The Urinary Citrate Excretion in Patients With Renal Calculi

Abstract

Summary It has been suggested that an important factor in the formation of renal calculi is a deficiency of citrate excretion by the kidney. This we have failed to confirm and consider rather that any gross diminution of urinary citrate is due simply to infection of the urinary tract. The proof of this is as follows:‐ 1. In seven patients with calculi and a sterile tract the average citrate content of the urine was comparable with that found in controls. 2. Seven patients with calculi, associated with infection, were all found to have less citrate in their urine than normals. 3. Experiments in vitro confirmed that in this latter group citrate was destroyed particularly by E. colz, although with Kosers medium this splitting action was not detectable.

Value of Routine Citrate Analysis and Calcium/Citrate Ratio in Calcium Urolithiasis

“…In the present study, we found only recurrent stone formers to have a reduced citrate excretion, while patients with a single stone episode showed no difference to the control group. It is known that citrate excretion is reduced in urine infected by certain organisms [ 19], in patients with impaired renal function [8], renal tubular acidosis [20], intestinal malabsorption [21], or potassium deficiency [22], Renal acidification or systemic acidosis are impor tant factors for reduced citrate excretion. All our patients were free of urinary tract infections, had normal renal function and no metabolic disorders.…”

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.…”

Renal tubular acidosis of pyelonephritis with renal stone disease.

“…There are at least three possible causes of the reduced citrate output that is known to be a feature of renal stone disease. It has been suggested that it is attributable to metabolism of citric acid in the urine by bacteria (Conway, Maitland, and Rennie, 1949). We have previously expressed the view that this is unlikely to be the explanation, since we have found no difference in the citrate output of infected and non-infected stone-formers (Nordin and Smith, 1963).…”