Introduction

Nephrolithiasis is a highly prevalent disease worldwide with rates ranging from 7 to 13% in North America, 5–9% in Europe, and 1–5% in Asia [1–3] There is growing evidence for an increasing incidence of stones in the United States (US) with recent data finding an overall prevalence of stone disease in 8.8% of the population (men 10.6%, women 7.1%) which is an increase from the 5.2% prevalence of kidney stone disease from 1988 to 1994 [4, 5]. This rise was also documented over a 40-year period in Japan where the estimated annual incidence of first-episode upper urinary tract stones in 2005 was 134.0 per 100,000 (192.0 in men and 79.3 in women) compared with 54.2 per 100,000 in 1965 [6]. The annual incidence has increased in all age groups except during the first three decades of life, and the peak age for both men and women has also increased [6]. Iceland also has documented an increase in prevalence from 7 to 24 per 100,000 for men over age 40 and from 7 to 21 per 100,000 for women over 50 years of age during a 24-year period [7, 8].

There is significant variation in rates based on geography, climate, diet, fluid intake, genetics, gender, occupation, and age. Due to the high rates of new and recurrent stones, management of stones is expensive and the disease has a high level of morbidity both acute and chronic. Understanding the epidemiology of stone disease can allow improved patient care and possibly prevention. The goal of this review is to update the work of the prior international consultation on urologic diseases (ICUD) regarding stone disease [9, 10]. A literature search was conducted through Pubmed®, Medline®, and Google Scholar® for English articles using keywords kidney stones, epidemiology, nephrolithiasis, diet intake and urolithiasis, fluid intake and urolithiasis, associated conditions of kidney stones, metabolic syndrome, obesity and nephrolithiasis, diabetes and nephrolithiasis, gout and nephrolithiasis, climate and nephrolithiasis, seasonal factors and nephrolithiasis, and occupation and nephrolithiasis. Studies identified through the search which evaluated current or new risk factors for stone disease internationally since the prior consultation updates comprised the bulk of this 2014 update. The current review is based on the evidence synthesis of the authors of this study highlighting studies which have added value to our understanding of stone disease. This review is limited given that it lacks formalized PRISMA guidelines and is based on expert opinion which may cause selection bias. This review was presented and peer-reviewed at the 3rd International Consultation on Stone Disease during the 2014 Société Internationale d’Urologie Congress in Glasgow.

Risk factors

Age

The incidence of stones varies by age with low incidence in childhood and the elderly and peaks in the fourth to sixth decades of life [11, 12]. An important factor to consider related to age is that incidence and prevalence of kidney stones represent two different entities. While incidence represents new stones, prevalence represents any stone during a period of time. As such, lifetime prevalence increases over time with age, and a population that is older may appear to have a higher stone prevalence when in fact, the incidence of stones is identical to a population that is younger on average. For example, in Japan, the prevalence increased from 4.7 and 2.1% for men and women in 1965, to 15.1 and 6.8% in 2005, respectively [13]. Over this time period, the percent of the population that was elderly increased from 9.7 to 27.9% which may have played a role [13].

There are several studies that found that stone disease is more common in working aged adults and then decreases in older individuals [14–16]. The increase in incidence of stones in middle age may be related to diet, work, and lifestyle changes [17].

There are differences in stone composition in different age groups. Calcium oxalate dihydrate (COD) stones are more common in young stone former in both sexes. In Europe, stone composition differs by age in addition to being affected by gender [16, 18] with COD being 5 times more common in younger people compared to elderly [15], while the contribution of COD declined (between 3 and 5%) for each decade from 20 to 80 years [15]. The amount of calcium oxalate monohydrate (COM) as the main component reached a peak somewhere between 40 and 70 years. In their series in patients up to 10 years of age, calcium phosphate constituted ~40% of cases, but then declined. In 20–29 year old females, calcium phosphate predominates (35% of stone) (mainly carbonate apatite). Infection stones occur at the two extremes of life.

Gender ratios and nephrolithiasis

Overall, there has been a persistent male predominance in prevalence and incidence of kidney stones over a century. Literature suggests a gender ratio (GR) of ~1.5–2.5 across the world [19, 20]. However, there has been some evidence of a narrowing of the gender gap which may be related to changes in diet and increase in metabolic syndrome including rates of obesity and diabetes. In the US, the GR moved from 3:1 to 1.3:1 in 30 years (1970–2000) with rates for women increasing annually at a rate of 1.9% and men decreasing by 1.7% annually [21]. Scales et al. noted a change in GR from 1.7:1 to 1.3:1 (over the period 1997–2002); Strope et al. noted a 52% increase in the nephrolithiasis-related discharges of women as compared to a 22% increase in men; and the GR of stone patients discharged from hospitals, changed from 2 (1998) to 1.6 (2004) [4, 22]. On the other hand, these changes are not consistent worldwide. An analysis of 224,085 stones from 22 German centers noted an increasing GR reaching 2.7 in 2006 (from 1.86 in 1977) [16]. There is not much evidence that socioeconomic issues explain gender disparities [23]. Higher GR is seen in affluent Saudi Arabia (4:1) and Taiwan (GR 3.94) and a low GR (1.91), for upper urinary tract stones in Ouagadougou (Burkina Faso) [24–26].

Geographic variation of incidence and prevalence of nephrolithiasis

There is clear geographic variation in stone incidence worldwide. Even throughout a particular country, the incidence may have a drastic range (Fig. 1). The variation in incidence and prevalence is impacted by many factors with differing magnitude of impact on stone formation. Factors such as seasonal temperature variation, genetics, water, environmental temperature, latitude, pollution, affluence, availability of technology, dietary habits, and age distribution among others interact with each other in complex ways.

Fig. 1
figure 1

Geographical distribution of various incidence rates of stone disease in Japan which have not changed in the last 20 years. Figure taken from Ref. [13], where it appears as “Figure 12.1, Geographical distribution of the annual incidence of urolithiasis in Japan…”

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There are also considerable issues with availability of data and sources of documentation for stones. Some countries have well-established sources of information such as the US but even the Urologic Diseases of America project used various databases for inpatient and outpatient care to try to capture the prevalence of disease since there is no centralized repository [27]. Differences in use of technology such as computed tomography (CT) can impact prevalence since CT scans have a higher sensitivity for stones than plain radiographs and ultrasound. On the other hand, routine use of ultrasound in examination may identify asymptomatic stones and can impact overall prevalence of disease. For example, ultrasound has been noted to identify asymptomatic stones in 2.1% of subjects in Denmark [28], 2% in Japan [29], and in 3% of subjects in Pakistan [30]. This may account for some of the increased prevalence noted in count in these countries.

One of the major problems in determining the prevalence of disease is that information from a third to a half of the population of the world is either non-existent or not accessible in the English speaking world. There is a lack of reliable large-scale studies from two major population blocks in South Central Asia and Sub-Saharan Africa (>1.8 billion people) and an inaccessibility of data for another 1 billion (+) population in China, because of language (Table 1).

Table 1 An assessment of what proportion of the world’s population [145] has extant figures on prevalence and incidence
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Even when available, comparisons are difficult: because of differences in period of study (years); per capita income changes which affect availability of technology; type of population studied (people accessing hospital, or sample of communities); method of study (self-reported, retrospective review of radiological evidence; population-based ultrasound); institutional characteristics (academic, community based, rural, or city); population demographics (ethnic mix, and age), access to care and changes in economy [13, 31]. Available data on incidence and prevalence rates in countries are summarized in Table 2, constructed by mostly adding pertinent information to and utilizing the template provided in the 2007 consultation. For completeness and comparison, some of previous data in that table are included as are data from Africa (though little is available on incidence).

Table 2 Prevalence and incidence of stones by continent incidence are reported as per 100,000 and prevalence as a percent, except where quoted
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There are also some unique populations who are predisposed to stones that can skew prevalence data independently of geography. For example there is a very high prevalence rate (46%) among Hmong (originally from the highlands of Lao) populations who have settled in US (in whom 24% of stones are staghorn) [32]. Similarly there is a high prevalence in the Hubei province in China (20%) in contrast to the rest of China [33] and in native Saudis who have 2.5 times the prevalence as compared to non-native Saudis in Saudi Arabia [34]. Some populations may be protected from upper urinary tract stone disease such as sub-Saharan Africans (see Fig. 2 map of Africa) who have persistently lower rate even after migration to North America, where they have a lower self-reported prevalence compared with Hispanic and non-Hispanic whites [4]. Other populations have demonstrated a rapid increase in stone disease such as in Kerala (South India) [35] from dietary changes on attaining affluence from job-related migration to United Arab Emirates and in Japan, where the incidence doubled over a 40-year time period, both in men and women [6, 13, 36].

Fig. 2
figure 2

Distribution of stone disease in Africa. Figure taken from Ref. [33], where it appears as “Figure 8.1 Distribution of Urinary tract stone disease in Africa)” p. 68

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The urinary metabolic evaluation and stone analysis reveal interesting variations from country to country. For example, hypercalciuria is common in US but rare in Thailand and South Asia. Hyperoxaluria is common in 61% of a cohort from NE Peninsular Malaysia, [37] in 25–29% in India, [38], and only 1.3% in Thailand [39]. This has a significant impact of types of stone disease which can also vary within countries. Figures 3 and 4 show different distributions of stones in China and Japan.

Fig. 3
figure 3

Distribution of stone type in China. Figure taken from Ref. [33], where it appears as “Figure 6.4 Types of stone in different territories of China”)

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Fig. 4
figure 4

Geographical distribution of stone type in Japan. Figure taken from Ref. [13], where it appears as “Figure 12.2, Geographical distribution of stone composition in Japan…”

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More efforts will be necessary to improve understanding of regional variation of stone disease and prevalence in countries with high populations but relatively sparse literature (China and India) in order to improve individualized recommendation based on risk factors of varying local, temperature, diet, and genetics.

Climate and seasonal factors

Regions with higher mean annual temperature have increased risk for stones due to the impact of temperature on fluid status and urine volume [40, 41]. In the US there is a twofold higher prevalence of stones in the Southeastern US compared to the Northern part of the country [40]. A study of individuals living in villages in Israel found that those living in hot climate formed more stones than those residing in temperate climate conditions [42]. Another study found higher stone incidence in British naval personnel stationed in tropical climates as compared with those posted in the UK [43]. The impact of change in temperature was also well documented in a study of military personal deployed to Kuwait from March through August 2003 where at one military hospital a total of 182 patients were diagnosed with 218 symptomatic stones [44]. The mean time to the formation of symptomatic urinary calculi was 93 days with a standard deviation of 42 days.

Within each geographic location there are variations in temperature related to seasonal changes which have been described as “stone season.” Several studies have found that increases in temperature in summer months result in an increase in stone formation. A study evaluating total admissions to emergency departments were obtained from the Taiwan National Health Insurance Research Database (1999–2003) which provided monthly urinary calculi attack rates per 100,000 of the population [45]. The seasonal trends in the monthly urinary calculi attack rates revealed a peak in July–September, followed by a sharp decline in October. Another study from Saudi Arabia evaluated 307 renal stones analyzed during 1 year period from September 2000 to August 2001 from different hospitals in Riyadh and found that maximum number of stones were analyzed in peak summer months [34].

Trends in global warming will likely result in shifting and expansion of areas at increased risk for stone formation [46]. A study modeling the impact of climate change on stone disease found that the fraction of the U.S. population living in high-risk zones for nephrolithiasis will grow from 40% in 2000 to 56% by 2050, and to 70% by 2095. There is a predicted increase of 1.6–2.2 million lifetime cases of nephrolithiasis by 2050, which increases expenditures by 25%.

Diet

In the ICUD consensus document published in 2008, aspects of the relationship between urolithiasis and diet are compared to the updated ICUD 2008–2014 recommendations combined with the American Urological Association (AUA) guidelines [47], which are presented in Table 3. Since 2008, our search identified 30 articles [48–78]. Only six studies involving human subjects have been published since this time and of these, only two of them were RCTs [70, 74]. Moreover, only the former investigation had stone recurrence as its end point for establishing the efficacy or otherwise of the dietary protocols under investigation. Scrutiny of the rest of the articles reveals that the core dietary risk factors—calcium, oxalate, animal protein, carbohydrates, and sodium—remain unchanged. There were no “new” dietary risk factors which were proposed as being significant, although dietary fat was mentioned in two articles [60, 65]. The implied recommendations which emerged from these articles were to reduce the intake of saturated fats and to increase the intake of omega-3 essential fatty acids.

Table 3 Summary of dietary and supplemental findings and recommendations from the ICUD Consensus Document 2008 compared with the updated literature and AUA guidelines
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Several additional details (qualitative and quantitative) which were not described in the 2008 Consensus Document emerged during the present review. Regarding the protective effect of (modestly) increasing dietary calcium, Sellaturay et al. suggested that adding two glasses of milk per day to the diet is strongly associated with a decreased risk of kidney stones [49]; Worcester and Coe provided a more quantitative recommendation of 800–1000 mg/day of dietary calcium [55]. The most recent AUA guidelines increased the recommendation to 1000–1200 mg/day of dietary calcium [47]. With respect to the intake of dietary oxalate, comprehensive lists of oxalate-rich foods were given in two articles [55, 65] and a guideline for the upper limit for oxalate intake was recommended [55]. The limits on protein intake which have been recommended since 2008 are fairly consistent [55, 60, 65]. Johri et al. reported that 40–50 g protein is approximately equivalent to 140–160 g animal flesh, irrespective of whether it is red meat, fish, or poultry [65]. Since sodium and salt (NaCl) are often used interchangeably, care has to be exercised in interpreting the suggested upper limits recommended in different articles: 2–3 g Na/day [79], 6 g NaCl/day (equivalent to 2.4 g Na/day) [60], and 100 mmol Na/day (equivalent to 2.3 g Na/day) [55]. Supplemental calcium is not regarded favorably [49, 55]. Restriction of vitamin C intake continues to be advised [56, 60, 61], with an upper limit of 1500 mg/day being recommended [60]. The role of vitamin D supplementation is controversial. Vitamin D supplementation is regarded as a risk factor [56] and over-repletion of vitamin D can be deleterious as noted in one study [60]. Others have noted that vitamin D therapy, if indicated, should not be withheld solely on the basis of stone disease [77]. Monitoring these patients may be difficult given that one study did not show a relationship between serum vitamin D level and 24-h urine calcium excretion in stone formers [78]. Therefore, repletion should be done carefully. The deleterious effects on urinary stone risk factors caused by high protein, low carbohydrate, ketogenic (Atkins) diets have been reinforced due to increase in urinary calcium and intracellular acidosis [51, 64, 80].

The associations between diet and stone disease are not always conclusive or consistent with several meta-analyses finding inconclusive results [52, 59]. Interestingly, Goldfarb et al. pointed out in the 2008 Consensus Document that the association of a high protein diet with stone prevalence has not been uniformly reported in epidemiological studies nor has any RCT demonstrated that a low animal protein diet has benefits with respect to prevention of stone formation [81]. While, Dussol et al. found that a low animal protein diet administered over 4 years, did not protect against stone recurrence in 175 idiopathic calcium stone formers, [70] the association between a high animal protein diet and nephrolithiasis continues to be widely reported and, as a result, restriction of dietary animal protein is commonly advocated and practiced [49, 50, 53–56, 60, 64, 65]. At this time, there is insufficient compelling evidence to either discount or advocate the beneficial effects of a reduced dietary intake of animal protein with respect to reducing stone formation.

In summary, the present review has shown that since publication of the 2008 Consensus Document, there has not been any major shift in global expert opinion about dietary risk factors for kidney stone formation, nor has there been any new compelling evidence to unambiguously demonstrate an association between dietary interventions and stone recurrence. The recommendations given in Table 4 must be regarded as guidelines, rather than rigid rules. As is common practice, each patient must be evaluated individually. Dietary interventions can then be tailored according to the patient’s specific metabolic profile.

Table 4 Summary of cited findings, authors’ interpretations, and authors’ recommendations
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Fluids

The impact of fluid intake on kidney stone pathogenesis and prophylaxis was briefly discussed in three chapters in the ICUD Consensus Document of 2008 (Table 4) [79–81]. Low fluid intake is a significant risk factor for kidney stone formation and that conversely, a regimen in which intake is increased will decrease the risk. This has been confirmed in more recent reviews. In those cases where authors provided recommendations, the desired urine output was recommended as being >2 l/day [48, 50, 60, 64, 65]. An output of >2.5 l day was advised in one article [68] and was strongly recommended in the most recent AUA guidelines [47]. In order to achieve output volumes of these magnitudes, fluid intake of 2.0–2.5 l/day was recommended [50, 64, 65]. A recent modeling study by Lotan et al. demonstrated that compliance with water intake in stone patients would result in significantly fewer stone recurrences with concomitant cost savings of millions of Euros/Dollars for the national budget [82]. Increasing water intake is therefore an established strategy in the treatment of kidney stone patients.

Four human studies have addressed changing composition of urine [83–86]. Some fruit juices (orange, apple, lime) have successfully raised urinary citrate excretion and urinary pH, both of which are regarded as favorable changes [87]. Inconsistent urinary responses have been reported for other juices such as grapefruit, cranberry and blackcurrant, and for sodas [87]. No updated literature on benefits of lemonade therapy have emerged since the 2nd ICUD statement. The previous literature has shown inconsistent results for lemonade therapy and benefits may be derived solely from maintaining adequate urine volume [88, 89]. Currently, there is insufficient evidence to recommend any forms of beverage (fruit juice, soda, energy drinks) for reduction of stone disease.

Occupational factors

Occupational history is considered an important component of stone formers’ evaluation. Occupation risk include heat exposure resulting in dehydration or conditions that do not permit frequent hydration due to lack of access to water, or bathroom facilities, which may result in lower fluid intake, decreased urine output, and susceptibility to stone formation [90, 91]. Certain occupations such as steel workers, glass makers, and machinists have been associated with increased stones due to exposure to high heat and humidity [92].

Direct occupational exposure to toxic substances may also predispose to stone formation. Cadmium, a well-known nephrotoxic agent, as well as oxalic acid contained in the paint have been suggested as potential examples of substances responsible for a higher prevalence of urolithiasis in welders and spray painters [93–98]. In addition, a recent study has provided evidence that occupational exposure to trimethyltin, a by-product of plastic stabilizers known to inhibit H+/K+ ATPase activity in renal intercalated cells and alter urinary pH, is associated with an increased prevalence of kidney stones, with positive associations seen between exposure levels at the workplace or employment length and the development of stones [99].

Inheritance and genetics

Urinary tract stone disease including the most common form, idiopathic calcium oxalate urolithiasis, is considered to result from the interaction of heritable factors (single or multiple genes; polygenic or monogenic forms of urolithiasis) and their interplay with environmental influences. Although the genetic component is often considered part of the stone formers’ differential diagnosis, people with known genetic causes appear to be few. The familial association of calcium oxalate urolithiasis and primary hypercalciuria, the most common metabolic risk factor, has been corroborated by several familial studies [100–102]. The collective estimation for the likelihood of kidney stone formers having affected first-degree or more distant family members is 15–65%; only 5–20% of non-stone formers have relatives with nephrolithiasis [103, 104]. Estimates of heritability in twin studies are higher (52–56%), with lower concordance in dizygotic than monozygotic twins (17 vs 32%, respectively) [105–107].

Recent genetic advances have revealed several candidate genes involved in renal calcium disorders/stone diseases such as NKCC2, ROMK, and ClCkb/Barttin, underlying renal salt excretion; claudin-14, -16, and -19, underlying renal calcium excretion; CaSR and KLOTHO that provide a sensing mechanism for renal salt, water, and calcium homeostasis regulation; F2, FN1, and HSPG2 encoding the stone inhibitor proteins prothrombin, fibronectin, and heparan sulfate proteoglycan, respectively; and MTNR1A, with unknown as yet mechanism [108–119]. The cellular mechanism for renal trans-epithelial calcium transport depends on these gene products’ concerted action. Despite the fact that their individual pathogenic contribution in stone formation remains obscure, perturbation of their expression/function compromises different steps in the integrated pathway for calcium reabsorption, providing a physiological basis for diagnosing/managing renal stone diseases.

Monogenic forms are characterized by more severe phenotypes and progressive renal function impairment. Dent’s disease, primary hyperoxaluria, adenine phosphoribosyl-transferase (APRT) deficiency (2,8-dihydroxyadeninuria), hypoxanthine–guanine phosphoribosyl-transferase (HPRT) deficiency, and familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) in particular are associated with end-stage renal disease. Defective transporter, channel, and receptor proteins in the renal tubule and in other non-renal epithelia, as well as enzymes have been recognized to be responsible for these phenotypes [120]. Recent literature has also emerged distinguishing between the more recognized homozygous and heterozygous form of cystinuria. Heterozygous patients presented at a later age for their first stone episode had mixed stone compositions, had higher male predominance, and lower incidence of hyperuricemia [121].

Associated diseases

While there are certainly many diseases that may lead to increased risk of kidney stones, we highlight ones based on population issues that are increasing in prevalence.

Obesity

The prevalence and incident risk of kidney stone disease was found to increase with weight and body mass index (BMI) in both men and women from two large prospective cohort studies [122, 123]. The relative risk for stone formation in men weighing more than 100.0 kg vs less than 68.2 kg was 1.44 [95% confidence interval (CI), 1.11–1.86; p = .002 for trend]. A higher risk was also reported for men who gained more than 15.9 kg from the age of 21 years and women from the age of 18 years than in those whose weight did not change: 1.39 (95% CI 1.14–1.70; p = .001 for trend) for men, 1.70 (95% CI 1.40–2.05; p < .001 for trend) for older women, and 1.82 (95% CI, 1.50–2.21; p < .001 for trend) for younger women.

Other studies have shown that obese stone formers (BMI ≥30 kg/m2) are more likely to have a lower urine pH, hyperuricosuria, hypercalciuria, and hypocitraturia than non-obese stone formers [124], and body weight was shown to be inversely related to urine pH in a large population of kidney stone formers [125]. The pathophysiological mechanisms underlying the increase in acid excretion may be related to obesity/insulin resistance [126]. A higher body weight has been linked to insulin resistance, which may be responsible for the more acidic urine of heavier individuals [125, 127]. Previous studies have also suggested that renal lipotoxicity may be an integral part of this complex pathophysiology by impairing Na+/H+ exchange and NH4 + secretion in the proximal tubules of obese individuals [128, 129].

Diabetes mellitus

Epidemiological studies have recently implicated diabetes mellitus (DM) as a risk factor for the development of kidney stones [130, 131]. The relationship between DM and kidney stones has been linked to lower urine pH due to the effects of insulin resistance on ammoniagenesis [127]. Regarding the composition of kidney stones, the formation of uric acid stones was shown to be significantly higher in patients with DM. A study of 2464 calculi from 272 (11%) patients with type 2 diabetes and 2192 without type 2 diabetes found that the proportion of uric acid stones was 35.7% in patients with type 2 diabetes and 11.3% in patients without type 2 diabetes (p < .0001) [132].

Hypertension

Evidence for the association between hypertension and kidney stone disease has been inconsistent. Two longitudinal studies with follow-ups of 8 years showed that the incidence of kidney stones was significantly higher in hypertensive patients [133, 134]. In contrast to these smaller studies in which a large number of patients were lost to the follow-up, the incidence of kidney stone disease was independent of hypertension in a prospective analysis of two large cohorts [135, 136]. The findings of the recent Third National Health and Nutrition Examination Survey (NHANES) found that the likelihood of self-reported hypertension was 69% higher in female stone formers than in non-stone formers but these differences were not seen in men [137]. Consumption of a Dietary Approaches to Stop Hypertension (DASH)-style diet was prospectively examined in three cohort studies (the Health Professionals Follow-Up Study, Nurses’ Health Study, and Nurses’ Health Study II) and was associated with a marked decrease in the risk of kidney stone formation and incident kidney stones [138]. A DASH-style diet may reduce the risk of kidney stone formation by increasing urinary citrate levels and volume [139].

Gout

The findings of a nationally representative sample of American adults showed that even after adjusting for current age and BMI, as well as gender, race, and hypertension, patients with gout were still 49% more likely to have a history of kidney stones [140]. These results were confirmed in men in the prospectively conducted Health Professionals Follow-up Study. The risk of subsequent incident kidney stones in age-adjusted (RR 2.06) and multivariate-adjusted models (RR 2.12) was higher in patients with a confirmed diagnosis of gout than in those without gout. Men with gout were shown to be twofold more likely to develop incident kidney stones than men without gout [141].

Metabolic syndrome

Metabolic syndrome (MetS) also has been associated with kidney stone disease. MetS is a disorder of energy utilization and storage, diagnosed by a co-occurrence of three out of five of the following medical conditions: abdominal (central) obesity, elevated blood pressure, elevated fasting plasma glucose, high serum triglycerides, and low high-density cholesterol (HDL) levels. The prevalence of a self-reported history of kidney stones was shown to increase with the number of MetS traits from 3% with 0 traits to 7.5% with 3 traits and 9.8% with 5 traits. After adjusting for age and other covariates, the presence of 2 or more traits significantly increased the likelihood of self-reported kidney stone disease. The presence of 4 or more traits was associated with an approximately twofold increase in the likelihood of self-reported kidney stone disease in the NHANES [142]. MetS was also associated with a twofold higher level of echographic evidence of kidney stones in Caucasians in Southern Italy [143], and the presence of MetS had an OR of 1.25 for kidney stone prevalence evaluated using computed tomography or ultrasonography in 34,895 individuals who underwent general health screening tests in Korea [144].

Conclusions

There has been a rising incidence in stone disease throughout the world with a narrowing of the gender gap. Increased stone prevalence has been attributed to population growth and increases in obesity and diabetes. There is need for more studies regarding stone prevalence in Asia and Africa as well as identification of regional and ethnic variation in risk. General dietary recommendations of increased fluid, decreased salt, and moderate intake of protein have not changed. However, improvements have been made as specific recommended values have either changed or are more frequently reported. Still, randomized controlled studies are necessary to improve future recommendations regarding diet and fluid intake. Further research into impact of age and gender on stone disease will allow improved recommendations for different age/gender groups. Understanding the impact of associated conditions, especially those such as metabolic syndrome which are rapidly increasing, will improve policy decisions and prevention of stone disease overall.