PTH - Chronic Renal Failure

Learning Objectives: • Describe the physiology of PTH and mineral metabolism in

patients with CKD • Discuss the available therapies for the disorders of PTH and

mineral metabolism in patients with CKD• Apply this information to the clinical management of patients

with CKD

PTH and Mineral Disorders in Patients With CKD: A Practical Case-Based

Approach for Renal Dietitians

Patient Case

• 53-year-old male with history of stage 5 CKD 2º ADPKD recently started on hemodialysis after failed renal transplant

• History of deceased donor renal transplant, 11/95

• Previously on hemodialysis, 6/95–11/95

• History of CVD, s/p CABG x 3 in 02/04

• History HTN; history basal cell carcinoma

• Social history: works as car mechanic; no history of alcohol, tobacco; married 21 years; 1 daughter, age 19

• Family history ADPKD on maternal side

Patient Case (cont)

• Presents with mild itching, bone pain• No history of fractures• Medications:

– Calcium acetate: 667 mg 3 tab tid– B-complex with C: 1 tab qd– Atorvastatin: 20 mg qd– Metoprolol: 50 mg bid– Prednisone: 2.5 mg qd

• Laboratory values:– Phosphorus: 8.0 mg/dl– Corrected calcium: 8.3 mg/dl– Intact PTH: 670 pg/ml– Ca x P: 66.4

• Concentration in blood/plasma is tightly regulated by PTH and vitamin D

• Calcium ions serve a variety of functions– Signal transduction: 1st and 2nd messengers

– Nerve and muscle function

– Major component of bone

• Serum calcium does not reflect total body calcium content

Overview of Calcium Physiology

Regulation of Plasma Calcium

PTglands

CaSR

Adapted from E Nemeth.

PTH

bone

PO4 reabsorption

Ca reabsorptionkidney

PTglands

CaSR

PO4 resorption

Ca resorption

Low plasma Ca2+

plasma Ca2+

intestine

1,25-dihydroxy-vitamin D3 PO4 absorption

Ca absorption

LiverLiver

KidneyKidney

SkinSkin

Pre-vitamin D

Vitamin D

7-dehydrocholesterol

25-OH calcidiol

1-hydroxylase

1,25 (OH)2 D

calcitriolmost potent metabolite

Low PO4

Low CaHigh PTH+

- High PO4

High CaLow PTH

Vitamin D Metabolism

DietDiet

Adapted from WG Goodman.

Principal Biological Effects of Vitamin D

• Increases absorption of Ca and P

• Maintains bone mineralization and turnover

• Indirectly reduces synthesis of calcitriol

• Reduces synthesis of PTH

Acute and Chronic Regulation of PTH Output

PROCESS TIME FRAME FACTORS

PTH secretion minutes Ca2+/CaSR

Gene expression

Transcription

mRNA stability

hours, days

Vit D / VDR VDRE

Ca2+ CaRE

low Ca (↑ half-life)

low PO4 (↓ half-life)

Tissue hyperplasiaweeks,

months, years

Ca2+/CaSR PO4

• Normal PO4 levels in plasma: 2.5–4.5 mg/dL1

• Total body PO4 content: 500–700 g1 (85% in bone)

• Dietary Reference Intake2: 700 mg

• Typical US dietary intake2: 1200 mg

• GI absorption Mainly passive, through Na/Pi transporter Fractional absorption 60–70% Enhanced by vitamin D

• Kidney is major regulator3 Mediated by brush border Na/Pi transporter PTH – increases excretion Vitamin D – decreases excretion

1. Merck Manual. 2006;Sec 2:Ch 12. 2. Food & Nutrition Board, Institute of Medicine. Washington D.C.: National Academy

Press; 1997:146-189. 3. Takeda E, et al. Adv Enzyme Regul. 2000;40:285-302.

Phosphorus Metabolism

Phosphorus Homeostasis

1200 mg

500 mg

130 mg700 mg

(< 1%)

(85%)

(15%)

Soft tissues

PlasmaBone

Kidney

Intestine

700 mg

Adapted from: Goodman WG. Med Clin North Am. 2005;89:631-647.

Physiology Summary

• PTH and vitamin D are central regulators of plasma Ca

• Calcium regulates serum PTH through the parathyroid CaSR

• PTH production is controlled at several levels:

• Kidney is crucial for calcitriol synthesis and phosphate secretion

• Calcitriol increases serum calcium through increased intestinal absorption

Calcium Vitamin D

Secretion

mRNA level

Hyperplasia

Secondary HPT Pathophysiology:Overview

• CKD disrupts calcium homeostasis High PTH Low calcitriol Reduced intestinal calcium absorption Low serum calcium at low GFR High serum phosphorus at low GFR

• Excess PTH synthesis and secretion Inhibition of PTH transcription is deficient Hyperplasia and parathyroid gland enlargement

contribute to elevated serum PTH

Serum Analytes Vary With Stage of Kidney Disease

Craver L, et al. Nephrol Dial Transpl. 2007;22:1171-1176..

50

40

30

20

10

0 CKD1 CKD2 CKD3 CKD4 CKD5

N = 15 87 221 156 43

1,25

-(O

H) 2

D (

pg

/mL

)

i PT

H (

pg

/mL

)

CKD1 CKD2 CKD3 CKD4 CKD5

N = 174 341 856 354 111

0

200

100

**

**

*

**

*P < 0.05

LLN ULN

LLN

Serum Analytes Vary With Stage of Kidney Disease (cont)


N = 174 341 856 354 111

9.7

9.6

9.5

9.4

9.3

9.2

9.1

9.0

8.9

Ser

um

Cal

ciu

m (

mg

/dL

)


N = 174 341 856 354 111

Ser

um

Ph

osp

hat

e (m

g/d

L)

5.5

5.0

4.5

4.0

3.5

3.0

*

*P < 0.05

*

*

All calcium values within normal range

ULN

Craver L, et al. Nephrol Dial Transpl. 2007;22:1171-1176.

Pathophysiology of sHPT in CKD

↓ 1,25(OH)2D3↑ P

Adapted from Skorecki K, et al. Harrison’s Principles of Internal Medicine. 15th ed. 2001:1551-1562.

↑ PTH

↓ Ca2+

1

1.5

2

0.9

All-

Cau

se D

eath

Haz

ard

Rat

io

Serum iPTH (pg/mL)

KDOQI recommended

range: 150-300 pg/mL

Risk of Death by Quarterly Varying iPTH

< 10

0

100-

200

200-

300

300-

400

400-

500

500-

600

600-

700

700

Time-dependent Case-Mix and MICS model

Kalantar-Zadeh K, et al. Kidney Int. 2006;70:771-780.

Corrected Serum Calcium (mg/dL)

< 8.0 8.0 to8.5

8.5 to9.0

9.0 to9.5

9.5 to10.0

10.0 to10.5

10.5 to11

11.00.7

2

3

1

All-

Cau

se D

eath

Haz

ard

Rat

io

8.0 to0.7

2

3

1

0.7

2

3

1

0.7

1.5

2

3

1

Risk of Death by Quarterly Varying Albumin-Adjusted Calcium

KDOQI recommended

range 8.4-9.5 mg/dL



Risk of Death by Quarterly Varying Phosphorus

0.7

2

3

4

1

Serum Phosphorus (mg/dL)

2

3

4

1

2

3

4

1

2

3

4

1

< 3.0 3.0 to3.99

4.0 to4.99

5.0 to5.99

6.0 to6.99

7.0 to7.99

8.0 to8.99

9.0

KDOQI recommended

range: 3.5-5.5 mg/dL

All-

Cau

se D

eath

Haz

ard

Rat

io



Clinical Consequences of Mineral Dysregulation

• Renal osteodystrophy

• Hyperphosphatemia

• Cardiovascular calcification

• Extraskeletal calcification

• Endocrine disturbances

• Neurobehavioral changes

• Compromised immune system

• Altered erythropoiesis

Forms of Vascular Calcification

London GM et al. Curr Opin Nephrol Hypertens. 2005;14:525–531.

Arterial Calcification

Intimal Calcification

Atherosclerosis

Stenosis, occlusions

Infarction, ischemia

Medial Calcification

Arteriosclerosis

Stiffening

Systolic and pulse pressures, early return of wave reflections

Altered coronary perfusion, left-ventricular

hypertrophy

Risk Factors for Soft Tissue Calcification

• Hyperphosphatemia

• Increased Ca x P product

• Excessive calcium load

• Secondary hyperparathyroidism

• Local tissue injury

• Rise in tissue pH

• Decreased levels of calcification inhibitors

• Systolic hypertension (average 1 year systolic bp 160 mm Hg vs 120)

• Adipose tissue (calcific uremic arteriolopathy)

Vascular Calcification in ESRD

Intimal CalcificationAtherosclerosis

Medial CalcificationArteriosclerosis

Available at: http://library.med.utah.edu/WebPath/CVHTML/CV007.html. Accessed May 2007.

Impact of Arterial Calcification in Stable Hemodialysis Patients with ESRD

London GM, et al. Nephrol Dial Transplant. 2003;18:1731.

Car

dio

vasc

ula

r S

urv

ival

2 = 34.9; P < 0.0001

0 25 50 75 1000.00

0.75

0.50

0.25

1.00

Time (months)

NCP < 0.01

P < 0.001

AMC

AIC

2 = 44.3; P < 0.00001

0 25 50 75 1000.00

0.75

0.50

0.25

1.00A

ll-C

ause

S

urv

ival

NC

P < 0.001

P < 0.01

AMC

AIC

0

0.25

0.5

0.75

1

0 20 40 60 80

Follow-up (months)

Probability of Survival

0 Arteries Calcified

1 Artery Calcified




N = 110 stable dialysis patients with ESRD

P < 0.0001 comparison among groups

Blacher J, et al. Hypertension. 2001;38:938-942.

Probability of Survival Decreases With Increasing Arterial Calcification

Valvular Calcification and Mortality

† P < 0.0005 vs no valvular calcification

0

0.2

0.4

0.6

0.8

1.0

0 6 12 18 24 30 36

Ove

rall

Su

rviv

al

Both Mitral and Aortic (n = 14)

Either Mitral or Aortic (n = 48)

Neither (n = 130)

Follow-Up Time (months)

†

Wang A, et al. J Am Soc Nephrol. 2003;14:159-168.

CAC Is Associated With Increased Mortality

Block GA, et al. Kidney Int. 2007;71:438-441.

0 6 12 18

CAC = 0CAC1 – 400CAC 400

240.00

0.25

0.50

0.75

1.00

30 36 42 48 54 60 66

P = 0.002

Months

Su

rviv

al D

istr

ibu

tio

n F

un

ctio

n

Calcification in Vascular Smooth Muscle Cells

Osteo/Chondrocytic VSMC

Death Signal VSMC Damage“Uremic Milieu”

Apoptotic Bodies

Matrix Vesicles

+ MGP / BMP7+ fetuin-A+ PPi

- MGP/ BMP2- fetuin-A- PPi/+ALK+ Ca/P

ClearanceCalcification

PhagocytosisDelayed or Impaired

Phagocytosis

Elastin

Shanahan CM. Curr Opin Nephrol Hypertens. 2005;14:361–367.

Vascular Calcification, Cardiovascular Complications, and CKD

• Vascular Calcification Associated With: – Accelerated risk of stroke, amputation, MI– Left ventricular hypertrophy– Poor coronary artery perfusion– Increased pulse wave velocity– Increased pulse pressure

• Contributory Factors:– Deranged bone and mineral metabolism– Decreased levels of inhibitors of calcification such as fetuin-A– Stimulation of osteogenic pathways in endothelial cells by

uremic “toxins” – Impaired endothelial repair mechanisms

Adapted from Lederer E and Ouseph R. Am J Kidney Dis. 2007;49:162-171.Block GA, et al. Kidney Int. 2007;71(5):438-441.

Serum PTH 150–300 pg/mLSerum Ca (albumin-corrected) 8.4–9.5 mg/dL

Serum P 3.5–5.5 mg/dLCa x P Product < 55 mg2/dL2

National Kidney Foundation. Am J Kidney Dis. 2002;39(Suppl 1):S1-S266.

KDOQI™ Goals for Stage 5 CKD

KDOQI guidelines recommend that Ca2+ and P should be monitored monthly and PTH quarterly after stabilization.

Patient Case Review/Update

• Medications: – Calcium acetate: 667 mg 3 tab tid– B-complex with C: 1 tab qd– Atorvastatin: 20 mg qd– Metoprolol: 50 mg bid– Prednisone: 2.5 mg qd

• Laboratory values:– Phosphorus: 8.0 mg/dl– Corrected calcium: 8.3 mg/dl– Intact PTH: 670 pg/ml– Ca x P: 66.4

Nutrition Guidelines

• Limit dietary phosphorus to 800-1000 mg/d with consideration for protein needs, ie, as low as possible while allowing for a recommended level of protein intake

• Limit elemental calcium from calcium-based binders to ≤ 1500 mg/d

• Limit total (dietary and medication) elemental calcium to ≤ 2000 mg/d

• Avoid calcium fortified foods as directed

• Moderate application of cardiovascular dietary recommendations, not to the detriment of nutrition status


Lifestyle Guidelines

• Exercise training

• Identify and address psychological issues (eg, depression)

• No smoking (help prevent CVD?)

Patient Case Review/Update

• Patient started on sevelamer HCl 800 mg 2 tablets tid with meals, Ca acetate discontinued to reduce vascular calcification risk

• Repeat labs after 2 weeks:

– Phosphorus: 6.5 mg/dl

– Corrected calcium: 8.3 mg/dl

– Ca x P: 54

• Diet reviewed; sevelamer increased to 3 tablets with meals, 2 tablets with snacks

Intervention Result

CaCa

PO4PO4

PTHPTH

Phosphate Binders

(Ca-based)

Therapeutic Interventions forManaging Secondary HPT

Adapted from Goodman WG. Nephrol Dial Transplant. 2003;18(suppl 3):iii2-iii8.

Managing Mineral Balance: Phosphate Binders

Sevelamer label: http://www.renagel.com/docs/renagel_pi.pdfBlock GA, et al. Kidney Int. 2007;71(5):438-441.

Serum Phosphate

SevelamerCalcium

Mortality

Ph

os

ph

oru

s C

ha

ng

e

Study Week

0 2 6 10 14 18 22 26 30 34 38 42 46 52

-5

-4

-

3

-2

-1

0

1

2

1.00

0.75

0.50

0.25

0.00

0 6 12 18 24 30 36 42 48 54 60 66

P = 0.016

Su

rviv

al

Fra

cti

on

SevelamerCalcium

Months

Use of Phosphate Binders

• Ca-based binder should not be used if patient has hypercalcemia or PTH < 150 pg/mL

• Non-Ca-based binder preferred if vascular or soft-tissue calcification is appreciable

1st line 2nd line 3rd line

Stage 3/4 Dietary P restriction Ca-based binder

Stage 5

Dietary P restriction,

Ca-based

or

other binder

Ca-based

and

other binder

Al-OH up to 4 wks


Phosphate Binders: Summary

Cannata-Andia JB. Dial Trans. 2002;17(Suppl 11):16–19; Ritz EJ. J Nephrol. 2005;18;221-228. Goodman WG. Neph Dial Trans. 2003;18(Suppl 3):iii2-iii8; Block GA, et al. Kidney Int. 2007; 71(5):438-441.

Binder Advantages Disadvantages

Aluminum-containing Effective

Tissue accumulation;

Bone disease, encephalopathy, anemia

Calcium-containing

Effective;

Widely used

Hyper-Ca, calcification risk;

High pill burden

Sevelamer

Less vascular calcification than Ca-containing binders; lower

mortality?

Reduction of TC & LDL

High pill burden

(moderate potency);

Cost; Tolerability

Lanthanum carbonate

Good potency;

Minimal absorption;

Not Hyper-Ca; Low pill burden

Cost; Taste fatigue; Unknown long term impact; Tolerability

Magnesium carbonate Potential to minimize Ca load Hyper-Mg; no long term

studies

Patient Case Update

• At 1 month, labs are checked

– Phosphorus: 5.5 mg/dL

– Corrected calcium: 8.3 mg/dL

– Ca x P: 46

– Intact PTH: 601 pg/mL

– 25-hydroxy vitamin D: 18 ng/mL

• Started on Vitamin D

– Ergocalciferol: 50,000 IU/month

– Active analog

Intervention Result

CaCa

PO4PO4

PTHPTHVitamin D

analog



Vitamin D Repletion in Stage 3 & 4 with Ergocalciferol: KDOQITM Recommendation

Serum 25(OH)D

(ng/mL)

Vitamin D Status Dose (IU) Route Duration

(months) Comment

< 5 Severe deficiency

50,000/wk X 12 wks; then

monthlypo

6

Assay 25(OH)D after 6 months

500,000 once im

Assure pt adherence;

assay 25(OH)D at 6 months

5-15 Mild deficiency

50,000/wk X 4 wks, then

monthlypo 6 Assay 25(OH)D

after 6 months

16-30 Insufficiency 50,000/mo po 6

National Kidney Foundation. Am J Kidney Dis. 2003;42(4 suppl 3):S1-S201.

Sprague SM, et al. Kidney Int. 2003;63:1483-1490.

Vitamin D Analogs Suppress PTH

Time (weeks)

PT

H (

pg

/mL

)

0

100

200

300

400

500

600

700

800

900

1000

Paricalcitol (n = 130)

Calcitriol (n = 133)

0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34

Vitamin D (n = 37,173)

No Vitamin D (n = 13,864)

Teng M, et al. J Am Soc Nephrol. 2005;16:1115-1125.

*P < 0.001

8

15

CVMortality

*

*

14

29

0

10

20

30

40

50

2-YearMortality

Mo

rtal

ity

per

100

Pat

ien

t-Y

ears

Infectious Cause Mortality

13*

Vitamin D Use Is Associated With Decreased Mortality in Incident HD Patients

Which Vitamin D Do We Use and Why?

• Calcitriol (Calcijex®, Rocaltrol®) active vitamin D

– Increased calcium and phosphorus absorption

– Increased serum levels

– Loses effectiveness with high serum P

• Paricalcitol (Zemplar®) active vitamin D analog

– Less calcemic

• Doxercalciferol (Hectorol®)

– Less calcemic

Recommended Vitamin D Dosing

PTH Ca P Ca x P Calcitriol Paricalcitol Doxercalciferol

300 – 600 < 9.5 < 5.5 < 55 IV 0.5 – 1.5

Oral same

2.5 – 5.0 mcg IV 2 mcg

Oral 5 mcg

600 – 1000 < 9.5 < 5.5 < 55 IV 1.0-3.0

Oral 1-4

6.0 – 10 mcg IV 2 – 4 mcg

Oral 5 – 10 mcg

> 1000 < 10 < 5.5 < 55 IV 3.0-5.0

Oral 3-7

10 – 15 mcg IV 4 – 8 mcg

Oral 10 - 20 mcg

• Serum Ca > 10.2 : stop all D, minimize Ca load• Ca = 9.5-10.2: change to non Ca-containing binder• Ca < 9.5: continue D or modify with P algorithm • P > 6.0: stop vitamin D• P = 5.5–6.0: increase binders, decrease Vitamin D• P < 5.5: continue or modify using Ca or PTH algorithm


• Laboratory data in one month:– Phosphorus: 6.1 mg/dl

– Calcium: 9.3 mg/dl

– Ca x P product: 57

– Intact PTH: 489 pg/ml

• Patient started on cinacalcet HCl 30 mg qd

Patient Case Update

Intervention Result

CaCa

PO4PO4

PTHPTHCalcimimetic



Targeting PTH Secretion With Cinacalcet

Control

Ser

um

PT

H (

% o

f m

axim

um

)

80

60

40

20

100

0 1.5

0

0.5 1.0 2.0

Extracellular Calcium (mM)

Cinacalcet

Cinacalcet Increases Calcium

Sensitivity

[Ca2+]ER [Cai2+]

CaSR

PTH

PTH

PTH

Cinacalcet

Adapted from Goodman WG, et al. Kidney Int. 1996;50:1834-1844.

Cinacalcet is Associated with a Reduction of PTH

Block GA, et al. New Engl J Med. 2004;350:1516-1525.

P < 0.001

Placebo

Cinacalcet

Dose titration Efficacy assessment

Week

PT

H le

ve

l (p

g/m

l)

800

700

600

500

400

300

200

100

00 2 4 6 8 10 12 14 16 18 20 22 24 26

~50

% r

edu

ctio

n

Cinacalcet Enables Patients to Achieve the KDOQI™ Targets

Adapted from Moe SM, et al. Kidney Int. 2005;67:760-771.

Me

dia

n i

PT

H (

pg

/mL

)

KDOQI™ Target

0

100

200

300

400

500

600

700

Week

Cinacalcet HCIPlacebo

n = 471n = 663

n = 366n = 473

B 2 4 6 8 12 14 16 18 20 22 24 2610

iPTH

Weekn = 471n = 663

n = 368n = 471

B 2 4 6 8 12 14 16 18 20 22 24 2610

Me

dia

n S

eru

m C

a (

mg

/dL

)

8.2

8.4

8.8

9.0

9.2

9.6

9.8

10.2

8.6

9.4

10.0

KDOQI™ Target

Serum Calcium

n = 410n = 547

n = 412n = 555

Weekn = 471n = 662

n = 363n = 466

B 2 4 6 8 12 14 16 18 20 22 24 2610

Me

dia

n C

a x

P (

mg

2/d

L2)

40

45

50

55

60

65Ca x P

KDOQI™ Target

n = 408n = 545

n = 363n = 466

Weekn = 471n = 663

B 2 4 6 8 12 14 16 18 20 22 24 26104.6

4.8

5.0

5.2

5.4

5.6

5.8

6.0

6.2

6.4

Me

dia

n S

eru

m P

(m

g/d

L) Serum Phosphorus

KDOQI™ Target

n = 409n = 547

Moe SM, et al. Nephrol Dial Transplant. 2005;20:2186-2193.

Cinacalcet Reduction of iPTH for 3 Years

Placebo n = 17

Cinacalcet n = 16

Cinacalcet Is Associated With Improved Outcomes

Cunningham J, et al. Kidney Int. 2005;68:1793-1800.

CV Hospitalization

FracturesPTX

Mortality

Week

Eve

nt-

Fre

e P

rob

abil

ity

0 4 8 12 16 20 24 28 32 36 40 44 48 52

0.75

0.95

1.00

Standard - 4.1 events / 100 pt yrs

Cinacalcet - 0.3 events / 100 pt yrs

0.90

0.85

0.80 Eve

nt-

Fre

e P

rob

abil

ity

Week 0 4 8 12 16 20 24 28 32 36 40 44 48 52

0.75

0.95

1.00

Standard - 6.9 events / 100 pt yrs

Cinacalcet - 3.2 events / 100 pt yrs

0.90

0.85

0.80

P = 0.04

Week

Eve

nt-

Fre

e P

rob

abil

ity

0 4 8 12 16 20 24 28 32 36 40 44 48 52

0.75

0.95

1.00

Standard – 19.7 events / 100 pt yrsCinacalcet – 15.0 events / 100 pt yrs

0.90

0.85

0.80

Week

Eve

nt-

Fre

e P

rob

abil

ity

0 4 8 12 16 20 24 28 32 36 40 44 48 52

0.75

0.95

1.00

Standard – 7.4 deaths / 100 pt yrs

Cinacalcet – 5.2 deaths / 100 pt yrs

0.90

0.85

0.80

P = NS

P = 0.009

P = 0.005

Diet/nutrition, Phosphate Binders, Vitamin D

CaCa

PO4PO4

PTHPTH

Diet/nutrition, Ca-based P-binders Vitamin D

Calcimimetics, Vitamin D



• Lab values checked at 1 week:– Phosphorus: 5.4 mg/dL


• Patient complains of mild nausea

• Advised to take cinacalcet with evening meal

• No other changes made at this time

Patient Case Update

• Labs rechecked at 1 month– Phosphorus: 5.4 mg/dL


– Intact PTH: 290 pg/ml

– Ca x P product: 47

• Nausea resolved

• No further changes warranted at present

Patient Case Update (cont)

Developing a Treatment Algorithm

• Promote patient safety and incorporate strategies for the fewest side effects

• Be consistent with current, valid research and update regularly as new information is available

• Reflect team consensus and consider facility needs or limitations

• Provide a schedule for changes (dose, meds, route of admin)• Provide logical, easy steps• Allow for therapy response time before making additional

changes • Minimize paperwork• Include mechanism to inform patient and team of progress• Define limits and provide mechanism to return management

to MD if treatment outside parameters is needed• Identify outcome measures and provide tracking mechanisms

Therapeutic Options for Secondary HPT: Conclusions

• New phosphate binders offer options for phosphorus reduction without increasing serum calcium

• Vitamin D analogs lower PTH and increase bone mineralization, but also raise calcium and phosphorus

• Cinacalcet can be used to lower PTH despite elevations in calcium and/or phosphorus

• Dialysis is a critical tool for managing ESRD

• Parathyroidectomy can be useful for lowering PTH when pharmacologic intervention fails

Health & Medicine

PTH - Chronic Renal Failure