Background and Aims Although renal transplantation improves survival, cardiovascular morbidity and mortality still remain as a significant problem compared with nonrenal populations. In end stage renal disease metabolic cardiovascular risk factors such as hypertension, hyperuricemia, obesity and diabetes mellitus have been confirmed to be positively correlated with arterial stiffness. Arterial stiffness is an important characteristic of the arterial wall and can be assessed noninvasively by the measurement of carotid-femoral pulse wave velocity (PWv). The aim of this study is to evaluate the risk factors for arterial stiffness in kidney transplant recipients. Method One hundred and forty nine kidney transplant recipients from our renal transplant outpatient clinic were enrolled into the study. All patients were evaluated for their standard clinical (age, gender, duration of hemodialysis, post-transplant time), biochemical parameters. Anthropometric and body composition analyses were performed for all patients. Body compositions were analyzed by using the Body Composition Analyzer (Tanita BC- 420MA). PWv was determined from pressure tracing over carotid and femoral arteries using the SphygmoCor system. Results Patients were divided into two groups according to PWv levels. The frequency of patients with PWv ≥ 7 m/s was higher in patients with new onset diabetes (55.9%), hyperuricemia (uric acid level type="Periodical" type="Periodical" type="Periodical" type="Periodical" type="Periodical" type="Periodical" type="Periodical" type="Periodical"> 7 mg/dl) (p:0.029, 0.05). Higher carotid-femoral PWv was significantly related with systolic (p:0.003) and diastolic blood pressure (p:0.002), uric acid (p:0.0001) and fasting glucose (p: 0.02) levels. According to body composition analyses, muscle mass, visceral fat ratio and body weight were significantly higher in patients with PWv ≥ 7 m/s (p < 0.005). In patients with high PWv, sagittal abdominal diameters and waist circumferences were significantly higher than patients with PWv < 7 m/s. When criteria for metabolic syndrome were assessed there were a significant increase in pulse wave velocity in patients with 0-1; 2-3; and 4-5criteria (p < 0.01). Conclusion In post transplantation period, metabolic syndrome indices as high blood pressure, hyperuricemia, hyperglycemia and increased waist and hip circumferences are closely related with arterial stiffness. For cardiovascular risk reduction after renal transplantation; blood pressure, serum glucose and uric acid levels should be under strict control.

Реферат. Цель-изучить влияние комбинированного комплексного лечения ингибитором АПФ (рамиприлом), ГМГ-КоА-редуктазой (аторвастатином) и β-адреноблокатором (небивалолом) на функциональное состояние эндотелия и почек при различных стадиях хронической болезни почек. Материал и методы. В исследование были включены больные с хронической болезнью почек, имеющие 1-4-ю стадии болезни. У обследованных больных причиной хронической болезни почек были следующие патологии: хронический гломерулонефрит, диабетическая нефропатия вследствие сахарного диабета II типа. Больные были разделены на 4 группы по уровню скорости клубочковой фильтрации. В свою очередь, каждая группа в зависимости от причины развития хронической болезни почек была разделена на 2 подгруппы: А-больные хроническим гломерулонефритом и В-больные диабетической нефропатией. Во время исследования во всех группах было изучено влияние комбинированного комплексного лечения рамиприлом, аторвастатином и небивалолом на функциональное состояние эндотелия и почек. В период проведения лечения в течение 3 мес были изучены ренопротективный эффект, изменения, происходящие в показателях эндотелиальной дисфункции. Полученные данные обрабатывались методами вариационной статистики с вычислением средней и ошибки средней (М±m). Результаты и обсуждение. После 3-месячного лечения у этих больных отмечалось статистически достоверное снижение уровня креатинина. Начиная со 2-й стадии хронической болезни почек, несмотря на уменьшение его уровня в обеих подгруппах, у больных с диабетической нефропатией его уменьшение было статистически незначимым. Несмотря на то что на 3-й стадии хронической болезни почек в обеих подгруппах были получены достоверные результаты, на 4-й стадии ни в одной из подгрупп положительных результатов достичь не удалось. Во 2-3-й стадиях хронической болезни почек наблюдалось повышение степени эндотелийзависимой вазодилатации. При хроническом гломерулонефрите в подгруппе 2А этот показатель в среднем составил 12%, а в подгруппе 3А-10,2%. В подгруппе 4А проводимое лечение не оказало на функцию эндотелия никакого влияния. Выводы. Трехмесячное лечение больных по схеме ингибитор АПФ + ингибитор ГMГ-KoA-редуктазы + β-адреноблокатор отмечалось улучшением функционального состояния почек, а также положительными изменениями вазодилатирующей реакции эндотелия сосудов. Ключевые слова: эндотелиальная дисфункция, хроническая болезнь почек, хронический гломерулонефрит, диабетическая нефропатия. Для ссылки: Влияние комбинированного комплексного лечения на эндотелий и функциональное состояние почек на различных стадиях хронической болезни почек / М.М. Агаев, Ш.Г. Исмайлова, И.М. Маммедова, М.С. Новрузова // Вестник современной клинической медицины.

concentration, 0.55 mmol/L; range: 0.5-0.6 mmol/L), despite high-dose of oral magnesium supplementation (~1.3 mmol/kg/day). She denied purging, diuretic or laxative abuse, or diarrhea. She was known to have a non-verbal learning disability (NVLD) and was subsequently diagnosed with social anxiety disorder. She continued to struggle in school and psycho-educational testing was performed at age 15, which assessed her verbal reasoning and comprehension, memory, and processing speed to be well below age expectations (0.4 th to 2 nd percentile). This was a notable change from her assessment at age 8, where these abilities were assessed in the low average to average ranges (13 th to 27 th percentile). Although significant regression in cognitive abilities did not occur, she did not demonstrate expected cognitive developments and progression. As a result, her cognitive presentation was in keeping with an Intellectual Disability, rather than NVLD. There was no significant family history of renal disease. Physical examination was unremarkable. Laboratory values revealed hypomagnesaemia with high fractional excretion of magnesium in urine repeated at least 3 times in spot as well as 24-hour urine collection (FeMg: 10%, normal <4%). Her renal function, other electrolytes, renal and brain imaging was normal. Due to high renal excretion of magnesium, her genetic evaluation was done to exclude hereditary hypomagnesaemia which revealed heterozygous mutation in CNNM2 at protein level (p.Arg366Pro). It is the first description of the CNNM2 mutation at this position causing hypomagnesaemia and neurological involvement. She continues to be on a high dose oral magnesium supplementation to maintain her serum magnesium around 0.56 mmol/L.Conclusions: CNNM2 mutations should be taken into account in patients with hypomagnesaemia and neurological impairment.

Background and Aims It is believed that septicemia and septicopyemia can lead to functional failure of many organs, including the kidneys. In this regard, it is important to study the morphological features of ultrastructural changes in kidney tissue. Method Structural changes in renal tissue of 30 patients who died as a result of sepsis were investigated by electron-microscopy. The burial was carried out at an early stage (1-6 hours after death). The sections obtained for ultrasonic examination were examined on “James 100 S ” electron microscope after contrasting with uranyl acetate and lead citrate solution. Results An ultrastructural study of the cells of the cortical and medial layers of the kidneys revealed that there are changes in extracellular contacts and cell fragmentation as a result of lysis of the cytoplasmic membrane of cells. The integrity of the basal membrane of epithelial cells of the proximal and distal tubules are preserved. However, the basal layer did not have a homogeneous structure, intersected and transparent in certain areas. Numerous vacuoles, lipid supplements and fragments of lysed intracellular proteins in the cytoplasm have been identified in the cytoplasm of cells. Most of the nucleus was in the collapse phase. The lumen of tubules is narrow and most of the microvilli of the brush border are destructed. It was revealed that in sepsis renal failure and severe destructive changes and the formation of necrosis sites in the structural elements of the nephron as a result of bacterial toxins were mainly observed in areas where bacteria were localized. Conclusion Abnormalities of podocytes, of endothelial cells, disruption of the basal membrane layers as a result of abnormal damage of organelles especially mitochondria, changes of proximal and distal tubules may be caused by severe renal failure due to sepsis.

E. coli is a gram-negative bacterium, which is present in normal intestinal microflora and indicates the toxic influence to many cells of the body as well as renal vascular endothelial cells in the kidneys and epithelial cells of proximal and distal renal tubules. The toxic effect of E. coli is related to lipopolysaccharide containing endotoxin placed in their wall. The needle biopsy had been taken from 10 patients (7 females, 3 males) complicated by pain in kidneys and nephrotic syndrome in anamnesis during the E. coli endotoxemia. The Araldite-Epon blocks had been prepared from biopsy materials. The semi-and ultrathin sections obtained from these resin blocks were examined by JEM-1400 Transmission Electron Microscope and the electron micrograms were taken. The titer of E. coli endotoxin was high in the microbiological analysis of the urine of the 10 patients with kidney disease (7 of them were female and 3 -male). The mixed infection of E. coli and Salmonella were found in bacteriological analysis of 1 female. Upon the result of toxemic influence of E. coli endotoxin to the epithelial cells of renal tubules, the severe structural abnormalities and necrosis were found. The different results of morphological research of renal structures during the E. coli endotoxemia pointed that there aren't same findings in epithelial cells of renal tubules in all patients. Finally, our findings can create a morphological basis for the future molecular investigations of acute endotoxemic kidney injury.