Alkali absorption and citrate excretion in calcium nephrolithiasis (original) (raw)
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Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas
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Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas
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Center for Hypertension and Renal Metabolic Disorders, State University of New York, Downstate Medical Center, Brooklyn
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Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas
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Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas
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National Aeronautics and Space Administration, Johnson Space Center, Houston, Texas
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Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas
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Received:
25 September 1991
Revision received:
17 December 1992
Accepted:
21 December 1992
Cite
Khashayar Sakhaee, Russel H. Williams, Man S. Oh, Paulette Padalino, Beverley Adams‐Huet, Peggy Whitson, Charles Y.C. Pak, Alkali absorption and citrate excretion in calcium nephrolithiasis, Journal of Bone and Mineral Research, Volume 8, Issue 7, 1 July 1993, Pages 789–794, https://doi.org/10.1002/jbmr.5650080703
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Abstract
The role of net gastrointestinal (GI) alkali absorption in the development of hypocitraturia was investigated. The net GI absorption of alkali was estimated from the difference between simple urinary cations (Ca, Mg, Na, and K) and anions (Cl and P). In 131 normal subjects, the 24 h urinary citrate was positively correlated with the net GI absorption of alkali (r = 0.49, p < 0.001). In 11 patients with distal renal tubular acidosis (RTA), urinary citrate excretion was subnormal relative to net GI alkali absorption, with data from most patients residing outside the 95% confidence ellipse described for normal subjects. However, the normal relationship between urinary citrate and net absorbed alkali was maintained in 11 patients with chronic diarrheal syndrome (CDS) and in 124 stone‐forming patients devoid of RTA or CDS, half of whom had “idiopathic” hypocitraturia. The 18 stone‐forming patients without RTA or CDS received potassium citrate (30–60 mEq/day). Both urinary citrate and net GI alkali absorption increased, yielding a significantly positive correlation (r = 0.62, p < 0.0001), with the slope indistinguishable from that of normal subjects. Thus, urinary citrate was normally dependent on the net GI absorption of alkali. This dependence was less marked in RTA, confirming the renal origin of hypocitraturia. However, the normal dependence was maintained in CDS and in idiopathic hypocitraturia, suggesting that reduced citrate excretion was largely dietary in origin as a result of low net alkali absorption (from a probable relative deficiency of vegetables and fruits or a relative excess of animal proteins).
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