Journals / Endokrinolojide Yönelişler / 2004 / Cilt: 13 - Sayı: 4

Comparison of treatment with enalapril and losartan in normotensive diabetic albuminuric patients

Normotansif diabetik albüminürili hastalarda enalapril ve losartan tedavilerinin karşılaştırılması

Pages
110–114
Publication Date
2022-10-17
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

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

As a result like ACE inhibitors, losartan, an All receptor antagonist can be used in the treatment of diabetic nephropathy.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Previous studies show that among patients with diabetes mellitus, ACE inhibitors decrease proteinuria and slow down the progression of nephropathy in hypertensive or normotensive type I and II diabetic patients by decreasing systemic hypertension and also by its positive effects on renal hemodynamics.
📊
Key Findings & Data:In general these effects are thought to be produced by blocking the reninangiotensin system and therefore decreasing the production of angioten-sihll.In recent years, some pharmacological agents which block All receptors and thus decrease All effects are developed.
💡
Conclusion & Impact:As a result like ACE inhibitors, losartan, an All receptor antagonist can be used in the treatment of diabetic nephropathy.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Previous studies show that among patients with diabetes mellitus, ACE inhibitors decrease proteinuria and slow down the progression of nephropathy in hypertensive or normotensive type I and II diabetic patients by decreasing systemic hypertension and also by its positive effects on renal hemodynamics. The mechanisms of the effects of ACE inhibitors are not fully explained. In general these effects are thought to be produced by blocking the reninangiotensin system and therefore decreasing the production of angioten-sihll.In recent years, some pharmacological agents which block All receptors and thus decrease All effects are developed. It is expected that these agents show the same effects in diabetic nephropathy.However in current literature there are not enough number of studies which investigate the effects of A II receptor antagonists in diabetic nephropathy. Therefore, in this study we compared the effects of Enalaprii, an ACE inhibitor with Losartan, an A II receptor antagonist. Both of the drugs are given alternatively to 20 normotensive diabetic patients. The patients are divided equally into two groups. Each group received these drugs alternatively for six weeks for two different treatment periods. The first group was given Enalaprii initially. They had four weeks of treatment free period and then they were given Losartan for six weeks. The second group was given Losartan first ; had no treatment for four weeks and than Losartan for six weeks.Proteinuria, blood pressure and renal functions were evaluated before the beginning and after the end of each treatment period. Both Enalaprii and Losartan created a similar decrease in proteinuria which was statistically significant. As a result like ACE inhibitors, losartan, an All receptor antagonist can be used in the treatment of diabetic nephropathy.

Özet

Yapılan çalışmalarda, ACE inhibitörlerinin diabetes mellituslu hastalarda sistemik hipertansiyonu düşürerek, ayrıca kan basıncı üzerindeki olumlu etkilerinden bağımsız olarak da renal hemodinamiye yaptıkları birçok olumlu etki ile; gerek hipertansif ve gerekse normotansif tip 1 ve tip II diyabetiklerde proteinüriyi azalttıkları ve nefropati gelişimini yavaşlattıkları gösterilmiştir. ACE inhibitörlerinin bu etkilerinin mekanizması tam olarak açıklık kazanmamıştır. Bu etkilerin genel olarak renin-anjiotensin sisteminin blokajı ile anjiotensin II (A II) oluşumunu ve sonuçta bunun etkinliğinin azaltılması ile elde edildiği düşünülmektedir. Son yıllarda A II reseptörlerini bloke ederek A ll'nin etkisini bu yolla da azaltabilen farmakolojik ajanlar geliştirilmiştir. Bu ajanların diyabetik hastalarda aynı mekanizma ile nefropati üzerine olumlu etkileri olması beklenir. Ancak bu konuda literatürde henüz A II reseptör blokerlerinin diyabetik nefropatideki etkinliğini araştıran yeterli miktarda çalışma bulunmamaktadır. Bu çalışmada bir ACE inhibitörü olan Enalaprii ile bir A II reseptör antagonisti olan Losartanın diyabetik nefropatideki etkinliklerini karşılaştırılmıştır. Bu amaçla kan basınçları normal olan 20 diabetik hasta çalışmaya alındı. Hastalar randomize eşit iki gruba ayrıldı; her gruba 6 haftalık 2 ayrı tedavi döneminde dönüşümlü olarak1 bu iki ilaç uygulandı. Bir gruba önce Enalaprii verildi, ara dönemde (4 hafta) ilaçsız bırakıldı, sonraki 6 haftalık dönemde ise Losartan uygulandı. Diğer gruba ise önce Losartan verildi, yine ara dönemde ilaçsız bırakıldı, sonra Enalaprii uygulandı. Her tedavi döneminin başında ve sonunda proteinüri, kan basıncı ve renal fonksiyonlar değerlendirildi. Enalaprii için proteinüride ortalama azalma başlangıç değer ile kıyaslama yapıldığında % 25.9 (p = 0.045 ), Losartan için % 15.5 (p = 0.014) olarak bulundu. Sonuç olarak bu çalışma bir A II reseptör antagonisti olan losartanın da ACE inhibitörleri gibi diyabetik nefropatinin tedavisinde kullanılabilecek potansiyel bir ajan olduğunu bir kez daha göstermiştir.

🔖

Cite This Article

CEYLAN, B., TİRYAKİOĞLU, Ö., MAZLUM, A., SEYAHİ, E. (2022). Comparison of treatment with enalapril and losartan in normotensive diabetic albuminuric patients. Endokrinolojide Yönelişler, Cilt: 13 - Sayı: 4, 110–114. https://ajindex.com/articles/500867

References (16)

  1. Pathogenesis, prevention, and treatment of diabetic nephropathy. (Seminar) Lancet 1998; 352: 213-219
  2. The Medical Clinics of North America; Essentia! Hypertension, Patt 1; September 1997: 1099-1112
  3. The Medical Clinics of North America; Essential Hypertension, Part 11; November 1997: 1319-1325; 1359- 1371
  4. Endocrinology and Metabolism Clinics of North America; Chronic complications of diabetes, June 1996: 255-267; 293-304
  5. Patophisiology of progressive nephropathies.The New England journal of Medicine. 339: 20; 1448-1456
  6. Sema -1, 2: J. lan S Robenson&Garry Nicholls. The Renin-Angiotensin System. Cower medical publishing 1993
  7. Şema -2: Messerli. Cardiovascular Driug Therapy, Second ed W.H. Saunders 1996 8. Angiotensin Converting Enzyme Inhibitors; Scientific Basis for Clinic Use; second edition. Lionel II. Opie; Wiley-Liss Authors' Publishing House
  8. Stephen Onh, Michal Nowicki, Andrej Wiecek and Eberhard Ritz Neuroprotective Effect of ACE Inhibitors, Drugs 46 (Suppl. 2h 189- 196, 1993
  9. Ron T. Gansevoon et al. Is the anliproteinutic effect of ACE inhibition mediated by interference in the renin-angiotensin system?. Kidney International, Vol. 45(1994). pp. 861-867
  10. Hutchinson EN, Webster SK. Effects of A II receptor antagonist on albuminuria and renal function in passive Heymann nephritis. American Journal of Phisiology 263: 311-318, 1992
  11. Ray PE, Aquilera G, Kopp JB,IIorokoshi S, Klotman PE.Angiotensin İI stimulates proliferation of human fetal inesangial cells by a receptor- mediated mechanism, journal of the American Society of Nephrology 1: 424, 1990 13. Kriz W.Elger M,Lemley K,Sakai T. Structure of the glomerular mesangium: a biomechanical interpretation. Kidney International 300: 2-9, 1990
  12. Orth S, Weinreich T, Weith M, Ritz E.Ang II induces cell hypertrophy and proliferation in human mesangial cells. Abstract. XIX Congress of EDTA-ERA, Paris, 1992
  13. Irzyniec T, Mali G.Ritz E. Effects cif enalapril on compensatory glomerular growth after subtotal nephrectomy. Abstract. XXVIll Congress of EDTA-ERA, Rimini Italy 1991
  14. Nagata M, Kriz W. Glomerular damage after uninephrectomy in young ruts
  15. Mechanichal stress on podocyies as a pathway to sclerosis. Kidney International 42: 148-160, 1992
  16. Rudberg S, Aperia A,Ereyschuss U, Persson B. Enalapril reduces microalbuminuria in young normotensive Type I( insulin dependent) diabetic patients irrespective of its hypotensive effect. Diabetologia 33: 470-176, 1990.