About secondary hyperparathyroidism
A balancing act
Vitamin D is crucial to homeostatic regulation of calcium, phosphorus, and parathyroid hormone (PTH), and by extension, bone health.1,2 In patients with chronic kidney disease (CKD), active vitamin D levels decline as kidney function diminishes.1 Low levels of active vitamin D lead to decreased absorption of calcium.1
To compensate for decreased calcium levels, the parathyroid gland increases production of PTH. This leads to inappropriate release of calcium and phosphorus from bone.3,4
To compensate for decreased calcium levels, the parathyroid gland increases production of PTH. This leads to inappropriate release of calcium and phosphorus from bone.3,4
As kidney failure progresses, the inhibition of active vitamin D synthesis increases.1
Calcium and phosphorus metabolism become further dysregulated, with notable decrease in gastrointestinal absorption of calcium.3,4
This series of dysregulations resulting in elevated levels of PTH is called secondary hyperparathyroidism (SHPT).1,5
Learn more about treating SHPT
As kidney failure progresses, the inhibition of active vitamin D synthesis increases.1
Calcium and phosphorus metabolism become further dysregulated, with notable decrease in gastrointestinal absorption of calcium.3,4
This series of dysregulations resulting in elevated levels of PTH is called secondary hyperparathyroidism (SHPT).1,5
Learn more about treating SHPTThe prevalence of SHPT
People with CKD are at risk for developing SHPT.5 In fact, 40% of people with stage 3 CKD and 82% of those with stage 4 CKD ultimately develop SHPT.5
Early diagnosis and management of SHPT is crucial
Patients may be asymptomatic or have mild or nonspecific symptoms, so obtaining lab values is key to diagnosing SHPT.3,6,7
Left untreated, SHPT can progress and lead to cardiovascular events, fractures, and increased morbidity and mortality.3,4
See the faces of SHPT
Patients may be asymptomatic or have mild or nonspecific symptoms, so obtaining lab values is key to diagnosing SHPT.3,6,7
Left untreated, SHPT can progress and lead to cardiovascular events, fractures, and increased morbidity and mortality.3,4
See the faces of SHPTReferences: 1. Cozzolino M, Covic A, Martinez-Placencia B, Xynos K. Treatment failure of active vitamin D therapy in chronic kidney disease: predictive factors. Am J Nephrol. 2015;42(3):228-236. 2. Ross AC, Taylor CL, Yaktine AL, Del Valle HB, eds. Dietary reference intakes for calcium and vitamin D. Washington, DC: National Academies Press; 2011. 3. Yuen NK, Ananthakrishnan S, Campbell MJ. Hyperparathyroidism of renal disease. Perm J. 2016 Summer;20(3):78-83. 4. Cunningham J, Locatelli F, Rodriguez M. Secondary hyperparathyroidism: pathogenesis, disease progression, and therapeutic options. Clin J Am Soc Nephrol. 2011;6:913-921. 5. Sprague SM, Crawford PW, Melnick JZ, et al. Use of extended-release calcifediol to treat secondary hyperparathyroidism in stages 3 and 4 chronic kidney disease. Am J Nephrol. 2016;44(4):316-325. 6. Lewis JL. Hyperparathyroidism. Merck Manual Professional Version. Updated September 2022. Accessed September 28, 2022. https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/parathyroid-disorders/hyperparathyroidism 7. Uhlig K, Berns JS, Kestenbaum B, et al. KDOQI US Commentary on the 2009 KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of CKD-Mineral and Bone Disorder (CKD-MBD). Am J Kidney Dis. 2010;55(5):773-799.