Georgian medical news · 2026
ASSESSMENT OF SUBCLINICAL RENAL INSULT IN SHORT- AND LONG-TERM UNCONTROLLED HYPERTENSION USING MOLECULAR BIOMARKERS OF NGAL AND KIM-1.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Alathary R, Jabbar N, Hamzah S
Аннотация
BACKGROUND: Uncontrolled Hypertension (UHTN) is a major cause of rapidly deteriorating kidney function. Typical clinical indicators often lack the sensitivity necessary for early detection of tubular changes preceding irreversible damage to the nephrons.
OBJECTIVE: To evaluate the diagnostic performance of a novel kidney damage index derived from the integrated values of Neutrophil gelatinase-associated lipocalin (NGAL) and Kidney injury molecule-1 (KIM-1), alongside Caspase-3 and Advanced protein oxidation products (AOPP), focusing on how disease duration of UHTN influences these molecular signatures of kidney injury.
METHODS: 90 participants were categorized into three groups (n=30): healthy controls, short-term UHTN (<5 years), and long-term UHTN (>10 years). NGAL, KIM-1, Caspase-3, and AOPP were quantified using ELISA.
RESULTS: Significant progressive elevations in serum NGAL, KIM-1, and Caspase-3 were observed in UHTN patients compared to controls (P<0.05).
CONCLUSION: UHTN triggers 'silent' tubular deterioration. These structural markers offer a superior diagnostic advantage by detecting subclinical damage at an early stage of UHTN. The clinical application of these sensitive biomarkers could be instrumental in preventing the rapid progression of HTN to overt chronic kidney disease and avoiding long-term complications.
OBJECTIVE: To evaluate the diagnostic performance of a novel kidney damage index derived from the integrated values of Neutrophil gelatinase-associated lipocalin (NGAL) and Kidney injury molecule-1 (KIM-1), alongside Caspase-3 and Advanced protein oxidation products (AOPP), focusing on how disease duration of UHTN influences these molecular signatures of kidney injury.
METHODS: 90 participants were categorized into three groups (n=30): healthy controls, short-term UHTN (<5 years), and long-term UHTN (>10 years). NGAL, KIM-1, Caspase-3, and AOPP were quantified using ELISA.
RESULTS: Significant progressive elevations in serum NGAL, KIM-1, and Caspase-3 were observed in UHTN patients compared to controls (P<0.05).
CONCLUSION: UHTN triggers 'silent' tubular deterioration. These structural markers offer a superior diagnostic advantage by detecting subclinical damage at an early stage of UHTN. The clinical application of these sensitive biomarkers could be instrumental in preventing the rapid progression of HTN to overt chronic kidney disease and avoiding long-term complications.