Bicarbonate re-absorption in renal stone patients with acidification defects.
A pathological renal response to ammonium chloride loading was found to be common in renal stone formers. In order to elicit further information about the impaired acidification capacity eight patients were investigated by bicarbonate loading. One patient with a mild acidification defect had normal tubular re-absorption of bicarbonate. Five of these eight patients with suspected proximal acidification defect and two patients with impaired distal acidification were found to have a low bicarbonate threshold and an increased, fractionated, bicarbonate excretion at a normal plasma bicarbonate level. Four of the patients with suspected, proximal, acidification defect reached a maximal re-absorption of bicarbonate (Tm) that was low, while three patients did not reach a Tm. These three factors indicate increased bicarbonate wastage from the kidneys. A constantly alkaline urine, such as exists in patients with proximal acidification defect may give rise to an increased risk of the precipitation of renal stones - primarily calcium-phosphate stones.
D000141:Acidosis, Renal Tubular / Q000150:complications / Q000378:metabolism*; D000328:Adult; D000471:Alkalosis / Q000378:metabolism; D001639:Bicarbonates / Q000097:blood / Q000378:metabolism* / Q000652:urine; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007669:Kidney Calculi / Q000150:complications / Q000378:metabolism*; D007686:Kidney Tubules, Distal; D007687:Kidney Tubules, Proximal; D008297:Male; D008875:Middle Aged
D001639:Bicarbonates