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2020, vol. 77, br. 6, str. 582-589
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Efekat vitamina D na proteinuriju, lipidni status, glikoregulaciju i C-reaktivni protein kod bolesnika sa dijabetes melitusom tip 2
Effect of vitamin D on proteinuria, lipid status, glycoregulation and C-reactive protein in patients with type-2 diabetes mellitus
Petrović Marijanaa  , Dragović Tamarab, Petrović Stankoc , Obrenčević Katarinad, Rančić Nemanjae , Đurašinović Tatjanaf, Petrović Dejang, Ignjatović Ljiljanaa, Rabrenović Violetaa, Nenezić Nemanjah, Marinković Dejanh, Maksić Đokoa
aVojnomedicinska akademija, Klinika za nefrologiju, Beograd + Univerzitet odbrane, Medicinski fakultet Vojnomedicinske akademije, Beograd bUniverzitet odbrane, Medicinski fakultet Vojnomedicinske akademije, Beograd + Vojnomedicinska akademija, Klinika za endokrinologiju, Beograd cUniverzitet odbrane, Medicinski fakultet Vojnomedicinske akademije, Beograd + Vojnomedicinska akademija, Klinika za gastroenterologiju i hepatologiju, Beograd dVojnomedicinska akademija, Klinika za nefrologiju, Beograd eVojnomedicinska akademija, Klinika za endokrinologiju, Beograd + Vojnomedicinska akademija, Centar za kliničku farmakologiju, Beograd fVojnomedicinska akademija, Institut za medicinsku biohemiju, Beograd gKlinički centar Kragujevac, Klinika za internu medicinu + Univerzitet u Kragujevcu, Medicinski fakultet hVojnomedicinska akademija, Klinika za endokrinologiju, Beograd
e-adresa: makystan@yahoo.com
Sažetak
Uvod/Cilj. Nedostatak vitamina D je često prisutan kod bolesnika sa dijabetes melitusom (DM) tip 2 i može biti faktor rizika od brže progresije dijabetesne nefropatije i veće incidencije kardiovaskularnih događaja. Cilj studije bio je da se ispita uticaj supstitucije vitamina D na proteinuriju, holesterol, trigliceride, C-reaktivni protein (CRP) i hemoglobin A1c kod bolesnika sa DM tip 2 i nedostatkom vitamina D. Metode. Prospektivnom, kohortnom studijom obuhvaćeno je 90 bolesnika sa DM tip 2 i nedostatkom (insuficijencija/deficijencija) vitamina D svrstanih u tri grupe po 30 bolesnika: I - sa normalnom proteinurijom, II - sa mikroproteinurijom i III - sa makroproteinurijom. Sprovedena je šestomesečna nadoknada vitamina D holekalciferol kapima: tokom prva dva meseca sa 20 000 i.j. dva puta nedeljno, a zatim, je kod bolesnika kod kojih je nivo vitamina D ostao snižen nastavljeno sa istom dozom još četiri meseca. Kod bolesnika kod kojih se nivo vitamina D normalizovao, nastavljeno je sa 5 000 i.j. dva puta nedeljno. Na početku i na kraju ispitivanja meren je nivo uree, kreatinina, jutarnje glikemije, kalcijuma, fosfora, holesterola, triglicerida, CRP, hemoglobina A1c, intaktnog paratireoidnog hormona, 24časovne proteinurije i klirensa kreatinina. Zbog eventualne korekcije doze holekalciferola vrednosti kalcijuma, fosfora i vitamina D proverene su i dva meseca posle započinjanja supstitucije. Rezultati. Najniži nivo vitamina D pre terapije imali su bolesnici u grupi sa makroproteinurijom, dok je na kraju ispitivanja utvrđen statistički značajno povišen nivo vitamina D, u sve tri grupe. Nakon šestomesečne primene vitamina D, postignuto je statistički značajno sniženje nivoa 24-časovne proteinurije, holesterola, triglicerida i hemoglobin A1c u sve tri ispitivane grupe, a CRP u grupi sa normalnom proteinurijom i mikroproteinurijom. Statistički značajna negativna korelacija između vitamina D i 24-časovne proteinurije, holesterola i CRP dokazana je u grupi sa makroproteinurijom. Statistički značajna negativna korelacija dokazana je između vitamina D i HBA1c u grupi sa normalnom proteinurijom i vitamina D i CRP u grupi sa miroproteinurijom. Zaključak. Supstitucija vitamina D visokim dozama holekalciferola i njegova preventivna primena kod bolesnika sa DM tip 2 (sa ili bez proteinurije) snižava holesterol, trigliceride, proteinuriju, CRP i hemoglobin A1c.
Abstract
Background/Aim. Vitamin D insufficiency/deficiency is often present in patients with type-2 diabetes mellitus (DM) and could present a risk factor for rapid progression of diabetic nephropathy and for higher incidence of cardiovascular events. The aim of this study was to examine the influence of vitamin D supplementation on proteinuria, cholesterol, triglycerides, C-reactive protein (CRP) and hemoglobin A1c in patients with type-2 DM and vitamin D insufficiency/deficiency. Methods. This prospective, cohort study included 90 patients with type-2 DM and vitamin D insufficiency/deficiency divided into 3 equal groups: with normal proteinura, with microproteinuria and with macroproteinuria. Therapy included six months of supplementation with cholecalciferol drops: first two months with 20,000 IU twice weekly, than if level of vitamin D was below normal the same dose was given next four months. If the level of vitamin D was normal 5,000 IU was given twice weekly. At the begining and at the end of the study the levels of urea, creatinine, fasting blood glucose, calcium, phosphorus, cholesterol, triglycerides, CRP, hemoglobin A1c, intact parathyroid hormone, 24-hour urine protein and creatinine clearance were determined. Levels of calcium, phosphorus and vitamin D were also checked 2 months after beginning of therapy due to possible correction of cholecalciferol dose. Results. The lowest level of vitamin D before therapy was found in patients with macroproteinuria, while at the end of the study the significantly higher level of vitamin D was found in all three groups. After 6 months of therapy a significant decrease of 24-hour urine protein, cholesterol, triglycerides, hemoglobin A1c in all three groups, and CRP in patients with normal proteinuria and microproteinuria were found. Significantly negative correlation between vitamin D and 24-hour urine protein, cholesterol and CRP was found in patients with macroproteinuria. Also, significantly negative correlation was found between vitamin D and hemoglobin A1c, in patients with normal proteinuria, vitamin D and CRP in patients with microproteinuria. Conclusion. A preventive use of high-dose cholecalciferol supplementation in patients with type-2 DM (with or without proteinuria) decreases cholesterol, triglycerides, proteinuria, CRP and hemoglobin A1c.
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