| Number | Risk factors | References |
| 1 | Lifestyle habits and dietary/nutritional factors: such as excessive intake of animal proteins and salt and deficiencies of chelating agents like citrate, fiber, and alkali foods | [9, 13, 19, 45] | 2 | Metabolic disorders: such as hypercalciuria, hypocitraturia, hyperoxaluria, hyperuricosuria, and history of gout (defective metabolism of uric acid) | [38, 46ā48] | 3 | Hypercalcemic disorders: primary hyperparathyroidism and other disturbances of calcium metabolism | [49] | 4 | Urine composition: excessive excretion of promoters of urinary crystallization and reduced excretion of inhibitors (urine deficient in inhibitory substances) | [1, 45, 49] | 5 | Low urine volume: inadequate water intake (dehydration and supersaturated urine) | [45, 49, 50] | 6 | Recurrent urinary tract infections: abnormalities of urinary pH and alkalinization of urine by bacterial urease (such as Proteus mirabilis) | [38, 49] | 7 | Genetic predisposition/inherited disorders: family history of stones (genetic susceptibility); genetic monogenic diseases (single abnormal gene disorders on the autosomes); renal tubular acidosis | [1, 9, 48, 49, 51] | 8 | Anatomical abnormalities: factors such as defects in medullary sponge kidney, ureteropelvic junction stenosis, pyeloureteral duplication, polycystic renal disease, and horseshoe kidney | [1, 48, 49, 52] | 9 | Hypertension | [46] | 10 | Obesity | [46ā48] | 11 | Climate change (global warming), occupation, geographic conditions, and seasonal variations (higher in summer than winter) | [1, 49] | 12 | Inflammatory bowel disease and other intestinal malabsorption or associated disease states | [9, 49] | 13 | Absence of intestinal oxalate-degrading bacteria | [53, 54] | 14 | Lithogenic drugs: such as indinavir (Crixivan), a protease inhibitor, sulfonamides (sulfadiazine), uricosuric agents, which have low solubility andpromotes the formation of calculi, and ceftriaxone (high dose on long terms) | [28, 38, 49, 50] |
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