Myeloma Kidney — Med2Date

📋 Key Information Summary

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Myeloma kidney (cast nephropathy) is the most common renal pathology in multiple myeloma, caused by intratubular light-chain casts and occurring in 20–50 % of patients at diagnosis.
Renal impairment (eGFR < 60 mL/min/1.73 m²) is present in up to 50 % of newly diagnosed myeloma patients; 20–25 % require dialysis at some point.
Cast nephropathy requires two simultaneous factors: high serum free light chain (sFLC) concentration AND enhanced proximal tubule delivery (volume depletion, nephrotoxins).
Hypercalcaemia worsens renal function through volume depletion and vasoconstriction; aggressive normal-saline rehydration is first-line therapy.
AL amyloidosis is a distinct renal mechanism (amyloid fibrils from monoclonal light chains); differentiated from cast nephropathy by Congo-red staining on renal biopsy.
Rapid reduction of pathogenic sFLC is the cornerstone of treatment — bortezomib-based regimens (e.g., CyBorD, VTD) achieve fastest sFLC responses.
High cut-off (HCO) haemodialysis or extended haemodiafiltration to remove sFLC remains investigational in Australia; not standard-of-care.
Avoid nephrotoxins — NSAIDs, IV contrast, aminoglycosides — in all myeloma patients with renal impairment.
Renal biopsy is indicated when the aetiology of renal impairment is uncertain or AL amyloidosis is suspected.
Dialysis-dependent patients can achieve dialysis independence with early, aggressive anti-myeloma therapy.
Daratumumab-based quadruple regimens are emerging as first-line in transplant-eligible and ineligible patients; PBS Authority Required.
Aboriginal and Torres Strait Islander peoples have higher rates of myeloma diagnosed at advanced stages with renal impairment, requiring culturally safe, locally accessible nephrology and haematology services.

Introduction & Australian Epidemiology

Multiple myeloma (MM) is a malignant proliferation of monoclonal plasma cells producing abnormal immunoglobulin or free light chains (FLCs). Renal involvement — collectively termed myeloma kidney — is one of the most frequent and impactful complications, present in 20–50 % of patients at diagnosis and contributing significantly to morbidity, mortality, and health-system cost.

In Australia, the estimated age-standardised incidence of MM is approximately 6–7 per 100 000 person-years, with around 1 800 new diagnoses annually. Renal impairment (eGFR < 60 mL/min/1.73 m²) is documented in up to half of newly diagnosed patients, and 20–25 % develop dialysis-dependent kidney failure during their disease course. Myeloma is more common in males, Aboriginal and Torres Strait Islander peoples, and individuals aged > 65 years.

The mechanisms of myeloma kidney are multifactorial and include:

Cast nephropathy (myeloma kidney) — the most common and specific mechanism, involving precipitation of monoclonal light chains with Tamm–Horsfall protein in distal tubules.
Hypercalcaemia — causes renal vasoconstriction, volume depletion, and nephrocalcinosis.
AL amyloidosis — deposition of amyloid fibrils derived from monoclonal light chains in glomeruli and vessels.
Direct tubular toxicity — free light chains are endocytosed by proximal tubular epithelial cells, triggering cytokine release, NF-κB activation, and apoptosis.
Monoclonal immunoglobulin deposition disease (MIDD) — non-amyloid deposits of light or heavy chains in glomerular and tubular basement membranes.
Cryoglobulinaemia and crystal-storing histiocytosis — rare mechanisms.

Early recognition and rapid intervention — particularly prompt reduction of pathogenic free light chains — remain the strongest modifiable determinants of renal recovery.

Cast Nephropathy (Myeloma Kidney)

Cast nephropathy is the hallmark renal lesion of multiple myeloma, accounting for the majority of myeloma-associated acute kidney injury (AKI). It results from the intratubular precipitation of monoclonal free light chains with Tamm–Horsfall protein (uromodulin) in the thick ascending limb of the loop of Henle.

Pathophysiology

Two concurrent conditions are required for cast formation:

High serum free light chain concentration — typically > 500 mg/L, often > 1 000 mg/L. The monoclonal FLC must be of a restricted charge–hydrophobicity profile that favours binding to uromodulin.
Enhanced distal delivery of FLC — promoted by volume depletion, hypercalcaemia, loop diuretics, NSAIDs, IV contrast, or any cause of reduced proximal tubular reabsorption.

The resulting casts obstruct tubular lumens, trigger interstitial inflammation, and produce a pattern of “flame-shaped” multinucleated giant cell reaction on histology. Progressive tubular atrophy and interstitial fibrosis lead to irreversible kidney damage if the FLC burden is not rapidly reduced.

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Key principle: Renal recovery is most likely when anti-myeloma treatment reduces sFLC by ≥ 50 % within 21 days of initiation. Delay beyond this window reduces the chance of dialysis independence.

Histological Features

Renal biopsy — when clinically indicated — demonstrates:

Dense, fractured, eosinophilic casts within distal tubules.
Giant cell reaction surrounding casts (foreign-body type).
Tubular rupture and interstitial inflammation.
Immunofluorescence staining for a single light chain type (κ or λ) within casts.
Absent glomerular deposits (distinguishes from amyloidosis / MIDD).

ℹ️

Renal biopsy indications: Consider biopsy when sFLC ratio is normal, when proteinuria pattern suggests glomerular disease (nephrotic syndrome), or when response to anti-myeloma therapy is poor.

Renal Biomarkers

Biomarker	Role in Cast Nephropathy	Australian Availability
Serum free light chains (sFLC)	Diagnostic and prognostic; FLC ratio identifies monoclonality; absolute level predicts cast risk	Freelite® assay; MBS item 69494
Serum & urine protein electrophoresis	Confirms monoclonal protein (M-spike)	MBS items 69488, 69491
eGFR / serum creatinine	Tracks AKI severity and response to therapy	Standard pathology
Urine protein-to-creatinine ratio	Quantifies proteinuria; disproportionately high in myeloma kidney	Standard pathology
NGAL / KIM-1 (urine)	Research biomarkers of tubular injury; not routine in Australia	Research use only

Hypercalcaemia & Direct Tubular Toxicity

Hypercalcaemia

Hypercalcaemia occurs in approximately 15–30 % of MM patients at diagnosis and is a major reversible contributor to renal impairment. Elevated calcium promotes:

Renal vasoconstriction and reduced glomerular filtration rate.
Volume depletion through nephrogenic diabetes insipidus (calcium blocks aquaporin-2 channels).
Nephrocalcinosis and medullary calcium deposition.
Enhanced Tamm–Horsfall protein–light chain binding, synergistically promoting cast nephropathy.

Mild

Corrected Ca²⁺ 2.60–2.85 mmol/L

Often asymptomatic or mild polydipsia. May exacerbate pre-existing renal impairment.

Setting: Outpatient — oral rehydration, monitor

Moderate

Corrected Ca²⁺ 2.85–3.20 mmol/L

Nausea, confusion, constipation, polyuria. Significant AKI risk.

Setting: Inpatient — IV normal saline, consider bisphosphonate

Severe

Corrected Ca²⁺ > 3.20 mmol/L

Coma, arrhythmia, renal failure. Medical emergency.

Setting: ICU / HDU — aggressive IV rehydration + zoledronic acid ± calcitonin ± dialysis

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Critical: Always calculate the corrected calcium: Corrected Ca²⁺ = measured Ca²⁺ + 0.02 × (40 − serum albumin in g/L). Use ionised calcium where available.

Hypercalcaemia Management

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0.9 % Sodium Chloride (Normal Saline)

IV Fluid · Volume repletion

Adult dose 200–500 mL/h IV for 2–4 L over first 24 h; titrate to urine output ≥ 100 mL/h

Renal adjustment Monitor closely if eGFR < 30; risk of fluid overload — consider loop diuretic after volume repletion

PBS status ✔ PBS General Benefit

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Zoledronic Acid

Zometa® · Bisphosphonate · Inhibits osteoclast-mediated bone resorption

Adult dose 4 mg IV over ≥ 15 minutes (reduce to 3 mg if eGFR 30–60; avoid if eGFR < 30)

Paediatric dose Not established in myeloma; paediatric oncology dosing as per local protocol

Renal adjustment 3 mg if CrCl 30–60 mL/min; contraindicated CrCl < 30 — use denosumab instead

PBS status ⚠ PBS Authority Required

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Denosumab

Prolia® / Xgeva® · RANK-L inhibitor

Adult dose 60 mg SC 6-monthly (Prolia®) or 120 mg SC every 4 weeks (Xgeva®) in malignancy

Renal adjustment No dose adjustment — preferred agent in eGFR < 30

PBS status ⚠ PBS Authority Required

Direct Tubular Toxicity

Free light chains are freely filtered at the glomerulus and reabsorbed by proximal tubular epithelial cells via megalin/cubilin receptor-mediated endocytosis. Intracellular accumulation triggers:

Activation of NF-κB signalling → pro-inflammatory cytokine release (IL-6, IL-8, TNF-α).
Lysosomal overload and cathepsin-B release → tubular cell apoptosis and necrosis.
Complement activation via the alternative pathway on tubular cell surfaces.
Reactive oxygen species generation and mitochondrial dysfunction.

This mechanism contributes to AKI independently of cast formation and is particularly relevant in patients with modest sFLC elevation but significant tubular injury biomarkers (e.g., elevated urine NGAL).

AL Amyloidosis vs Other Mechanisms

AL Amyloidosis

Systemic AL (immunoglobulin light chain) amyloidosis occurs when misfolded monoclonal light chains — most commonly λ (lambda) — form β-pleated-sheet amyloid fibrils that deposit in organs including the kidney, heart, liver, and peripheral nerves. It is distinct from cast nephropathy and is present in approximately 5–10 % of myeloma patients.

Feature	Cast Nephropathy	AL Amyloidosis	MIDD
Primary lesion	Intratubular light chain casts	Glomerular & vascular amyloid deposits	Glomerular & tubular basement membrane deposits
Typical presentation	Acute kidney injury	Nephrotic syndrome, gradual eGFR decline	Proteinuria, renal impairment, often monoclonal gammopathy
Light chain isotype	κ or λ (often κ)	Mostly λ (λ:κ ~ 3:1)	Mostly κ
Congo-red staining	Negative	Apple-green birefringence	Negative
Biopsy features	Fractured casts, giant cells	Congo-red positive amorphous deposits in mesangium, vessels	PAS-positive linear deposits on GBM / TBM by EM
Ultrastructure (EM)	Dense amorphous casts	Randomly oriented fibrils (8–12 nm)	Powdery electron-dense deposits
Nephrotic-range proteinuria	Uncommon	Common	Common
Cardiac involvement	Rare	Frequent (major prognostic determinant)	Rare

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Diagnostic pitfall: AL amyloidosis may coexist with myeloma. In any myeloma patient with nephrotic-range proteinuria or gradual eGFR decline, AL amyloidosis and MIDD should be actively excluded — sFLC ratio, Congo-red staining, and electron microscopy are essential.

Other Renal Mechanisms in Myeloma

Monoclonal immunoglobulin deposition disease (MIDD): Non-amyloid, Congo-red-negative deposits of light chains (LCDD), heavy chains (HCDD), or both (LHCDD) on glomerular and tubular basement membranes. Produces nodular sclerosing glomerulopathy resembling diabetic nephropathy.
Cryoglobulinaemic glomerulonephritis: Type I cryoglobulins (monoclonal IgG or IgM) can cause membranoproliferative GN. Managed with anti-myeloma therapy and plasma exchange.
Crystal-storing histiocytosis: Rare; intracellular crystal accumulation of monoclonal light chains in histiocytes, occasionally involving the kidney.
Proximal tubular dysfunction (Fanconi syndrome): Light chain-mediated damage to proximal tubule causing glycosuria, aminoaciduria, phosphaturia, and type 2 (proximal) RTA.
Direct plasma cell infiltration: Rare; renal parenchymal infiltration by myeloma cells causing mass lesions and AKI.

Management — Hydration, Myeloma Treatment, Dialysis

1. Supportive Measures & Hydration

Immediate supportive care is critical to limit ongoing renal injury and optimise the chance of renal recovery:

1

Aggressive IV rehydration

0.9 % NaCl at 200–300 mL/h initially; target urine output ≥ 2–3 L/day. Adjust rate based on volume status and cardiac function. Avoid hypotonic fluids.

2

Correct hypercalcaemia

IV normal saline + zoledronic acid (or denosumab if eGFR < 30). Calcitonin for rapid effect in severe cases.

3

Avoid nephrotoxins

Stop NSAIDs, IV iodinated contrast, aminoglycosides, ACE inhibitors/ARBs if haemodynamically unstable.

4

Alkalinise urine (controversial)

Sodium bicarbonate IV (target urine pH > 6.5) to reduce cast formation. Use with caution in hypercalcaemia (may promote calcium-phosphate precipitation). Not universally recommended.

5

Thromboprophylaxis

Enoxaparin 40 mg SC daily (or 20 mg if eGFR < 30) or unfractionated heparin if on haemodialysis. Myeloma carries high VTE risk.

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Never use: NSAIDs, nephrotoxic antibiotics (gentamicin), or IV contrast in myeloma patients with AKI. Ensure any radiological imaging uses low-osmolality or iso-osmolality contrast only when essential, with pre- and post-hydration.

2. Anti-Myeloma Therapy — Rapid FLC Reduction

The primary goal is rapid and sustained reduction of pathogenic serum free light chains. Bortezomib-based regimens produce the fastest FLC responses (median time to best FLC response: 21 days).

First-Line Regimens (Transplant-Ineligible or Transplant-Eligible Induction)

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CyBorD (VCD)

Cyclophosphamide + Bortezomib + Dexamethasone

Bortezomib dose 1.3 mg/m² SC Days 1, 4, 8, 11 (21-day cycle)

Cyclophosphamide dose 500 mg PO weekly or 300 mg/m² IV Day 1 (21-day cycle)

Dexamethasone dose 20 mg PO Days 1, 2, 4, 5, 8, 9, 11, 12 (Cycle 1); reduce to 10 mg from Cycle 2 in elderly / renal impairment

Renal adjustment No bortezomib dose adjustment for renal impairment; reduce cyclophosphamide if eGFR < 30 (dose per local protocol)

PBS status ⚠ PBS Authority Required

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Dara-VTD

Daratumumab + Bortezomib + Thalidomide + Dexamethasone

Daratumumab dose 1 800 mg SC weekly × 6, then 3-weekly × 8, then 4-weekly (or as per PBS authority schedule)

Thalidomide dose 100 mg PO daily; reduce to 50 mg in elderly

Renal adjustment Thalidomide: no renal dose adjustment; monitor for peripheral neuropathy. Daratumumab: no renal adjustment.

PBS status ⛔ PBS Authority Required — Restricted Benefit

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Dara-Rd

Daratumumab + Lenalidomide + Dexamethasone

Lenalidomide dose 25 mg PO Days 1–21 (28-day cycle); adjust for renal impairment (see below)

Renal adjustment eGFR 30–59: 10 mg daily; eGFR < 30 (not on dialysis): 15 mg every 48 h; on dialysis: 5 mg daily post-dialysis

PBS status ⛔ PBS Authority Required — Restricted Benefit

✅

Bortezomib is preferred in myeloma kidney: It is not renally cleared, has rapid onset, and does not require dose adjustment in renal impairment. In Australia, bortezomib is PBS-listed (Authority Required) for newly diagnosed and relapsed myeloma.

3. Plasmapheresis & High Cut-Off Dialysis

The role of plasma exchange (PLEX) to remove circulating FLCs remains uncertain. The largest RCT (Clark et al., 2005) showed no significant benefit of PLEX over standard care, but was underpowered. Meta-analyses suggest a possible trend toward reduced dialysis dependence. Australian practice: PLEX may be considered in severe AKI (eGFR < 15 or dialysis-dependent) with very high sFLC levels (> 10 000 mg/L), in conjunction with anti-myeloma therapy.

High cut-off (HCO) haemodialysis using membranes with a 45–60 kDa molecular weight cut-off can remove FLCs more efficiently than standard HD. The European EuLITE trial demonstrated improved dialysis independence rates with HCO dialysis + bortezomib vs conventional HD + bortezomib. However, HCO dialysis is not currently standard-of-care in Australia and is available only at select tertiary centres as part of clinical research protocols.

4. Renal Replacement Therapy (Dialysis)

Indications for dialysis in myeloma kidney are the same as for other causes of AKI:

Refractory hyperkalaemia (> 6.5 mmol/L despite medical therapy).
Severe metabolic acidosis (pH < 7.1) unresponsive to bicarbonate.
Pulmonary oedema / fluid overload unresponsive to diuretics.
Uraemic symptoms (encephalopathy, pericarditis, intractable nausea).
Refractory hypercalcaemia (> 3.5 mmol/L).

Modality: Intermittent haemodialysis (IHD) is standard. Extended haemodiafiltration (HDF) may offer improved FLC clearance. Continuous renal replacement therapy (CRRT) is used in haemodynamically unstable patients in ICU.

Prognosis on dialysis: With effective anti-myeloma therapy, approximately 20–40 % of dialysis-dependent patients achieve dialysis independence, usually within 2–6 months. Factors predicting renal recovery include early initiation of bortezomib therapy, sFLC reduction ≥ 50 % within 21 days, and shorter duration of dialysis dependence (< 30 days).

⚠️

Dialysis catheter care: Patients with myeloma are immunocompromised and at high risk of catheter-related bloodstream infections. Use subcutaneous tunnelling and strict aseptic technique. Avoid femoral catheters where possible.

5. Monitoring Response

Day 1–3

Initiate IV rehydration, correct hypercalcaemia, start anti-myeloma therapy. Baseline sFLC, calcium, eGFR, U&E, FBC, LDH.

Day 7–14

Repeat sFLC — target ≥ 50 % reduction from baseline. Monitor creatinine trend, fluid balance, electrolytes.

Day 21

Critical assessment point — sFLC reduction ≥ 50 % strongly predicts renal recovery. If not achieved, consider intensifying therapy.

Week 4–6

Assess eGFR trajectory. If improving, continue therapy. If static or worsening, consider renal biopsy to exclude alternative diagnoses.

Month 3–6

Reassess for dialysis independence. Evaluate ongoing need for renal replacement therapy. Transition to maintenance myeloma therapy.

Special Populations

🤰 Pregnancy

General: Myeloma in pregnancy is extremely rare. Diagnosis requires coordination between haematology, obstetrics, nephrology, and neonatology.

Bortezomib: Category D — teratogenic. Avoid in pregnancy unless life-threatening disease.

Lenalidomide / Thalidomide: Absolutely contraindicated — severe teratogenicity. Pregnancy prevention programme mandatory.

Dexamethasone: May be used short-term for hypercalcaemia; avoid prolonged courses.

Dialysis: Safe in pregnancy; increase frequency to maintain urea < 15 mmol/L.

👶 Paediatrics

General: Multiple myeloma is exceedingly rare in children (< 1 % of all myeloma cases). Paediatric cases should be managed at a specialist paediatric oncology centre.

Bortezomib: Limited paediatric data; used in paediatric leukaemia protocols. Dose: 1.3 mg/m² SC.

Renal biopsy: More readily pursued in children when diagnosis is uncertain.

👴 Elderly (> 75 years)

Epidemiology: Median age at myeloma diagnosis is ~70 years. Most patients are not transplant-eligible.

Dexamethasone: Reduce dose (20 mg rather than 40 mg) to minimise steroid toxicity — hyperglycaemia, infection risk, psychosis.

Thalidomide: Increased peripheral neuropathy and VTE risk; consider dose reduction to 50 mg.

Frailty assessment: Use IMWG frailty score to guide treatment intensity.

Dialysis: Consider patient goals of care; conservative management may be appropriate in frail patients.

🩺 Renal Impairment (eGFR < 30 / Dialysis)

Bortezomib: No dose adjustment required.

Cyclophosphamide: Reduce dose by 25–50 % if eGFR < 30.

Lenalidomide: Significant dose reduction required (see drug card above).

Daratumumab: No renal dose adjustment.

Bisphosphonates: Zoledronic acid 3 mg if eGFR 30–60; avoid if eGFR < 30 — switch to denosumab.

Dialysis: Use post-dialysis dosing for renally cleared drugs. Monitor drug levels where available.

🫁 Hepatic Impairment

Bortezomib: Hepatic impairment increases exposure — use with caution; no specific dose recommendation.

Thalidomide: Primarily hepatically metabolised; use with caution in significant liver disease.

Daratumumab: No hepatic dose adjustment.

🦠 Immunocompromised

Infection risk: Myeloma patients are hypogammaglobulinaemic and immunosuppressed from therapy. High risk of bacterial, viral (VZV reactivation), and fungal infections.

Antimicrobial prophylaxis: Aciclovir 400 mg PO BD (HSV/VZV prophylaxis) while on bortezomib. Consider co-trimoxazole for PJP prophylaxis if prolonged steroids. IVIg replacement if IgG < 4 g/L with recurrent infections.

Vaccination: Annual influenza, pneumococcal (Prevenar 13 then Pneumovax 23), COVID-19. Avoid live vaccines.

Sepsis: Treat aggressively — myeloma patients with sepsis and AKI have high mortality.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience a higher incidence of myeloma compared with non-Indigenous Australians, with evidence of later-stage presentation, higher rates of renal impairment at diagnosis, and poorer survival outcomes. Myeloma kidney in this population is compounded by the high background prevalence of chronic kidney disease (CKD), diabetes, and limited access to specialist haematology and nephrology services in regional and remote areas.

Incidence & burden

Age-standardised incidence of myeloma is approximately 1.5–2× higher in Aboriginal and Torres Strait Islander peoples. CKD prevalence is 2–3× higher, compounding renal risk.

Diagnostic delay

Later presentation with more advanced disease — higher rates of renal failure, anaemia, and hypercalcaemia at diagnosis. Contributing factors include reduced access to primary care, delayed pathology investigation, and systemic barriers.

Remote & rural access

Specialist haematology and nephrology services are concentrated in major cities. Patients in remote communities may require aeromedical retrieval for dialysis initiation or bortezomib therapy. Telehealth and visiting specialist outreach are essential.

Dialysis access

Aboriginal and Torres Strait Islander peoples are disproportionately represented in dialysis populations. Community-based dialysis units and patient-assisted travel schemes (PATS) are critical for access. Home dialysis is often not feasible in remote settings due to infrastructure limitations.

Cultural safety

Engagement with Aboriginal Health Workers and Aboriginal Liaison Officers is essential. Incorporate cultural practices, family-centred decision-making, and language-appropriate communication. Respect Sorry Business and cultural obligations.

Medication access

PBS authority applications may require specialist sign-off that is difficult to obtain remotely. Ensure medication supply chains (cold-chain for bortezomib SC) are viable in the patient's location. Coordinate with local hospital pharmacies.

Recommended approach

Early screening for myeloma in unexplained CKD (check sFLC, SPEP). Use shared-care models with local Aboriginal Medical Services. Prioritise culturally safe nephrology and haematology pathways via RFDS, PATS, and telehealth. Engage with RHDAustralia guidelines for chronic disease management.

📚 References

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2. Dimopoulos MA, Sonneveld P, Leung N, et al. International Myeloma Working Group recommendations for the diagnosis and management of myeloma-related renal impairment. Journal of Clinical Oncology. 2016;34(13):1544–1557.
3. Clark WF, Stewart AK, Rock GA, et al. Plasma exchange when myeloma presents as acute renal failure: a randomized, controlled trial. Annals of Internal Medicine. 2005;143(11):777–784.
4. Hutchison CA, Bradwell AR, Cook M, et al. Treatment of acute renal failure secondary to multiple myeloma with chemotherapy and extended high cut-off hemodialysis. Clinical Journal of the American Society of Nephrology. 2009;4(4):745–754.
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6. Australian Institute of Health and Welfare (AIHW). Cancer data in Australia: Myeloma. Canberra: AIHW; 2023. Available from: https://www.aihw.gov.au/reports/cancer/cancer-data-in-australia
7. RACGP. Red Book — Investigation of suspected monoclonal gammopathy. In: Guidelines for Preventive Activities in General Practice. 9th ed. Melbourne: RACGP; 2016.
8. Rajkumar SV, Dimopoulos MA, Palumbo A, et al. International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma. The Lancet Oncology. 2014;15(12):e538–e548.
9. Rajkumar SV, Jacobus S, Callander NS, et al. Lenalidomide plus high-dose dexamethasone versus lenalidomide plus low-dose dexamethasone as initial therapy for newly diagnosed multiple myeloma: an open-label randomised controlled trial. The Lancet Oncology. 2010;11(1):29–37.
10. Facon T, Kumar S, Plesner T, et al. Daratumumab plus lenalidomide and dexamethasone for untreated myeloma. New England Journal of Medicine. 2019;380(22):2104–2115.
11. Morie A, Gertz MA, Dispenzieri A. End-stage renal disease in AL amyloidosis: clinical characteristics and outcomes. Blood Cancer Journal. 2021;11:152.
12. RHDAustralia. National Guide to a Preventive Health Assessment for Aboriginal and Torres Strait Islander People. 3rd ed. Darwin: RACGP; 2018.
13. Singhal S, Mehta J, Desikan R, et al. Antitumor activity of thalidomide in refractory multiple myeloma. New England Journal of Medicine. 1999;341(21):1565–1571.
14. Corso A, Barbarano L, Mangiacavalli S, et al. Bortezomib plus dexamethasone can improve stem cell collection and overcome the need for additional chemotherapy before autologous transplant in patients with myeloma. Leukemia & Lymphoma. 2010;51(2):236–242.