Diabetic Kidney Disease 3rd stage – laboratory markers of mineral bone disorder
Authors:
Adriana Klimentová; Ivana Ságová; Dana Prídavková; Daniela Kantárová; Pavol Makovický; Jurina Sadloňová; Marián Mokáň
Authors‘ workplace:
I. interná klinika Jesseniovej LF UK a UN Martin, Slovenská republika
Published in:
Vnitř Lék 2016; 62(6): 442-448
Category:
Original Contributions
Overview
Background:
Diabetes mellitus is the most common cause of end stage kidney disease in the developed countries. Chronic kidney disease-mineral and bone disorder (CKD-MBD) develops with deteriorating of the renal functions. Diabetic patients on hemodialysis are characterized by low bone turnover, higher prevalence of severe and progressive vascular calcification with increased cardiovascular morbidity and mortality. The main factor which causes vascular calcification in patients with diabetic kidney disease (DKD) is poor glycemic control. The recent trial findings describe an inverse correlation between intact parathyroid hormone (iPTH) serum levels and glycemic control in a group of diabetic patients on hemodialysis.
Aim:
The objective of the proposed project is to access the difference of the laboratory markers MBD in the group of patients with 3rd stage DKD depending on glycemic control. We focused on the relationship between the glycemic compensation of diabetes (HbA1c) and iPTH serum level.
Patients and method:
Ninety one patients with 3rd stage DKD were investigated. There were 46 women (50.5 %) and 45 men (49.5 %), average age of patients was 71.2 ± 7.0 years, with creatinine level 128 ± 30 μmol/l and estimated glomerular filtration (eGF, MDRD) 0.82 ± 0.16 ml/s. There were 60 patients with better glycemic control of diabetes (HbA1c < 7 %) vs 29 patients with poorly controlled diabetes (HbA1c > 7 %). MBD markers were compared in both groups. Patients were further stratified into subgroups based on the serum level of iPTH (iPTH < 35 pg/ml vs iPTH > 35 pg/ml) and MBD markers compared. Statistical analysis was performed using and Mann-Whitney test.
Results:
We have found the statistical significance in the serum phosphate and proteinuria levels in between groups with HbA1c < 7 % vs patients with HbA1c > 7 %. Diabetics with better glycemic control had significant reduction in serum phosphate level (1.14 ± 0.20 vs 1.23 ± 0.18 mmol/l, p = 0.038) and in 24 hrs proteinuria level (0.56 ± 1.35 vs 1.30 ± 1.61 g/day, p = 0.007). In the group of presumed low bone turnover (iPTH < 35 pg/ml) we have found the trend towards increased serum calcium level (2.49 ± 0.12 vs 2.43 ± 0.10 mmol/l, p = 0.063) and increased HbA1c value (7.5 ± 1.8 vs 6.4 ± 1.6 %, p = 0.023).
Conclusion:
Our results suggest the closer relationship between glycemic control of diabetes and mineral-bone disorder in earlier stages of DKD.
Key words:
diabetes mellitus type 2 (DM2T) – chronic kidney disease (CKD) – mineral and bone disorder (MBD)
Sources
1. Dusilová Sulková S, Opatrná S, Ryšavá R et al. KDIGO doporučení pro diagnostiku a léčbu CKD-MBD: komentovaný návod pro klinickou praxi. Aktuality v nefrologii 2010; 16(4): 113–126.
2. Dusilová Sulková S. Renální osteopatie. Maxdorf: Praha 2007: 20 -21. ISBN 978–80–7345–119–6.
3. Moe SM, Druek T, Cunningham J et al. Definition, evaluation and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes. Kidney Int 2006; 69(11): 1945–1953.
4. Dusilová Sulková S. Co prinášejí nová KDIGO doporučení zamĕřená na CKD-MBD? 1. část. Aktuality v nefrologii 2009; 15(4): 159–165.
5. KDIGO Clinical Practice Guideline for the diagnosis, evaluation, prevention and treatment of chronic kidney disease – mineral bone disorder (CKD-MBD). Kidney Int Suppl 2009; (113): S1-S130.
6. Sotorník I, Kutílek Š et al. Kostní minerály a skelet pri chronickém onemocnení ledvin. Galén: Praha 2011: 103–106. ISBN 978–80–7262–769–1.
7. Bouček P, Kvapil M, Monhart V et al. Doporučené postupy při diabetickém onemocnění ledvin. Aktuality v nefrologii 2012;18,(1):18–26.
8. Okša A, Spústová V. Nefropatia pri diabetes mellitus – skríning, prevencia a liečba v spolupráci diabetológa a nefrológa. Diabetes a Obezita 2007; 7(Suppl): 6–13.
9. Alicic RZ, Tuttle KR. Management of the diabetic patient with advanced chronic kidney disease. Semin Dial 2010; 23(2): 140–147.
10. Tuttle KR, Bakris GL, Bilous RW et al. Diabetic Kidney Disease: A Report From an ADA Consensus Conference. Diabetes Care 2014; 37(10): 2864–2883.
11. Sotorník I, Kutílek Š et al. Kostní minerály a skelet pri chronickém onemocnení ledvin. Galén: Praha 2011: 337–349. ISBN 978–80–7262–769–1.
12. Sun YM, Su Y, Li J et al. Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropaty. Biochem Biophys Res Commun 2013; 433(4): 359–361.
13. Inaba M. Chronic kidney disease (CKD) and bone. Impact of diabetes mellitus on the development of CKD-MBD. Clin Calcium 2009; 19(4): 502–507.
14. Inaba M, Okuno S, Nagasue K et al. Impaired secretion of parathyroid hormone is coherent to diabetic hemodialyzed patients. Am J Kidney Dis 2001; 38(4 Suppl. 1): S139-S142.
15. Nasri H, Kheiri S. Effect of diabetes mellitus, age, and duration of dialysis on parathormone in chronic hemodialysis patients. Saudi J Kidney Dis Transpl 2008; 19(4): 608–613.
16. Dusilová Sulková S. Renální osteopatie. Maxdorf: Praha 2007. ISBN 978–80–7345–119–6.
17. Kestenbaum B, Sampson JN, Rudser KD et al. Serum Phosphate Levels and Mortality Risk among People with Chronic Kidney Disease. J Am Soc Nephrol 2005; 16(2): 520–528.
18. Sotorník I, Kutílek Š et al. Kostní minerály a skelet pri chronickém onemocnení ledvin. Galén: Praha 2011: 344–345. ISBN 978–80–7262–769–1.
19. Spasovski GB, Bervoets AR, Behets GJS et al. Spectrum of renal bone disease in end-stage renal failure patients not yet on dialysis. Nephrol Dial Transplant 2003; 18(6): 1159–1166.
20. Dusilová Sulková S. Kostní choroba u chronického selhání ledvin a její moderní terapie. Vnitř Lék 2011; 57(7–8): 620–625.
21. Inaba M Chronic kidney disease (CKD) and bone. Impact of diabetes of mellitus on the development of CKD-MBD. Clin Calcium 2009; 19(4): 502–507.
22. Žamboch K, Zahálková J, Kosatíkova Z Minerálová a kostní nemoc při chronickém onemocnění ledvin. Interní Med 2010; 12(7–8): 357–360.
23. London GM, Marchais SJ, Guérin AP et al. Association of bone activity, calcium load, aortic stiffness, and calcifications in ESRD. J Am Soc Nephrol 2008; 19(9): 1827–1835.
24. Blahoš J, Sotorník I. Změny kalcium-fosfátového metabolizmu při chronických nefropatiách. Vnitř Lék 2012; 58(7–8): 12–18.
25. Park J, Lertdumrongluk P, Molnar MZ et al. Glycemic control in diabetic dialysis patients and the burnt-out diabetes phenomenon. Curr Diab Rep 2012; 12(4): 432–439.
26. Dan S, Aditya P, Samanta M et al. Effect of glycemic control on intact parathyroid hormone level in end stage renal disease patients on maintenance hemodialysis. Diabetes Res Clin Pract 2014; 105(3): 352–355.
27. Error in Text in: Role of Intensive Glucose Control in Development of Renal End Points in Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis. Arch Intern Med 2012; 172(14): 1095.
28. Rhee MC, Leung AM, Kovesdy PC et al. Updates on the Management of Diabetes in Dialysis Patients. Semin Dial 2014; 27(2): 135–145.
29. Perkovic V, Heerspink HL, Chalmers J et al. Intensive glucose control improves kidney outcomes in patients with type 2 diabetes. Kidney Int 2013; 83(3): 517–523.
30. Murakami R, Murakami S, Tsushima R et al. Glycaemic control and serum intact parathyroid hormone levels in diabetic patients on haemodialysis therapy. Nephrol Dial Transplant 2008; 23(1): 315–320.
31. Gnudi L Serum Intact Parathyroid Hormone in Diabetic Patients on Haemodialysis: What is the Treatment Goal? Nephrol Dial Transplant 2008; 23(1): 24–26.
32. Odborné usmernenie Ministerstva zdravotníctva Slovenskej republiky na liečbu porúch minerálového a kostného metabolizmu u pacientov s chronickým ochorením obličiek. Aktuality v nefrologii 2009; 15(3): 121–126.
33. Dusilová Sulková S. Renální osteopatie. Maxdorf: Praha 2007. ISBN 978–80–7345–119–6.
34. Levin A, Bakris GL, Molitch M et al. Prevalence of abnormal serum vitamin D, PTH, calcium and phosphorus in patients with chronic kidney disease: results of the study to evaluate early kidney disease. Kidney Int 2007; 71(1): 31–38.
35. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease‘. Kidney Int Suppl 2013; 3(1): 136–150.
36. Bover J, Urena P, Brandenburg V et al. Adynamic bone disease: from bone to vessels in chronic kidney disease. Semin Nephrol 2014; 34(6): 626–640.
Labels
Diabetology Endocrinology Internal medicineArticle was published in
Internal Medicine
2016 Issue 6
Most read in this issue
- Sinus histiocytosis with massive lymphadenopathy: FDG-PET/CT documented partial remission after treatment with 2-chlorodeoxyadenosine
- Insulin application techniques in adult patients with diabetes
- Cardiomyopathy in MR image
- Acute causes of sudden deaths in patients with severe hypoglycemia