- Calcium oxalate
- Calcium oxalate: risk factors
- Diet to prevent calcium oxalate calculations
- Calcium oxalate calculation medicines
About 10% of people are the subject of a lifetime kidney calculus episode, and about 70% of these people experience relapses.
About 80% ofkidney stonescontains calcium, of which about 80% is calcium oxalate, in pure form or associated with calcium phosphate.
We can therefore say that in most cases (about 65%)kidney stonesare formed by important concentrations of calcium oxalate. Knowing its metabolism is therefore important to prevent the onset of nephrolithiasis and recurrence.
Calcium oxalate
Calcium oxalate (CaC)2O4) is a calcium salt of oxalic acid, a compound that occurs in aghiform crystals, known in botany as rafids.
In plants these pointed needles at the ends and enclosed in vacuoles, represent a defense mechanism against herbivores; particularly rich are its plants such as Rhubarb, Altea, Dieffenbachia and Pastinaca.
As for food sources, in addition to rhubarb (fowls), spinach, leaves of you, kiwi, beetroot are remembered: the presence of these microscopic crystals is responsible for the intense burning sensation in the mouth and throat that some people warn after ingesting these foods.
At high doses, calcium oxalate is a real poison for the human body, triggering severe digestive disorders and breathing difficulties to the coma.
Calcium oxalate present in the body comes both from the direct supply of plants that are rich in it, and from the saltification of calcium dietary with the oxalic acid contained in food, and from the endogenous production (e.g. from vitamin C).
Therefore, in addition to removing calcium from the body, frequent ingestion of foods rich in oxalic acid may encourage the occurrence of renal calculus in predisposed subjects.
Calcium oxalate: risk factors
Both genetic and behavioural factors contribute to the formation of calcium oxalate calculations. These may be corrected to prevent their occurrence at various levels.
| RISK FACTORS | CAUSES | Treatment |
| Reduced urine volume | Exercise, intense sweating, decreased fluid intake with diet, heat, diarrhea, vomiting | Increased fluid intake to 2.5-3.0 L/day |
| Hypercalciuria (↑↑ calcium in urine) | Idiopathic, vitamin D poisoning, excess calcium in diet (e.g. abuse of supplements) | Reduction of sodium intake; thiazide chondriuretic therapy; do not reduce calcium intake except in extreme cases; increase calcium intake to 1000 mg |
| Hyperedoluria (↑↑ oxalic acid in urine) | Dietary ingestion (dioxalated rich foods) and metabolism; inflammatory bowel diseases | Reduce oxalate intake; increase the intake of milk and derivatives when consuming foods rich in oxalic acid |
| Hypocytraturia (↓↓ citric acid in urine) | Tubular acidosis, other metabolic acidosis, eynthestinal inflammatory diseases, often idiopathic | Start a specific supplementation with citrate |
| Hyperuricosuria (↑↑ uric acid in urine) | Excessive ingestion of purines and animal proteins | Reduce the ingestion of purines (see gout diet); starting allopurinol therapy |
| Increased sodium excretion | Excessive sodium intake with diet (kitchen salt and salty food) | Reduce sodium intake |
| Obesity, overweight and insulinor existence | Reduction of citrate excretion, increased calcium excretion and oxalates | Normocaloric or hypocaloric diet associated with regular physical exercise |
Of all these risk factors for the calculation of calcium oxalate, hypercalciuria is the most common, although its origins are not clearly identifiable in many patients, where the adjective "idiopathic" is forged.
Diet to prevent calcium oxalate calculations
| FOODS MORE COMMONLY RESPONSIBILIABLE TO THE IMPROVEMENT OF LEVELS OF OXALATES IN URINS |
| Rhubarb
Dark green plantations (spinach, beet, rocket) Beetroot Wheat bran Nuts Soya and its derivatives Chocolate Tea Strawberries |
1) Increase fluid intake to stimulate frequent diuresis with clear urine: in this way the urine will be less concentrated, and calcium and oxalate more diluted, therefore less likely to precipitate;
2) Limit the intake of foods rich in animal proteins, in particular of purins (sea fruit, anchovies, sardines under oil, herring, caviar, strawberries, meat extracts, meat broth, game, ripples, meats and fat fish), avoiding hyperprothetic, ketogenic or low carb diets. Ingestion of animal protein increases urinary excretion of calcium and uric acid, the latter can promote the formation of stones of uric acid and calcium oxalate
3) Limiting the consumption of oxalate-rich foods and possiblyassociate them with calcium-rich sources(e.g. spinach + grated cheese) as a useful strategy to limit the absorption of oxalates; In addition, increase the intake of liquids for dilution
4) Reduce sodium intakeless than 2-3 grams per day: prefer food without added salt(n.a., therefore, attention to the water of the softener that is rich in sodium); cook the food with little salt, possibly replacing it with spices; If necessary, replace traditional salt with hyposodium salt; read food labels, avoiding those containing more than 250 mg sodium per 100 grams of product
5) Avoid vitamin C megadosis, which may increase oxalate concentration in urine: any supplement should be made at doses below 1000 mg per day
6) The restriction of dietary calcium is not necessary to prevent the formation of calcium oxalate calculations; the dietary intake of the mineral should be around gram per day to avoid possible deficiencies, which would lead to increased absorption of oxalates during digestion; do not abuse supplements that contain vitamin D and calcium, although from some studies it seems that – despite what is thought in the past – they can protect against kidney calculus. .
7) Conseuma foods rich in citric acid, such as citrus and lemon juice, which tend to alkaline the urine by preventing the formation of stones of uric acid and calcium oxalates.
Calcium oxalate calculation medicines
Among the drugs potentially useful to prevent the appearance of osylic nephrolithiasis:
- thiazide diuretics (e.g. hydrochlorothiazide, chlorthalidone and indapamide): have been shown to be useful in reducing calcium and nephrolithiasis. These drugs also induce a positive balance of calcium, thereby promoting an increase in bone mineral density. During therapy, sodium dietary restriction is indicated, while potassium intake should be increased to avoid hypokalaemia, which may in turn lead to hypocytraturia. The usual starting dose is 12.5-25 mg chlortalidone or hydrochlorothiazide. Most patients should receive potassium citrate supplementation. Potassium-sparing diuretics such as amyloride may help to avoid hypokalaemia, but triamterene should be avoided due to its low solubility.
- alkalinizing agents: citrates inhibit the formation and growth of calcium crystals; generally the potassium citrate is preferred, since sodium can favour hypercalciuria
- allopurinol: in case of concurrent presence of hyperuricosuria, since uric acid favors the precipitation of calcium oxalate crystals, allopurinol is useful because it suppresses the synthesis of uric acid, reducing the urinary excretion
- fish oil: reduces calcium concentration in the urine, and renal calculus is very rare among Greenland Inuits; it could therefore be useful in preventing calcium oxalate kidney stones











