Who is at risk of developing kidney stones, considering factors such as family history, underlying medical conditions like gout, inflammatory bowel disease, and primary hyperparathyroidism, dietary habits, demographics, and past medical history?

Who Is at Risk of Developing Kidney Stones

Men are at substantially higher risk than women, with lifetime incidence of approximately 13% for men versus 7% for women, though this gender gap is narrowing as stone prevalence increases more rapidly in women. 1, 2

Demographic Risk Factors

• Male sex confers higher risk, with prevalence of 10.6% in men versus 7.1% in women in the United States 3
• Older age increases stone risk progressively 3, 4
• White race has higher prevalence compared to other racial groups 3
• Family history is one of the most powerful risk factors, with a relative risk of 2.57 for incident stone formation in those with positive family history compared to those without, and prevalence odds ratio of 3.16 in those with existing stones 5, 6, 2

Medical Conditions That Increase Risk

• Obesity significantly increases stone risk, with particularly pronounced effects in females where the impact is greater than in men 1, 7, 2, 4
• Diabetes mellitus (type 2) is commonly associated with stone disease as part of metabolic syndrome 1, 2, 4
• Hypertension increases risk and is frequently present alongside other metabolic abnormalities 1, 2, 3, 4
• Metabolic syndrome encompasses multiple risk factors that collectively promote stone formation 7, 2, 3, 4
• Gout elevates risk through hyperuricemia and hyperuricosuria [1, @21@]
• Primary hyperparathyroidism causes hypercalciuria and hypercalcemia, identified when serum calcium is high or high-normal 1, 2
• Inflammatory bowel disease and intestinal malabsorption increase risk through multiple mechanisms including chronic volume contraction, decreased citrate and magnesium absorption, and in cases with intact colon, enteric hyperoxaluria from increased colonic oxalate absorption 1, 8
• Renal tubular acidosis type 1 leads to persistently alkaline urine, hypocitraturia, and nephrocalcinosis 2
• Chronic kidney disease is both a risk factor for and consequence of stone disease 4

Genetic and Inherited Conditions

• Cystinuria, an inherited disorder causing cystine stone formation, requires lifelong management with aggressive fluid intake of at least 4 liters daily 6, 2
• Primary hyperoxaluria, a genetic disorder causing severe hyperoxaluria exceeding 75 mg/day 2
• Medullary sponge kidney predisposes to stones through urinary stasis 2

Anatomic Abnormalities

• Renal and ureteral anatomic abnormalities that cause urinary stasis increase stone risk 3, 2
• Nephrocalcinosis implies underlying metabolic disorders 2

Dietary and Lifestyle Risk Factors

• Inadequate fluid intake resulting in urine output below 2 liters daily is a critical modifiable risk factor 2
• High sodium intake (common in processed foods consumed by obese individuals) reduces renal tubular calcium reabsorption and increases urinary calcium excretion, with intake above 2 grams (90 mmol) per day promoting stone formation 7, 6, 2
• Excessive animal protein consumption generates sulfuric acid, increasing urinary calcium and reducing protective urinary citrate 6, 2
• Low dietary calcium intake paradoxically increases stone risk by reducing gastrointestinal oxalate binding, leading to increased oxalate absorption and urinary excretion 1, 6, 2
• Sugar-sweetened beverages, particularly colas acidified with phosphoric acid, increase stone recurrence risk 2
• High oxalate foods (spinach, rhubarb, nuts, chocolate, tea) increase risk in susceptible individuals with hyperoxaluria 6, 2
• Excessive vitamin C supplementation increases oxalate generation through metabolism 2

Metabolic Abnormalities

• Hypercalciuria (elevated urinary calcium excretion) is a common metabolic abnormality in recurrent stone formers 2
• Hypocitraturia (low urinary citrate) predisposes to recurrent calcium stones 2
• Hyperoxaluria increases calcium oxalate supersaturation and stone risk 2
• Hyperuricosuria can promote calcium oxalate stone formation even without forming uric acid stones 1, 2
• Low urine volume or concentrated urine increases supersaturation of all stone-forming salts 2
• Abnormal urine pH affects stone type, with acidic urine (common in obesity and metabolic syndrome) promoting uric acid stones and alkaline urine promoting calcium phosphate stones 7, 2

Medication-Induced Risk

• Calcium supplements may increase stone risk 2
• Topiramate and other carbonic anhydrase inhibitors increase calcium phosphate stone risk 2
• Loop diuretics can cause hypercalciuria 2
• Thiazide diuretics are listed among medications requiring careful monitoring 9

Infectious Causes

• Recurrent urinary tract infections with urea-splitting organisms (such as Proteus) produce struvite stones, requiring complete stone removal and antimicrobial therapy 6, 2

Clinical Context and Recurrence Risk

• Previous kidney stones dramatically increase risk, with recurrence rates of 35-50% within 5 years without specific preventive treatment, and at least 50% of individuals experiencing another stone within 10 years without preventive measures 1, 6, 10, 4
• The 5-year recurrence rate after a symptomatic stone event is 35-50% without treatment, and 30-50% even with some interventions 1, 2, 10
• Modifiable lifestyle factors collectively account for approximately 55-57% of all incident kidney stones across multiple large prospective cohorts 2