Under the action of exogenous, androgenic, genetically determined factors, the metabolism of stone-forming salts of calcium, phosphorus, magnesium, oxalates, uric acid in the blood serum and their active excretion by the kidneys to the state of hypersaturation (oversaturation) is disturbed) urine is formed. When the level of crystallization inhibitors is disturbed, a saturated salt solution crystallizes with the formation of microliths. The formation of stones in the kidneys is possible only in the presence of «building material» – supersaturated saturated urine, therefore, hyperoxaluria is a pre-stone condition. Treatment measures should be aimed at correcting mineral metabolism in the body after establishing the type of hyperoxaluria using laboratory tests: salt transport, calcium load, dietary test – low-calcium diet, thiazide test and determination of the mineral composition of the removed (removed) stone. Genetically consequential conditions (10–15%) count about 30 varieties in which the main sign or symptom in the manifestation of the disease is urolithiasis. Unfortunately, congenital tubulopathies are not sufficiently studied, so the treatment is symptomatic, in some cases simultaneous kidney and liver transplantation options are possible. Clinically, 4 main forms of hypercrystalluria are distinguished: hypercalciuria, hyperoxaluria, hyperuricuria, phosphaturia and mixed forms of crystalluria. Acquired forms of hypercrystalluria, of which they are absorptive (type II intestinal hyperabsorption – absorptive hypercalciuria and absorptive hyperoxaluria), are of main clinical interest, which is characteristic of the course of calcium-oxalate urolithiasis. Metaphylaxis of calcium-oxalate urolithiasis is formed on the basis of these data.