ALKALI ABSORPTION AND CITRATE EXCRETION IN CALCIUM NEPHROLITHIASIS

The role of net gastrointestinal (GI) alkali absorption in the develop ment of hypocitraturia was investigated. The net GI absorption of alka li was estimated from the difference between simple urinary cations (C a, Mg, Na, and K) and anions (Cl and P). In 131 normal subjects, the 2 4 h urinary citrate was positively correlated with the net GI absorpti on of alkali (r = 0.49, p < 0.001). In 11 patients with distal renal t ubular acidosis (RTA), urinary citrate excretion was subnormal relativ e to net GI alkali absorption, with data from most patients residing o utside the 95% confidence ellipse described for normal subjects. Howev er, the normal relationship between urinary citrate and net absorbed a lkali was maintained in 11 patients with chronic diarrheal syndrome (C DS) and in 124 stone-forming patients devoid of RTA or CDS, half of wh om had ''idiopathic'' hypocitraturia. The 18 stone-forming patients wi thout RTA or CDS received potassium citrate (30-60 mEq/day). Both urin ary citrate and net GI alkali absorption increased, yielding a signifi cantly positive correlation (r = 0.62, p < 0.0001), with the slope ind istinguishable from that of normal subjects. Thus, urinary citrate was normally dependent on the net GI absorption of alkali. This dependenc e was less marked in RTA, confirming the renal origin of hypocitraturi a. However, the normal dependence was maintained in CDS and in idiopat hic hypocitraturia, suggesting that reduced citrate excretion was larg ely dietary in origin as a result of low net alkali absorption (from a probable relative deficiency of vegetables and fruits or a relative e xcess of animal proteins).