Сечокам'яна хвороба як наслідок вторинної гіперурикемії у пацієнтів з діабетичним ураженням нирок

Abstract

Urolithiasis is currently one of the most pressing problems of modern urology and medicine in general. The pathogenesis of urolithiasis is multifactorial and caused by various metabolic disorders, in particular carbohydrate, the main manifestation of which is diabetes mellitus. In connection with the above, a comparative approach to the study of metabolic disorders in patients with diabetic kidney damage, in particular hyperuricemia, is relevant in order to identify possible causes of lithogenesis. The purpose of the study is to study the effect of secondary hyperuricemia on the formation of urinary stones in patients with diabetic kidney damage, compared with non-diabetic nephropathies. Materials and methods. The study included 59 patients with chronic kidney disease, including 27 with diabetic nephropathy and 32 with non-diabetic nephropathy. All patients underwent a comprehensive clinical and laboratory study, which included glycosylated hemoglobin, glycemic profile, lipid complex, C-reactive protein, serum creatinine, urea, electrolytes, uric acid, uric acid clearance, glomerular filtration rate, and ultrasound examination of the urinary system. Results and discussion. Urolithiasis was detected in 70.3 % patients with diabetic kidney disease and in 29.6% patients with non-diabetic pathology. The stones had a renal localization: pelvic stones occurred in 38.9% patients, stones in calyces – in 61.1% patients. When assessing the biochemical parameters, the average level of uric acid in the blood serum of patients with diabetes mellitus significantly exceeded the same indicator in the group of patients with non-diabetic pathology. Also, the level of hyperuricemia was higher in diabetic patients with a glycosylated hemoglobin content of more than 8.5%, compared with patients with an HbA1 concentration of less than 7.5%. In patients of both groups compared with serum uric acid concentrations exceeding the level of 498.5 mmol/l in men and 384.2 mmol/L in women, there was a progression of arterial hypertension. In patients with diabetic nephropathy, there was a significant increase in the level of cholesterol, low-density lipoproteins and triglycerides, which provided an increase in the value of the atherogenicity index to 5.7±1.2. Conclusion. In patients with diabetic kidney damage, there are prerequisites for the development of urolithiasis, due to the development of a number of metabolic disorders that affect kidney function and the composition of urine. The key links in the pathogenesis of more frequent development of urolithiasis in this category of patients are secondary hyperuricemia, as well as disorders of carbohydrate and lipid metabolism in the form of hyperglycemia and hyperlipidemia