Abstract
Elevated urine oxalate (hyperoxaluria) is a risk factor for kidney stones. Normally eliminated by the kidneys, oxalate originates from endogenous metabolism and dietary absorption but secretion into the intestine remains an open question. We considered saliva and bile as two potential sources. Previous studies report ≥100 μmol/L oxalate in saliva, far exceeding blood (1-3 μmol/L), implying secretion. With the liver being the main site of oxalate synthesis, bile is another path into the intestine. We set out to (1) Verify these salivary oxalate concentrations and rates of secretion. (2) Measure oxalate concentrations in bile. Saliva was obtained from healthy volunteers and bile from patients undergoing endoscopic retrograde cholangiopancreatography. Oxalate was determined by commercial assay and ion chromatography coupled with mass spectrometry (IC-MS). With the assay, salivary oxalate averaged 21 μmol/L. However, using IC-MS, values were ~1 μmol/L, comparable to plasma. This disparity resulted from positive interference with the enzyme-based assay by one or more constituents in saliva. The rate of salivary secretion thus proved negligible. Bile oxalate averaged 14 μmol/L, suggesting hepatocyte secretion but biliary clearance is minor (<5%), relative to urine. We conclude saliva and bile are insignificant sources of secretion and unnecessary for determining oxalate clearance.