis in proximal tubules generates NH3, crucial for acid-base balance.

Purpose of the Study:

  • To investigate if free fatty acids (FFAs) reduce renal ammoniagenesis in uric acid stone formers (UASFs) versus controls (Ctrls).
  • To assess the impact of a dietary fat load as an alternative energy substrate on renal ammoniagenesis.

Main Methods:

  • Seven UASFs and 8 Ctrls underwent a 4-day fixed metabolic diet.
  • Fasting urine and blood samples were collected, followed by a 10-hour oral fat load with serial sampling.

Main Results:

  • Both groups showed similar increases in serum FFAs.
  • UASFs had a persistently lower baseline UpH (5.3) compared to Ctrls (6.6), which decreased significantly in Ctrls but not UASFs during the fat load.
  • The ammonium (NH4+) to net acid excretion (NAE) ratio was lower at baseline in UASFs and decreased in both groups during the fat load.

Conclusions:

  • Controls demonstrated reduced NH4+ excretion with fat load, suggesting a substrate switch.
  • UASFs exhibited a chronic defect in NH4+ excretion, indicative of lipotoxic impairment of proximal tubule function.
  • Dietary fat restriction alone may be insufficient for managing aciduria in UASFs.