ONADAGI GIPOPARATIREOZ SHAROITIDA AVLOD BUYRAKLARIDA NEFRON MORFOLOGIK O‘ZGARISHLARI: PATOGENEZ, DASTLABKI DALILLAR
- Авторы:Axmedova Sayora Muxammadiyevna. Avezova Gulshod Sattarovna
- Дата публикации:December 1, 2025
- Тип:Статья
- DOI: 10.64156/mju.8720 Скопировано
- Том / № Выпуска:Toм 1_6_Спец выпуск 2025
Аннотация
Annotatsiya
Maqsad: Onadagi gipoparatireoz sharoitida avlod buyragida nefrogenes va nefro-morfologiyaga ta’sir etuvchi mexanizmlarni (PTH/PTHrP, vitamin D, platsentar Ca tashuvi) tizimlashtirish.Usul: 1996–2025 yy. oralig‘ida 10–15 ta asosiy ish ko‘rib chiqildi (hayvon modellar, mexanistik va klinik sharhlar). Natija: Bevosita “ona gipoparatireozi → buyrak morfologiyasi” bo‘yicha inson dalillari kam. Biroq PTHrP ning platsentar Ca tashuvi va buyrak rivojlanishida ishtiroki, hamda onadagi vitamin D tanqisligi modellarida avlodda glomerulalar soni ko‘payib, kattaligi kichrayishi va yetilish kechikishi ko‘rsatildi. Nutritiv va uteroplatsentar omillar nefro-endoumentni pasaytirishi mumkin. Xulosa: Gipoparatireozli homiladorlarda Ca–D o‘qi barqarorligini ta’minlash va perinataldan keyin avlodning uzoq muddatli buyrak kuzatuvi maqsadga muvofiq.
Kalit so‘zlar
Gipoparatireoz, PTH, PTHrP, D vitamini, nefrogenez, buyrak morfologiyasi, platsentar kalsiy tashilishi, homila, ona–homila o‘qi, glomerulyar yetilish, perinatal nefroprotektsiya.
Аннотация.
Цель: Систематизировать механизмы влияния материнского гипопаратиреоза на нефрогенез и морфологию нефронов у потомства. Методы: Анализ 10–15 ключевых исследований (модельные эксперименты на животных, механистические работы, клинические обзоры; 1996–2025). Результаты: Прямые данные у людей крайне ограничены. Однако показана ключевая роль PTHrP в плацентарном переносе кальция и развитии почки; при дефиците витамина D у матери у потомства отмечены увеличение числа клубочков при их меньшем размере и задержка зрелости. Нутритивный стресс и утероплацентарная недостаточность снижают нефронный эндоумент. Вывод: Поддержание стабильности оси Ca–витамин D при беременности с гипопаратиреозом и последующее долгосрочное наблюдение функции и морфологии почек у детей представляются целесообразными.
Ключевые слова:
Гипопаратиреоз, паратиреоидный гормон (ПТГ), пептид, подобный ПТГ (PTHrP), витамин D, нефрогенез, морфология нефрона, плацентарный транспорт кальция, плод, ось мать–плод, гломерулярное созревание, перинатальная нефропротекция.
Abstract
Objective: To synthesize evidence on how maternal hypoparathyroidism may influence offspring renal nephron morphology via PTH/PTHrP and vitamin-D–dependent pathways. Methods: Narrative review of 10–15 pivotal studies spanning animal models, mechanistic work, and clinical reviews (1996–2025). Results: Direct human evidence on nephron morphology after maternal hypoparathyroidism is scarce. Experimental data indicate that PTHrP governs placental calcium transport and is expressed during kidney maturation; maternal vitamin-D deficiency increases nephron number but yields smaller, less mature glomeruli. Maternal nutritional stress and uteroplacental insufficiency reduce nephron endowment. Conclusions: In pregnancies complicated by hypoparathyroidism, optimizing Ca–vitamin-D homeostasis and arranging long-term renal follow-up in offspring are prudent.
Key words:
Hypoparathyroidism, parathyroid hormone (PTH), parathyroid hormone-related peptide (PTHrP), vitamin D, nephrogenesis, nephron morphology, placental calcium transport, fetus, maternal–fetal axis, glomerular maturation, perinatal nephroprotection.
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