Hypocitraturia in Patients with Gastrointestinal Malabsorption

Abstract

We measured serum and urinary citrate, oxalate, calcium, and magnesium in 22 normal subjects and in 16 patients with malabsorption. The patients had subnormal levels of serum citrate and magnesium during fasting, subnormal 24-hour levels of urinary citrate, magnesium, and calcium, and excessive levels of urinary oxalate. Daily citrate excretion averaged only 15 per cent of normal. The hypocitraturia in the patients resulted from a subnormal filtered load of citrate and abnormally high net tubular reabsorption of the anion. An oral citrate supplement raised both the serum concentration and the filtered load of citrate to normal fasting values, but net tubular reabsorption remained abnormally high and urinary excretion abnormally low. Intramuscular magnesium sulfate, which corrected the hypomagnesemia and hypomagnesuria, had no effect on serum citrate or its filtered load. Nevertheless the injection restored net tubular reabsorption of citrate to normal and partially improved the hypocitraturia. Full correction of the hypocitraturia was achieved by combined treatment with oral citrate and intramuscular magnesium sulfate. Hypocitraturia may contribute to the formation of oxalate stones in these patients, and therefore our treatment may help to prevent this complication.

Management of patients with a short bowel

“…Hypocitraturia is common in patients with malabsorption or jejunoileal bypass [195][196][197] . Citrate excretion and urine pH are reduced by systemic acidosis, including that caused by gastrointestinal bicarbonate wastage, and by hypomagnesaemia.…”

“…Citrate excretion and urine pH are reduced by systemic acidosis, including that caused by gastrointestinal bicarbonate wastage, and by hypomagnesaemia. Hypocitraturia in patients with malabsorption can be corrected by oral citrate supplementation and magnesium injections [196] .…”

Risk factors for low urinary citrate in calcium nephrolithiasis: low vegetable fibre intake and low urine volume to be added to the list

“…From the patients routinely seen for metabolic work-up at our renal stone clinic, 34 consecutive male recurrent idiopathic calcium stone formers (RCSF) meeting the following criteria were studied: (1) passage or removal of at least two calcium-containing stones, defined either by stone analysis (X-ray diffraction) or disappearance of opaque material on conventional radiographs or excretory urograms; (2) no established cause of calcium stone formation such as primary hyperparathyroidism, medullary sponge kidney, overt distal renal tubular acidosis, sarcoidosis, excessive vitamin D intake, and hypercalciuria due to hypercalcaemia of malignancy or immobilization; (3) absence of obvious causes of hypocitraturia such as malabsorption with steatorrhoea [13], hypokalaemia (serum K<3.5 mmol/1) due to acetazolamide or thiazide treatment, or urinary tract infection [14]; and (4) C crcm >70ml/min/1.73m 2 . Ml RCSF were referred after ESWL or endourolegical treatment of their stone disease, and they were asked to keep unchanged the free-choice diet they used to have before stone treatment.…”

The&lt;i&gt; I&lt;/i&gt;550&lt;i&gt;V&lt;/i&gt; polymorphism in the renal human sodium/dicarboxylate cotransporter 1 (&lt;i&gt;hNaDC&lt;/i&gt;-1) gene is associated with the risk for urolithiasis in adults from Southeastern, Mexico

“…The presence of this protein in the intestine was documented by Northern blot analysis, in which, mRNA of NaDC-1 was detected in intestinal tissue [9]. The fact that the same protein regulates citrate absorption in both the intestine as in the renal proximal tubules is interesting in the sense that one SNP affecting the recognition of the NaDC-1 substrate would result in a poor citrate absorption at the intestine level, which could be reflected with the onset of hypocitraturia [20]. Poor intestinal citrate absorption should not be dismissed as a possible cause for the high frequency of hypocitraturia in the Yucatan population.…”