GOUT NEPHROPATHY: CHOICE OF INITIAL THERAPY IN A COMORBID PATIENT

Gout is one of the most common inflammatory diseases of the joints, which is often accompanied by comorbid pathology, most often diseases of the cardiovascular system and metabolic disorders. This fact reflects the influence of hyperuricemia and the lack of compensation for purine metabolism disorders. Most researchers explain the lack of effective control of purine metabolism in gout with patients’ low adherence to treatment. This idea led to the formation of the concept of insufficient use of hypouricemic therapy and, as a result, to the lack of control over the course of the disease and the possibility of preventing the deterioration of the general state of the patient’s health, which is largely due to the progression of concomitant pathology. Many retrospective studies demonstrate a low frequency of timely appointment of hypouricemic therapy, inefficient dosage, which does not allow to reach target levels of SC in blood serum and effectively control the disease. Febuxostat is an effective means of reducing the level of SC in the blood serum in this disease. The literature provides data on the serious advantages of febuxostat over other hypouricemic agents. The purpose of this work was to study the possibility of obtaining a clinical and laboratory effect in a short time after the start of febuxostat therapy (up to 3 months) in patients with gouty nephropathy who have concomitant pathology. A study of the efficacy and safety of febuxostat (tablets of 80 or 120 mg) was conducted in gout patients with concomitant diseases. The observation period was 3 months, during which time the possibility of patients achieving the target level of SC (≤360 μmol/l) was evaluated. 6 patients reached the target SC level within 1.5 months of treatment. In 19 (30%) patients, the SC level decreased to ≤360 μmol/L after 3 months of therapy. Exacerbations of gout were noted in the first 2 months of therapy in individual patients and were characterized by less activity of joint syndrome. It is known that hyperuricemia is one of the main risk factors for endothelial dysfunction, which, in turn, contributes to the development of arterial hypertension and damage to target organs. Regardless of hypertension, an increase in the level of SC in the blood serum affects the cells of the endothelium and vascular smooth muscle, leading to the formation of microvascular damage to the kidneys. According to our data, the presence of CKD, DM and/or hypertension significantly reduces the speed