What causes recurrent kidney stones?

Causes of Recurrent Kidney Stones

Recurrent kidney stones result from a combination of metabolic abnormalities, dietary factors, genetic predisposition, and systemic conditions that create persistent urinary supersaturation of stone-forming salts.

Metabolic and Urinary Abnormalities

The primary metabolic causes identified through 24-hour urine testing include:

• Hypercalciuria (elevated urinary calcium excretion) is one of the most common metabolic abnormalities in recurrent stone formers 1
• Hypocitraturia (low urinary citrate, which normally inhibits stone formation) predisposes to recurrent calcium stones 1, 2
• Hyperoxaluria (elevated urinary oxalate) increases calcium oxalate supersaturation and stone risk 1
• Hyperuricosuria (elevated urinary uric acid) can promote calcium oxalate stone formation even without forming uric acid stones 1, 2
• Low urine volume (concentrated urine) increases supersaturation of all stone-forming salts 1
• Abnormal urine pH affects stone type—acidic urine promotes uric acid stones while alkaline urine promotes calcium phosphate stones 1

Dietary Risk Factors

Specific dietary patterns substantially increase recurrence risk:

• Inadequate fluid intake resulting in urine output below 2 liters daily is a critical modifiable risk factor 1
• High sodium intake (>2,300 mg/day) reduces renal tubular calcium reabsorption and increases urinary calcium excretion 1, 2
• Excessive animal protein consumption generates sulfuric acid, increasing urinary calcium and reducing urinary citrate 2
• Low dietary calcium intake paradoxically increases stone risk by reducing gastrointestinal oxalate binding, leading to increased oxalate absorption and urinary excretion 1, 3
• Sugar-sweetened beverages, particularly colas acidified with phosphoric acid, increase stone recurrence risk 1, 4
• High oxalate foods (spinach, nuts, chocolate, tea) in susceptible individuals with hyperoxaluria 2
• Excessive vitamin C supplementation (>1,000 mg/day) increases oxalate generation through metabolism 2, 5

Genetic and Familial Factors

• Family history of kidney stones increases risk substantially, with a relative risk of 2.57 for incident stone formation compared to those without family history 6
• The age-adjusted prevalence odds ratio for having a family history is 3.16 in men with personal stone history versus those without 6
• Genetic predisposition interacts with environmental and dietary factors to determine individual susceptibility 5, 7

Underlying Medical Conditions

Several systemic conditions predispose to recurrent stones:

• Primary hyperparathyroidism causes hypercalciuria and hypercalcemia, identified when serum calcium is high or high-normal 1
• Renal tubular acidosis type 1 leads to persistently alkaline urine, hypocitraturia, and nephrocalcinosis 1
• Primary hyperoxaluria (genetic disorder) causes severe hyperoxaluria exceeding 75 mg/day 1
• Cystinuria (inherited disorder) results in cystine stone formation 1
• Obesity and metabolic syndrome are increasingly recognized as risk factors, with greater impact in women than men 1
• Type 2 diabetes, hypertension, and dyslipidemia are commonly associated with stone disease as part of a larger metabolic picture 1, 7
• Chronic bowel disease (inflammatory bowel disease, malabsorption) increases oxalate absorption 2

Anatomic and Infectious Causes

• Medullary sponge kidney predisposes to stone formation through urinary stasis 1
• Nephrocalcinosis implies underlying metabolic disorders 1
• Recurrent urinary tract infections with urea-splitting organisms (Proteus) produce struvite stones 1
• Urinary stasis from any anatomic obstruction increases stone risk 1

Medication-Induced Stone Formation

Certain medications directly promote stone formation:

• Calcium supplements (as opposed to dietary calcium) may increase stone risk 2, 5
• Topiramate and other carbonic anhydrase inhibitors increase calcium phosphate stone risk 1
• Loop diuretics can cause hypercalciuria 1
• Patients should be queried about stone-provoking medications during evaluation 1

Age and Sex-Related Variations

• Risk factors vary by age and sex, requiring individualized assessment 1
• The gender gap is closing, with stone prevalence increasing more rapidly in women 1
• Age of onset is decreasing in developed populations 7

Key Clinical Pitfall

The recurrence rate without prophylactic intervention is 30-50% within 5 years 1, 5. Simply removing stones without addressing underlying metabolic and dietary causes does not prevent recurrence, as stone removal does not treat the fundamental abnormalities driving stone formation 7. This emphasizes the critical importance of comprehensive metabolic evaluation and long-term preventive management in all recurrent stone formers 1.