Differences in 24-h urine profiles and stone composition among stone formers with and without coronary heart disease


Kidney stones are a common condition, with an estimated prevalence of about 8% (Croppi E – 2012 [1]). Kidney stone disease seems to be associated with systemic conditions including diabetes mellitus, high blood pressure and increased risk of incident cardiovascular outcomes (Ferraro PM – 2013 [2]). The reasons for this association are still unknown. A subgroup of stone formers might have characteristic metabolic abnormalities that in turn could be associated with increased cardiovascular risk. We analyzed differences in 24-h excretory profiles and stone composition among stone formers with and without heart disease (HD).


We used data from patients attending the UCL Centre for Nephrology’s metabolic stone clinic in London from 1995 to 2012. We divided the sample into two groups according to the presence or absence of a history of HD (defined as self-reported history of myocardial infarction, angina, coronary revascularization, or surgery for calcified heart valves) and analyzed 24-h urines and stone composition measurements for differences between groups with univariate and multivariate regression models.


1826 patients had available data for 24-h urine analysis. Among these, 108 (5.9%) had a history of HD. Those with HD were older (59±13 vs 46±13 years, p<0.001), whereas the prevalence of males was similar among the two groups (73 vs 70%, p=0.52).

Univariate analyses showed that patients with HD had significantly lower urinary excretions for citrate (2.4±1.5 vs 2.6±1.4 mmol, p=0.04) and magnesium (3.9±1.3 vs 4.2±1.3 mmol, p=0.03); adjustment for age and sex did not change these findings. The 24-h urine comparisons between groups are reported in Figure 1.

A subgroup of 677 patients had available data for stone composition analysis. The proportion of calcium oxalate (57 vs 53%, p=0.99), calcium phosphate (19 vs 28%, p=0.76), and uric acid (16 vs 12%, p=0.64) in analyzed stones was similar for those with and without HD.


Stone formers with HD have lower urinary excretions for citrate and magnesium. Since both citrate and magnesium have been implicated in the pathogenesis of arterial plaque formation (“McCarty MF – 2014” [3]“Reid DG – 2013” [4]), as well as being protective factors in nephrolithiasis, this may indicate a common mechanism underlying the processes of kidney stone formation and of arterial calcification and plaque formation.