CC BY
37
the underlying disease of the total boundaries of the field narrowed below baseline by the end of the observation period. In the control group 6 months total field of view narrowed (from 225.5° ± 22.8° to 169.0° ± 22.8°).
Ultrasound biomicroscopy structures responsible for the drainage fUnction of the eyes, carried out after antiglaucomatous surgery showed significantly higher values of the parameters indicators of filter pads and intrascleral cavity height, area and volume, in the study group compared with the control group. On 2 (5 %) eyes of the control group patients filtration cushion completely isn't. In other cases researches parameters in patients of the control group was lower than in patients of the main group. In 2 eyes (5 %) in the control group revealed blockade anterior chamber iris root angle. At the same time it was combined with the disappearance of the filter pad.
Thus, a comparative assessment of the immediate and long-term results in the treatment of NVG, revealed the lack of effectiveness of the immediate outcomes and low efficiency deep sclerectomy in long-term period, in comparison with deep sclerectomy implantation xenokollagen drainage. Implementation of the developed modified surgery with implantation xenokollagen drainage at NVG will ensure the long-term normalization of intraocular pressure, the stabilization ofvisual function and decrease the intensity of antihy-pertensive therapy.
Conclusion
The use of a modified method of surgical treatment of neovas-cular glaucoma helps reduce the number of postoperative complications, not only provides a stable hypotensive effect, but also increase visual function in most patients.
References:
1. Wand M. Neovascular glaucoma. Ed. by R. Riteh, M. B. Shilds. - StLouis: C. V. Mosby Co., 2002.
2. Shmireva V. F. Causes of long-term decrease of glaucoma surgery hypotensive effect and possibilities of its enhancement//Glaucoma. -2010. - 2: 43-49. (In Russ.).
3. Madsen P. H. Rubeosis of the iris and haemorrhagic glaucoma in patients with proliferative diabetic retinopathy//Br J Ophthalmol. - 2001. - 55.
4. Nesterov A. P. Glaukoma. - Moscow: MIA, 2008. - 357 p. (In Russ.).
5. Shields M. B. Textbook of glaucoma. - Baltimore, 1997.
Rakhimova Gulnara Nishanovna, D. M., Head of the Department «Endocrinology», Tashkent Institute of Post-graduate Medical Education, Head of Science Department of «<Child endocrinology», Republic Specialized Scientific Research Center of Endocrinology of the Ministry of Healthcare of the Republic of Uzbekistan,
Uzbekistan, Tashkent E-mail: [email protected] Sadykova Akida Sattarovna, D. M. at Science Department of «<Child Endocrinology», Republic Specialized Scientific Research Center of Endocrinology of the Ministry of Healthcare of the Republic of Uzbekistan
E-mail: [email protected]
Study of interrelation of I/D polymorphism in ace gene with a stage of chronic kidney disease in children and teenagers of Uzbek population with D1 according to guidelines K/DOQI (2012)
Abstract: The aim of the research was the evaluation of the functional condition of kidneys and the study of interrelation of I/D polymorphism in ACE gene with a stage of chronic kidney disease in children and teenagers of Uzbek population with D1 according to new guidelines K/DOQI (2012). 120 children and teenagers with type 1 diabetes, 53 (44.2 %) males and 67 (55.8 %) females, were examined. The average age of the patients was 13.8 ± 2.7 years old (Me 15.0; IQR 13.0-16.0). The stages of the chronic kidney disease were classified in accordance with guidelines K/DOQI (2012). In the course of work, it was revealed that the use of new classification K/DOQI (2012) for children and teenagers with D1of Uzbek population allows detecting the decrease in kidney function at earlier stages: 61.9 % of children and teenagers with D1 showed GFR 80.6 ± 7.5 ml/min/1.73m 2 at the stage of normal albuminuria, which corresponds to stage II of CKD and 16.7 % had GFR 45.1 ± 9.5 ml/min/1.73m 2, which corresponds to stage III of CKD. Also, 28.6 % of children and teenagers at MAU stage showed stage II of CKD and 75.0 % showed stage III of KCD respectively. Frequency distribution of ACE genotypes in children and teenagers with D1 was characterized by significant correlation of DD genotype interrelated with the severity of KCD of GFR reduction, which confirms the influence of genetic factors in KCD development. I/D polymorphism in ACE gene is a molecular-genetic marker of disposition to CKD D1 in children and teenagers of Uzbek population.
Keywords: diabetes, children and teenagers, CKD, polymorphism in ACE gene.
Type 1 diabetes (D1) is one ofthe most severe endocrinal diseases in children and teenagers. The dramatic nature ofthe problem ofD1 in the population of children and teenagers is determined by expressed disruption of quality of a child's life, early development of complications with disability in patients and reduction oflife expectancy [7; 10].
The main risk is posed by late complications of diabetes, particularly, diabetic nephropathy (DN). DN mainly develops in 5-10 years from the beginning of the disease and leads to chronic kidney insufficiency (CKI) quite quickly — every 4th-5th patient with D1 dies of CKI [6; 11].
According to the screening conducted in Uzbekistan in 2012, the distribution of DN of4th-5th category was 4.8 % among children and 10.8 % among teenagers with D1 [21].
To develop an optimal strategy ofpatient management with progressive reduction of kidney function, unified, agreed in the entire nephrology world, definitions and classification were required. The creation of guidelines within the Kidney Disease Outcomes Quality Initiative — KDOQI of the National kidney fund of the USA in 2002 (with revision in 2012), the first part of which contained definition and division into stages of a new over-nosological notion «chronic kidney disease» (CKD) contributed to it [2; 15; 16; 17].
The term CKD was used in pediatrics for the first time in 2003 by Hogg R.; definition and classification of the given state are not different from such in adults [14]. K/DOQI guidelines define CKD, regardless the age of the patient, as kidney lesion for 3 or more months characterized by structural and functional disruptions ofkidneys with or without reduction of glomerular filtration rate (GFR) [16].
One of the leading directions in the development of nephrol-ogy is a molecular-genetic study of the role of hereditary endo-genic/genetic factors leading to the disease. The definition of polymorphic markers of genes-candidates is used to study the role of heritable factors in the disease development [8]. Genes coding the components of renin-angiotensin-aldosterone system are primarily viewed as genes-candidates, products, the expressions of which can define the speed ofprogression ofkidney insufficiency [1; 3; 5]. The study of clinical-genetic peculiarities of CKD in order to understand the pathogenic mechanisms of formation of nephrosclerosis and improvement of preventive measures is relevant. The study of polymorphic markers of genes coding regulators and receptors of renin-angiotensin system allows detecting a group of patients with increased risk of development of progression of pathological process, micro-vascular complications. Genetic studies may become a basis for personalization of kidney diseases.
In the literature for the last 5-10 years, there is no data on the evaluation of GFR depending on I/D polymorphism in ACE gene in diabetes. The interrelation of I/D polymorphism in ACE gene with a stage of chronic kidney disease in children and teenagers of Uzbek population with D1 according to new guidelines K/DOQI (2012) will be studied for the first time.
Aim of research: to evaluate functional condition of kidneys and study the interrelation of I/D polymorphism in ACE gene with a stage of chronic kidney disease in children and teenagers of Uzbek population with D1 according to new guidelines K/DOQI (2012).
Materials and methods
120 children and teenagers with type 1 diabetes, 53 (44.2 %) males and 67 (55.8 %) females, were examined. The average age of the patients was 13.8 ± 2.7 years old (Me 15.0; IQR 13.0-16.0).
For the quick evaluation and monitoring of kidney function, a GFR value that reflects the condition of kidneys very informatively was assessed. There is a close connection between the GFR level and presence of these or those manifestations or complications of CKD.
GFR (eGFR) for all children was calculated according to Schwarz formula considering sex and age:
GFR = (0.0484* height (cm.))/blood creatinine (^mol/l), the obtained data was standardized to body surface [4].
Stages of the chronic kidney disease were classified in accordance with guidelines K/DOQI (2012) on GFR:
I stage — GFR > 90 ml/min/1.73m 2;
II — GFR 89-60 ml/min/1.73m 2;
III — GFR 59-30 ml/min/1.73m 2;
IV — GFR 29-15 ml/min/1.73m 2;
V — GFR 15 and less ml/min/1.73m 2.
Isolation of genomic DNA and genotyping under I/D polymorphic marker of ACE gene (was conducted at the laboratory of Functional Genomics of a Man of the Institute of genetics and experimental biology of plants of the Academy of Sciences of the Republic of Uzbekistan). Isolation of DNA according to the method of R. Higuchi, H. Erlich (1989) with the use of a dry set of reagents Diatom™ DNA Prep 200.
Statistical processing of the results was conducted with the help of STATISTICA 6 and Biostat programs. Odd ration (OR) and 95 % confidential interval (95 % CI) were calculated with the use of logistic regression. The significance of differences of indicators was evaluated with the help of non-parametric test x2 (Pearson's test). The quantitative indicators were presented in the form of M ± SD, as well as a median (Me) and 25 and 75 percentiles (IQR). The differences between groups were considered statistically significant at p = 0.05.
Results
According to CKD concept, the evaluation of a stage of kidney pathology is done according to the value of GFR accepted as the one that reflects quantity and total volume of nephron work, including the one related to the execution of non-excretory functions, to the fullest (Table 1).
During the analysis of CKD stage depending on the age of disease onset, significant differences between the groups of the examined were not revealed. During the analysis of duration of the disease, it was revealed that as the duration of the disease increases, the occurrence of progression of CKD III and IV stages increases.
The analysis of HbA1 c level depending on CKD stage showed that even the children with diabetes in the stage of compensation (HbA1 c < 7.5 %) show CKD II (23.8 %) and III (8.3 %) stages.
It was revealed that the use of new classification K/DOQI (2012) allows detecting the decrease in kidney function at earlier stages: 61.9 % of children and teenagers with D1 showed CKD II stage at the stage of normal albuminuria and 16.7 % had stage III of CKD. Also, 28.6 % of children and teenagers at MAU stage showed stage II of CKD and 75.0 % showed stage III of KCD respectively (Table 2).
Conducted studies showed that 69 (57.5 %) patients with D1 showed high and optimal GFR at CKD I stage (> 90 ml/min/1.73m 2). The average value of GFR corresponded to 168.9 ± 58.4 ml/min/1.73m 2 (Me 157.2; IQR 126.2-200.1).
Insignificant reduction of GFR at CKD II stage (60-89 ml/min/1.73m 2) was revealed in 21 (17.5 %) patients and average GFR was 78.4 ± 8.6 ml/min/1.73m 2 (Me 78.7; IQR 74.3-87.4). Moderate reduction of GFR at CKD III stage (59-30 ml/min/1.73m 2) was observed in 12 (10.0 %) patients and average GFR was 38.2 ± 5.9 ml/min/1.73m 2 (Me 38.3; IQR 33.5-40.5). CKD IV stage (15-29 ml/min/1.73m 2) was revealed in 18 (15.0 %) patients. The average GFR was 22.8 ± 3.8 ml/min/1.73m 2 (Me 22.6; IQR 19.7-26.8).
CKD V stage (< 15 ml/min/1.73m 2) was not reveled in the examined patients with D1.
Table 1. - Clinical indicators depending on CKD stage
Indicators CKD stag e, n = 120
I, n = 69 (57.5 %) II, n = 21 (17.5 %) III, n = 12 (10.0 %) IV, n = 18 (15.0 %)
n % n % n % n %
Sex male 34 49.3 7 33.3 5 41.7 7 38.9
female 35 50.7 14 66.7 7 58.3 11 61.1
Age of disease onset
from 1 to 5 17 24.6 5 23.8 2 16.7 3 16.7
from 5 to 10 30 43.5 11 52.4 6 50.0 10 55.6
> 10 22 31.9 5 23.8 4 33.3 5 27.8
Duration of disease
Up to 1 year 5 7.3 3 14.3 1 8.3 - -
from 1 to 5 21 30.4 1 4.8 4 33.3 3 16.7
from 5 to 10 23 33.3 5 23.8 2 16.8 6 33.3
> 10 20 29.0 12 57.1 5 41.7 9 50.0
HbA1 c < 7.5 % 22 31.9 5 23.8 1 8.3 - -
HbA1 c > 7.5 % 47 68.1 16 76.2 11 91.7 18 100.0
Age, years 13.2 ± 3.1 14.5 ± 1.6 p. = 0.07 14.2 ± 2.2 p. = 0.28 14.9 ± 1.6 p. = 0.03
Age of disease onset, years 7.3 ± 3.7 7.1 ± 3.4 p. = 0.83 7.9 ± 4.0 p. = 0.61 6.9 ± 2.8 p. = 0.67
Duration of disease, years 6.1 ± 3.9 7.4 ± 3.9 Pi = 0.19 6.2 ± 3.9 p. = 0.94 8.1 ± 3.2 p. = 0.05
Note: pI — significance towards the indicator in the group CKD I stage.
Table 2. - GFR depending on the stage of albuminuria and CKD
Indicators CKD stage, n=120
I, n = 69 (57.5 %) II, n = 21 (17.5 %) III, n = 12(10.0 %) IV, n = 18 (15.0 %)
n % n % n % n %
NAU (A1) 37 53.6 13 61.9 2 16.7
MAU (A2) 32 46.4 6 28.6 9 75.0 3 16.7
HPU (A3) 2 9.5 1 8.3 15 83.3
GFR (ml/min/1.73 m2)
Average indicators 168.9 ± 58.4 78.4 ± 8.6 p. = 0.0001 38.2 ± 5.9 p. = 0.0001 22.8 ± 3.8 p. = 0.0001
NAU (A1) 181.6 ± 61.4 80.6 ± 7.5 p. = 0.0001 45.1 ± 9.5 p. = 0.0001
MAU (A2) 154.1 ± 51.8 76.4 ± 10.6 p. = 0.0001 36.6 ± 4.6 p. = 0.0001 20.3 ± 2.4 p. = 0.0001
HPU (A3) 70.6 ± 5.2 38.2 ± 5.9 p.. = 0.0001 23.3 ± 3.9 p.. = 0.0001
Note: pI — significance against the indicator in the group with CKD stage I; pII — significance against the indicator in the group with CKD stage II; NAU — normal albuminuria; MAU — microalbuminuria; HPU — heavy proteinuria.
Thus, the majority ofexamined (75.0 % OR 9.0; 95 % CI 5.02-16.1; p < 0.0001) children and teenagers with D1 is classified into I and II stages of chronic kidney disease according to guidelines K/DOQI (2012).
During the analysis of GFR depending on the stage of albuminuria and CKD, it was established that even at the stage of normal albuminuria, when there are no clinical signs of development and progression of diabetic nephropathy, the level of GFR may be significantly reduced against the group of CKD I stage in 61.9 %.
The analysis of ACE gene distribution demonstrated that 49 (40.8 %) patients are the carriers of II genotype; I/D genotype was revealed in 28 (23.4 %) and DD genotype was revealed in 43 (35.8 %) patients with D1 (Table 3).
The homozygous carriers of genotypes II (40.8 %) and DD (35.8 %) of ACE gene prevail among the examined children and teenagers of Uzbek population with D1.
The analysis of distribution of genotypes ofACE gene depending on the onset of disease showed the absence of statistically significant differences between groups with various age of the onset of the disease and polymorphism of ACE gene.
During the analysis of distribution of polymorphism of ACE gene depending on the duration of the disease, it was established that the occurrence of polymorph alleles of ACE gene were not significantly different between the groups, i. e. the occurrence of genotypes is identical in all groups with various duration of the disease.
Genotype II was established in the majority, 46 (66.7 % OR 4.0; 95 % CI 1.97-8.12; p = 0.0002), of the examined with stage I CKD. Genotype DD was revealed in the same percentage (66.7 % OR 4.0; 95 % CI 1.11-14.4; p = 0.06) of the patients with stage II CKD (Table 4).
Note: pI — significance against the indicator in the group with CKD stage I; pII — significance against the indicator in the group with CKD stage II; NAU — normal albuminuria; MAU — microalbuminuria; HPU — heavy proteinuria.
Table 4. - Frequency of occurrence of polymorphism of ACE gene and level of GFR depending on the stage of CKD
Table 3. - Clinical indicators depending on I/D polymorphism in ACE gene
Indicators Genotype
II n = 49 (40.8 %) ID n = 28 (23.3 %) DD n = 43 (35.8 %)
n % n % n %
Sex male 25 51.0 12 42.9 16 37.2
female 24 49.0 16 57.1 27 62.8
Age of disease onset
from 1 to 5 30.6 3 10.7 9 20.9
from 5 to 10 40.8 13 46.4 24 55.8
> 10 28.6 12 42.9 10 23.3
Duration of disease
Up to 1 year 8.2 3 10.7 2 4.6
from 1 to 5 24.5 10 35.7 7 16.3
from 5 to 10 30.6 10 35.7 11 25.6
> 10 36.7 5 17.9 23 53.5
Age, years 13.3 ± 3.2 13.3 ± 2.6 Pi = 1.0 14.6 ± 1.8 p. = 0.02
Age of disease onset, years 6.9 ± 3.8 8.4 ± 3.7 Pi = 0.10 6.9 ± 3.0 P. = 1.0
Duration of disease, years 6.7 ± 4.0 4.9 ± 3.7 pI = 0.06 7.8 ± 3.4 p. = 0.16
NAU (A1) 29 59.2 11 39.3 12 27.9
MAU (A2) 20 40.8 14 50.0 16 37.2
HPU (A3) 3 10.7 15 34.9
Albuminuria, mg/ml
NAU (A1) 13.2 ± 2.8 14.6 ± 3.5 pI = 0.06 31.7 ± 44.9 p. = 0.005
MAU (A2) 29.8 ± 15.3 27.9 ± 14.6 pI = 0.60 101.2 ± 50.8 p. = 0.0001
HPU (A3) - 83.3 ± 57.7 374.0 ± 189.8 p. = 0.0001
^\_CKD stage Genotype I n = 69 II n = 21 III n = 12 IV n = 18
abs. % abs. % abs. % abs. %
II 46 66.7 3 14.3
ID 23 33.3 4 19.0 1 8.3
DD 14 66.7 11 91.7 18 100
GFR (ml/min/1.73 m 2)
II 166.9 ± 56.1 77.1 ± 13.5 p. = 0.0001
ID 172.9 ± 63.8 77.3 ± 9.6 p. = 0.0001 38.2
DD 79.0 ± 8.0 38.2 ± 6.2 p.. = 0.0001 22.8 ± 3.8 p.. = 0.0001
Note: pI — significance against the indicator in the group with CKD stage I; pu — significance against the indicator in the group with CKD stage II.
Among the patients with CKD stage III, the majority (91,7 %) were the carriers of genotype DD, whereas the patients with CKD IV showed no case of presence of allele I (genotypes ID and DD), and all patients (100 %) were the carriers of genotype DD, which once again proves the significance of the role of polymorphism of ACE gene in development and progression of CKD in children and teenagers with D1.
In average, the GFR indicator in patients with genotype II was 161.4 ± 58.6 ml/min/1.73m 2 (Me 151.0; IQR 124.7-195.4)
at average; in the carriers of heterozygous genotype — 154.4 ± 70.7 ml/min/1.73m 2 (Me 135.0; IQR 110.7-181.7); in patients with genotype DD — 45.0 ± 25.4 ml/min/1.73m 2 (Me 33.6; IQR 24.0-74.2).
Herewith, the presence of genotype DD correlated with the severity of CKD (r = 0.66; P < 0.05). Consequently, the presence of genotype DD predisposes an increased risk of development or progression of CDK, whereas, genotype II is a predictor in the development and progression of CKD in children and teenagers with D1.
Discussion
Thus, we confirm that as the duration of the disease increases, the occurrence of progression of CKD III and IV stages increases (which corresponds to the literature data) [9]. Dependences of CKD stages on the age of onset were not detected.
The reduction of GFR was observed in one third (31.7 %) of children and teenagers with the inclination to the disease up to 5 years. Similarly, (31.6 %) of children and teenagers with D1 showed the reduction of GFR, which corresponds to CKD II, III and IV stages.
Intensive glycemic control significantly reduces the risk of microvascular disorders both in D1 and in D2, although, optimal level of HbA1 c required for prevention of the progression of CKD at diabetes hasn't been defined yet. According to Oh S. et al. 2011 [20], the level of HbA1 c < 6.50 % is associated with the reduced risk of development of terminal stage of CKD, which certifies about the importance of glycemic control in patients with high risk of progression of nephropathy. In DCCT research, it was proved in patients with D1 that HbA1 c < 7.5 % reduces the risk of DN to 55 %.
The analysis conducted by us showed that even children with diabetes in the stage of compensation (HbA1 c < 7.5 %) demonstrate CKD II (28.6 %) and III (4.8 %) stages. The duration of the disease in children with HbA1 c < 7.5 % was 5.53 ± 4.09 years (Me 5.0; IQR 2.0-10.0 years).
Modern classification of CKD (K/DOQI, 2012) promotes the detection of kidney disease at earlier stages and allows timely correction of therapy and improvement of the patient's forecast.
The results of our research showed that in significant number of children and teenagers with D1, the patients with II (61.9 % and 28.6 % respectively) and III (16.7 % and 75.0 % respectively) CKD stages were already detected at the stages of NAU and MAU.
Genetic factors, including ethnic or inter-population differences, play a notable role in CKD pathogenesis. In the recent years, more attention has been paid to the impact of genetic polymorphisms of ACE genes on the development of kidney complications [13; 18; 22].
We established that homozygous carriers of genotypes II (40.8 %) and DD (35.8) ofACE gene prevail among the examined children and teenagers of Uzbek population with D1. It was revealed for the first time that the frequency of genotype DD was 91.7 % in children and teenagers with D1 of Uzbek population at CKD III
stage, and the frequency of genotype DD was 100 % at CKD stage IV. The occurrence of CKD stage V was not observed among the examined.
The results obtained by us correspond to the data of the studies that relate D allele of GFR gene with the disease occurrence and progression of chronic (glomerular and tubulo-interstitial) kidney diseases [12; 19].
It was established for the first time that the frequency of genotype DD was 91.7 % in children and teenagers with D1 of Uzbek population at CKD III stage, and the frequency of genotype DD was 100 % at CKD stage IV. The occurrence of CKD stage V was not observed among the examined.
Thus, guidelines K/DOQI (2012) in relation with polymorphism of ACE gene and calculation of GFR allowed performing a new assessment of frequency of kidney lesion in children and teenagers with D1 of Uzbek population. The conducted research showed that the development and progression of CKD in children and teenagers with D1 is associated with I/D polymorphism ofACE gene; herewith, DD genotype is the marker of progression of CKD.
Conclusions
1. The use of new classification K/DOQI (2012) for children and teenagers with D1of Uzbek population allows detecting the decrease in kidney function at earlier stages: 61.9 % of children and teenagers with D1 showed GFR 80.6 ± 7.5 ml/min/1.73m 2 at the stage of normal albuminuria, which corresponds to stage II of CKD and 16.7 % had GFR 45.1 ± 9.5 ml/min/1.73m 2, which corresponds to stage III of CKD. Also, 28.6 % of children and teenagers at MAU stage showed stage II of CKD and 75.0 % showed stage III of KCD respectively.
2. The conducted analysis shows that GFR reduction can be observed even at the duration of the disease up to 5 years (38 children and teenagers — 31,7 %). Among children and teenagers with D1, 31.6 % (12 patients) showed GFR reduction, which corresponds to CKD II, III and IV stages.
3. Frequency distribution of ACE genotypes in children and teenagers with D1 was characterized by significant correlation of DD genotype interrelated with the severity of KCD of GFR reduction, which confirms the influence of genetic factors in KCD development. I/D polymorphism in ACE gene is a molecular-genetic marker of disposition to CKD D1 in children and teenagers of Uzbek population.
References:
1. Vikulova O. K. Clinical-laboratory and genetic factors of development and progression of diabetic nephropathy in patients with type 1 diabetes. Author's dissertation for the degree of the Candidate of medical sciences. - Moscow, 2003.
2. Zemchenko A. Yu., Konakova I. N. Classification of chronic kidney disease: isn't it time for reconsideration?//Doctor. - 2009. - № 7: 2-7.
3. Zyablitsev S. V., Chernobrivtsev P. A., Kishenya M. S., Pishchulina S. V. Role of the genetic marker of endothelial dysfunction ofACE gene in the pathogenesis of glomerular nephritis//Tauric medical and biological herald. - 2012. - Vol. 15, № 3. - P. 105-108.
4. Ivanova I. E., Rodionov V. A., Semenova L. V. Chronic kidney disease in children of the Republic of Chuvashia//Pediatrics. - 2011. -Vol. 90, № 3. - P. 138-144.
5. Kaliev R. R., Budaichieva A. B., Aldashev A. A. Interrelation of I/D polymorphism ofACE gene with progression of chronic glomerular nephritis//Therapeutic archive. - 2005. - Vol. 77, № 6. - P. 12-15.
6. Kuraeva T. L. Insulin resistance at type 1 diabetes in teenagers: treatment with Siofor (metformin)//DiabetesT. - 2003. - № 1. - P. 26-28.
7. Panfilova V. N. Type 1 diabetes: management and control of the disease (according to the results of a prospect trial): Author's dissertation... Doctor of medical sciences. - Krasnoyarsk, 2010. - 46 p.
8. Rakhimova G. N., Sadykova A. S. Clinical-genetic factors of risk of development of chronic kidney disease in children and teenagers with D1 of Uzbek population//Theoretical and clinical medicine. - 2014. - P. 124-128.
9. Semidotskaya Zh. D., Chernyakova I. A. etc. Chronic kidney disease and factors of progression//News of medicine and pharmacy. -2010. - № 8(321)// [Electronic resource]. - Available from: http://www.mif-ua.com
10. Surikova S. V. Peculiarities of fuctional condition of endothelium in children with type 1 diabetes before development of microvascular complications: Author's dissertation. Candidate of medical sciences - Tyumen, 2008. - 24 p.
Prediction role of risk factors assessment to immediate results of surgical treatment of concomitant lesions
11. Shestakova M. V., Dedov I. I. Diabetes and chronic kidney disease. - Moscow, 2009.
12. Akman B., Tarhan C., Arat Z., Sezer S., Ozdemir F. Renin-angiotensin system polymorphisms: A risk factor for progression to end-stage renal disease in vesicoureteral reflux patients//Ren Fail. - 2009. - 31: 196-200.
13. Elshamaa M., Sabry S., Bazaraa H. et al. Genetic polymorphism of ACE and the angiotensin II type1 receptor genes in children with chronic kidney disease//J Inflamm (Lond). - 2011. - 8: 20.
14. Hogg R., Furth S., Lemeley K. National Kidney Foundation's Kidney Disease Outcomes Quality Initiative clinical practice guidelines for chronic kidney disease in children and adolescents: evaluation, classification and stratisfaction//Pediatrics. - 2003. - 111: 1416-1421.
15. Coresh J., Selvin E., Stevens L. A. et al. Prevalence of chronic kidney disease in the United States//JAMA. - 2007. - 298: 2028-2047.
16. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease//Kidney International Supplements. - 2013. - 3(1): 1-150.
17. Levey A., Atkins R., Coresh J. et al. Chronic kidney disease as a global public health problem: approaches and initiatives - a position statement from Kidney Disease: Improving Global Outcomes//Kidney Int. - 2007. - 72: 247-259.
18. McClellan W., Warnock D., Judd S. et al. Association of family history of ESRD, prevalent albuminuria, and reduced GFR with incident ESRD//Am J Kidney Dis. - 2012. - 59: 25-31.
19. Morsy M., Abdelaziz N., Boghdady A. et al. Angiotensin converting enzyme DD genotype is associated with development of rheumatic heart disease in Egyptian children//Rheumatol Int. - 2011. - 31: 17-21.
20. Oh S., Kim Y., Koo H. et al. Glycated haemoglobin and the incidence of end-stage renal disease in diabetics//Nephrol Dial Transplant. - 2011. - 26(7): 2238-2244.
21. Rakhimova G. N., Alimova N. U. Decrease in prevalence of diabetic nephropathy in children and adolescents as per republic of Uzbekistan national register. Abstracts of 54th Annual Meeting of the European Society for Paediatric Endocrinology. - P. 364.
22. Shanmuganathan R., Kumaresan R., Giri P. Prevalence of angiotensin converting enzyme (ACE) gene insertion/deletion polymorphism in South Indian population with hypertension and chronic kidney disease//J Postgrad Med. - 2015. - 61: 230-234.
Sobirov Jasur Gaybillaevich, MD, Senior Researcher, Department of Vascular Surgery, JSC «Republican Specialized Surgery Center named after academician V. Vakhidov» E-mail: [email protected] Bahritdinov Fazliddin Shamsitdinovich, MD, PhD, Head of the Department of Vascular Surgery E-mail: [email protected]
Prediction role of risk factors assessment to immediate results of surgical treatment of concomitant lesions
Abstract: The authors aim was to investigate the impact of risk factors by SMART assessing tool, on the immediate results of surgical treatment of patients with concomitant lesions of the aortic arch branches, terminal part of abdominal aorta and lower limb arteries.
Keywords: atherosclerosis, risk factors, tools of the scoring.
Introduction
There are a lot of ways of assessing the impact of both — various risk factors within the development processes of the course and outcomes from treatments taken for atherosclerosis. Assessing risks for each individual patient is crucial. Moreover, most of risk factors have an independent effect on atherosclerosis and related complications, which can be reduced through a course of treatment of the latter. Risk assessment tools help review the impact of individual risk factors and their focus on selection of an appropriate treatment which is based on the diagnostic methods applied [1; 2; 3; 4].
In the last 25-30 years developed dozens of risk assessment tools (methods, calculators) which include main predictors such as age, gender, systolic blood pressure, diabetes, smoking, cardiovascular diseases (myocardial infarction, angina pectoralis, stroke, arrhythmia (arterial fibrillation), left ventricular hypertrophy, cholesterol, etc. [4; 5; 6; 7; 8].
SMART study group (Second Manifestations ofARTerial disease) (2009) looked into the impact ofvarious risk factors in 800 patients with peripheral atherosclerosis and developed a sensitive
method for determining of a 1-5-year long risk of stroke, heart attack and death, with a statistical certainty (95 %CI) (tab. 2) [4].
Accordingly, the aim of study was to investigate the impact of risk factors by SMART assessing tool, on the immediate results of surgical treatment of patients with concomitant lesions of the aortic arch branches, terminal part of abdominal aorta and lower limb arteries.
Material and methods
Analyzed results of the assessment of risk factors by SMART of 181 patients operated with combined lesions of the aortic arch branches and lower limb arteries. All of them were operated in the Department of Vascular Surgery from 2000 to 2015. Patients were divided into three groups exposed to different surgical interventions at the initial stage: Group I — patients exposed to reconstruction of the aortic arch branches (31 patients); Group II — those operated on the terminal portion of the abdominal aorta and the arteries of the lower limb arteries (120 patients); and Group III — patients operated simultaneously on both arterial beds (30 patients). The age of the patients ranged between 51 and 70 years (average 60 ± 1), it is noteworthy that 97.2 % of all subjects were male patients (tab. 1).
