Calcium pyrophosphate deposition disease

Australian GP guideline on the diagnosis and management of calcium pyrophosphate deposition (CPPD) disease, including acute CPP crystal arthritis, chronic CPPD, and investigation for secondary metabolic causes.

Introduction and Overview

Calcium pyrophosphate deposition (CPPD) disease is a crystal arthropathy caused by the deposition of calcium pyrophosphate dihydrate (CPP) crystals in articular cartilage, fibrocartilage, synovium, and periarticular soft tissues. It encompasses a spectrum of clinical presentations, from asymptomatic chondrocalcinosis discovered incidentally on imaging to acute CPP crystal arthritis (formerly "pseudogout") and chronic CPP crystal inflammatory arthritis. It is the most common cause of acute monoarthritis in older adults and is frequently underdiagnosed.

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Key Point: The terminology "pseudogout" is now discouraged in favour of "acute CPP crystal arthritis." CPPD encompasses multiple clinical syndromes. Management depends on the clinical presentation — acute arthritis, chronic arthritis, or incidental chondrocalcinosis — and requires distinguishing from gout, septic arthritis, and other arthritides.

Parameter	Detail
Peak incidence	Adults >60 years; prevalence increases steeply with age
Sex distribution	Slight female predominance in chronic forms; equal in acute presentations
Most common joints	Knee (most common), wrist, hip, shoulder, ankle, symphysis pubis
Crystal type	Calcium pyrophosphate dihydrate (CPP) — weakly positive birefringent, rhomboid-shaped under polarised light
Chondrocalcinosis	Radiographic calcification of cartilage — marker of CPP deposition, may be asymptomatic

Pathophysiology

CPP crystals form in cartilage matrix when inorganic pyrophosphate (PPi) levels exceed the solubility threshold. PPi is generated by chondrocytes via ENPP1 (ectonucleotide pyrophosphatase/phosphodiesterase 1) and transported out of cells by ANKH (ankylosis protein homologue). Elevated extracellular PPi leads to CPP crystal nucleation in the cartilage matrix.

Causes and Risk Factors

Category	Details
Age-related (primary)	Most cases — age-related changes in cartilage matrix and pyrophosphate metabolism; no identifiable metabolic cause
Hyperparathyroidism	Elevated calcium promotes CPP crystallisation; consider in younger patients (<55 years) or with florid chondrocalcinosis
Haemochromatosis	Iron deposition inhibits pyrophosphatase enzymes; chondrocalcinosis a recognised feature; check ferritin and transferrin saturation
Hypomagnesaemia	Magnesium required for pyrophosphatase activity — deficiency promotes CPP accumulation; seen in loop diuretic use, malabsorption
Hypophosphataemia	Inhibits pyrophosphatase; seen in X-linked hypophosphataemia
Hypothyroidism	Association recognised; mechanism unclear
Familial CPPD	Rare autosomal dominant mutations in ANKH; florid chondrocalcinosis in young adults
Joint trauma / surgery	Local tissue damage may precipitate acute CPP crystal arthritis ("acute attack after procedure")

Acute Inflammatory Mechanism

CPP crystals shed from cartilage into joint space — triggers NLRP3 inflammasome activation in macrophages and neutrophils
IL-1β is a central mediator — explains why IL-1 inhibitors are effective in refractory cases
Acute CPP crystal arthritis is clinically indistinguishable from gout without synovial fluid analysis
Triggers include: intercurrent illness, surgery, dehydration, hyaluronic acid injection, bisphosphonate infusion

Clinical Presentation

CPPD presents across a wide spectrum from asymptomatic chondrocalcinosis to debilitating chronic inflammatory arthritis. Recognition of the clinical syndrome guides management.

Clinical Phenotypes

Phenotype	Features	Notes
Asymptomatic chondrocalcinosis	Incidental calcification on X-ray; no symptoms	Most common; no treatment required; investigate for secondary causes if <55 years or florid
Acute CPP crystal arthritis (formerly pseudogout)	Sudden severe monoarthritis; red, swollen, hot joint; fever; elevated inflammatory markers	Most common acute monoarthritis in elderly; knee most common; confirm with joint aspiration
Chronic CPP crystal inflammatory arthritis	Persistent or episodic polyarthritis resembling RA; symmetric or asymmetric; may have synovitis	Can be seronegative; distinguish from RA — RF/CCP usually negative; X-ray chondrocalcinosis helpful
Osteoarthritis with CPPD	Premature or severe OA with superimposed CPP crystal inflammation; subchondral cysts, hook-shaped osteophytes in MCP joints	Common pattern in elderly; mixed inflammatory and OA features
Crowned dens syndrome	Acute severe neck pain and fever; CPP crystal deposition around the dens of C2	Mimics meningitis, giant cell arteritis; CT shows calcification around dens

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Must Exclude Septic Arthritis: Acute monoarthritis with fever in an elderly patient requires urgent synovial fluid analysis and Gram stain/culture to exclude septic arthritis before attributing to CPP crystal arthritis. Septic arthritis and crystal arthritis can co-exist.

Investigations

Diagnosis requires a combination of clinical assessment, synovial fluid analysis, and imaging. Crucially, metabolic causes of CPPD should be screened for — particularly in patients under 55 years or with florid chondrocalcinosis.

Synovial Fluid Analysis

Essential
Synovial fluid microscopy (polarised light)
CPP crystals: weakly positive birefringent, rhomboid-shaped, intracellular and extracellular. WCC >2,000/mm³ (usually 5,000–50,000) in acute arthritis. Send simultaneously for MC&S to exclude septic arthritis.
Essential
Synovial fluid MC&S
Gram stain and culture mandatory — septic arthritis must be excluded in every acute monoarthritis. Negative culture does not completely exclude infection in early or treated cases.
Essential
Serum inflammatory markers (CRP, ESR)
Markedly elevated in acute CPP crystal arthritis. ESR >100 mm/hr may occur. Elevated but non-specific — does not distinguish from infection.
Essential
FBC, UEC
Leucocytosis common in acute flare. Renal function relevant for NSAID/colchicine dosing.

Imaging

Essential
Plain X-ray of affected joint(s)
Chondrocalcinosis — linear calcification within cartilage (menisci, articular cartilage, triangular fibrocartilage of wrist, symphysis pubis). Not required to make diagnosis of acute CPP crystal arthritis if crystals confirmed on aspiration.
Recommended
Ultrasound of joints
Detects CPP crystals as hyperechoic deposits within cartilage (deep to cartilage surface, unlike gout tophi). Increasingly used in specialist practice for diagnosis and aspiration guidance.
Available
CT (cervical spine)
If crowned dens syndrome suspected — CT of C1–C2 shows calcification around dens. Preferred over MRI for calcification detection.
Available
Dual-energy CT (DECT)
Research tool for crystal differentiation; not routinely available in Australian practice.

Metabolic Screen (Important — Do Not Miss)

Essential if <55 years or florid
Serum calcium, PTH
Hyperparathyroidism — most important secondary cause. Elevated calcium and PTH.
Essential if <55 years or florid
Serum ferritin, transferrin saturation
Haemochromatosis — florid chondrocalcinosis, hook-shaped MCP osteophytes. Elevated ferritin and transferrin saturation. HFE gene testing if suspected.
Recommended
Serum magnesium
Hypomagnesaemia — seen with loop diuretics, malabsorption, alcoholism.
Recommended
TFTs
Hypothyroidism association.
Recommended
Serum phosphate, ALP
Hypophosphataemia. ALP low in hypophosphatasia.

Risk Stratification

Clinical management of CPPD is guided by the clinical phenotype, frequency of attacks, and degree of functional impairment. There is no validated severity scoring tool for CPPD, but a pragmatic approach based on attack frequency and joint damage guides treatment escalation.

Category	Features	Management Approach
Asymptomatic chondrocalcinosis	Incidental finding; no symptoms; no inflammatory markers	No treatment; screen for secondary causes if <55 years or florid; patient education
Acute CPP crystal arthritis — single/infrequent	Episodic monoarthritis; <3 attacks per year; good between-attack function	Treat acute flare (NSAIDs/corticosteroids/colchicine); identify and treat triggers; prophylaxis generally not required
Acute CPP crystal arthritis — recurrent	≥3 attacks per year; significant morbidity; poor between-attack function	Treat acute flare; consider low-dose colchicine prophylaxis; rheumatology referral
Chronic CPP inflammatory arthritis	Persistent synovitis; multiple joints; elevated inflammatory markers; functional impairment	Treat like inflammatory arthritis — low-dose colchicine, hydroxychloroquine, low-dose corticosteroids; rheumatology referral
CPPD with secondary cause	Any phenotype with identifiable metabolic cause	Treat underlying cause (e.g., parathyroidectomy for hyperPTH, treat haemochromatosis, correct hypomagnesaemia)

Pharmacological Management

Pharmacological management targets the specific clinical phenotype. Acute CPP crystal arthritis is treated similarly to acute gout. Chronic inflammatory CPPD requires longer-term anti-inflammatory approaches. Unlike gout, there is no equivalent of allopurinol — no proven crystal-dissolving therapy exists for CPPD.

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No Crystal-Dissolving Therapy Available: Unlike gout, there is no proven pharmacological agent that dissolves CPP crystals or prevents their deposition. Management is targeted at controlling inflammation. Treating secondary metabolic causes (e.g., hyperparathyroidism) may slow progression but does not reliably resolve established chondrocalcinosis.

Acute CPP Crystal Arthritis Treatment

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Naproxen

Various generics | Acute CPP crystal arthritis — first line

Adult Dose500 mg twice daily for 5–7 days

FrequencyTwice daily

RouteOral

PBS Status✓ PBS: General benefit for arthritis indications

NotesNSAIDs are first-line for acute CPP crystal arthritis if no contraindications. Use with gastroprotection (PPI). Avoid in CKD eGFR <30, heart failure, active peptic ulcer, anticoagulation without careful review.

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Colchicine

Colgout® | Acute CPP crystal arthritis — alternative/adjunct

Adult Dose1 mg then 0.5 mg 1 hour later (low-dose regimen)

FrequencyAs above; can repeat next day if needed

RouteOral

PBS Status✓ PBS: Authority required for gout (may be used off-label for CPPD)

NotesEffective for acute CPP crystal arthritis; similar efficacy to low-dose regimen in gout. Reduce dose in CKD. Avoid with strong CYP3A4 inhibitors (clarithromycin, cyclosporin). Diarrhoea common.

Intra-articular Corticosteroids (Preferred When NSAIDs Contraindicated)

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Triamcinolone acetonide

Kenacort-A® | Intra-articular injection — acute CPP crystal arthritis

Adult Dose20–40 mg intra-articular (dose depends on joint size)

FrequencySingle injection; may repeat after 4–6 weeks if needed

RouteIntra-articular

PBS Status✓ PBS: Not listed for intra-articular use (requires private prescription or hospital supply)

NotesHighly effective in acute CPP crystal arthritis — particularly useful when NSAIDs and oral steroids are contraindicated. Must confirm no joint infection before injecting. Requires aspiration to dryness before injection.

Systemic Corticosteroids (When Other Agents Contraindicated)

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Prednisolone

Various generics | Acute CPP crystal arthritis — when NSAIDs/intra-articular route not feasible

Adult Dose20–40 mg/day tapered over 7–14 days

FrequencyOnce daily (morning)

RouteOral

PBS Status✓ PBS: General benefit — inflammatory conditions

NotesUse when NSAIDs contraindicated and intra-articular route not feasible (polyarticular flare, inaccessible joint). Short course only. Monitor glucose, BP. Use with gastroprotection.

Prophylaxis and Chronic CPPD Management

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Colchicine (low-dose prophylaxis)

Colgout® | Recurrent CPP crystal arthritis — prophylaxis

Adult Dose0.5 mg once or twice daily

FrequencyDaily (long-term)

RouteOral

PBS Status✓ PBS: Authority required for gout (off-label for CPPD prophylaxis)

NotesReduces frequency of recurrent CPP crystal arthritis attacks. Evidence from small RCTs and case series. Reduce dose in CKD. Appropriate for patients with ≥3 attacks/year or chronic CPPD arthritis.

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Hydroxychloroquine

Plaquenil® | Chronic CPP inflammatory arthritis

Adult Dose200–400 mg/day

FrequencyOnce or twice daily

RouteOral

PBS Status✓ PBS: Authority required — inflammatory conditions (off-label for CPPD)

NotesUsed in chronic CPPD inflammatory arthritis refractory to colchicine. Evidence limited but practice-based. Baseline and annual ophthalmology review for retinopathy. Safe in renal impairment with dose adjustment.

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Methotrexate

Various generics | Refractory chronic CPP inflammatory arthritis

Adult Dose7.5–15 mg once weekly (escalate to 20–25 mg if needed)

FrequencyOnce weekly with daily folic acid 5 mg

RouteOral (or SC if tolerability issue)

PBS Status✓ PBS: Authority required — rheumatoid arthritis/inflammatory arthritis

NotesFor severe refractory chronic CPPD inflammatory arthritis — specialist-initiated. Requires monitoring (FBC, LFTs, creatinine monthly). Avoid in significant renal impairment, hepatic disease, alcohol excess, pregnancy.

Directed Therapy — Treating Secondary Causes

Identifying and treating secondary metabolic causes of CPPD is important. Correction of the underlying cause may reduce attack frequency and slow the progression of chondrocalcinosis, though established crystal deposits rarely dissolve completely.

Secondary Cause Management

Cause	Investigation	Treatment
Primary hyperparathyroidism	Serum calcium, PTH	Parathyroidectomy for symptomatic or appropriate cases — reduces attack frequency in CPPD
Haemochromatosis	Ferritin, transferrin saturation, HFE gene	Venesection — reduces iron burden; may reduce CPPD flares but established chondrocalcinosis persists
Hypomagnesaemia	Serum magnesium	Oral magnesium supplementation (e.g., magnesium glycinate 300–600 mg/day); review causative medications (loop diuretics)
Hypothyroidism	TFTs	Thyroid hormone replacement
Hypophosphataemia	Serum phosphate, ALP	Treat underlying cause; phosphate supplementation as appropriate

Trigger Avoidance

Acute CPP crystal arthritis can be triggered by intercurrent illness, surgery, dehydration, and procedures
Hyaluronic acid intra-articular injections have been associated with acute CPP crystal arthritis flares — warn patients
Bisphosphonate infusions (e.g., zoledronic acid) can precipitate acute CPP crystal arthritis — monitor post-infusion
Ensure adequate hydration during intercurrent illness and perioperatively
Consider prophylactic colchicine cover for major surgery in patients with recurrent CPPD

Non-Pharmacological Management

Non-pharmacological management is adjunctive for acute attacks and supportive for chronic CPPD. Unlike gout, there is no equivalent dietary modification that reliably reduces CPP crystal burden. Joint aspiration is both diagnostic and therapeutic.

Joint Aspiration

Aspiration of acute monoarthritis is mandatory — provides definitive diagnosis (crystal identification and exclusion of septic arthritis) and is therapeutic (removes crystals, reduces joint pressure, and relieves pain)
Aspiration should be performed before initiating anti-inflammatory treatment in undifferentiated acute monoarthritis
In confirmed recurrent CPPD without diagnostic uncertainty, aspiration may be combined with intra-articular corticosteroid injection
Ultrasound guidance improves aspiration yield for small or difficult joints

Physical and Supportive Measures

Rest and elevation of affected joint during acute attack — reduces pain and swelling
Ice application — 15–20 minutes several times daily during acute flare
Walking aids (cane, crutch) for lower limb involvement during acute attack
Physical therapy for chronic CPPD — range of motion exercises, quadriceps strengthening for knee CPPD reduces mechanical stress
Weight management — reduces mechanical load on affected joints

Patient Education

Explain the difference between chondrocalcinosis (incidental X-ray finding) and CPPD disease (symptomatic crystal arthritis)
Advise patients to present early during acute attacks — early treatment reduces attack duration
For patients on prophylactic colchicine — explain long-term nature of treatment and importance of compliance
Emphasise that joint aspiration is both diagnostic and therapeutic — address needle phobia early
Inform about potential attack triggers (dehydration, illness, procedures) and the importance of maintaining hydration

Monitoring Parameters

Monitoring in CPPD is directed at disease activity, treatment response, and medication safety. There is no serum biomarker equivalent to serum urate in gout for tracking disease burden.

Parameter	Frequency	Purpose
Inflammatory markers (CRP, ESR)	During acute attacks; periodically in chronic CPPD	Assess response to treatment; monitor disease activity in chronic inflammatory CPPD
Renal function (UEC, eGFR)	Annually; before and during NSAID use	NSAIDs and colchicine require renal dose adjustment in CKD; haemochromatosis nephropathy
FBC, LFTs	Annually; monthly initially if on methotrexate	Methotrexate hepatotoxicity and bone marrow suppression monitoring; haemochromatosis follow-up
Serum calcium, PTH	Annually if hyperparathyroidism established or post-parathyroidectomy	Monitor treatment response for secondary cause
Serum ferritin, transferrin saturation	Annually if haemochromatosis being treated	Monitor iron depletion with venesection therapy
Ophthalmology review	Annually if on hydroxychloroquine >5 years	Screen for hydroxychloroquine retinopathy
Joint X-ray	As clinically indicated; not routinely for monitoring	Progressive chondrocalcinosis or joint damage assessment if clinical uncertainty

When to Refer

Rheumatology: Diagnostic uncertainty (first presentation of acute monoarthritis), refractory or recurrent CPPD, chronic CPP inflammatory arthritis requiring DMARDs, suspected familial CPPD, or age <55 years
Orthopaedics/Interventional radiology: For joint aspiration or injection if GP not confident with the procedure, or for joints not accessible in general practice
Endocrinology/Endocrine surgery: Confirmed secondary cause (hyperparathyroidism, haemochromatosis) requiring specialist management
Haematology: Haemochromatosis management — venesection programme coordination

Special Populations

Several populations require modified approaches to CPPD management.

Young Patients (<55 Years) with Chondrocalcinosis

Florid chondrocalcinosis under age 55 warrants a thorough search for metabolic secondary cause — routine screening may miss familial CPPD and haemochromatosis
Screen: calcium, PTH, ferritin, transferrin saturation, magnesium, phosphate, TSH, ALP
Consider HFE gene testing and hepatology referral if haemochromatosis confirmed
Genetic counselling if familial CPPD suspected (autosomal dominant inheritance — ANKH mutations)

Elderly Patients with Multiple Comorbidities

NSAIDs are often contraindicated — CKD, heart failure, anticoagulation, peptic ulcer disease
Intra-articular corticosteroids are the preferred treatment for acute monoarthritis in elderly patients with NSAID contraindications
Systemic corticosteroids (prednisolone) for polyarticular flares — short course, monitor glucose (especially in diabetes)
Colchicine dose adjustment required in CKD: eGFR 30–60: reduce dose by 50%; eGFR <30: avoid or use with caution under specialist guidance
Consider falls risk when treating acute lower limb arthritis in frail elderly patients

CPPD in the Setting of Septic Arthritis Concern

The two conditions can co-exist — crystal arthritis does NOT exclude septic arthritis
If clinical suspicion of septic arthritis: admit, aspirate, send for MC&S and crystals, commence empirical antibiotics while awaiting results
Never initiate intra-articular corticosteroids until infection has been excluded

Post-surgical and Post-procedural CPPD

Acute CPP crystal arthritis is a recognised complication after major surgery, particularly joint replacement and parathyroidectomy
In the post-operative patient with acute joint inflammation — aspirate to distinguish CPP crystal arthritis from septic arthritis/prosthetic joint infection
Treatment as per standard acute CPPD, but intra-articular corticosteroids near surgical site require careful consideration

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

CPPD is less well-characterised in Aboriginal and Torres Strait Islander (ATSI) populations compared to gout. However, the high prevalence of secondary causes — particularly haemochromatosis variants, renal disease, and metabolic conditions — means that CPPD in ATSI patients warrants thorough investigation for metabolic secondary causes. Acute monoarthritis in ATSI patients should always prompt joint aspiration to distinguish CPP crystal arthritis from gout and septic arthritis.

Septic Arthritis Vigilance

ATSI communities have higher rates of Staphylococcal and streptococcal infections. Acute monoarthritis in ATSI patients requires a low threshold for aspiration and empirical antibiotic treatment until septic arthritis is excluded.

Secondary Cause Screening

Haemochromatosis (including non-HFE variants) may be underdiagnosed in ATSI populations. Metabolic screening including ferritin, transferrin saturation, calcium, and PTH should be performed for any ATSI patient presenting with chondrocalcinosis.

Access to Joint Aspiration

In remote and rural areas, access to joint aspiration may be limited. Telehealth consultation with a rheumatologist or physician may help guide empirical management when aspiration is not feasible, while ensuring the patient is transferred for aspiration if clinical suspicion of septic arthritis is high.

NSAID Use

NSAIDs should be used cautiously in ATSI patients given high background rates of CKD, hypertension, and cardiovascular disease. Intra-articular corticosteroids and short-course systemic prednisolone are often safer alternatives.

Appropriate Use of Medicine and Stewardship

The key stewardship concerns in CPPD relate to appropriate aspiration and diagnostic workup, avoidance of unnecessary investigations and treatments, and the appropriate use of long-term therapies.

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Common Stewardship Issues:

Treating acute monoarthritis without aspiration: Crystal arthritis and septic arthritis cannot be reliably distinguished clinically. Aspiration is required before initiating treatment for any undifferentiated acute monoarthritis.
Failing to screen for secondary causes: Hyperparathyroidism and haemochromatosis are treatable causes of CPPD. Screening should be performed, particularly in patients <55 years or with florid chondrocalcinosis.
Long-term NSAIDs for CPPD: NSAIDs should be used for acute flares only, not as long-term suppressive therapy. Chronic use leads to GI, renal, and cardiovascular harm.
Injecting a potentially infected joint: Intra-articular corticosteroids are contraindicated if septic arthritis has not been excluded. Aspirate first, send MC&S, then inject only when infection is excluded.

GP Role

Aspirate acute monoarthritis — diagnosis cannot be made without synovial fluid analysis
Screen for secondary metabolic causes in all new CPPD diagnoses, particularly if <55 years
Treat acute flares with NSAIDs, colchicine, or intra-articular corticosteroids depending on the clinical situation — avoid defaulting to systemic corticosteroids without considering safer alternatives
Refer to rheumatology for recurrent or refractory CPPD, chronic inflammatory arthritis, or diagnostic uncertainty
Do not prescribe long-term NSAIDs for CPPD prevention — use low-dose colchicine prophylaxis if prophylaxis is indicated

Follow-up and Prevention

Follow-up in CPPD depends on the clinical phenotype. Acute episodic CPPD may need only opportunistic review, while chronic inflammatory CPPD requires regular surveillance.

Acute attack — 1–2 weeks

Confirm resolution of attack. Review diagnosis. Perform metabolic screen if not done. Discuss recurrence risk.

3 months post-diagnosis

Repeat inflammatory markers if elevated. Review metabolic screen results. Consider prophylaxis if ≥2 attacks. Refer to rheumatology if chronic phenotype suspected.

Annually (stable disease)

Review attack frequency. Medication review (NSAID safety, colchicine dose in CKD). Renal function if on chronic NSAID or colchicine. Ophthalmology if on hydroxychloroquine.

If attacks increasing in frequency

Increase monitoring to 3–6 monthly. Intensify prophylaxis or escalate to DMARDs. Rheumatology referral.

Prevention Strategies

Treat identified secondary causes — parathyroidectomy, haemochromatosis venesection, magnesium replacement
Low-dose colchicine prophylaxis for patients with ≥3 attacks/year — reduces attack frequency significantly
Avoid known triggers where possible — maintain hydration, prophylactic colchicine cover for major surgery in susceptible patients
Patient education — early presentation at attack onset allows earlier treatment and shorter attack duration
Regular metabolic review for patients with known secondary cause — monitor calcium, PTH, ferritin as appropriate

References

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