Epidemiology

The lifetime prevalence of nephrolithiasis is estimated to be about 10%.[3] The probability of having a stone varies according to age, sex, race, and geographical location.[3][4][5] Nephrolithiasis typically affects adult men more commonly than adult women; however, there is evidence that this difference in incidence between men and women is narrowing.[4] In US men, the highest prevalence of nephrolithiasis is found in white men, followed by Hispanic men, non-Hispanic men, and black men.[3] However, the rate of stone incidence is increasing at a faster rate for black people compared to white, and particularly for black women compared to men.[6] Historically, stone occurrence was relatively uncommon before age 20 years but the incidence of stones in children and adolescents is rising.[6] In adults, stone incidence peaks between the ages of 40 and 50 years.[7]

Nephrolithiasis has a higher prevalence in hot, arid, or dry climates such as the mountains, desert, or tropical areas.[4][8] Worldwide, regions of high stone prevalence include the US, UK, Scandinavian and Mediterranean countries, northern India and Pakistan, northern Australia, central Europe, portions of the Malay peninsula, and China.[4] Heat exposure and dehydration are risk factors for nephrolithiasis. The prevalence and incident risk of nephrolithiasis are directly correlated with type 2 diabetes, obesity, and adiposity variables including higher waist circumference and BMI in both sexes, although the magnitude of this association is greater in women than in men.[9][10][11]

Risk factors

Fluid intake is very important and should be 2.5 to 3 litres (adults) or 1 to 2 litres (children) per day.[15] In two large observational studies, fluid intake was found to be inversely related to the risk of renal stone formation.[16][17] A low urine output can produce a higher concentration of urinary solutes, therefore leading to stone formation.

Higher sodium intake is associated with higher urinary sodium and calcium levels, and decreased urinary citrate.[18] This promotes calcium salt crystallisation due to urinary saturation of monosodium urate and calcium oxalate/calcium phosphate being increased. Salt excess can also lead to bone loss, thereby worsening hypercalciuria.

In US men, the highest prevalence of nephrolithiasis is found in white men, followed by Hispanic men, Asian men, and black men.[19] Among US women, the prevalence is highest among white women but lowest among Asian women.[20]

Nephrolithiasis typically affects adult men more commonly than adult women, with a male to female ratio of 2 or 3:1.[21][19][22] However, there is evidence that this difference in incidence between men and women is narrowing.[23]

Two large prospective cohort studies of men and women found that the prevalence and incident risk of nephrolithiasis were directly correlated with higher weight and BMI in both genders, although the magnitude of the association was greater in women than in men.[16][17]

Evidence linking obesity with low urine pH and uric acid stones and an association with hypercalciuria could account for an increased risk of uric acid and/or calcium stones in obese patients.[2]

Stone formers (especially calcium oxalate stones) frequently excrete more calcium oxalate crystals in the urine. Increased urinary excretion of cystine, struvite, and uric acid crystals is also a risk factor for stone formation.[2][24]

Dehydration and heat exposure are risk factors for nephrolithiasis. Those exposed to high temperatures demonstrate lower urine volumes and pH, higher uric acid levels, and higher urine specific gravity, leading to higher urinary saturation of uric acid, as well as calcium oxalate. As a result, people exposed to dehydration and heat are at increased risk for forming stones.[4][25]

Seasonal variation in nephrolithiasis is likely related to temperature because of fluid losses through perspiration. It has been reported that the highest incidence of nephrolithiasis is in the summer months, with the peak occurring within 1 to 2 months of maximal mean temperatures.[4][25]

In the US, prevalence of nephrolithiasis in the south-eastern states ('stone belt') is nearly double that in other areas.[8]

A positive family history of nephrolithiasis is associated with an increased risk of forming stones. A stone former is twice as likely as a non-stone former to have a first-degree relative with a history of stones. Patients with a family history have a higher incidence of multiple stones and early recurrence.[24] Studies into possible genetic mutations responsible for inherited forms of nephrolithiasis are ongoing.[26]

Medications that are associated with an increased risk of stone formation include calcium-containing antacids, carbonic anhydrase inhibitors, sodium and calcium-containing medications, vitamin C, and vitamin D. Most of these medications lead to higher urinary levels of calcium, uric acid, sodium, or oxalate, in turn promoting stone formation. Other medications are poorly soluble with high urinary excretion, favouring direct crystallisation and stone formation in urine. These include protease inhibitors (e.g., indinavir, atazanavir), ephedrine, guaifenesin, triamterene, and sulfadiazine.[27] Antibiotic exposure (sulfas, cephalosporins, fluoroquinolones, nitrofurantoin, broad-spectrum penicillins) is associated with an increased likelihood for nephrolithiasis, with the greatest odds for recent exposure and exposure at younger age.[28]

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