About secondary hyperparathyroidism

A balancing act

Bar graph showing vitamin D goes up and PTH goes down.

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

Bar graph showing vitamin D goes up and PTH goes down.
Bone losing calcium and phosphorus.
Gray background layout rectangle.

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

Bone losing calcium and phosphorus.

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  Gastrointestinal tract highlighted showing the decreased calcium absorption.
Gastrointestinal tract highlighted showing the decreased calcium absorption.

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

Gastrointestinal tract highlighted showing the decreased calcium absorption.

This series of dysregulations resulting in elevated levels of PTH is called secondary hyperparathyroidism (SHPT).1,5

Learn more about treating SHPT 

The prevalence of SHPT

Circular chart showing that 40% of patients with CKD stage 3 and 82% stage 3 or 4 develop SHPT.
Gray background layout rectangle.

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 
Vials used to collect the lab work that is key to diagnosing SHPT.

Patients may be asymptomatic or have mild or nonspecific symptoms, so obtaining lab values is key to diagnosing SHPT.3,6,7

Vials used to collect the lab work that is key to diagnosing SHPT.

Left untreated, SHPT can progress and lead to cardiovascular events, fractures, and increased morbidity and mortality.3,4

See the faces of SHPT 

References: 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. Hyperparathyroidism. Mayo Clinic Web site. https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-causes/syc-20356194. Accessed July 1, 2019. 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.

Important Safety Information

Hypercalcemia: Excessive administration of vitamin D compounds, including Rayaldee, can cause hypercalcemia and hypercalciuria. Severe hypercalcemia due to substantial overdosage of vitamin D and its metabolites may require emergency attention. Patients should be informed about the symptoms of elevated calcium.
Digitalis toxicity: Potentiated by hypercalcemia of any cause. Monitor serum calcium and signs and symptoms of digitalis toxicity more frequently when initiating or adjusting the dose of Rayaldee.
Adynamic Bone Disease: Monitor for abnormally low levels of intact parathyroid hormone (iPTH) levels when using Rayaldee, and adjust dose if needed.
The most common adverse reactions (≥3% and more frequent than placebo) were anemia, nasopharyngitis, increased blood creatinine, dyspnea, cough, congestive heart failure and constipation.
Care should be taken while dosing Rayaldee with cytochrome P450 inhibitors, thiazides, cholestyramine or drugs stimulating microsomal hydroxylation due to the potential for drug interactions.
Serum calcium should be below 9.8 mg/dL before initiating treatment.
Monitor serum calcium, phosphorus, 25-hydroxyvitamin D and iPTH 3 months after starting therapy or changing dose.

Indication and Limitations of Use

Rayaldee® (calcifediol) extended-release 30 mcg capsules is indicated for the treatment of secondary hyperparathyroidism in adults with stage 3 or 4 chronic kidney disease and serum total 25-hydroxyvitamin D levels less than 30 ng/mL. Rayaldee is not indicated in patients with stage 5 chronic kidney disease or end-stage renal disease on dialysis.

Important Safety Information

Hypercalcemia: Excessive administration of vitamin D compounds, including Rayaldee, can cause hypercalcemia and hypercalciuria. Severe hypercalcemia due to substantial overdosage of vitamin D and its metabolites may require emergency attention. Patients should be informed about the symptoms of elevated calcium.
Digitalis toxicity: Potentiated by hypercalcemia of any cause. Monitor serum calcium and signs and symptoms of digitalis toxicity more frequently when initiating or adjusting the dose of Rayaldee.
Adynamic Bone Disease: Monitor for abnormally low levels of intact parathyroid hormone (iPTH) levels when using Rayaldee, and adjust dose if needed.
The most common adverse reactions (≥3% and more frequent than placebo) were anemia, nasopharyngitis, increased blood creatinine, dyspnea, cough, congestive heart failure and constipation.
Care should be taken while dosing Rayaldee with cytochrome P450 inhibitors, thiazides, cholestyramine or drugs stimulating microsomal hydroxylation due to the potential for drug interactions.
Serum calcium should be below 9.8 mg/dL before initiating treatment.
Monitor serum calcium, phosphorus, 25-hydroxyvitamin D and iPTH 3 months after starting therapy or changing dose.