nidНефрология и диализNephrology and Dialysis1680-44222618-9801Российское диализное общество10.28996/2618-9801-2022-3-480-485nid-83Research ArticleОРИГИНАЛЬНЫЕ СТАТЬИORIGINAL ARTICLESИнтраназальный вазопрессин (DDAVP) и частота внутридиализной гипотензии при терминальной стадии почечной недостаточностиIntranasal vasopressin (DDAVP) and intra-dialysis hypotension incidence in end-stage renal diseaseАлидадиАлиAlidadiALiresearch1376@gmail.comФатидеТахере МохаммадиFatidehTahereh Mohammadi30stana@gmail.comЗахеданский университет медицинских наукРоссияZahedan University of Medical SciencesRussian Federation202221062024243480485Copyright © Алидади А., Фатиде Т.М., 20242024Алидади А., Фатиде Т.М.Alidadi A., Fatideh T.M.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephro.ru/jour/article/view/83

Введение. Интрадиализная гипотензия (ИДГ) остается одним из наиболее частых и потенциально смертельных острых осложнений, с которыми сталкиваются пациенты, находящиеся на гемодиализе. Цель исследования - определить влияние интраназального DDAVP (вазопрессина) на частоту ИДГ и объем физиологического раствора, необходимого для лечения гипотонии у склонных к гипотензии пациентов с хронической болезнью почек 5 стадии, получающих лечение гемодиализом (ХБП 5D). Методы. Включено десять пациентов с ХБП 5D, предрасположенных к гипотензии. ИДГ фиксировалась как минимум в 30% случаев гемодиализа в предыдущем месяце. В течение 30 дней они получали интраназальный спрей плацебо. В течение следующего месяца они получали 2 впрыскивания (каждое содержало 10 мкг) вазопрессина (DDAVP) за 30 минут до начала гемодиализа. ИДГ определяли как симптоматическое снижение систолического артериального давления (АД) более чем на 20 мм рт.ст. или падение среднего артериального давления (САД) более чем на 10 мм рт. Результаты. ИДГ была зарегистрирована в 68 сеансах гемодиализа в группе плацебо (63,6%) и в 53 сеансах в группе вазопрессина (49,5%) со статистически незначимой разницей (P =0,07). Между двумя группами существовали достоверные различия (P =0,04) в отношении снижения систолического АД, и оно было более выраженным в группе плацебо. Средний (±SD) объем физиологического раствора, вводимого внутривенно, был значительно ниже в группе вазопрессина (34±68 мл) по сравнению с группой плацебо (77±90 мл); P<0,001. Гипертонический раствор не требовался ни в одной из групп. Заключение. Хотя статистически значимых различий в частоте ИДГ между группой плацебо и группой интраназального введения вазопрессина не наблюдалось, средние значения систолического АД и САД были значительно выше в группе вазопрессина. Кроме того, группе вазопрессина требовались значительно меньшие объемы внутривенного введения физиологического раствора для лечения ИДГ. Хотя мы предлагаем интраназальный вазопрессин в качестве возможного фармакологического лечения для предотвращения ИДГ, необходимо учитывать, что небольшой размер выборки и статистически незначимая разница в частоте ИДГ сделали наши результаты не обобщаемыми. Чтобы сделать это утверждение убедительным, необходимы дальнейшие исследования с большим числом наблюдений.

Introduction: intradialytic hypotension (IDH) remains one of the most common and potentially lethal acute complications encountered by patients under hemodialysis. To determine the effect of intranasal DDAVP (vasopressin) on IDH incidence and the volume of normal saline required to manage hypotension in hypotension-prone patients with chronic kidney disease stage 5 receiving hemodialysis treatment (CKD 5D). Material and Methods: ten hypotension-prone CKD 5D patients were included in the study. They had experienced IDH for at least 30% of hemodialysis treatments in the preceding month. For 30 days, they received a placebo intranasal spray. For the next month, they received 2 puffs (each containing 10 μg) of vasopressin (DDAVP) 30 minutes before hemodialysis. IDH was defined as a symptomatic decrease in systolic blood pressure (BP) by more than 20 mmHg or a drop in mean arterial pressure (MAP) by more than 10 mmHg. Results: IDH was observed in 68 hemodialysis sessions in the placebo group (63.6%) and 53 sessions in the vasopressin group (49.5%) with a marginally significant difference (P =0.07). A significant difference (P =0.04) was found between the two groups regarding the decrease in systolic BP that was more pronounced in the placebo group. Mean (±SD) normal saline volume administered intravenously was significantly lower in the vasopressin group (34±67.6 mL) compared to the placebo group (77.1±89.8 mL); P<0.001. Hypertonic saline was not required in either group. Conclusion: Although no statistically significant difference was observed between the placebo and intranasal vasopressin groups in terms of IDH incidence, mean systolic BP and MAP measurements were significantly higher in the vasopressin group. Also, the vasopressin group required significantly lower volumes of intravenous normal saline to manage IDH. Although we suggest intranasal vasopressin as a possible pharmacologic treatment to prevent IDH, it must be considered that the low sample size and non-significant difference in IDH frequency made our results non-generalizable. Further studies with a larger number of observations are required to make this statement convincing.

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The authors declare that there are no conflicts of interest present.