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Hematology›Condition·Updated Jul 11, 2026·v1

Amyloidosis

Amyloidosis is a protein misfolding disease with systemic organ involvement. AL type is the most common and requires hematologic management. Diagnosis depends on tissue biopsy with Congo red staining and precise typing. Treatment for AL is daratumumab-based chemotherapy, with early deep response predicting survival. Cardiac involvement is the main prognostic factor.

High Evidence309 references·2,138 words·9 min read·v1
amyloidosisAL amyloidosisATTR amyloidosismonoclonal gammopathycardiac amyloidosishematologyplasma cell disorder

Quick Reference

RxDrug of choiceDaratumumab + cyclophosphamide + bortezomib + dexamethasone (Dara-CyBorD)
AltAlternativesBortezomib-melphalan-dexamethasone, lenalidomide-based regimens, BCMA-directed therapies (CAR-T, bispecific antibodies)
⊘AvoidNon-dihydropyridine calcium channel blockers (diltiazem, verapamil) in cardiac amyloidosis; high-dose melphalan/ASCT in unselected patients; digoxin; avoid bortezomib in NYHA III/IV HF without caution
DxTest of choiceTissue biopsy with Congo red staining and laser microdissection/mass spectrometry (LC-MS/MS) for amyloid typing
ScKey scoreMayo 2012 staging system (NT-proBNP, troponin T, dFLC) - stages I-IV with median OS 94.1 to 5.8 months
→When to referTo hematology at diagnosis of AL amyloidosis; to cardiology for suspected cardiac amyloidosis; to nephrology for renal involvement; to neurology for neuropathy
Early diagnosis and deep hematologic response (≥VGPR) within 3 months are the strongest predictors of survival; Dara-CyBorD is the standard of care for AL; cardiac involvement determines prognosis.
Amyloidosis is a heterogeneous group of diseases characterized by extracellular deposition of insoluble fibrillar proteins derived from misfolded precursors. Accurate identification of the fibril type is paramount as treatment differs fundamentally. This summary covers classification, pathophysiology, clinical presentation, diagnosis, staging, and management, focusing on AL, ATTR, and AA types.

Overview and Recommendations

Background

  • •Amyloidosis is a heterogeneous group of diseases defined by extracellular deposition of insoluble fibrils from misfolded precursor proteins. The most common systemic type is AL (immunoglobulin light chain) amyloidosis, with an incidence of 8-12 per million, followed by ATTR (transthyretin) and AA (serum amyloid A).
  • •AL amyloidosis originates from a small clonal plasma cell population, often harboring t(11;14) (50% of cases), that secretes amyloidogenic monoclonal light chains. The bone marrow plasma cell burden is typically low but can overlap with multiple myeloma.
  • •Cardiac involvement dominates prognosis: 60-75% of AL patients have cardiac amyloidosis, presenting as HFpEF with restrictive physiology. Untreated median survival is 12-18 months; modern therapy achieves 5-year survival >70% with deep hematologic response.
  • •Other major types: ATTRwt (wild-type, older men, carpal tunnel syndrome, cardiomyopathy), ATTRv (hereditary, neuropathy/cardiomyopathy), and AA (secondary to chronic inflammation, primarily renal). Accurate typing dictates treatment, making mass spectrometry the gold standard.
  • •Pathophysiology involves misfolding of normally soluble proteins into beta-pleated sheet fibrils; oligomeric intermediates are the primary cytotoxic species, causing oxidative stress and organ dysfunction even before fibril deposition.

Evaluation

  • •Suspect AL amyloidosis in patients >50 years with unexplained nephrotic syndrome, restrictive cardiomyopathy, peripheral neuropathy, hepatomegaly, macroglossia, or periorbital purpura. Also consider ATTRwt in older men with carpal tunnel syndrome preceding heart failure.
  • •Ask about exertional dyspnea, orthopnea, edema, weight loss, early satiety, orthostatic dizziness, paresthesias, and family history of neuropathy or cardiomyopathy.
  • •Examine for orthostatic hypotension, jugular venous distension, peripheral edema, hepatomegaly, macroglossia, periorbital purpura, and length-dependent sensory loss with diminished ankle reflexes.
  • •Order serum immunofixation, urine immunofixation, and serum free light chain (FLC) assay as initial screen. The combination detects 92% of AL cases. Also obtain NT-proBNP and cardiac troponin for staging.
  • •Perform transthoracic echocardiography with global longitudinal strain and cardiac MRI with T1 mapping to assess cardiac involvement. Fat pad aspirate and bone marrow biopsy with Congo red staining diagnose amyloid; mass spectrometry (LC-MS/MS) is the gold standard for typing.
  • •Apply Mayo 2012 staging: NT-proBNP ≥1800 pg/mL, troponin T ≥0.025 ng/mL, dFLC ≥18 mg/dL. Stage IIIb (NT-proBNP >8500 ng/L) identifies ultra-high risk with median OS 9 months despite therapy.
  • •Consider genetic testing for TTR mutations in patients with atypical features, no clonal dominance, or family history. Cardiac biopsy may be needed if non-invasive tests are inconclusive.
  • •Assess renal function (eGFR, proteinuria) and coagulation profile (fibrinogen, D-dimer) due to bleeding risk from hyperfibrinolysis and factor X deficiency.

Management

  • •Initiate daratumumab-CyBorD for newly diagnosed AL. Daratumumab 1800 mg SC weekly cycles 1-2, then q2w cycles 3-6, then q4w up to 2 years. CyBorD: bortezomib 1.3 mg/m² SC, cyclophosphamide 300 mg/m² PO/IV, dexamethasone 40 mg PO/IV on days 1,8,15,22 of a 28-day cycle for 6 cycles.
  • •Titrate doses: reduce bortezomib for neuropathy, cyclophosphamide for renal impairment (CrCl 10-50: 75% dose), dexamethasone to 20 mg weekly in frail patients to avoid volume overload and infections.
  • •Monitor hematologic response after each cycle: CR requires normal FLC ratio and negative immunofixation; VGPR is dFLC <40 mg/L; PR is >50% dFLC reduction. Aim for VGPR or better within 3 months.
  • •Assess cardiac response: NT-proBNP decrease >30% and >300 ng/L defines cardiac response. Graded criteria (cardiac CR, VGPR, PR, NR) predict 5-year survival (93%, 79%, 65%, 33% respectively).
  • •For ATTR cardiomyopathy, vutrisiran 25 mg SC q12w or patisiran 0.3 mg/kg IV q3w. In octogenarians, tafamidis reduces all-cause mortality (HR 0.51). For ATTR polyneuropathy, inotersen 300 mg SC weekly.
  • •For AA, aggressively control underlying inflammation to achieve SAA <10 mg/L; target <4 mg/L for optimal survival.
  • •What NOT to do: avoid ASCT as first-line in unselected patients; avoid dexamethasone 40 mg beyond 6 cycles; avoid bortezomib in NYHA III/IV HF without caution; avoid digoxin in cardiac amyloidosis.
  • •When to refer: to hematology for AL; to cardiology for advanced cardiac imaging; to nephrology for renal biopsy or dialysis; to neurology for neuropathy.
  • •For acute bleeding, tranexamic acid 1 g IV q8h (adjust for eGFR <30). For AF with cardiac amyloidosis, use DOACs over warfarin; LAAC is alternative for high bleeding risk.
  • •Escalation: if no PR after 2-3 cycles, switch to bortezomib-melphalan-dexamethasone, lenalidomide-based therapy, or BCMA-directed therapy. Anti-BCMA CAR-T achieves 94% ORR but with high early mortality in advanced cardiac disease.
  • •Discharge criteria: hemodynamic stability, controlled heart failure, no active bleeding, plan for ongoing chemotherapy. Re-stage at 3 and 6 months; stage migration predicts worse survival.

Board Review — High Yield

  • •Congo red stain - apple-green birefringence under polarized light is diagnostic for amyloid.
  • •t(11;14) - most common cytogenetic abnormality in AL, present in ~50%, associated with adverse prognosis and targetable with venetoclax.
  • •Mayo 2012 staging - uses NT-proBNP, troponin T, and dFLC to stratify prognosis; stage IV median OS 5.8 months.
  • •Dara-CyBorD - standard first-line therapy for AL; ANDROMEDA trial showed CR 53% vs 18% and reduced organ deterioration (HR 0.58).
  • •Mass spectrometry - gold standard for amyloid typing, sensitivity 98-100%; immunofixation is complementary.
  • •ATTRwt - often misdiagnosed as HFpEF; consider in older men with carpal tunnel syndrome and thick LV walls.
  • •SAA target - in AA, maintain SAA <4 mg/L for optimal survival; risk of death 18-fold higher if SAA >155 mg/L.
  • •Hyperfibrinolysis - dominant bleeding mechanism in AL; treat with tranexamic acid 1 g IV q8h.
  • •DOACs preferred - for atrial fibrillation in cardiac amyloidosis over warfarin; meta-analysis shows reduced thromboembolism without increased major bleeding.
  • •Cardiac response - NT-proBNP decrease >30% and >300 ng/L defines cardiac response; 5-year OS 93% for cardiac CR vs 33% for no response.

Deep Dive — Evidence Details

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