Version July 2025
INTRODUCTION —
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a systemic disorder characterized by biochemical abnormalities (calcium, phosphate, parathyroid hormone [PTH], and vitamin D), abnormalities in bone turnover and mineralization, and extraskeletal (ie, vascular and soft tissue) calcification.
Secondary hyperparathyroidism refers to the elevated circulating levels of PTH that typically occur in patients with CKD-MBD.
This topic reviews the management of secondary hyperparathyroidism in patients on dialysis. The management of secondary hyperparathyroidism in the predialysis patient with CKD, treatment of hyperphosphatemia in patients with CKD, and indications for parathyroidectomy in patients with end-stage kidney disease (ESKD) are presented separately.
●(See "Management of hyperphosphatemia in adults with chronic kidney disease".)
●(See "Refractory hyperparathyroidism and indications for parathyroidectomy in adult patients on dialysis".)
RATIONALE FOR TREATMENT —
For patients on dialysis, secondary hyperparathyroidism is treated to prevent severe bone disease (osteitis fibrosa) and reduce the risk of bone fracture. In the era prior to current therapies, these mineral metabolism sequelae of end-stage kidney disease (ESKD) were common [1]. (See "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)", section on 'Abnormalities in bone turnover, mineralization, volume linear growth, or strength'.)
An additional rationale for treating secondary hyperparathyroidism is based on observational studies reporting an association between higher parathyroid hormone (PTH) levels and increased mortality, possibly mediated by excess PTH contributing to hyperphosphatemia and vascular calcification (see "Vascular calcification in chronic kidney disease"). For example, in a study of over 25,000 patients on maintenance hemodialysis, PTH levels greater than 600 pg/mL were associated with a 21 percent increase in mortality compared with PTH levels between 100 and 300 pg/mL [2].
MONITORING —
To monitor secondary hyperparathyroidism, we routinely measure serum levels of intact parathyroid hormone (PTH), phosphorus, and calcium [3]. We also measure serum 25-hydroxyvitamin D levels. The optimal frequency of monitoring these biomarkers is unknown. We measure these serum parameters as follows:
●Intact PTH at least every 6 months and every 3 months if the baseline concentration is elevated or if the patient is being treated for secondary hyperparathyroidism. PTH levels are assessed more frequently (eg, monthly) when changes are made to PTH lowering therapy (eg, calcitriol or cinacalcet).
●Phosphorus and calcium at least every three months and every month if the patient has or is being treated for hyperparathyroidism or hyperphosphatemia.
●25-hydroxyvitamin D every 12 months and every 6 months if the patient is being treated for vitamin D deficiency.
Some clinicians also measure bone-specific alkaline phosphatase in addition to PTH as a marker of bone response to elevated PTH.
TARGET PTH RANGE —
The goal of secondary hyperparathyroidism management is to maintain parathyroid hormone (PTH) levels in a range associated with optimal bone health and overall survival. However, the ideal PTH range for patients on dialysis is unknown and is a matter of disagreement. By contrast, there is general consensus that an absolute PTH threshold for treatment should not be specified because of variability in PTH assays, and that decisions regarding treatment should be based upon trends rather than single laboratory values [3].
For most patients on dialysis, we suggest the following target:
●Intact PTH values should be maintained between two to seven times the upper normal limit for the PTH assay.
However, some patients may benefit from PTH values substantially less than seven times the upper limit of normal. For example, a patient with PTH values at the higher end of the target range who has symptoms of bone pain or unexplained hypercalcemia, in conjunction with high serum levels of bone-specific alkaline phosphatase, likely has a component of inadequately controlled high-turnover bone disease (see "Evaluation of renal osteodystrophy", section on 'Evaluation'). In such a patient, it would be reasonable to narrow the desired PTH range (eg, to two to approximately four times the upper normal limit for the PTH assay).
Our suggested upper limit for the PTH target range is below that of the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines, which recommend that intact PTH values should be maintained between two to nine times the upper normal limit for the PTH assay [3,4]. The higher upper limit for PTH in these guidelines was due to concerns that aggressive use of PTH-lowering therapy would lead to over suppression of bone turnover and the subsequent development of adynamic bone disease. However, we believe such concerns have led to undertreatment and to higher rates of progressive, severe hyperparathyroidism [5]. Furthermore, PTH levels greater than approximately seven times the upper limit of normal generally indicate high-turnover bone disorders (see "Evaluation of renal osteodystrophy", section on 'Evaluation'), and observational data suggest that targeting PTH levels lower than that recommended by current guidelines may improve survival [6].
Suppression of PTH to less than two times the upper limit for the specific PTH assay is not desirable, since it is associated with a higher prevalence of adynamic bone disease [1,7]. (See "Adynamic bone disease associated with chronic kidney disease".)
GENERAL MEASURES IN ALL PATIENTS
Manage hyperphosphatemia — Management of high serum phosphorus (ie, >5.5 mg/dL [1.78 mmol/L]) is an integral part of the management of secondary hyperparathyroidism and is presented separately. (See "Management of hyperphosphatemia in adults with chronic kidney disease", section on 'Treatment'.)
The use of calcitriol and synthetic vitamin D analogs to lower parathyroid hormone (PTH) levels (see 'Treatment options' below) may increase serum phosphorus concentrations, and higher phosphorus is associated with excess mortality among patients on dialysis [8-12]. In addition, higher serum phosphorus levels can contribute to the development and severity of secondary hyperparathyroidism.
Maintain normocalcemia — We avoid both higher and lower levels of serum calcium that may result from the treatment of secondary hyperparathyroidism. Calcitriol and synthetic vitamin D analogs may increase and calcimimetics typically decrease serum calcium (see 'Treatment options' below). Higher levels of serum calcium are associated with the development of adverse cardiovascular events among patients on dialysis [3]. Hypocalcemia, especially if moderate or severe (ie, corrected total serum calcium ≤7.5 mg/dL [1.87 mmol/L]), may result in serious complications if untreated [13]. (See "Clinical manifestations of hypocalcemia".)
Treat vitamin D deficiency — Although there is no conclusive evidence to support a benefit of vitamin D replacement in patients on dialysis, we correct vitamin D deficiency [3], even in patients treated with calcitriol or a synthetic vitamin D analog (see 'Treatment' below). We use a similar treatment strategy as is recommended for the general population. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on 'Vitamin D replacement'.)
Among patients on hemodialysis, both ergocalciferol and cholecalciferol are effective in repleting vitamin D levels [14-17].
In contrast to secondary hyperparathyroidism in patients with nondialysis chronic kidney disease (CKD), secondary hyperparathyroidism in patients on dialysis generally does not improve after treatment of vitamin D deficiency [14,17]. However, observational data suggest that low vitamin D levels are associated with increased mortality among patients on hemodialysis [18]. Furthermore, there is no significant toxicity associated with its use in this setting, although long-term studies have not been performed. In particular, studies have shown little or no difference in risk of hypercalcemia, hyperphosphatemia, or vascular calcification among vitamin-D-treated patients [14-17].
TREATMENT OPTIONS —
Treatment options for increased parathryroid hormone (PTH) include calcimimetics, calcitriol or synthetic vitamin D analogs, or a combination of these therapies [1].
Calcitriol and synthetic vitamin D analogs — Calcitriol (oral or intravenous [IV]) and synthetic vitamin D analogs all reduce serum levels of PTH [18-21] by suppressing PTH production; however, these agents may not be sufficiently effective as monotherapy if the PTH is very high [22,23]. Major potential adverse effects include elevated levels of serum phosphorus and calcium, which can cause vascular calcification.
Six active (ie, 1-hydroxylated) vitamin D derivatives are available. These include calcitriol [24,25] and five synthetic vitamin D analogs: paricalcitol [20,26], doxercalciferol [27-29], alfacalcidol (not available in the United States) [30-32], falecalcitriol (not available in the United States), and 22-oxacalcitriol (not available in the United States) [25,33-35]. All of the available vitamin D derivatives are considered acceptable, and there are no convincing studies that support one particular agent over another [36]. As an example, in one observational study of patients on hemodialysis, three vitamin D derivatives (calcitriol, paricalcitol, and doxercalciferol) were associated with similar rates of calcium, phosphate, and PTH control, as well as similar rates of hospitalization and survival [37].
No randomized trials have shown a convincing benefit of calcitriol or synthetic vitamin D analogs on survival, bone pain, in preventing parathyroidectomy, or other important clinical outcomes [38,39].
Calcimimetics — Calcimimetics reduce PTH by increasing the sensitivity of the calcium-sensing receptor (CaSR) to calcium [40]; they also decrease serum calcium and, to a lesser extent, serum phosphorus [41-56]. (See "Parathyroid hormone secretion and action", section on 'Calcimimetic drugs'.)
Widely available calcimimetics include cinacalcet (oral) and etelcalcetide (intravenous with hemodialysis). When a calcimimetic is indicated, we prefer cinacalcet over etelcalcetide because it is relatively inexpensive. However, we use etelcalcetide in patients who fail to respond sufficiently to cinacalcet, or in patients who have poor adherence to oral medications.
Potential adverse effects of calcimimetics include hypocalcemia, which is more common with etelcalcetide, and gastrointestinal symptoms (eg, nausea, vomiting, or diarrhea), which are similar with etelcalcetide and cinacalcet.
Despite effective control of hyperparathyroidism, the use of calcimimetics has not been shown to improve cardiovascular or all-cause mortality among patients on dialysis [56]. Data regarding the efficacy and side effects of cinacalcet and etelcalcetide are provided below:
●Cinacalcet ─ The addition of cinacalcet to existing treatment regimens (usually calcitriol or an active vitamin D analog plus phosphate binder) increases the chances of decreasing PTH to target values without causing hypercalcemia or hyperphosphatemia [48,52,54,55,57]. Cinacalcet also decreases the chances of requiring a parathyroidectomy [58]. However, for patients with advanced secondary hyperparathyroidism (baseline PTH levels above 800 pg/mL), monotherapy with cinacalcet may be inadequate to control PTH [59].
Cinacalcet does not appear to provide a benefit on mortality and cardiovascular outcomes, at least among patients <65 years of age [58,60]. In the Evaluation of Cinacalcet Hydrochloride Therapy to Lower Cardiovascular Events (EVOLVE) randomized trial, patients were assigned to receive cinacalcet or placebo in addition to conventional therapy including phosphate binders and/or active vitamin D or synthetic analogs [60]. At a median follow-up of less than two years, a difference between groups in the composite outcome of time until death or the first nonfatal cardiovascular event was not shown.
The interpretation of this trial is limited by both a high dropout rate in the cinacalcet group (62 percent) and a high rate of crossover in the placebo group: Nearly 20 percent of patients in the placebo group ended up taking commercially available cinacalcet. The high rate of crossover may have diminished between-group differences.
Cinacalcet may provide a benefit to older individuals, who are at higher cardiovascular risk compared with younger patients. In EVOLVE, the effect of cinacalcet was examined among patients on hemodialysis who were ≥65 years (n = 1005) and <65 years (n = 2878) [61]. Among older patients, cinacalcet was associated with a reduced risk of major cardiovascular events (adjusted hazard ratio [AHR] 0.70, 95% CI 0.60-0.81) and death (AHR 0.68, 95% CI 0.51-0.81). Among younger patients, the cinacalcet-associated AHRs for cardiovascular events and mortality were 0.97 (95% CI 0.86-1.09) and 0.99 (95% CI 0.86-1.13), respectively. The effect of cinacalcet on severe hyperparathyroidism was the same between older and younger individuals.
Among EVOLVE participants aged ≥65 years, cinacalcet was associated with lower risk of fracture (AHR 0.69, 95% CI 0.49-0.95) [62].
Side effects of cinacalcet noted in the EVOLVE trial included hypocalcemia and gastrointestinal symptoms [60]. Hypocalcemia was mostly asymptomatic and usually resolved spontaneously [63].
●Etelcalcetide ─ Intravenous etelcalcetide was compared with placebo and with oral cinacalcet in three randomized trials [64,65]. All trials were of short duration and did not examine patient-important outcomes [66].
In two parallel randomized trials, etelcalcetide was compared with placebo among a total of 1023 patients on hemodialysis with hyperparathyroidism [64]. Etelcalcetide was more effective than placebo in reducing PTH (with 74 to 75 percent of patients achieving >30 percent reduction in PTH versus 8.3 to 9.6 percent in placebo) by 27 weeks. However, etelcalcetide-treated patients had more side effects compared with placebo (hypocalcemia, muscle spasms, nausea and vomiting).
A randomized trial compared intravenous etelcalcetide versus oral placebo (n = 340) and oral cinacalcet versus intravenous placebo (n = 343) among patients on hemodialysis with hyperparathyroidism [65]. Etelcalcetide was superior to cinacalcet in reducing PTH by greater than 30 percent (68 in etelcalcetide groups versus 58 percent in cinacalcet group).
Nausea and vomiting were comparable between groups. However, hypocalcemia was more common in the etelcalcetide group and required interventions to increase serum calcium concentrations (such as raising the dialysate calcium concentrations and prescribing calcium-containing phosphate binders, oral calcium supplements, calcitriol, and active vitamin D analogs). Etelcalcetide administration led to prolongation of corrected QT intervals in many patients.
In a subsequent pilot trial that included 13 patients on hemodialysis, etecalcetide therapy resulted in significant improvements in central skeleton bone mineral density, trabecular quality, and bone turnover [67].
TREATMENT —
Several therapeutic approaches effectively reduce levels of parathyroid hormone (PTH) among patients on dialysis. Calcitriol/synthetic vitamin D analogs, calcimimetics, or a combination of the two can be used as first-line therapy [3]. However, no randomized trials have determined the optimal approach, or whether medical treatment of secondary hyperparathyroidism improves patient-centered outcomes. (See 'Rationale for treatment' above.)
Initial therapy — Our initial management is based on correcting the deficit of active vitamin D (ie, 1,25-dihydroxyvitamin D) present in most patients on dialysis.
Start and titrate active vitamin D — We treat most patients with calcitriol or a synthetic vitamin D analog; calcimimetic therapy is added when active vitamin D therapy fails to adequately control PTH at doses that avoid elevated serum calcium or phosphorus levels. Calcimimetic monotherapy is generally reserved for patients with hypercalcemia or for patients who are not adherent to phosphorus lowering therapies.
We administer increasing doses of calcitriol or synthetic vitamin D analogs with the goal of achieving target plasma PTH level (see 'Target PTH range' above) while avoiding hypercalcemia and maintaining serum phosphorus ≤5.5 mg/dL (1.78 mmol/L) [4]. Measures to control serum phosphorus are used concurrently with these agents. (See "Management of hyperphosphatemia in adults with chronic kidney disease".)
Our preference for an active vitamin D based approach is based largely on physiology. Although the pathogenesis of secondary hyperparathyroidism is complex and multifactorial, a major contributor among patients on dialysis is impaired kidney production of 1,25-dihydroxyvitamin D (see "Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)"). However, up to one-half of patients with severe hyperparathyroidism show little or no decline in plasma PTH levels with calcitriol therapy [22,23].
Control calcium and phosphorus — Our approaches to patients with increasing or elevated levels of serum calcium and elevated levels of phosphorus in the setting of active vitamin D therapy are as follows:
●Increasing serum calcium – For patients who have increasing and higher levels of corrected total serum calcium (eg, >9.5 mg/dL [2.37 mmol/L]) during up-titration of calcitriol or synthetic vitamin D analogs, we typically add a calcimimetic to prevent the development of frank hypercalcemia that may occur with higher doses of active vitamin D therapy.
●Hypercalcemia – Hypercalcemia (ie, corrected total serum calcium >10.2 mg/dL [2.54 mmol/L]) is a contraindication to treatment with calcitriol or synthetic vitamin D analogs [4]. However, these agents may be continued for patients in whom a clearly reversible cause of hypercalcemia is identified (eg, treatment with calcium-based phosphorus binders or nonadherence to cinacalcet for patients on combination therapy). If treatment with calcitriol or a synthetic vitamin D analog is discontinued, it can be resumed at one-half the previous dose after resolution of hypercalcemia.
●Elevated serum phosphorus – Calcitriol or synthetic vitamin D analogs should not be up-titrated if the serum phosphorus persistently exceeds 5.5 mg/dL (1.78 mmol/L) despite maximal therapies to treat hyperphosphatemia [4] (see "Management of hyperphosphatemia in adults with chronic kidney disease"). For such patients, we add calcimimetic therapy provided the corrected total serum calcium is ≥8.4 mg/dL (2.10 mmol/L). In addition to lowering PTH, calcimimetic therapy modestly lowers serum phosphorus [68].
Persistent and severe hyperphosphatemia (eg, >6.5 mg/dL [2.10 mmol/L]) despite maximal phosphorus lowering therapies is a contraindication to active vitamin D therapy. If treatment with calcitriol or a synthetic vitamin D analog is discontinued, it can be resumed at one-half the previous dose after improvement of hyperphosphatemia.
Active vitamin D dosing — In general, the starting dose of active vitamin D formulations (ie, calcitriol, whether oral or IV, or synthetic vitamin D analogs) should be low (eg, 0.25 mcg of calcitriol thrice weekly). Provided hypercalcemia and hyperphosphatemia are avoided, the dose may be increased at four- to eight-week intervals. Patients who are responsive to therapy typically show significant reductions in PTH levels within the first three to six months of therapy [7,22,28,69-76]. Some clinicians limit the maximal dose of calcitriol or synthetic vitamin D analogs to a dose equivalent to the physiological production rate of approximately 0.5 to 1 mcg of calcitriol per day and add calcimimetics to lower PTH further if needed. (See 'Add calcimetic if PTH uncontrolled' below.)
Subsequent therapy — Many patients treated with active vitamin D therapy will require the addition of a calcimimetic.
Add calcimetic if PTH uncontrolled — For patients in whom calcitriol or synthetic vitamin D analogs fail to adequately control PTH at doses that avoid elevated serum calcium or phosphorus levels, we add calcimimetic therapy and up-titrate as necessary, provided the corrected total serum calcium is ≥8.4 mg/dL (2.10 mmol/L). Our preferred initial calcimimetic agent is cinacalcet; we use etelcalcetide among patients who fail to respond sufficiently to cinacalcet. (See 'Calcimimetics' above.)
The addition of cinacalcet to active vitamin D therapy increases the chances of achieving target PTH values (see 'Target PTH range' above) and allows the use of lower doses of the vitamin D analog, which are less likely to cause hypercalcemia or hyperphosphatemia [48,52,54,55,57,77,78].
Patients with hypocalcemia — Hypocalcemia should be avoided during calcimimetic therapy (see 'Maintain normocalcemia' above). Calcimimetics should not be started or the dose increased if the corrected total serum calcium is <8.4 mg/dL (2.10 mmol/L) [79]. We do not specifically treat asymptomatic and mild hypocalcemia (ie, >7.5 mg/dL [1.87 mmol/L] in the setting of normal albumin) with either calcium or escalating doses of calcitriol or synthetic vitamin D analogs since mild calcimimetic-associated hypocalcemia often resolves spontaneously (see 'Calcimimetics' above). If corrected total serum calcium is <7.5 mg/dL (1.87 mmol/L), or if the patient is symptomatic, we increase the active vitamin D dose (if possible) and withhold calcimimetic therapy until the serum calcium reaches 8.0 mg/dL (2.00 mmol/L) and/or symptoms have resolved. Calcimimetic treatment is subsequently reinitiated using the next lowest dose.
Calcimimetic dosing — Specific dosing regimens for cinacalcet and etecalcitide are discussed below (see 'Treatment options' above):
●Cinacalcet – Cinacalcet is initiated at a dose of 30 mg/day orally, with stepwise increments to 60, 90, and 180 mg/day. Provided hypocalcemia is avoided, the dose can be increased every four weeks until goals are achieved.
Due to payor limitations, many patients receiving in-center dialysis take cinacalcet thrice weekly rather than daily. However, we do not endorse this approach. There are no high-quality data to support thrice-weekly dosing regimens, and pharmacokinetic studies suggest dosing intervals longer than one day may be suboptimal. After a cinacalcet dose, plasma PTH levels reach nadir in two to three hours and then rebound substantially over the rest of the day [47,80].
●Etecalcetide – We use etelcalcetide among patients who fail to respond sufficiently to cinacalcet. Cinacalcet should be discontinued for at least 7 days prior to starting etecalcetide. Etecalcetide is started intravenously at 5 mg three times per week at hemodialysis. The dose may be increased in increments of 2.5 to 5 mg no more frequently than every four weeks to a maximum dose of 15 mg three times per week, as long as hypocalcemia is not present.
Refractory hyperparathyroidism — We define refractory hyperparathyroidism as severe, persistent, and progressive elevation of serum PTH that cannot be treated adequately by medical therapy (including both vitamin D analogs and calcimimetics) without causing significant hyperphosphatemia or hypercalcemia. Patients with severe disease may require parathyroidectomy [4]. (See "Refractory hyperparathyroidism and indications for parathyroidectomy in adult patients on dialysis".)
Treatment following parathyroidectomy — The prevention and medical management of parathyroidectomy-associated complications among patients on dialysis are discussed elsewhere (see "Hungry bone syndrome following parathyroidectomy in patients with end-stage kidney disease"). With respect to treatment thresholds/targets and medical therapy for secondary hyperparathyroidism, the long-term management of patients on dialysis who had a parathyroidectomy is the same as that for patients who did not.
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic kidney disease-mineral and bone disorder".)
SUMMARY AND RECOMMENDATIONS
●Rationale for treatment – For patients on dialysis, secondary hyperparathyroidism is treated to prevent severe bone disease (osteitis fibrosa) and reduce the risk of bone fracture. An additional rationale for treating secondary hyperparathyroidism is based on observational studies reporting an association between higher parathyroid hormone (PTH) levels and increased mortality. (See 'Rationale for treatment' above.)
●Monitoring – To monitor secondary hyperparathyroidism, we routinely measure serum levels of intact PTH, phosphorus, and calcium [3]. We also measure serum 25-hydroxyvitamin D levels. The frequency of monitoring depends on whether baseline abnormalities are present or therapeutic measures have been taken. (See 'Monitoring' above.)
●Goals of treatment – The goal of secondary hyperparathyroidism management is to maintain PTH levels in a range associated with optimal bone health and overall survival. However, the ideal PTH range for patients on dialysis is unknown. For most patients on dialysis, we suggest that serum levels of intact PTH should be maintained between two to seven times the upper normal limit for the PTH assay (Grade 2C). (See 'Target PTH range' above.)
●General measures – Management of high serum phosphorus is an integral part of the management of secondary hyperparathyroidism. We avoid both higher and lower levels of serum calcium that may result from the treatment of secondary hyperparathyroidism. (See "Management of hyperphosphatemia in adults with chronic kidney disease" and 'General measures in all patients' above.)
●Treatment options – Treatment with active vitamin D (ie, calcitriol or a synthetic vitamin D analog) reduces serum levels of PTH by suppressing PTH production. Major potential adverse effects of active vitamin D therapy include elevated levels of serum calcium and phosphorus. Calcimimetics reduce PTH by increasing the sensitivity of the calcium-sensing receptor (CaSR) to calcium; they also decrease serum calcium and, to a lesser extent, serum phosphorus. (See 'Treatment options' above.)
●Treatment approach – Several therapeutic approaches effectively reduce levels of PTH among patients on dialysis. However, no randomized trials have determined the optimal approach, or whether medical treatment of secondary hyperparathyroidism improves patient-centered outcomes. (See 'Treatment' above.)
•Initial therapy – For most patients on dialysis treated for secondary hyperparathyroidism, we suggest initial therapy with calcitriol or a synthetic vitamin D analog alone rather than combination therapy with a calcimimetic or a calcimimetic alone (Grade 2C). Initial therapy with a calcimimetic is generally reserved for patients with hypercalcemia or for patients who are not adherent to phosphorus lowering therapies. (See 'Start and titrate active vitamin D' above.)
We administer increasing doses of calcitriol or a synthetic vitamin D analog with the goal of achieving target plasma PTH levels while avoiding hypercalcemia and maintaining serum phosphorus ≤5.5 mg/dL (1.78 mmol/L). Measures to control serum phosphorus are used concurrently with these agents. (See 'Control calcium and phosphorus' above and 'Active vitamin D dosing' above.)
•Subsequent therapy – For patients in whom calcitriol or synthetic vitamin D analogs fail to adequately control PTH at doses that avoid elevated serum calcium or phosphorus levels, we suggest adding a calcimimetic rather than switching to calcimimetic monotherapy (Grade 2C). Calcimimetics should not be started or the dose increased if the corrected total serum calcium is <8.4 mg/dL (2.10 mmol/L). (See 'Subsequent therapy' above.)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges Robert E Cronin, MD, and Michael Berkoben, MD, who contributed to earlier versions of this topic review.
