R/f of associated with urolithiasis
| Factor | Detail |
|---|---|
| Sex | Males > Females (prevalence ~10.6% vs. 7.1%); gap is narrowing |
| Race/Ethnicity | Whites > Mexican Americans > African Americans |
| Age | Higher in aging population |
| Geography | "Stone belt" = Southeastern USA, Middle East, Saudi Arabia (highest prevalence worldwide) |
| Family history | First-degree relatives with stones significantly increase risk |
| Genetics | Monogenic disorders (cystinuria, primary hyperoxaluria, Dent disease) plus polygenic susceptibility |
| Condition | Mechanism |
|---|---|
| Obesity / BMI | Only strong independent predictor of stone recurrence; associated with low urinary pH → uric acid stones |
| Type 2 Diabetes Mellitus | Impaired ammoniagenesis → persistently acidic urine → uric acid stones |
| Metabolic syndrome | Combination of obesity, insulin resistance, hypertension → uric acid nephrolithiasis |
| Gout / Hyperuricemia | High purine load → hyperuricosuria + acidic urine |
| Hypertension | Independent association; low income also correlates |
| Hypercalciuria (idiopathic) | Most common metabolic abnormality in calcium stone formers |
| Hyperoxaluria | Primary (genetic), enteric (bowel disease), or dietary |
| Hypocitraturia | Citrate is a key inhibitor; deficiency promotes crystallization |
| Hyperuricosuria | Promotes nucleation of calcium oxalate crystals |
| Hypomagnesuria | Magnesium inhibits oxalate crystallization |
| Renal tubular acidosis (distal) | Alkaline urine + hypocitraturia → calcium phosphate stones |
| Primary hyperparathyroidism | Hypercalcemia → hypercalciuria → calcium stones |
| Gout | Uric acid stones |
| Factor | Effect |
|---|---|
| Low fluid intake / Dehydration | Low urine volume → supersaturation of lithogenic solutes |
| High animal protein intake | ↑ urinary calcium, oxalate, uric acid; ↓ urinary citrate |
| High sodium intake | ↑ urinary calcium excretion |
| High oxalate diet | Spinach, nuts, chocolate → calcium oxalate stones |
| Low calcium intake | Paradoxically increases stone risk (unbound oxalate absorbed in gut) |
| High purine diet | Red meat, organ meat, shellfish → hyperuricosuria |
| High fructose / sugar-sweetened beverages | Promotes uric acid stone formation |
| Low potassium intake | Associated with hypocitraturia |
| Factor | Mechanism |
|---|---|
| Small bowel resection / Crohn's disease / Ileostomy | Fat malabsorption → saponification of calcium → unbound oxalate absorbed → enteric hyperoxaluria → calcium oxalate stones |
| Bariatric surgery (Roux-en-Y) | ↑ oxalate absorption |
| Medullary sponge kidney | Urinary stasis in dilated collecting ducts |
| Horseshoe kidney / Ureteropelvic junction obstruction | Urinary stasis |
| Urinary diversion / Ileal conduit | Altered pH, bacterial colonization, stasis |
| Factor | Mechanism |
|---|---|
| Recurrent UTI with urease-producing organisms | Proteus, Klebsiella, Pseudomonas → urea → NH₃ + HCO₃⁻ → alkaline urine (pH >7) → struvite (magnesium ammonium phosphate) stones / staghorn calculi |
| Drug | Stone Type |
|---|---|
| Indinavir (HIV antiretroviral) | Indinavir crystalluria |
| Atazanavir | Drug crystal stones |
| Topiramate | Carbonic anhydrase inhibition → ↑ urinary pH → calcium phosphate stones |
| Triamterene | Radiolucent stones |
| Calcium/Vitamin D supplements (excess) | Hypercalciuria |
| Acetazolamide | Metabolic acidosis; alkaline urine |
| Loop diuretics (furosemide) | ↑ urinary calcium |
| Stone | Key Risk Factors |
|---|---|
| Calcium oxalate (most common, ~70%) | Hypercalciuria, hyperoxaluria, hypocitraturia, low fluid intake, enteric disease |
| Calcium phosphate (~15%) | Distal RTA, hyperparathyroidism, alkaline urine, topiramate |
| Uric acid (~8–10%) | Obesity, T2DM, metabolic syndrome, gout, acidic urine, high purine diet |
| Struvite / Infectious | Recurrent UTI with urease-producing bacteria |
| Cystine | Cystinuria (autosomal recessive, SLC3A1/SLC7A9 mutations) |