O‘Zbekistondagi Mavjud Suv Muammolari Va Uning Jiddiy Oqibatlari Mavzusini O‘Qitish Metodikasi

Key words
:
uric acid, hyperfiltration, metabolic 
syndrome, tubulointerstitial tissue. 

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JOURNAL OF ADVANCED
RESEARCH AND STABILITY (JARS) 
Volume: 01 Issue: 06 | 2021 
ISSN: 2181-2608
470 
There is literary evidence that hyperuricemia leads to changes in the afferent arteriole, changes in the 
structure of the smooth muscle cells of renal arterioles and, as a consequence, can cause an increase in 
blood pressure and / or progression of arterial hypertension (AH) [1]. On the other hand, a fairly 
frequent combination of metabolic syndrome with hypertension, metabolic syndrome (MS), insulin 
resistance, type 2 diabetes mellitus can independently make a certain contribution to damage to the 
glomerular apparatus of the kidneys. 
Not only TIT, but also the glomerular apparatus is involved in the mechanisms of kidney damage in 
metabolic syndrome. Therefore, in the diagnosis of urate nephropathy, it is important to study the 
partial functions of the kidneys [2]. 
This vascular endothelial growth factor plays an important role in maintaining endothelial stability and 
physiological neoangiogenesis, and also takes an active part in the processes of neovascularization in 
pathological situations. Many studies, including those in various kidney diseases, have demonstrated its 
leading role as a marker of endothelial dysfunction [9]. It is normally expressed by podocytes, tubular 
epithelial cells, and renal endothelial cells [10,11]. 
One of the informative indicators of the functional state of the kidneys is the assessment of the renal 
reserve, the absence of which is regarded as equivalent to the existing hyperfiltration, even with normal 
indicators of the glomerular filtration rate (GFR) [12,17,18]. 
Currently, the role of hyperfiltration has been established not only in the late stages of nephropathy, but 
also in renal patients without impaired renal function due to pathological activation of hormonal 
factors. [13,17,24]. 
To detect intraglomerular hypertension, it is proposed to use the method for determining the RPF with 
a protein (glucagon, dopamine, amino acid) load. [15,18].