Secondary hyperparathyroidism in patient with type 2 diabetes and stages 3–4 chronic kidney disease
Abstract
Secondary hyperparathyroidism is an early complication of chronic kidney disease, with increasing severity as the glomerular filtration rate decreases and characterized by a progressive increase in parathyroid hormone and growth of the parathyroid glands. It is generally accepted that a deficiency in active form of vitamin D or calcitriol levels seems to play a relevant role in its development and progression of secondary hyperparathyroidism. A reduction in plasma calcitriol levels occurs early in renal disease. Major renal guidelines recommend use of vitamin D for secondary hyperparathyroidism in chronic kidney disease. In the treatment vitamin D receptor activation inhibit glandular hyperplasia; reduce parathyroid hormone levels impact on bone turnover and mineral density. Treatment with calcitriol can occasionally result in hypercalcemia and hyperphosphatemia in renal patients due promotes intestinal calcium and phosphorus absorption. This limits its suitability for the treatment. But next generation vitamin-D analogs such as paricalcitol have lower intestinal absorption of calcium, phosphorous and significantly lowers renin levels, albuminuria and blood pressure.
In this article, we present the case of a Caucasian male with type 2 diabetes and secondary hyperparathyroidism in stages 3–4 chronic kidney disease. Our case study shows that in treating for secondary hyperparathyroidisms selective vitamin D receptor activation with paricalcitol reduction of levels parathyroid hormone, albuminuria, offering low chance hypercalcemia, hyperphosphatemia and other side effects.
About the Authors
Lilit V. EgshatyanEndocrinology Research Centre; А.I. Evdokimov Moscow State University of Medicine and Dentistry
Russian Federation
MD, PhD
Natalya G. Mokrisheva
Endocrinology Research Centre
MD, PhD
References
1. Abe M, Okada K, Soma M. Mineral metabolic abnormalities and mortality in dialysis patients. Nutrients. 2013;5(3):1002-1023. doi: 10.3390/nu5031002
2. Coresh J, Selvin E, Stevens LA, et al. Prevalence of chronic kidney disease in the United States. JAMA. 2007;298(17):2038-2047. doi: 10.1001/jama.298.17.2038
3. Wen CP, Cheng TYD, Tsai MK, et al. All-cause mortality attributable to chronic kidney disease: a prospective cohort study based on 462 293 adults in Taiwan. Lancet. 2008;371(9631):2173-2182. doi: 10.1016/s0140-6736(08)60952-6
4. Go AS, Chertow GM, Fan D, et al. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351(13):1296-1305. doi: 10.1056/NEJMoa041031
5. United States Renal Data System. USRDS 2004 Annual Data Report: Atlas of End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2004.
6. Levin A. Clinical Epidemiology of Cardiovascular Disease in Chronic Kidney Disease Prior to Dialysis. Semin Dial. 2008;16(2):101-105. doi: 10.1046/j.1525-139X.2003.16025.x
7. Kidney Disease: Improving Global Outcomes CKDMBDWG. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. 2009(113):S1-130. doi: 10.1038/ki.2009.188
8. Bouillon R, Norman AW, Lips P. Vitamin D deficiency. N Engl J Med. 2007;357(19):1980-1981. doi: 10.1056/NEJMc072359
9. Lips P, Hosking D, Lippuner K, et al. The prevalence of vitamin D inadequacy amongst women with osteoporosis: an international epidemiological investigation. J Intern Med. 2006;260(3):245-254. doi: 10.1111/j.1365-2796.2006.01685.x
10. Greene-Finestone LS, Berger C, de Groh M, et al. 25-Hydroxyvitamin D in Canadian adults: biological, environmental, and behavioral correlates. Osteoporos Int. 2011;22(5):1389-1399. doi: 10.1007/s00198-010-1362-7
11. Hagenau T, Vest R, Gissel TN, et al. Global vitamin D levels in relation to age, gender, skin pigmentation and latitude: an ecologic meta-regression analysis. Osteoporos Int. 2009;20(1):133-140. doi: 10.1007/s00198-008-0626-y
12. van Schoor NM, Lips P. Worldwide vitamin D status. Best Pract Res Clin Endocrinol Metab. 2011;25(4):671-680. doi: 10.1016/j.beem.2011.06.007
13. Mehrotra R, Kermah DA, Salusky IB, et al. Chronic kidney disease, hypovitaminosis D, and mortality in the United States. Kidney Int. 2009;76(9):977-983. doi: 10.1038/ki.2009.288
14. Аляев Ю.Г., Егшатян Л.В., Рапопорт Л.М., Ларцова Е.В. Гормонально-метаболические нарушения как системный фактор формирования мочевых камней // Урология. — 2014. — №5. — С. 35-39. [Alyaev YG, Egshatyan LV, Rapoport LM, Lartsova EV. Hormonal and metabolic disorders as systemic factor for the formation of uroliths. Urologiia. 2014;(5):35-39. (In Russ.)]
15. Fernandez-Juarez G, Luno J, Barrio V, et al. 25 (OH) vitamin D levels and renal disease progression in patients with type 2 diabetic nephropathy and blockade of the renin-angiotensin system. Clin J Am Soc Nephrol. 2013;8(11):1870-1876. doi: 10.2215/CJN.00910113
16. Elamin MB, Abu Elnour NO, Elamin KB, et al. Vitamin D and cardiovascular outcomes: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2011;96(7):1931-1942. doi: 10.1210/jc.2011-0398
17. Alborzi P, Patel NA, Peterson C, et al. Paricalcitol reduces albuminuria and inflammation in chronic kidney disease: a randomized double-blind pilot trial. Hypertension. 2008;52(2):249-255. doi: 10.1161/HYPERTENSIONAHA.108.113159
18. Ketteler M, Block GA, Evenepoel P, et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters. Kidney Int. 2017;92(1):26-36. doi: 10.1016/j.kint.2017.04.006
19. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42(4 Suppl 3):S1-201.
20. Alem AM, Sherrard DJ, Gillen DL, et al. Increased risk of hip fracture among patients with end-stage renal disease. Kidney Int. 2000;58(1):396-399. doi: 10.1046/j.1523-1755.2000.00178.x
21. Panda DK, Miao D, Bolivar I, et al. Inactivation of the 25-hydroxyvitamin D 1alpha-hydroxylase and vitamin D receptor demonstrates independent and interdependent effects of calcium and vitamin D on skeletal and mineral homeostasis. J Biol Chem. 2004;279(16):16754-16766. doi: 10.1074/jbc.M310271200
22. Научное общество нефрологов России, Ассоциация нефрологов. России. Клинические рекомендации «Диагностика и лечение артериальной гипертензии при хронической болезни почек». — М.; 2014. [Nauchnoe obshchestvo nefrologov Rossii, Assotsiatsiya nefrologov. Rossii. Klinicheskie rekomendatsii «Diagnostika i lechenie arterial'noy gipertenzii pri khronicheskoy bolezni pochek». Moscow; 2014. (In Russ.)]
23. Sprague SM, Llach F, Amdahl M, et al. Paricalcitol versus calcitriol in the treatment of secondary hyperparathyroidism. Kidney Int. 2003;63(4):1483-1490. doi: 10.1046/j.1523-1755.2003.00878.x
24. de Zeeuw D, Agarwal R, Amdahl M, et al. Selective vitamin D receptor activation with paricalcitol for reduction of albuminuria in patients with type 2 diabetes (VITAL study): a randomised controlled trial. Lancet. 2010;376(9752):1543-1551. doi: 10.1016/s0140-6736(10)61032-x
Review
For citations:
Egshatyan L.V., Mokrisheva N.G. Secondary hyperparathyroidism in patient with type 2 diabetes and stages 3–4 chronic kidney disease. Diabetes mellitus. 2018;21(2):128-134. (In Russ.)