Urinary Stones (Urolithiasis): Causes

Pathogenesis (development of disease)

The cause of urinary stone formation is not yet fully understood. However, it is clear that it is a multifactorial event. Two hypotheses are discussed

  • Crystallization theory – concretion formation in a supersaturated solution.
  • Colloid theory – accumulation of urinary salts on urinary organic substances.

Probably a combination of both theories is present.Undisputed is the fact that a supersaturated solution must be present. In addition, there is the fact that in all types of stones urinary organic substances.

Notice:

  • Most stones consist of calcium oxalate (80% of cases).
  • Urinary stones without calcium oxalate are associated with an increased risk of complications, as such stones can become very large. These were stones made of uric acid in about 10% of cases and carbapatite (carbonate hydroxylapatite, dahlite) in 8% and struvite (infectious stone, magnesium ammonium phosphate hexahydrate), brushite (calcium hydrogen phosphate dihydrate) and cystine in 2% of cases.The largest were the rare stones: struvite (7.9 mm), cystine (6.8 mm) and brushite (6.2 mm). In comparison, stones with calcium oxalate monohydrate had an average diameter of 3.6 mm, those with calcium oxalate dihydrate of 4.5 mm.
  • Kidney stones containing uric acid, calcium phosphate or ammonium urate always indicate a systemic acid-base disorder.

Etiology (causes)

Biographical causes

  • Genetic diseases
    • Cystinuria – genetic metabolic disorder with autosomal recessive inheritance; results in increased excretion of the amino acid cystine, as well as the related amino acids arginine, lysine, and ornithine, in the urine.
    • Fructose transporter gene SLC2A9: genetic disorder of renal excretion of uric acid due to a gene variant.
    • Hereditary hyperoxaluria (primary hyperoxaluria) – inborn error of metabolism with autosomal recessive inheritance, in which there is too much oxalate in the urine.
    • Infantile hypercalcemia (infantile hypercalcemia) – genetic disorder with autosomal recessive inheritance; age of manifestation: Infancy, neonatal period; children develop symptomatic hypercalcemia after administration of higher doses of vitamin D for rickets prophylaxis, in part, with suppressed parathyroid hormone (PTH), as well as hypercalciuria (increased excretion of calcium in the urine) and nephrocalcinosis (accumulation of multiple small, radiopaque calcifications distributed in the renal parenchyma).
    • Lesch-Nyhan syndrome (LNS; synonyms: hyperuricemia syndrome; hyperuricosis) – X-linked recessive inherited metabolic disorder of the rheumatic type (disorder in purine metabolism).
    • Cystic fibrosis (cystic fibrosis) – genetic disease with autosomal dominant inheritance, characterized by the production of secretions in various organs to be tamed.
    • Renal tubular acidosis (RTA) – genetic disease with autosomal recessive inheritance, leading to a defect defect H+ ion secretion in the tubular system of the kidney and, as a result, demineralization of bone (hypercalciuria and hyperphosphaturia/increased excretion of calcium and phosphate in the urine).
    • Xanthinuria – inborn error of metabolism with autosomal recessive inheritance, disorder in purine metabolism with greatly reduced activity of xanthine oxidase.
    • 2,8-Dihydroxyadeninuria (deficiency of arginine phosphoribosyltransferase (APRT); autosomal recessive inheritance.
  • Pregnancies – for nulligravidae 5.2% and increases to 12.4% for women with three or more pregnancies
  • Professions – physicians, especially surgeons (due topoor fluid balance).

Behavioral causes

  • Nutrition
    • Dehydration (dehydration of the body) – due to fluid loss or lack of fluid intake (drinking amount).
    • Malnutrition
    • High-protein (high-protein) diet (animal protein).
    • High fat diet
    • High intake of oxalic acid-containing foods (chard, cocoa powder, spinach, rhubarb).
    • High intake of calcium
    • High purine intake (offal, herring, mackerel).
    • High consumption of table salt (eg, canned and convenience foods).
    • Fructose-containing beverages lead to an increase in uric acid serum levels in approximately 5% of patients – due to the presence of a gene variant of the fructose transporter gene SLC2A9 – this leads to the disturbance of the renal excretion of uric acid
    • Micronutrient deficiency (vital substances) – see prevention with micronutrients.
  • Consumption of stimulants
    • Alcohol (woman: > 20 g/day; man > 30 g/day).
    • Tobacco (smoking)
  • Physical activity
    • Physical inactivity
    • Immobility or immobilization
  • Psycho-social situation
    • Chronic stress
  • Overweight (BMI ≥ 25; obesity).

Disease-related causes

Laboratory diagnoses – laboratory parameters that are considered independent risk factors.

Medication

  • Chronic antibiotic therapy – medications used to treat bacterial infections; three to twelve months after prescription, the risk of kidney stones increases by 30-130%:
  • Laxative abuse – dependence on laxatives.
  • Vitamin D intoxication (e.g. due torickets prophylaxis/prevention of bone softening in children).

Operations

  • Urological procedures or operations

Further

  • Single kidney situation
  • Pregnancy – having been pregnant leads to a doubling of the risk of developing the disease