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Nephrology Education Series

Systemic AL Amyloidosis with Cardiac and Renal Involvement: Inpatient Case Report and Clinical Framework

Andrew Bland, MD, FACP, FAAP UICOMP · UDPA · Butler COM 2026-03-06 19 min read

Systemic AL Amyloidosis with Cardiac and Renal Involvement

Inpatient Case Report and Clinical Decision Framework

Medical Associates Department of Nephrology | University of Illinois College of Medicine at Peoria | Butler College of Osteopathic Medicine

Andrew Bland, MD, FACP, FAAP

Executive Summary

Key Points - A patient presenting with massive albuminuria (protein/Cr 7.9), hypoalbuminemia, 3+ edema, and worsening renal function should prompt immediate evaluation for plasma cell dyscrasia regardless of the absence of CRAB features. - Free light chains reported as kappa 17.4 / lambda 3.24 / ratio 5.37 in mg/dL correspond to kappa 174 mg/L and lambda 32.4 mg/L in standard units — both the ratio and the absolute kappa are elevated above the renal-adjusted reference range, confirming a true clonal kappa-dominant process, not a CKD artifact (1,2). - BNP 4,598 pg/mL and troponin I 59 ng/L with echocardiographic LVH, impaired relaxation, and EF 45% meet criteria for advanced cardiac involvement. This is an oncologic and cardiorenal emergency (3). - The differential diagnosis in a kappa-dominant FLC pattern with nephrotic-range albuminuria is led by Light Chain Deposition Disease (LCDD), followed by kappa AL amyloidosis; kidney biopsy is the only test that resolves this distinction (4). - Daratumumab, bortezomib, cyclophosphamide, and dexamethasone (Dara-VCd) is the FDA-approved standard of care for newly diagnosed AL amyloidosis, established in the phase 3 ANDROMEDA trial (5). - Multi-disciplinary care involving nephrology, cardiology, and hematology/oncology with amyloid expertise is required within 24 hours of biomarker confirmation.

1. Case Presentation

1.1 Presenting Clinical Data

The patient presented with a clinical syndrome characterized by progressive renal insufficiency and volume overload in the setting of prior evaluation by an outside oncologist for severe anemia. The following data were collected at the time of nephrology involvement:

Admission data: - Creatinine: 2.5 mg/dL (rising to 4.0 with aggressive diuresis) - Bicarbonate: 21 mEq/L (mild metabolic acidosis) - Albumin: 3.1 g/dL - Hemoglobin: 8.2 g/dL (prior range 7–9 g/dL, worked up by outside oncology) - Platelets: 192 × 10³/µL (normal) - Calcium: 8.8 mg/dL (normal) - Edema: 3+ bilateral - Urine albumin-to-creatinine ratio: >4 - Urine protein-to-creatinine ratio: 7.9 - Volume response: Minimal fluid removed with aggressive loop diuretic therapy; creatinine worsened

Subsequent evaluation: - Free light chain kappa: 17.4 mg/dL (= 174 mg/L) - Free light chain lambda: 3.24 mg/dL (= 32.4 mg/L) - κ/λ ratio: 5.37 - Echocardiogram: EF 45%, LVH, impaired relaxation (Grade I–II diastolic dysfunction) - BNP: 4,598 pg/mL - Troponin I: 59 ng/L - Monoclonal evaluation: Pending at time of nephrology consultation (no prior SPEP, immunofixation, or FLC had been obtained)

1.2 Initial Clinical Impression

The combination of massive albuminuria, hypoalbuminemia, preserved platelet count, normal calcium, and absent bone pain placed this patient outside the classical CRAB (hypercalcemia, renal failure, anemia, bone lesions) framework of symptomatic multiple myeloma. The outside oncologic workup had not specifically addressed plasma cell dyscrasia with renal-organ manifestation. Nephrology involvement reframed the presentation from “anemia workup with CKD” to a potential monoclonal gammopathy of renal significance (MGRS) or systemic AL amyloidosis.

2. Proteinuria Phenotyping — Glomerular Disease, Not Cast Nephropathy

The urine protein/Cr of 7.9 with albumin/Cr >4 establishes that the proteinuria is albumin-predominant and glomerular in origin. This is the first and most diagnostically decisive point in the case.

Differential by proteinuria phenotype:

Feature Cast Nephropathy (Myeloma Kidney) Glomerular Amyloid / LCDD
Primary pathology Distal tubular casts Mesangial/GBM fibril or non-fibrillar deposits
Proteinuria type Bence Jones (light chains) Albumin-dominant
Urine dipstick Trace or negative (misses light chains) 3-4+ positive
Serum albumin Usually preserved Low — hypoalbuminemia
FLC threshold Typically >500–1,500 mg/L Often lower (<500 mg/L)
Volume physiology Variable Oncotic-driven underfilling

Cast nephropathy presents with predominantly tubular proteinuria and low albumin excretion, often with a trace-positive or negative dipstick despite elevated total protein, because standard urine dipstick detects albumin rather than immunoglobulin light chains. This patient’s pattern — heavy dipstick-positive, albumin-rich proteinuria with hypoalbuminemia and massive edema — is the inverse of that phenotype and confirms glomerular rather than tubular injury as the primary lesion (6).

Clinical Pearl: When a patient with a suspected plasma cell dyscrasia has 3-4+ dipstick proteinuria with hypoalbuminemia and edema, the lesion is glomerular (amyloid, LCDD, or membranoproliferative pattern), not tubular cast nephropathy. Aggressive loop diuresis without this distinction risks AKI from intravascular depletion in a patient who cannot refill from the interstitium due to insufficient oncotic pressure.

3. Free Light Chain Interpretation in Renal Failure

3.1 Unit Conversion — A Critical Potential Error Source

Serum free light chains are measured and reported in mg/L at most reference laboratories, including Mayo Clinic. When values are reported in mg/dL (as in this case), conversion is mandatory before clinical interpretation:

1 mg/dL = 10 mg/L

Analyte Reported (mg/dL) Converted (mg/L) Standard Reference (mg/L)
Kappa (κ) 17.4 174 3.3–19.4
Lambda (λ) 3.24 32.4 5.7–26.3
κ/λ Ratio 5.37 5.37 0.26–1.65

The kappa of 174 mg/L is approximately 9× the upper limit of normal. The lambda of 32.4 mg/L is only mildly above the standard reference upper limit, and this mild elevation is entirely attributable to reduced renal clearance (kappa clears faster than lambda in normal renal function; impaired GFR raises both proportionally, but the smaller monomer kappa typically rises more in CKD as a non-clonal artifact).

3.2 Renal-Adjusted Reference Range

The standard κ/λ FLC reference range (0.26–1.65) was established in patients with normal renal function. In CKD, differential renal clearance of κ vs. λ light chains alters the ratio independent of clonality. The extended reference range for renal impairment is approximately 0.37–3.1. This patient’s ratio of 5.37 exceeds the renal-adjusted upper limit of 3.1, confirming a true clonal process rather than a CKD artifact (1,2).

3.3 Delta FLC (dFLC) Calculation

The dFLC (involved minus uninvolved FLC) = 174 − 32.4 = 141.6 mg/L

The Mayo 2012 revised staging system uses a dFLC threshold of 180 mg/L (approximately 18 mg/dL) as a high-risk marker. This patient’s dFLC of 141.6 mg/L falls below that threshold — but critically, this is almost certainly an underestimate. With protein/Cr of 7.9, the patient is excreting massive quantities of kappa light chain in the urine daily, reducing the serum concentration relative to actual clone production. The measured dFLC should be interpreted as a floor, not a ceiling.

⚠️ Warning: In patients with heavy nephrotic-range proteinuria, serum FLC levels are spuriously lowered by urinary losses. The degree of clonal disease burden is likely greater than the serum FLC values imply. Do not use the dFLC alone to assess clone burden in this setting.

4. Differential Diagnosis — Kappa-Dominant FLC Pattern

The kappa-dominant FLC pattern changes the differential hierarchy compared to a lambda-dominant presentation. Lambda accounts for approximately 70–75% of AL amyloidosis cases, while kappa predominates in multiple myeloma (approximately 60–65%). A kappa-dominant low-burden clonal process with nephrotic-range albuminuria and absent CRAB features raises the following diagnoses in order of probability:

1. Light Chain Deposition Disease (LCDD) — Leading Diagnosis LCDD most commonly involves kappa light chains (approximately 60–70% of LCDD cases), producing a non-fibrillar, Congo red–negative glomerular deposit along the GBM and mesangium. Presentation is nephrotic-range albuminuria with preserved or mildly reduced GFR and absent CRAB features — precisely this patient’s profile at baseline presentation. The Vκ4 and Vλ6 germline gene subsets are overrepresented in LCDD. LCDD deposits are non-fibrillar and will be Congo red negative on biopsy, differentiating LCDD from AL amyloidosis.

2. Kappa AL Amyloidosis — Close Second Kappa AL amyloidosis accounts for approximately 25–30% of AL cases. Kappa AL tends to have more hepatic involvement compared to lambda AL (which is more associated with cardiac and renal organ tropism), though renal amyloid deposition does occur. Congo red staining of kidney biopsy will be positive with apple-green birefringence under polarized light if this is the diagnosis.

3. MGRS-class disease — Broadest Category Either of the above may represent a Monoclonal Gammopathy of Renal Significance (MGRS) — renal disease caused by a clonal immunoglobulin that does not meet criteria for overt myeloma. A nephrologist who identifies a monoclonal protein in the setting of unexplained renal disease should not assume the paraprotein is an innocent MGUS simply because the M-protein is small and the marrow involvement is <10%. Renal biopsy is essential to determine whether the monoclonal protein is directly causing renal injury (7).

SLiM Myeloma-Defining Criteria Assessment:

The involved/uninvolved FLC ratio criterion for a myeloma-defining biomarker event requires ≥100 (kappa direction). This patient’s ratio of 5.37 does not meet that threshold. This does not diminish the urgency of evaluation; MGRS-class disease causes dialysis-driving renal failure from clones that by definition do not qualify as myeloma.

Clinical Pearl: Do not wait for a myeloma-defining event to pursue tissue diagnosis. In the presence of confirmed clonal FLC with heavy glomerular proteinuria, the clone is causing organ-level injury and requires treatment regardless of whether MM criteria are formally met.

5. Cardiac Evaluation — Confirmed Advanced Involvement

5.1 Biomarker Staging

Biomarker Patient Value Mayo 2004 Threshold Mayo 2004 Stage
BNP 4,598 pg/mL >81 pg/mL (BNP equivalent) Positive
Troponin I (hs) 59 ng/L >54 ng/L (hs-TnI equivalent) Positive
Overall Stage Both positive — Stage III

The Mayo 2004 cardiac staging system established that both biomarker elevation (Stage III) carries a historically poor median survival of approximately 3.5–4.1 months without effective therapy (3). The patient’s BNP of 4,598 pg/mL is markedly elevated. Using the BNP-adapted staging system (BNP threshold of 81 pg/mL), cardiac involvement is unequivocal (8).

An important caveat: this patient has a creatinine of 4.0 mg/dL. Natriuretic peptides are renally cleared, and NT-proBNP in particular rises as a function of reduced GFR. However, a BNP of 4,598 pg/mL far exceeds what renal failure alone produces. Published data suggest that in impaired renal function (CKD Stage III+), BNP thresholds for cardiac amyloid involvement shift to approximately 427 pg/mL — still orders of magnitude below this patient’s value. The biomarker elevation is cardiac, not purely renal (8).

5.2 Echocardiographic Reinterpretation

The echocardiogram showing EF 45%, LVH, and impaired relaxation was initially framed as hypertensive heart disease. With confirmed Stage III cardiac biomarker elevation, this interpretation requires revision:

  • EF 45% in cardiac amyloidosis does not represent mild systolic dysfunction — it represents the transition point where systolic reserve is becoming exhausted. Early cardiac amyloidosis presents with preserved EF; declining EF below 50% reflects progression into the systolic failure phase.
  • “LVH” in amyloidosis is infiltrative pseudohypertrophy — amyloid fibrils depositing in the myocardial interstitium — not true myocyte hypertrophy driven by pressure overload. These walls appear thick but are physiologically hostile: stiff, non-compliant, and dependent on elevated filling pressures to maintain stroke volume.
  • The echocardiogram should be re-read with a dedicated amyloid protocol including: posterior wall + septal thickness, mitral annular velocity (e’), E/e’ ratio, and most importantly global longitudinal strain (GLS) with apical sparing pattern. The relative apical sparing pattern on strain imaging (Bull’s-eye map) is highly specific for cardiac amyloidosis (sensitivity and specificity both exceeding 80%).

⚠️ Warning: A patient with suspected cardiac amyloidosis and EF 45% has already lost significant systolic reserve. Standard heart failure medications that reduce preload (aggressive diuretics), afterload (ACE-inhibitors, ARBs), or heart rate (beta-blockers, non-dihydropyridine calcium channel blockers) may be poorly tolerated or harmful. Cardiology co-management with amyloid expertise is required before titrating any cardiac medications.

5.3 The European IIIB Substage

The European modification of the Mayo staging system subdivides Stage III into IIIA (NT-proBNP 332–8,500 ng/L or BNP equivalent) and IIIB (NT-proBNP >8,500 ng/L). BNP and NT-proBNP are different molecules and not interchangeable by simple ratio, but a BNP of 4,598 pg/mL corresponds to a very high-risk profile. Whether this patient meets IIIB criteria requires NT-proBNP confirmation. Stage IIIB disease carries a median survival of approximately 5 months — the extreme high-risk category where speed of hematologic response is the dominant modifiable outcome predictor.

6. Renal Staging (Palladini 2014 System)

The Palladini renal staging system stratifies risk of progression to dialysis using two thresholds: eGFR <50 mL/min/1.73m² and 24-hour proteinuria >5 g/day (9).

Risk Factor Patient Status
eGFR <50 mL/min/1.73m² YES — Cr 4.0, eGFR estimated 15–20 mL/min
Proteinuria >5 g/day YES — Protein/Cr 7.9, consistent with >15–20 g/day
Renal Stage Stage III (both adverse criteria present)

Patients with Palladini Renal Stage III have a 60–85% probability of requiring dialysis within 3 years at diagnosis; this patient is presenting at Palladini Stage III with an acutely rising creatinine (9). Combined cardiac Stage III and renal Stage III represents the highest-burden systemic AL amyloidosis presentation.

Clinical Pearl: The 5-year cumulative incidence of renal replacement therapy for Stage III patients in revised staging models approaches 51%. This does not mean dialysis is inevitable — rapid and deep hematologic response to Dara-VCd can halt amyloid production and allow gradual clearance of fibril deposits. However, the window for meaningful renal recovery is time-dependent and narrows with further injury.

7. The Diuresis Problem — Cardiorenal Physiology of Amyloidosis

7.1 Why Diuresis Failed

Creatinine rising from 2.5 to 4.0 during aggressive loop diuretic therapy with minimal fluid removal is the pathognomonic hemodynamic signature of advanced cardiorenal amyloidosis:

  1. Oncotic failure: With albumin at 3.1 g/dL, plasma oncotic pressure is insufficient to draw interstitial edema fluid back into the intravascular compartment. Diuresis removes intravascular volume faster than it can be refilled.
  2. Stiff ventricle dependence on preload: The amyloid-infiltrated left ventricle requires elevated filling pressures to maintain stroke volume. Reduction of preload through diuresis drops cardiac output, reducing renal perfusion.
  3. Tubular light chain toxicity: Loop diuretics concentrate tubular fluid, potentially increasing tubular light chain concentration and promoting Tamm-Horsfall protein binding — the same mechanism driving cast nephropathy. In a patient with heavy kappa light chain burden, aggressive furosemide may simultaneously worsen tubular injury.

7.2 Right Heart Catheterization — The Case For and Against

The diagnostic question (is this cardiac amyloidosis?) is answered. RHC is not needed to establish the diagnosis.

The management question (how do we safely manage volume?) remains open. RHC is justified to define: - Cardiac output and index (CI <2.0 L/min/m² confirms low-output state driving pre-renal AKI) - Right atrial pressure and PCWP (defining safe operating filling pressures) - Pulmonary vascular resistance (relevant if cardiac transplant consideration arises later)

If CI is markedly reduced, the appropriate response is not diuretic escalation but rather a shift to slow ultrafiltration or continuous renal replacement therapy with carefully defined net negative fluid removal rates that the ventricle can tolerate.

⚠️ Warning: Screen for Factor X deficiency before any invasive procedure. Systemic AL amyloid fibrils adsorb and sequester clotting Factor X, producing an acquired Factor X deficiency in up to 14% of AL amyloidosis patients. This causes procedure-related hemorrhage risk independent of platelet count and INR. A Factor X activity level should be sent before kidney biopsy or RHC.

8. Tissue Diagnosis — Required, Not Optional

Kidney biopsy is necessary to differentiate between the entities with identical laboratory profiles but distinct pathology and treatment nuance:

Finding AL Amyloidosis LCDD
Congo red stain Positive — apple-green birefringence under polarized light Negative
Electron microscopy Fibrils 8–12 nm, randomly arranged Non-fibrillar, organized, granular deposits
Immunofluorescence Restricted light chain (Congo red confirms fibril) Linear kappa or lambda staining along GBM
Mass spectrometry amyloid typing Required — confirms AL vs. AA vs. ATTR N/A
Treatment implication Dara-VCd Clone-directed therapy (similar but biopsy defines urgency)

Abdominal fat pad biopsy is a less invasive alternative with approximately 60–80% sensitivity for systemic AL amyloidosis. It can be performed bedside and may yield a positive result while awaiting definitive kidney biopsy, or if kidney biopsy is deferred due to coagulopathy concerns.

Bone marrow biopsy is required for clone characterization, cytogenetics, and assessment of plasma cell percentage — all of which define transplant eligibility and inform chemotherapy selection.

9. Treatment Framework

9.1 Standard of Care: Dara-VCd

The ANDROMEDA phase 3 randomized controlled trial established daratumumab, bortezomib, cyclophosphamide, and dexamethasone (Dara-VCd) as the first FDA-approved therapy for newly diagnosed AL amyloidosis (January 2021). In 388 patients, the addition of subcutaneous daratumumab to VCd resulted in a hematologic complete response rate of 53.3% versus 18.1% in the VCd-alone arm, with significantly superior survival free from major organ deterioration or hematologic progression (5).

Key ANDROMEDA eligibility nuances relevant to this patient: - Patients with cardiac Stage IIIB (NT-proBNP >8,500 ng/L) were excluded from ANDROMEDA — this patient’s NT-proBNP equivalent needs verification - eGFR ≥20 mL/min was required — this patient’s current eGFR is borderline - Symptomatic multiple myeloma (meeting CRAB criteria) was an exclusion

These nuances underscore why a hematologist with specific AL amyloidosis expertise — not general oncology — is required for treatment planning. The dosing of bortezomib and cyclophosphamide, the management of fluid overload from IV infusions, and the decision-making around early mortality risk all require specialized experience.

9.2 Three Pillars of Outcome Improvement

Three pillars have been identified for improving AL amyloidosis outcomes: 1. Early disease recognition before advanced organ damage — partially failed here (delayed diagnosis with Cr already 4.0 and cardiac Stage III) 2. Rapid and deep hematologic response — the dominant modifiable variable going forward 3. Comprehensive multi-specialty supportive care — cardiology, nephrology, hematology working in parallel, not sequentially

9.3 Supportive Care Considerations

  • Diuresis: Hold or dramatically reduce; if volume management is mandatory, consider ultrafiltration after RHC-guided hemodynamic assessment.
  • Albumin infusions: Physiologically intuitive but not proven to improve outcomes; may precipitate pulmonary edema if cardiac function is compromised — use with caution and only with cardiac monitoring.
  • Avoid: ACE inhibitors, ARBs, beta-blockers, non-dihydropyridine calcium channel blockers (poorly tolerated with amyloid cardiomyopathy).
  • Coagulopathy surveillance: Factor X level, CBC, INR before procedures.
  • Renal support: If creatinine continues to rise and the patient cannot tolerate adequate fluid removal for pulmonary protection, early renal replacement therapy planning should begin.

10. Priority Diagnostic and Management Checklist

Immediate (within 24 hours): - [ ] Hematology/oncology consultation — amyloid-experienced center preferred - [ ] Cardiology consultation with dedicated amyloid echo re-read (GLS, strain imaging) - [ ] NT-proBNP to complement BNP (define IIIA vs. IIIB status) - [ ] Factor X activity level (pre-procedure coagulopathy screen) - [ ] Serum immunofixation + urine immunofixation (characterize M-protein isotype) - [ ] 24-hour urine protein (formal Palladini renal staging) - [ ] Alkaline phosphatase (hepatic amyloid screening)

Within 48–72 hours: - [ ] Bone marrow biopsy (clone characterization, cytogenetics, plasma cell percentage) - [ ] Kidney biopsy (or fat pad biopsy as interim) - [ ] RHC consideration (hemodynamic-guided volume management) - [ ] Echocardiogram with dedicated amyloid protocol including GLS - [ ] Nerve conduction study if neuropathic symptoms present - [ ] Consider cardiac MRI if echocardiogram is technically limited

Pending test to follow specifically: - [ ] Serum and urine immunofixation — characterize heavy/light chain of M-protein - [ ] MASS-FIX (if accessible via Mayo) for superior sensitivity to conventional SPEP

11. Summary

This case represents systemic AL amyloidosis (or LCDD — tissue biopsy will distinguish) with confirmed multi-organ involvement. The key diagnostic milestones and their clinical implications are:

The proteinuria phenotype (albumin/Cr >4, protein/Cr 7.9, hypoalbuminemia, 3+ edema) established glomerular disease and excluded cast nephropathy as the primary lesion. The kappa FLC of 174 mg/L with ratio 5.37 above the renal-adjusted reference range confirmed a clonal kappa-dominant plasma cell dyscrasia. The cardiac biomarkers (BNP 4,598, TnI 59) with echocardiographic changes confirmed Mayo Stage III cardiac involvement. The combination of absent CRAB features with glomerular nephrotic syndrome and a small-to-moderate kappa clone makes LCDD the leading tissue diagnosis, with kappa AL amyloidosis as a close alternative — only the kidney biopsy resolves this. The diuresis failure reflects the hemodynamic paradox of the amyloid cardiorenal phenotype: simultaneous total body volume overload and intravascular depletion from oncotic failure and a stiff, preload-dependent ventricle. Multidisciplinary emergent care coordination is the clinical priority.

References

  1. Dispenzieri A, Kyle RA, Katzmann JA, et al. Immunoglobulin free light chain ratio is an independent risk factor for progression of smoldering (asymptomatic) multiple myeloma. Blood. 2008;111(2):785-789. doi:10.1182/blood-2007-08-108357. PMID: 17942755

  2. Hutchison CA, Plant T, Drayson M, et al. Serum free light chain measurement aids the diagnosis of myeloma in patients with severe renal failure. BMC Nephrol. 2008;9:11. doi:10.1186/1471-2369-9-11. PMID: 18928561

  3. Dispenzieri A, Gertz MA, Kyle RA, et al. Serum cardiac troponins and N-terminal pro-brain natriuretic peptide: a staging system for primary systemic amyloidosis. J Clin Oncol. 2004;22(18):3751-3757. doi:10.1200/JCO.2004.03.029. PMID: 15365071

  4. Palladini G, Hegenbart U, Milani P, et al. A staging system for renal outcome and early markers of renal response to chemotherapy in AL amyloidosis. Blood. 2014;124(15):2325-2332. doi:10.1182/blood-2014-04-570010. PMID: 25115890

  5. Kastritis E, Palladini G, Minnema MC, et al. Daratumumab-based treatment for immunoglobulin light-chain amyloidosis. N Engl J Med. 2021;385(1):46-58. doi:10.1056/NEJMoa2028631. PMID: 34192431

  6. Leung N, Bridoux F, Batuman V, et al. The evaluation of monoclonal gammopathy of renal significance: a consensus report of the International Kidney and Monoclonal Gammopathy Research Group. Nat Rev Nephrol. 2019;15(1):45-59. doi:10.1038/s41581-018-0077-4. PMID: 30510265

  7. Rajkumar SV, Dimopoulos MA, Palumbo A, et al. International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma. Lancet Oncol. 2014;15(12):e538-e548. doi:10.1016/S1470-2045(14)70442-5. PMID: 25439696

  8. Lilleness B, Ruberg FL, Mussinelli R, Doros G, Sanchorawala V. Development and validation of a survival staging system incorporating BNP in patients with light chain amyloidosis. Blood. 2019;133(3):215-223. doi:10.1182/blood-2018-06-858951. PMID: 30401706

  9. Kumar S, Dispenzieri A, Lacy MQ, et al. Revised prognostic staging system for light chain amyloidosis incorporating cardiac biomarkers and serum free light chain measurements. J Clin Oncol. 2012;30(9):989-995. doi:10.1200/JCO.2011.38.5724. PMID: 22331953

  10. Merlini G, Dispenzieri A, Sanchorawala V, et al. Systemic immunoglobulin light chain amyloidosis. Nat Rev Dis Primers. 2018;4(1):38. doi:10.1038/s41572-018-0034-3. PMID: 30361501