Abstract:
AIM:To study the urinary excretion of the molecular factors regulating angiogenesis, such as vascular endothelial growth factor type A (VEGF-A), thrombospondin 1 (THBS1), and angiopoietin 2 (ANGPT2), versus that of the urinary markers of renal injury and fibrogenesis, such as neutrophil gelatinase-associated lipocalin (NGAL), type IV collagen (COL4), and known clinical risk factors for accelerated disease progression to estimate the prognostic value of urinary excretion in patients with chronic glomerulonephritis (CGN). SUBJECTS AND METHODS:Eighty-two patients (45% men, 55% women; mean age, 36.5 years) with a clinical diagnosis of CGN were examined. 31.7% of the examinees presented with nephrotic syndrome; 31.7% had a glomerular filtration rate (GFR) of less than 60 ml/min/1.73 m2. Morning urine samples were analyzed by Elisa to determine the urinary excretion of biomarkers (VEGF-A, THBS1, ANGPT2, NGAL, and COL4). The results were adjusted to urinary creatinine concentrations. RESULTS:The urinary excretion of the angiogenesis regulators VEGF-A, THBS1, and ANGPT2 correlated between them, with that of the renal injury markers NGAL and COL4, with the level of proteinuria. That was found to be unassociated with blood pressure and GFR. In the presence and absence of nephrotic syndrome, high (> 75th percentile) urinary excretion rates were 46.2 and 14.8% for VEGF-A (p < 0.01); 50 and 13% for THBS1 (p < 0.001); and 46.2 and 14.8% for ANGPT2 (p < 0.01), respectively. That for ANGPT2 was also high in the presence of anemia (63.2 versus 11.7%; p < 0.001). CONCLUSION:The finding of the high urinary excretion of the angiogenesis regulators VEGF-A, THBS1, and ANGPT2 and its association with that of kidney injury markers in the patients with the proteinuric forms of CGN suggest that this excretion may be considered as an integral index that displays glomerular injury and indicates tubulointerstitial proteinuric/hypoxic remodeling. :Цель исследования. У больных хроническим гломерулонефритом (ХГН) изучить мочевую экскрецию молекулярных факторов, регулирующих ангиогенез - фактора роста эндотелия сосудов A типа (VEGF-A), тромбоспондина 1-го типа (THBS1) и ангиопоэтина 2-го типа (ANGPT2) по сравнению с мочевыми маркерами повреждения и фиброгенеза почек - липокалином, ассоциированным с желатиназой нейтрофилов (NGAL), коллагеном IV типа (COL4) и известными клиническими факторами риска ускоренного прогрессирования заболевания для оценки ее прогностического значения. Материалы и методы. Обследовали 82 больных с клиническим диагнозом ХГН, средний возраст 36,5 года, 45% мужчин, 55% женщин. У 31,7% обследованных имелся нефротический синдром, у 31,7% - скорость клубочковой фильтрации (СКФ) ниже 60 мл/мин/1,73 м2. Для определения мочевой экскреции биомаркеров (VEGF-A, THBS1, ANGPT2, NGAL, COL4) исследовали утреннюю пробу мочи методом ELISA. Результат стандартизовали на концентрацию креатинина в моче. Результаты. Уровни мочевой экскреции регуляторов ангиогенеза VEGF-A, THBS1, ANGPT2 коррелировали между собой, с уровнем мочевой экскреции маркеров повреждения почек NGAL и COL4, уровнем протеинурии. Связи с уровнем артериального давления и СКФ не отмечено. При наличии и отсутствии нефротического синдрома частота высокого (>75-й процентиль) уровня мочевой экскреции регуляторов ангиогенеза соответственно составляла: для VEGF-A 46,2 и 14,8% (р<0,01); THBS1 50 и 13% (р<0,001); ANGPT2 46,2 и 14,8% (р<0,01). Частота высокого уровня ANGPT2 также была выше при наличии анемии - 63,2% против 11,7% (р<0,001). Заключение. Полученные данные о высокой экскреции с мочой у больных с протеинурическими формами ХГН регуляторов ангиогенеза VEGF-A, THBS1 и ANGPT2 и ее связи с экскрецией маркеров повреждения почек свидетельствуют, что такая экскреция может рассматриваться как интегральный показатель, отражающий повреждение почечных клубочков и свидетельствующий о протеинурическом/гипоксическом ремоделировании тубулоинтерстиция.
journal_name
Ter Arkhjournal_title
Terapevticheskii arkhivauthors
Shvetsov MY,Zheng A,Kozlovskaya LV,Serova AG,Travkina EV,Mukhin NAdoi
10.17116/terarkh201587675-82subject
Has Abstractpub_date
2015-01-01 00:00:00pages
75-82issue
6eissn
0040-3660issn
2309-5342journal_volume
87pub_type
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