ArticleCureus2025
Multisystem Light Chain Amyloidosis: Diagnostic and Therapeutic Challenges.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid light (AL) chain amyloidosis is a rare, progressive multisystem disorder caused by the deposition of misfolded monoclonal light chains, which are produced by clonal plasma cells and commonly affect the kidneys and heart. The overall prognosis depends on the extent of organ involvement and timely diagnosis. A previously healthy 57-year-old man presented with a two-month history of progressive lower limb edema and exertional dyspnea. Initial investigations revealed elevated troponin, hypoalbuminemia, and nephrotic-range proteinuria. Coronary angiography was normal, but echocardiography showed restrictive cardiomyopathy. Renal biopsy after light and immunofluorescence microscopy was reported as membranous nephropathy. However, there was no response to proteinuria to sacubitril/valsartan, sodium-glucose co-transporter 2 (SGL2) inhibitor, and steroid therapy. The treatment was escalated with additional immunosuppressive treatments, including cyclosporine and rituximab. Subsequently, Congo red staining of the renal biopsy confirmed a diagnosis of amyloidosis. Further, a hematologic workup showed marked lambda (λ) light chain predominance with a suppressed kappa (κ)/λ ratio, and fluorescence in situ hybridization (FISH) analysis revealed a t (11;14) translocation, confirming AL amyloidosis. The patient was treated with daratumumab, bortezomib, cyclophosphamide, and dexamethasone (Dara-VCD), which was complicated by cytomegalovirus (CMV) gastritis. Despite receiving three cycles of therapy, the patient's condition deteriorated due to advanced cardiac failure, autonomic neuropathy, and a severe CMV infection. He ultimately succumbed to the illness 18 months after the initial presentation. This case highlights the diagnostic complexity of AL amyloidosis and the importance of early recognition. Clinicians should consider AL amyloidosis in patients with unexplained nephrotic syndrome and heart failure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.