Urinary stone disease (USD) is one of the most common urological diseases occurring mainly in people of working age. USD is associated with metabolic disorders, the causes of which include endogenous and exogenous factors. Metabolic syndrome (MS) is a “non-infectious epidemic” that manifests itself in diabetes, hypertension, atherosclerosis, and obesity. The bidirectionality of metabolic processes is an important factor of USD and MS. Aim. The paper aims at reviewing modern literary sources regarding the determination of pathogenetic links between the comorbidity of USD and MS. Results. Nephrolithiasis spreads and recurs simultaneously with obesity. A decrease in urine pH, which is the basis for the formation of urate stones, is associated with the presence of obesity, insulin resistance, and MS. Under such conditions, urine alkalinization is the main treatment for urolithiasis. The risk of stone formation increases when the body mass index is more than 30 kg/m2. Among patients with insulin resistance, nephrolithiasis is more severe, and kidney stones occur more often. The relationship between the hypertensive component of MS and USD has been established. Disorders of lipid metabolism have a negative prognosis, causing physicochemical aberrations in urine and the development of nephrolithiasis. Hyperuricemia is related to both the ability of insulin to reduce uric acid clearance in the proximal renal tubules and insulin resistance. The link between USD and chronic inflammation is based on an increase in the endogenous synthesis of oxalates from endogenous glycogenic amino acids, which leads to the development of hyperoxaluria in patients with MS. Clinical studies show the formation of kidney stones in conditions of oxidative stress, an association between stone formation and the development of MS, coronary heart disease, arterial hypertension, which is the result of common pathogenetic characteristics. Conclusions. The comorbidity of USD and MS is a systemic disorder. Kidney stone formation is associated with a decrease in urine pH against the background of MS. Hyperuricemia is comorbid with insulin resistance, dyslipoproteinemia, arterial hypertension, and abdominal obesity. Systemic chronic inflammation, comorbid with obesity and USD, based on an increase in the endogenous synthesis of oxalates from endogenous glycogenic amino acids. Oxidative stress has a common pathogenetic link between stone formation and insulin resistance, atherosclerosis, hypertension, and obesity.

Urinary stone disease (USD) is a polyetiological urological disease caused by both exogenous and endogenous factors, including hereditary ones. It is characterized by the appearance of stones in the kidneys and urinary tract, and a tendency to relapse, often with a severe course. Almost 25 % of stones consist of uric acid (UA). The leading role in the pathogenesis of urate nephrolithiasis (UN) is played by disorders of purine metabolism, which are characterized by the development of hyperuricemia (HU) and hyperuricuria. The aim of the work is to review modern literary sources on the role of purine metabolism disorders in the etiopathogenesis of UN. Results. The development of UN depends on the constancy of the acidic urine pH, as well as on a decrease in diuresis, HU and hyperuricuria. UA is the final metabolite of purine metabolism and the main stone-forming substance in patients with UN. HU develops both due to uncompensated disorders of purine metabolism with a decrease in renal secretion and intestinal uricolysis (excretion pathway) and excessive intake of purine bases in the body and their increased synthesis in vivo (metabolic pathway). Citric acid, as one of the main metabolites of the tricarboxylic acid (TCA) cycle, is connected through the corresponding substrates to the formation of purines and the metabolite of amino acid metabolism, glutamine. TCA is connected to the cycles of urea, glyoxylate and purine bases through α-ketaglutaric acid. It is a substrate of citric acid, and it affects the synthesis of glutamate, which combines with ammonia to form glutamine, used in the cycle of purine synthesis. Conclusions. The role and diagnostic value of purine metabolism upsets, disorders of the TCA (citric acid), amino acid metabolism (glutamine), the activity of xanthine oxidase is a key enzyme in purine synthesis which passes through TCA with the participation of its metabolite α-ketaglutarate, have been established. TCA is bound to glutamine, rich in nitrogen, which is necessary for the synthesis of purine bases.