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Journals / Sağlık Bilimlerinde Değer / 2026 / Volume: 11 Issue: 2

Endocrine Functions of Kidneys

Böbreklerin Endokrin Fonksiyonları

Hanife Yavuz(istanbul şişli hamidiye etfal eğitim ve araştırma hastanesi)0000-0002-6191-4282
Seyit Ankaralı(İSTANBUL MEDENİYET ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0003-3752-0846
Pages
265–272
Publication Date
2021-05-07
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

The risk of peptic ulcers due to disorders in gastrin metabolism is increased in patients with acute and chronic kidney disease.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Hormonal functions of the kidneys play a key role in regulating and maintaining basal body functions.
📊
Key Findings & Data:Some of the thrombopoietine that is produced in various parts of the body such as liver, spleen and bone marrow; and 90% of erythropoietine are prodeuced by kidneys.
💡
Conclusion & Impact:The risk of peptic ulcers due to disorders in gastrin metabolism is increased in patients with acute and chronic kidney disease.
🔬Design:Derleme
📍Scope:Comprehensive Sample
⚙️Variables:böbrek · endokrin fonksiyon · hormon

Abstract

Hormonal functions of the kidneys play a key role in regulating and maintaining basal body functions. The renin-angiotensin-aldosterone system balances plasma Na+ levels, protects the body fluid volume and regulates blood pressure. The Kallikrein-kinine system also works in conjunction with the RAAS system. Some of the thrombopoietine that is produced in various parts of the body such as liver, spleen and bone marrow; and 90% of erythropoietine are prodeuced by kidneys. The active form of vitamin D metabolized by the kidneys and PTH plasma are essential for maintaining Ca+ levels. ADH, which allows fluid retention by the kidneys, ensures the preservation of plasma osmolarity and fluid volume. Prostaglandins prevent excessive reabsorption of Na+ and water with vasodilator effects on the kidneys. The primary effect of atrial natriuretic peptide on the kidneys is to increase GFH and provide natriuresis. In addition, endothelin-I also causes renal vasoconstriction as GFH and reduces diuresis. The exact mechanisms of effects of urotensin II, which has more vasoconstrictor effects on the kidneys than endothelin-I, are still being investigated. insulin is largely metabolized from the kidneys, and in cases where kidney function is impaired, insulin resistance develops and blood glucose levels increase. The kidneys are also responsible for gastrin metabolism. The risk of peptic ulcers due to disorders in gastrin metabolism is increased in patients with acute and chronic kidney disease.

Özet

Bazal vücut fonksiyonlarının düzenlenmesinde ve sürdürülmesinde böbreklerin hormonal fonksiyonları anahtar rol oynar. Renin-anjiyotensin-aldosteron sistemi plazma Na+ düzeyini dengede tutarak, vücut sıvı hacmini korur, kan basıncını düzenler. Kallikrein-kinin sistemi de RAAS sistemi ile birlikte çalışır. Vücutta karaciğer, dalak, kemik iliği gibi vücudun çeşitli bölgelerinde yapılan trombopoietinin bir kısmının ve eritropoietinin % 90’ının yapım yeri böbreklerdir. Böbrekler tarafından metabolize edilen D vitaminin aktif formu ve PTH plazma Ca+’nın düzeylerinin korunması için gereklidir. Böbrekler tarafından sıvı tutulmasını sağlayan ADH, plazma ozmolaritesinin ve sıvı hacminin korunmasını sağlar. Prostaglandinler böbrekler üzerindeki vazodilatatör etkileri ile Na+ ve suyun aşırı geri emilimini önlerler. Atriyal natriüretik peptidin böbrekler üzerindeki birincil etkisi GFH artışı ve natriürezi sağlamaktır. Bunun yanında endotelin-I de renal vazokonstriksiyona neden olarak GFH ve diürezi azaltır. Böbrekler üzerinde endotelin-I’den daha fazla vazokonstriktör etkisi olan ürotensin II’nin böbrekler üzerindeki kesin etki mekanizmaları araştırılmaya devam etmektedir. İnsülin büyük oranda böbreklerden metabolize edilir ve böbrek fonksiyonlarının bozulduğu durumlarda insülin direnci gelişerek kan glukoz düzeyi yükselir. Böbrekler gastrin metabolizmasından da sorumludur. Akut ve kronik böbrek hastalığı olanlarda gastrin metabolizmasındaki bozukluklara bağlı peptik ülser riskinin arttığı görülür.

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Cite This Article

Yavuz, H., Ankaralı, S. (2021). Endocrine Functions of Kidneys. Sağlık Bilimlerinde Değer, Volume: 11 Issue: 2, 265–272. https://doi.org/10.33631/duzcesbed.671445

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  37. Jeffrey A, Kraut GTN. Metabolic Acidosis of Chronic Kidney Disease. Textbook of Nephro-Endocrinology. 2018;17 291-318.s
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  44. Hall J. Guyton and Hall Textbook of Medical Physiology. PA, The U.S: Saunders; 2010
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  49. Silverthorn DU. Human Physiology. CA, The U.S: Pearson Education, Inc.; 2010
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  51. Anette Fiebeler DNM, Erdenechimeg Shagdarsuren, Friedrich C.Luft. Aldosteron, Mineralokortikoid Reseptörleri ve Vasküler İnflamasyon. Türkiye Klinikleri J Nephrol. 2008;3:25-35.s
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  53. Hanukoglu I. Introduction to Epithelial sodium channel (ENaC). IUPHAR/BPS Guide to Pharmacology Database. 2019;4.s
  54. James Matthew Luther NJB. Renin-angiotensin-aldosterone system and glucose homeostasis. Trends Pharmacol Sci. 2011;32(12):734–9.s
  55. Pommering TL. Erythropoietin and Other Blood-Boosting Methods. Pediatr Clin North Am. 2007;54(4):691-9.s
  56. Shoskes DA, McMahon AW. Renal Physiology and Pathophysiology. Campbell-Walsh Urology Elsevier Inc,; 2016
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  59. Fouad Kutuby SW, Desai C, Lerma EV. Anemia of chronic kidney disease. Dis Mon. 2015;61(10):421-4.s
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  62. Liesbet Lieben GC, Masuyama R. Calcemic actions of vitamin D: Effects on the intestine, kidney and bone. Best Pract Res Clin Endocrinol Metab. 2011;25(4):561-72.s
  63. Paçacı G. Dahili Yoğun Bakım Ünitesine Kabul Edilen Kritik Hastalarda Erken Dönemde Vitamin D Düzeyi Değişimi ve Buna Etki Edebilecek Faktörler [Uzmanlık]. Ankara: Ankara Üniversitesi; 2015
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  65. Soysal Ö. Hemodiyaliz Hastalarında Sekonder Hiperparatiroidinin Kalp Yapısı Ve Fonksiyonları Üzerine Etkisi. İstanbul: İstanbul Göztepe Eğitim ve Araştırma Hastanesi; 2006
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  69. Lynn E, Schlanger JLB, Jeff M.S. Electrolytes in the Aging. Arch Biochem Biophys 2010;17(4):308-19.s
  70. Líbano-Soares J.D, Landgraf S.S, Gomes-Quintana E, Lopes A.G, C. Caruso-Neves C. Prostaglandin E2 modulates proximal tubule Na+-ATPase activity: Cooperative effect between protein kinase A and protein kinase C. Arch Biochem Biophys. 2011;507(2):281-6.s
  71. Vinay Acharya JO. The Kidney as an Endocrine Organ. Methodist Debakey Cardiovasc J. 2018(4):305-7.s
  72. Henderson J, Henderson IW. The endocrine functions of the kidney. J Biol Educ 1994;28(4):245-54.s
  73. Tamar S, Polonsky GLB. Alterations in Kidney Function Associated With Heart Failure. In: G. Michael Felker DLM, editor. Heart Failure: A Companion to Braunwald's Heart Disease E-Book: Elsevier Inc; 2016
  74. Richard E, Gilbert AA. Vasoactive Molecules and the Kidney. In: Alan S. L, Yu GMC, Valerie Luyckx, Philip A. Marsden, Karl Skorecki, Maarten W. Taal,, editor. Brenner and Rector's The Kidney E-Book: Saunders; 2011
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  78. Jeffrey A, Kraut GTN. Metabolic Acidosis of Chronic Kidney Disease. Textbook of Nephro-Endocrinology. 2018;17 291-318.s
  79. Mukoyama M, Nakao K. Hormones of the Kidney. In: Shlomo Melmed PMC, editor. Endocrinology Basic and Clinical Principles 2005. s. 353-65
  80. Pär M, Kathleen M, Giacomini D, Craig B. Renal Disposition of Drugs and Translation to Dosing Strategies. Seldin and Gielbisch's The Kidney. 952013. s. 3185-214
  81. Rosa M, Montero DJAG. Management of the Diabetic Patient With Chronic Kidney Disease Comph Clin Nephrol. 2019;32:385-95.s
  82. Armin Kurtz RHW, Kai-Uwe E. Hematopoiesis and the Kidney. In: Robert J. Alpern OWM, Michael Caplan, editor. Seldin and Giebisch's The Kidney: Elsevier B.V.; 2013. s. 3087-124.