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Kidney Week

Abstract: SA-PO300

Controls but Not Patients with Calcium Nephrolithiasis Secrete Less Urinary Uromodulin After Salt Loading

Session Information

Category: Bone and Mineral Metabolism

  • 502 Bone and Mineral Metabolism: Clinical

Authors

  • Bani Hani, Salar, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Wolf, Matthias Tilmann, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Sakhaee, Khashayar, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Background

Calcium is the most common constituent of kidney stones. Uromodulin (UMOD) enhances TRPV5 membrane abundance increasing renal Ca2+ absorption thus reducing hypercalciuria. UMOD stimulates Na+absorption via NKCC2 causing hypertension. High salt intake is also risk factor for nephrolithiasis. We hypothesize that a higher urinary UMOD secretion with a high salt diet compensates for the higher stone risk by improving hypercalciuria.

Methods

This is a prospective, randomized, cross-over study. Stone-formers and controls were randomized to a control or a high salt diet for 2 days. After washout, the participants received the diet they were not exposed to previously. After each diet, we obtained 24-hour urine and fasting serum studies.

Results

At baseline, there was no significant difference for urinary UMOD secretion between stone-formers and controls. In contrast to our hypothesis, we found that urinary UMOD secretion was significantly reduced after the salt load in controls but not in stone-formers.

Conclusion

There was no lower baseline urine UMOD level in stone-formers. After salt loading, we show lower urinary UMOD secretion in controls but not in stone-formers. As UMOD enhances NKCC2 contributing to hypertension, acute downregulation of UMOD after a salt loading makes physiologically sense.

Salt-loading reduces uUMOD in controls only (P<0.05).

Baseline.