nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.36485/1561-6274-2021-25-3-20-27nefr-1971Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESАртериальная гипертензия у детей с нефротическим синдромомArterial hypertension in children with nephrotic syndromehttps://orcid.org/0000-0002-9356-4870КаримджановИ. А.KarimdzhanovI. A.

Каримджанов Ильхамджан Асамович, проф, д-р мед. наук, кафедра детских болезней №2, нефрологическое отделение.

100102, г. Ташкент, ул. Фароби, д. 2. 

 Тел.: (+998) 90-351-53-46

 Ilkhamdzhan A. Karimdzhanov, MD, PhD, DMedSci, Prof. Department of Children's Diseases №2 and nephrology

100102,  Tashkent, Farobi St., 2.

 Phone: (+998) 90-351-53-46

dr.ilhomjon@mail.ruhttps://orcid.org/0000-0003-3577-499XИскановаГ. Х.IskanovaG. Kh.

Исканова Гулшан Холдоровна, канд. мед. наук, доц., кафедра детских болезней №2, нефрологическое отделение

100102, г. Ташкент, ул. Фароби, д. 2.

 Тел.: (+998) 90-370-64-40

Gulshan Kh. Iskanova, MD, PhD, Associate professor, Department of Children's Diseases №2 and nephrology

100102,  Tashkent, Farobi st., 2.

Phone: (+998) 90-370-64-40

gulshan1972iskanova@gmail.comhttps://orcid.org/0000-0002-1234-9475ИсраиловаН. А.IsrailovaN. A.

Исроилова Нигора Амануллаевна, канд. мед. наук, асс., кафедра детских болезней №2.

100102,  г. Ташкент, ул. Фароби, д. 2.

Тел.: (+998) 90-175-71-80

Nigora A.Isroilova, MD, PhD, Assistant,  Department of Children's Diseases №2 and nephrology

100102, Tashkent, Farobi st., 2.

Phone: (+998) 90-175-71-80

Nigora99@gmail.comТашкентская медицинская академияУзбекистанTashkent Medical AcademyUzbekistan2021220420212532027Copyright © Каримджанов И.А., Исканова Г.Х., Исраилова Н.А., 20212021Каримджанов И.А., Исканова Г.Х., Исраилова Н.А.Karimdzhanov I.A., Iskanova G.K., Israilova N.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephrolog.ru/jour/article/view/1971

В обзоре приведены материалы распространенности НС у детей, варианты его течения: стероидочувствительный (СЧНС) и стероидрезистентный (СРНС), стероидзависимый (СЗНС). Нефротический синдром с минимальными изменениями (НСМИ) является наиболее распространенной патологией клубочков. Хотя НСМИ имеет отличный прогноз с низким риском прогрессирования в т-ХПН, его рецидивирующий характер требует, чтобы дети получали частые курсы стероидной терапии и другие лекарства, многие из которых, как известно, влияют на артериальное давление (АД). Показана взаимосвязь НС у детей с артериальной гипертензией (АГ). Приведена распространенность АГ у детей с СЧНС, СРНС, СЗНС. Регулирование АГ у детей является обязательным в лечении НС в связи с тем, что АГ своевременно не устанавливается, недостаточно контролируется и часто маскируется. Нарушение регуляции сосудов, перегрузка жидкостью, повышенный сердечный выброс и периферическое сосудистое сопротивление в отдельности или в комбинации могут привести к АГ при ХБП. Использование современных методов для мониторинга и контроля АД имеет решающее значение для улучшения управления АГ и предотвращения повреждения органов-мишеней у детей. Круглосуточные измерения АД являются важным инструментом в определении прогноза и лечения детей с НС. Многие сопутствующие заболевания увеличивают риск возникновения сердечно-сосудистых заболеваний, включая ожирение, гипертрофию левого желудочка (ГЛЖ), повышение показателей артериальной ригидности (увеличение сИМТ, эндотелиальная дисфункция), нарушение метаболизма глюкозы и гиперлипидемию. Рассмотрены патофизиологические аспекты АГ при НС у детей. Патофизиология АГ при НС является сложной, с множеством почечных и внеченочных факторов. Среди почечных факторов можно выделить задержку натрия, фиброз / снижение СКФ и прогрессирование заболевания почек, и в последнее время описана прямая связь между альбуминурией и артериальным давлением. Среди других факторов приводятся побочные эффекты лекарств, сопутствующие заболевания и генетическая предрасположенность. Важную роль в развитии отека и регуляции АД при НС играет обмен натрия. Приведены две основные гипотезы удержания натрия при НС, гипотеза недостаточного заполнения и переполнения. Также рассмотрены роли эпителиально-натриевого канала (ЭНК), предсердного натрийуретического пептида (ПНП), оксида азота (NO), стероидных гормонов и других препаратов в задержке натрия и патогенезе АГ. У детей с НС АГ приводит к повреждению органов-мишеней (ПОМ): гипертрофии левого желудочка (ГЛЖ), поражению органа зрения, когнитивным нарушениям и более быстрому прогрессированию хронических заболеваний почек. Ограничение соли и ингибирование РААС считаются неотъемлемой частью лечения детей с протеинурией, и, как известно, оба имеют эффект снижения артериального давления. Блокада РААС обладает ренопротекторным эффектом у больных с поражением клубочков. Исследованиями установлено большее снижение протеинурии при комбинированной терапии АПФ / БРА. Этот рено-протекторный эффект объясняется как снижением АД, так и независимыми от АД механизмами. Модификации образа жизни, контроль массы тела, здоровое питание, снижение потребления натрия, поддерживающие упражнения и основная лекарственная терапия с использованием ингибиторов ангиотензинпревращающего фермента (ИАПФ), локаторов рецепторов ангиотензина (БРА), диуретиков могут замедлить прогрессирование НС у детей.

The review presents materials on the prevalence of NS in children, variants of its course: steroid-sensitive (SSNS) and steroidresistant (SRNS) steroid-dependent (SSNS). Minimal change nephrotic syndrome minimal changes (NSMC) is the most common glomerular disorder. Although NSMC has an excellent prognosis with a low risk of progression to t-CRF, its recurrent nature requires children to receive frequent courses of steroid therapy and other medications, many of which are known to affect blood pressure (BP). The interrelation of NS in children with arterial hypertension (AH) is shown. Prevalence of hypertension in children with SCNS, SRNS, SZNS is given. The regulation of hypertension in children is mandatory in the treatment of NS, due to the fact that hypertension is not established in a timely manner, is insufficiently controlled and is often masked. Vascular dysregulation, fluid overload, increased cardiac output and peripheral vascular resistance, alone or in combination, can lead to hypertension in CKD. The use of modern methods to monitor and control blood pressure is critical for improving hypertension management and preventing target organ damage in children. 24-hour blood pressure measurements are an important tool in determining the prognosis and treatment of children with HC. Many comorbidities increase the risk of cardiovascular disease, including obesity, left ventricular hypertrophy (LVH), increased arterial stiffness (increased BMI, endothelial dysfunction), impaired glucose metabolism, and hyperlipidemia. The pathophysiological aspects of hypertension in children with NS are considered. The pathophysiology of hypertension in NS is complex, with many renal and extrarenal factors. Renal factors include sodium retention, fibrosis / decreased GFR, and progression of kidney disease, and a direct link between albuminuria and blood pressure has recently been described. Other factors include drug side effects, comorbidities and genetic predisposition. Sodium metabolism plays an important role in the development of edema and blood pressure regulation in NS. There are two main hypotheses for sodium retention in NS, the hypothesis of underfilling and overfilling. The role of the epithelial sodium channel (ENC), atrial natriuretic peptide (ANP), nitric oxide (NO), steroid hormones and other drugs in sodium retention and the pathogenesis of hypertension is also considered. In children with NS, hypertension leads to target organs damage (TOD): left ventricular hypertrophy (LVH), damage to the organ of vision, cognitive impairment and more rapid progression of chronic kidney disease. Salt restriction and RAAS inhibition are considered integral parts of the treatment of children with proteinuria, and both are known to have blood pressure lowering effects. The RAAS blockade has a renoprotective effect in patients with glomerular damage. Studies have found greater reductions in proteinuria with ACE / ARB combination therapy. This renoprotective effect is explained by both a decrease in blood pressure and mechanisms independent of blood pressure. Lifestyle modifications, weight control, healthy eating, reduced sodium intake, supportive exercise, and basic drug therapy using angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), diuretics can slow the progression of NS in children.

детинефротический синдромартериальная гипертензияренин-ангиотензин-альдостероновая системаchildrenchronic kidney diseasearterial hypertensionangiotensin converting enzyme inhibitorReferencesСавенкова НД, Папаян АВ, Батракова ИВ. Нефротический синдром с минимальными изменениями у детей. Клиническая нефрология детского возраста. Ред: АВ Папаян, НД Савенкова. Левша. Санкт-Петербург, СПб., 2008; 259–282Savenkova ND, Papayan AV. Nephrotic syndrome with minimal changes in children. Clinical nephrology of childhood. AV Papayan, ND Savenkova. Levsha. Saint-Petersburg, 2008; 259–282 (In Russ.)Хронический гломерулонефрит. Детская нефрология: Руководство для врачей. Ред. МС Игнатова. Медицинское информационное агентство, М., 2011; 269–282Chronic glomerulonephritis. Pediatric nephrology: A manual for physician. Edited by M Ignatova. Medical News Agency Ltd., M., 2011; 269–282. (In Russ.)Chanchlani R, Parekh RS. Ethnic differences in childhood nephrotic syndrome. Front Pediatr2016;4:39. doi: 10.3389/fped.2016.00039Chanchlani R, Parekh RS. Ethnic differences in childhood nephrotic syndrome. Front Pediatr2016;4:39. doi: 10.3389/fped.2016.00039Цыгин АН. Артериальная гипертензия у детей. Детская нефрология. Ред. Э Лойманн, АН Цыгин, АА Саркисян. Литтерра, M., 2010; 244–251Cygin AN. Arterial hypertension in children. Detskajа nefrologijа. Ye. Loimann, AN Cygin, AA. Sarkisjаn (eds). Litterra, Moscow, 2010; 244–251 (In Russ.)Avner ED et al. Chronic Kidney Disease. Pediatric Nephrology. 7th ed. Springer Reference, New York, 2016; 2061–2064Avner ED et al. Chronic Kidney Disease. Pediatric Nephrology. 7th ed. Springer Reference, New York, 2016; 2061–2064Игнатова МС, Длин ВВ. Нефротический синдром: прошлое, настоящее и будущее. Рос вестн перинатол и педиатр2017;62:(6):29–44. doi: 10.21508/1027–4065–2017–62–6–29–44Ignatova MS, Dlin VV. Nephrotic syndrom: Past, Present and future. Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics)2017;62(6):29–44 (In Russ.). doi: 10.21508/1027-4065-2017-62-6-29-44Shatat IF, Becton LJ, Woroniecki RP. Hypertension in Childhood Nephrotic Syndrome. Front Pediatr2019;7:287. doi: 10.3389/fped.2019.00287Shatat IF, Becton LJ, Woroniecki RP. Hypertension in Childhood Nephrotic Syndrome. Front Pediatr2019;7:287. doi: 10.3389/fped.2019.00287Trautmann A, Bodria M, Ozaltin F et al. Spectrum of steroidresistant and congenital nephrotic syndrome in children: the PodoNet registry cohort. Clin J Am Soc Nephrol 2015;10(4):592–600. doi: 10.2215/CJN.06260614Trautmann A, Bodria M, Ozaltin F et al. Spectrum of steroidresistant and congenital nephrotic syndrome in children: the PodoNet registry cohort. Clin J Am Soc Nephrol 2015;10(4):592–600. doi: 10.2215/CJN.06260614Савенкова НД. Наследственный нефротический синдром у педиатрических и взрослых пациентов. Нефрология2020;24(3):15–27. doi: 10.36485/1561-6274-2020-24-3-15-27Savenkova ND. The hereditary nephrotic syndrome in children and adults. Nephrology (Saint-Petersburg 2020;24(3):15–27 (In Russ.). doi: 10.36485/1561-6274-2020-24-3-15-27Keshri S, Sharma S, Agrawal N et al. Hypertension and its severity in children with steroid sensitive nephrotic syndrome during remission. Clin Exp Nephrol2018;22:1157–1162. doi: 10.1007/s10157-018-1565-3Keshri S, Sharma S, Agrawal N et al. Hypertension and its severity in children with steroid sensitive nephrotic syndrome during remission. Clin Exp Nephrol2018;22:1157–1162. doi: 10.1007/s10157-018-1565-3Kontchou LM, Liccioli G, Pela I. Blood pressure in children with minimal change nephrotic syndrome during oedema and after steroid therapy: the influence of familial essential hypertension. Kidney Blood Press Res2009;32:258–262. doi: 10.1159/000238823.Kontchou LM, Liccioli G, Pela I. Blood pressure in children with minimal change nephrotic syndrome during oedema and after steroid therapy: the influence of familial essential hypertension. Kidney Blood Press Res2009;32:258–262. doi: 10.1159/000238823.Mitsnefes M, Ho PL, McEnery PT. Hypertension and progression of chronic renal insufficiency in children: a report of the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS). J Am Soc Nephrol2003;14:2618–2622. doi: 10.1097/01.ASN.0000089565.04535.4BMitsnefes M, Ho PL, McEnery PT. Hypertension and progression of chronic renal insufficiency in children: a report of the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS). J Am Soc Nephrol2003;14:2618–2622. doi: 10.1097/01.ASN.0000089565.04535.4BFlynn JT, Mitsnefes M, Pierce C et al. Blood pressure in children with chronic kidney disease: a report from the chronic kidney disease in children study. Hypertension2008;52:631–637. doi: 10.1161/HYPERTENSIONAHA.108.110635Flynn JT, Mitsnefes M, Pierce C et al. Blood pressure in children with chronic kidney disease: a report from the chronic kidney disease in children study. Hypertension2008;52:631–637. doi: 10.1161/HYPERTENSIONAHA.108.110635Sethna CB, Meyers KEC, Mariani LH et al. Blood pressure and visit-to-visit blood pressure variability among individuals with primary proteinuric glomerulopathies. Hypertension 2017;70:315–23. doi: 10.1161/HYPERTENSIONAHA.117.09475. 09475Sethna CB, Meyers KEC, Mariani LH et al. Blood pressure and visit-to-visit blood pressure variability among individuals with primary proteinuric glomerulopathies. Hypertension 2017;70:315–23. doi: 10.1161/HYPERTENSIONAHA.117.09475. 09475Gabban NIAl, Abdullah EA, Abd HN. Nephrotic syndrome and hypertension. Iraqi J Comm Med2010;4:271–276Gabban NIAl, Abdullah EA, Abd HN. Nephrotic syndrome and hypertension. Iraqi J Comm Med2010;4:271–276Inaba A, Hamasaki Y, Ishikura K et al. Long-term outcome of idiopathic steroid-resistant nephrotic syndrome in children. Pediatr Nephrol2016;31:425–434. doi: 10.1007/s00467-015-3174-7Inaba A, Hamasaki Y, Ishikura K et al. Long-term outcome of idiopathic steroid-resistant nephrotic syndrome in children. Pediatr Nephrol2016;31:425–434. doi: 10.1007/s00467-015-3174-7Sarkar S, Sinha A, Lakshmy R et al. Ambulatory blood pressure monitoring in frequently relapsing nephrotic syndrome. Indian J Pediatr2017;84:31–35. doi: 10.1007/s12098-016-2207-y.19Sarkar S, Sinha A, Lakshmy R et al. Ambulatory blood pressure monitoring in frequently relapsing nephrotic syndrome. Indian J Pediatr2017;84:31–35. doi: 10.1007/s12098-016-2207-y.19Haruhara K, Tsuboi N, Koike K et al. Circadian blood pressure abnormalities in patients with primary nephrotic syndrome. Clin Exp Hypertens2017;39:155–159. doi: 10.1080/10641963.2016.1235179 20Haruhara K, Tsuboi N, Koike K et al. Circadian blood pressure abnormalities in patients with primary nephrotic syndrome. Clin Exp Hypertens2017;39:155–159. doi: 10.1080/10641963.2016.1235179 20Sethna CB, Meyers KEC, Mariani LH et al. Blood pressure and visit-to-visit blood pressure variability among individuals with primary proteinuric glomerulopathies. Hypertension2017;70:315–323. doi: 10.1161/HYPERTENSIONAHA.117.0947516.21Sethna CB, Meyers KEC, Mariani LH et al. Blood pressure and visit-to-visit blood pressure variability among individuals with primary proteinuric glomerulopathies. Hypertension2017;70:315–323. doi: 10.1161/HYPERTENSIONAHA.117.0947516.21Ishikura K, Yoshikawa N, Nakazato H et al. Morbidity in children with frequently relapsing nephrosis: 10-year follow-up of a randomized controlled trial. Pediatr Nephrol2015;30:459–468. doi: 10.1007/s00467-014-2955-8Ishikura K, Yoshikawa N, Nakazato H et al. Morbidity in children with frequently relapsing nephrosis: 10-year follow-up of a randomized controlled trial. Pediatr Nephrol2015;30:459–468. doi: 10.1007/s00467-014-2955-8Skrzypczyk P, Panczyk-Tomaszewska M, Roszkowska-Blaim M et al. Long-term outcomes in idiopathic nephrotic syndrome: from childhood to adulthood. Clin Nephrol 2014;81:166–173. doi: 10.5414/CN108044Skrzypczyk P, Panczyk-Tomaszewska M, Roszkowska-Blaim M et al. Long-term outcomes in idiopathic nephrotic syndrome: from childhood to adulthood. Clin Nephrol 2014;81:166–173. doi: 10.5414/CN108044Vaziri ND. Disorders of lipid metabolism in nephrotic syndrome: mechanisms and consequences. Kidney Int2016;90:41–52. doi: 10.1016/j.kint.2016.02.026Vaziri ND. Disorders of lipid metabolism in nephrotic syndrome: mechanisms and consequences. Kidney Int2016;90:41–52. doi: 10.1016/j.kint.2016.02.026Gungor O, Demirci MS, Kircelli F et al. Increased arterial stiffness in patients with nephrotic syndrome. Clin Nephrol 2013;79:1–6. doi: 10.5414/CN107760Gungor O, Demirci MS, Kircelli F et al. Increased arterial stiffness in patients with nephrotic syndrome. Clin Nephrol 2013;79:1–6. doi: 10.5414/CN107760Rahul I, Krishnamurthy S, Satheesh S et al. Brachial artery flow-mediated dilatation and carotid intima medial thickness in pediatric nephrotic syndrome: a cross-sectional case-control study. Clin Exp Nephrol2015;19:125–132. doi: 10.1007/s10157-014-0958-1Rahul I, Krishnamurthy S, Satheesh S et al. Brachial artery flow-mediated dilatation and carotid intima medial thickness in pediatric nephrotic syndrome: a cross-sectional case-control study. Clin Exp Nephrol2015;19:125–132. doi: 10.1007/s10157-014-0958-1Hooman N, Isa-Tafreshi R, Otukesh H et al. Carotid artery function in children with idiopathic nephrotic syndrome. Nefrologia 2013;33:650–656. doi: 10.3265/Nefrologia.pre2013.May.12036Hooman N, Isa-Tafreshi R, Otukesh H et al. Carotid artery function in children with idiopathic nephrotic syndrome. Nefrologia 2013;33:650–656. doi: 10.3265/Nefrologia.pre2013.May.12036Candan C, Canpolat N, Gökalp S et al. Subclinical cardiovascular disease and its association with risk factors in children with steroid-resistant nephrotic syndrome. Pediatr Nephrol 2014;29:95–102. doi: 10.1007/s00467-013-2608-3Candan C, Canpolat N, Gökalp S et al. Subclinical cardiovascular disease and its association with risk factors in children with steroid-resistant nephrotic syndrome. Pediatr Nephrol 2014;29:95–102. doi: 10.1007/s00467-013-2608-3Haas ME, Aragam KG, Emdin CA et al. Genetic association of albuminuria with cardiometabolic disease and blood pressure. Am J Hum Genet2018;103:461–473. doi: 10.1016/j.ajhg.2018.08.004Haas ME, Aragam KG, Emdin CA et al. Genetic association of albuminuria with cardiometabolic disease and blood pressure. Am J Hum Genet2018;103:461–473. doi: 10.1016/j.ajhg.2018.08.004Ray EC, Rondon-Berrios H, Boyd CR, Kleyman TR. Sodium retention and volume expansion in nephrotic syndrome: implications for hypertension. Adv Chronic Kidney Dis2015;22:179–184. doi: 10.1053/j.ackd.2014.11.006Ray EC, Rondon-Berrios H, Boyd CR, Kleyman TR. Sodium retention and volume expansion in nephrotic syndrome: implications for hypertension. Adv Chronic Kidney Dis2015;22:179–184. doi: 10.1053/j.ackd.2014.11.006Andersen RF, Buhl KB, Jensen BL et al. Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC. Pediatr Nephrol2013; 28:1227–1234. doi: 10.1007/s00467-013-2439-2Andersen RF, Buhl KB, Jensen BL et al. Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC. Pediatr Nephrol2013; 28:1227–1234. doi: 10.1007/s00467-013-2439-2Ray EC, Rondon-Berrios H, Boyd CR, Kleyman TR. Sodium retention and volume expansion in nephrotic syndrome: implications for hypertension. Adv Chronic Kidney Dis2015;22:179–184. doi: 10.1053/j.ackd.2014.11.006Ray EC, Rondon-Berrios H, Boyd CR, Kleyman TR. Sodium retention and volume expansion in nephrotic syndrome: implications for hypertension. Adv Chronic Kidney Dis2015;22:179–184. doi: 10.1053/j.ackd.2014.11.006Küster S, Mehls O, Seidel C, Ritz E. Blood pressure in minimal change and other types of nephrotic syndrome. Am J Nephrol 1990;10 (Suppl. 1):76–80. doi: 10.1159/000168198Küster S, Mehls O, Seidel C, Ritz E. Blood pressure in minimal change and other types of nephrotic syndrome. Am J Nephrol 1990;10 (Suppl. 1):76–80. doi: 10.1159/000168198Peterson C, Madsen B, Perlman A, Chan AY, Myers BD. Atrial natriuretic peptide and the renal response to hypervolemia in nephrotic humans. Kidney Int. 1988;34:825–831. doi: 10.1038/ki.1988.256Peterson C, Madsen B, Perlman A, Chan AY, Myers BD. Atrial natriuretic peptide and the renal response to hypervolemia in nephrotic humans. Kidney Int. 1988;34:825–831. doi: 10.1038/ki.1988.256Polzin D, Kaminski HJ, Kastner C, Wang W, Krämer S, Gambaryan S, et al. Decreased renal corin expression contributes to sodium retention in proteinuric kidney diseases. Kidney Int 2010;78:650–659. doi: 10.1038/ki.2010.197Polzin D, Kaminski HJ, Kastner C, Wang W, Krämer S, Gambaryan S, et al. Decreased renal corin expression contributes to sodium retention in proteinuric kidney diseases. Kidney Int 2010;78:650–659. doi: 10.1038/ki.2010.197Ni Z, Vaziri ND. Downregulation of nitric oxide synthase in nephrotic syndrome: role of proteinuria. Biochim Biophys Acta. 2003;1638:129–137. doi: 10.1016/S0925-4439(03)00061-9Ni Z, Vaziri ND. Downregulation of nitric oxide synthase in nephrotic syndrome: role of proteinuria. Biochim Biophys Acta. 2003;1638:129–137. doi: 10.1016/S0925-4439(03)00061-9HoškováL, Málek I, Kopkan L, Kautzner J. Pathophysiological mechanisms of calcineurin inhibitor-induced nephrotoxicity and arterial hypertension. Physiol Res2017;66:167–180HoškováL, Málek I, Kopkan L, Kautzner J. Pathophysiological mechanisms of calcineurin inhibitor-induced nephrotoxicity and arterial hypertension. Physiol Res2017;66:167–180Hoorn EJ, Walsh SB, McCormick JA, Zietse R, Unwin RJ, Ellison DH. Pathogenesis of calcineurin inhibitor-induced hypertension.J Nephrol 2012;25:269–275. doi: 10.5301/jn.5000174Hoorn EJ, Walsh SB, McCormick JA, Zietse R, Unwin RJ, Ellison DH. Pathogenesis of calcineurin inhibitor-induced hypertension.J Nephrol 2012;25:269–275. doi: 10.5301/jn.5000174Shatat IF, Schoeneman M, Flynn JT, Woroniecki RP. Association of steroid and cyclosporin resistance in focal segmental glomerulosclerosis. Pediatr Nephrol2007;22:834–839. doi: 10.1007/s00467-006-0413-yShatat IF, Schoeneman M, Flynn JT, Woroniecki RP. Association of steroid and cyclosporin resistance in focal segmental glomerulosclerosis. Pediatr Nephrol2007;22:834–839. doi: 10.1007/s00467-006-0413-yLoeffler K, Gowrishankar M, Yiu V. Tacrolimus therapy in pediatric patients with treatment-resistant nephrotic syndrome. Pediatr Nephrol 2004;19:281–287. doi: 10.1007/s00467-003-1370-3Loeffler K, Gowrishankar M, Yiu V. Tacrolimus therapy in pediatric patients with treatment-resistant nephrotic syndrome. Pediatr Nephrol 2004;19:281–287. doi: 10.1007/s00467-003-1370-3El-Husseini A, El-Basuony F, Mahmoud I, Sheashaa H, Sabry A, Hassan R, et al. Long-term effects of cyclosporine in children with idiopathic nephrotic syndrome: a single-centre experience.Nephrol Dial Transplant 2005;20:2433–2438. doi: 10.1093/ndt/gfi059El-Husseini A, El-Basuony F, Mahmoud I, Sheashaa H, Sabry A, Hassan R, et al. Long-term effects of cyclosporine in children with idiopathic nephrotic syndrome: a single-centre experience.Nephrol Dial Transplant 2005;20:2433–2438. doi: 10.1093/ndt/gfi059Saruta T. Mechanism of glucocorticoid-induced hypertension.Hypertens Res1996;19:1–8. doi: 10.1291/hypres.19.1Saruta T. Mechanism of glucocorticoid-induced hypertension.Hypertens Res1996;19:1–8. doi: 10.1291/hypres.19.1Kornel L, Prancan AV, Kanamarlapudi N et al. Study on the mechanisms of glucocorticoid-induced hypertension: glucocorticoids increase transmembrane Ca2+ influx in vascular smooth muscle in vivo. Endocr Res1995;21:203–210. doi: 10.3109/07435809509030436Kornel L, Prancan AV, Kanamarlapudi N et al. Study on the mechanisms of glucocorticoid-induced hypertension: glucocorticoids increase transmembrane Ca2+ influx in vascular smooth muscle in vivo. Endocr Res1995;21:203–210. doi: 10.3109/07435809509030436Whitworth JA. Studies on the mechanisms of glucocorticoid hypertension in humans. Blood Press1994;3:24–32. doi: 10.3109/08037059409101518Whitworth JA. Studies on the mechanisms of glucocorticoid hypertension in humans. Blood Press1994;3:24–32. doi: 10.3109/08037059409101518Ong SL, Whitworth JA. How do glucocorticoids cause hypertension: role of nitric oxide deficiency, oxidative stress, and eicosanoids. Endocrinol Metab Clin North Am2011;40:393–407. doi: 10.1016/j.ecl.2011.01.010Ong SL, Whitworth JA. How do glucocorticoids cause hypertension: role of nitric oxide deficiency, oxidative stress, and eicosanoids. Endocrinol Metab Clin North Am2011;40:393–407. doi: 10.1016/j.ecl.2011.01.010Klepikov PV, Kutyrina IM, Tareyeva IE. Steroid-induced hypertension in patients with nephrotic syndrome. Nephron1988; 48:286–290. doi: 10.1159/000184944Klepikov PV, Kutyrina IM, Tareyeva IE. Steroid-induced hypertension in patients with nephrotic syndrome. Nephron1988; 48:286–290. doi: 10.1159/000184944Савенкова НД. Нефрогенная артериальная гипертензия у детей и подростков: причины, классификация, диагностика. Рос вестн перинатол и педиатр2017; 62:(4): 43–48. doi: 10.21508/1027–4065–2017–62–4–43–48Savenkova ND. Renal Arterial Hypertension in children and adolescents: causes, classification, diagnosis. Ros Vestn Perinatol i Pediatr 2017;62:(4):43–48 (In Russ.). doi: 10.21508/1027–4065–2017–62–4–43–48Tylicki L, Rutkowski P, Renke M, Rutkowski B. Renoprotective effect of small doses of losartan and enalapril in patients with primary glomerulonephritis. Short-term observation. Am J Nephrol 2002;22:356–362. doi: 10.1159/000065227Tylicki L, Rutkowski P, Renke M, Rutkowski B. Renoprotective effect of small doses of losartan and enalapril in patients with primary glomerulonephritis. Short-term observation. Am J Nephrol 2002;22:356–362. doi: 10.1159/000065227Wühl E, Trivelli A, Picca S et al. Strict blood-pressure control and progression of renal failure in children. N Engl J Med 2009;361:1639–1650. doi: 10.1056/NEJMoa0902066Wühl E, Trivelli A, Picca S et al. Strict blood-pressure control and progression of renal failure in children. N Engl J Med 2009;361:1639–1650. doi: 10.1056/NEJMoa0902066Shapiro MD, Hasbargen J, Hensen J, Schrier RW. Role of aldosterone in the sodium retention of patients with nephrotic syndrome. Am J Nephrol1990;10:44–48. doi: 10.1159/000168052Shapiro MD, Hasbargen J, Hensen J, Schrier RW. Role of aldosterone in the sodium retention of patients with nephrotic syndrome. Am J Nephrol1990;10:44–48. doi: 10.1159/000168052Schrier RW, Masoumi A, Elhassan E. Aldosterone: role in edematous disorders, hypertension, chronic renal failure, and metabolic syndrome. Clin J Am Soc Nephrol2010;5:1132–1140. doi: 10.2215/CJN.01410210Schrier RW, Masoumi A, Elhassan E. Aldosterone: role in edematous disorders, hypertension, chronic renal failure, and metabolic syndrome. Clin J Am Soc Nephrol2010;5:1132–1140. doi: 10.2215/CJN.01410210Bianchi S, Bigazzi R, Campese VM. Long-term effects of spironolactone on proteinuria and kidney function in patients with chronic kidney disease. Kidney Int2006;70:2116–2123. doi: 10.1038/sj.ki.5001854Bianchi S, Bigazzi R, Campese VM. Long-term effects of spironolactone on proteinuria and kidney function in patients with chronic kidney disease. Kidney Int2006;70:2116–2123. doi: 10.1038/sj.ki.5001854Trachtman H, Nelson P, Adler S et al. DUET: a phase 2 study evaluating the efficacy and safety of sparsentan in patients with FSGS. J Am Soc Nephrol2018;29:2745–2754. doi: 10.1681/ASN.2018010091Trachtman H, Nelson P, Adler S et al. DUET: a phase 2 study evaluating the efficacy and safety of sparsentan in patients with FSGS. J Am Soc Nephrol2018;29:2745–2754. doi: 10.1681/ASN.2018010091Duffy M, Jain S, Harrell N et al. Albumin and furosemide combination for management of edema in nephrotic syndrome: a review of clinical studies. Cells2015;4:622–630. doi: 10.3390/cells4040622Duffy M, Jain S, Harrell N et al. Albumin and furosemide combination for management of edema in nephrotic syndrome: a review of clinical studies. Cells2015;4:622–630. doi: 10.3390/cells4040622Oxlund CS, Buhl KB, Jacobsen IA et al. Amiloride lowers blood pressure and attenuates urine plasminogen activation in patients with treatment-resistant hypertension. J Am Soc Hypertens 2014;8:872–881. doi: 10.1016/j.jash.2014.09.019Oxlund CS, Buhl KB, Jacobsen IA et al. Amiloride lowers blood pressure and attenuates urine plasminogen activation in patients with treatment-resistant hypertension. J Am Soc Hypertens 2014;8:872–881. doi: 10.1016/j.jash.2014.09.019

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