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, 46–48] |
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
|
[46–48] |
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] |