Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Keep Your Urine Dilute: Concentrated urine lets calcium oxalate and other salts reach saturation and crystallise, and stone formers in this study had lower baseline urine volumes than stone-free controls (about 1,057 ml a day versus 1,401 ml in men). In a five-year randomised trial, 199 people after a first idiopathic calcium stone were assigned either to a high intake of water with no other dietary change, or to no treatment. Over five years 12 of 99 in the water group had a recurrence against 27 of 100 in the untreated group, and the recurrences that did happen came later (38.7 months versus 25.1 months). The authors concluded that urine volume is a genuine stone risk factor rather than a marker of one. Journal of Urology (PubMed)
Keep Calcium In Your Food: Cutting calcium out of the diet to prevent calcium stones appears to backfire, because calcium eaten with a meal binds oxalate in the gut so less oxalate is absorbed and excreted in urine. A five-year randomised trial in 120 men with recurrent calcium oxalate stones and idiopathic hypercalciuria compared a diet with normal calcium but reduced animal protein and reduced salt against the traditional low-calcium diet. Twelve of 60 men relapsed on the normal-calcium, low-protein, low-salt diet versus 23 of 60 on the low-calcium diet, an unadjusted relative risk of 0.49 (95% CI 0.24 to 0.98). Urinary oxalate excretion rose on the low-calcium diet and fell on the other one, which is the mechanism the authors point to. New England Journal of Medicine (PubMed)
Skip Sugar-Sweetened Drinks: Fructose has been shown to increase urinary excretion of calcium, oxalate and uric acid, which is the proposed route from sweetened drinks to stones. Across three prospective cohorts totalling 194,095 people and 4,462 incident stones, a serving a day or more of sugar-sweetened cola was associated with 23% higher risk and sugar-sweetened non-cola with 33% higher risk, compared with less than one serving a week, though the confidence interval for cola was wide. In the same cohorts coffee was associated with lower risk (26% lower for caffeinated, 16% for decaffeinated) as were tea (11% lower) and orange juice. Beer and wine also tracked with lower risk, but that is observational and heavily confounded by who drinks what, so it is not a reason to start drinking. Clinical Journal of the American Society of Nephrology (PMC)
Watch Weight And Waist Size: Larger body size is associated with higher urinary excretion of calcium, oxalate and uric acid, which raises the chance those salts crystallise. In three prospective cohorts covering 241,623 participants and 4,827 incident stones, men over 220 lb had about 1.44 times the risk of men under 150 lb, while women at those same weights had roughly 1.9 times the risk. Gaining more than 35 lb since early adulthood was associated with about 1.39 times the risk in men and 1.70 to 1.82 times in women, and waist circumference tracked with risk in both sexes. The authors concluded that obesity and weight gain are associated with stone formation, and that the increase may be larger in women than in men. JAMA (PubMed)
Find Out Your Stone Type: Which of the above matters most depends on what the stones are actually made of, since most dietary evidence comes from calcium oxalate stones in particular study populations and does not transfer to uric acid, struvite or cystine stones. The evidence base is also thinner than it looks: a 2017 review notes that only one randomised controlled trial has tested increased fluid intake for preventing recurrence, that it enrolled only first-time stone formers, and that the heterogeneity of stone disease has limited opportunities for large randomised trials. Recurrence stays common regardless, with rates in one cohort of 11%, 20%, 31% and 39% at 2, 5, 10 and 15 years. Analyzing a passed stone and measuring what is in the urine are how the relevant risk factors get identified, and that is a conversation to have with a doctor. Clinical Journal of the American Society of Nephrology (PMC)
How much of this is genetic?
Genetics explains 56% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Goldfarb et al. 2005, Kidney International
Background and further reading
Nephrolithiasis is the formation of hard mineral and salt deposits, known as kidney stones, within the kidneys or urinary tract. It is common, with an estimated lifetime prevalence of roughly 10% and rising in many countries [1]. Most stones (about 80%) are composed primarily of calcium oxalate, with the remainder made up of calcium phosphate, uric acid, struvite, or cystine. Small stones may pass unnoticed, but larger ones can cause severe flank pain (renal colic), blood in the urine, nausea, and urinary tract obstruction. Stones frequently recur, with roughly half of affected people forming another stone within 5 to 10 years [2].
Genetic Basis: Twin and family studies estimate the heritability of kidney stone disease at roughly 45 to 56%, indicating that inherited factors contribute substantially alongside diet and environment [3]. The trait is highly polygenic, but a handful of genes involved in mineral handling stand out. Common variants near CLDN14 (claudin-14), which regulates calcium reabsorption in the kidney tubule, were among the first robust genome-wide associations and also relate to urinary calcium levels [4]. Additional signals implicate CASR (the calcium-sensing receptor), ALPL, SLC34A1 (a renal phosphate transporter), and the vitamin D and oxalate metabolism pathways [5]. Rare highly penetrant mutations in genes such as SLC3A1/SLC7A9 (cystinuria) and AGXT (primary hyperoxaluria) cause distinct monogenic stone diseases that a polygenic score does not capture.
Environmental Factors: Kidney stone formation is strongly influenced by modifiable factors, which is why genetics is only part of the picture. Low fluid intake and concentrated urine are the leading risk factors, while high dietary sodium, high animal protein intake, and low dietary calcium each raise the concentration of stone-forming salts in urine [2]. Obesity, diabetes, gout, and metabolic syndrome are associated with higher stone risk, and hot or dry climates increase risk through dehydration [1]. Adequate hydration and dietary adjustments are the cornerstone of prevention, and these measures can meaningfully lower risk even in people with a genetic predisposition.
The published research behind your score, and the variants it draws on.
4 published scores from 2 studies
The nephrolithiasis score combines 4 polygenic scores drawn from 2 published studies.
Scales CD Jr, et al. Prevalence of kidney stones in the United States. European Urology (2012)
Khan SR, et al. Kidney stones. Nature Reviews Disease Primers (2016)
Howles SA, Thakker RV. Genetics of kidney stone disease. Nature Reviews Urology (2020)
These traits are influenced by some of the same genes and variants as this one
Venous Thromboembolism: Blood clots that form in the deep veins and can travel to the lungs.
Content updated August 2026.
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