S-13-00837 Expedited IRB approval pending
PI: J Lowenstein, MD
While it has long been recognized that some patients with renal disease exhibit stable metabolic acidosis . Estimation of the rate of acid production, based on measurements of urinary sulfate and organic acid excretion, and urinary acid excretion, estimated from measurements of titratable acidity (TA) and urinary ammonium excretion, have consistently been reported to reveal an excess of acid production over excretion of about 20 mEq ( 1,2 ). Most texts of renal disease and acid - base physiology assume that the excess acid is buffered by the skeleton ( 3 ). Oh and Uribarri ( 4, ) have presented strong evidence that this cannot be the explanation as there is not sufficient buffer capacity in bone to sustain a stable metabolic acidosis for more than one year.
The study will examine the hypothesis that glutamine excretion, not measured in the assessment of metabolic acidosis, represents the “missing acid excreted”. Urinary glutamine excretion will be measured, by a standard colorimetric assay, in 10 subjects with stable renal metabolic acidosis, identified in the Renal Clinic of Bellevue Hospital. Glutamine measurements will also be performed on the urine of 3 normal volunteers. 24 hour urine collections will permit calculation of the apparent gap between acid production and excretion (in a further study of the same samples) if the hypothesis of glutamine excretion is confirmed.