Abstract: FR-PO1265
AA Amyloidosis in the Setting of Metastatic Carcinoid Tumor
Session Information
- Onconephrology: Diagnostic Dilemmas, Therapy-Related Toxicities, and Clinical Cases
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Kurian, Rebecca, Yale University, New Haven, Connecticut, United States
- El Mouhayyar, Christopher, Yale University, New Haven, Connecticut, United States
- Shirali, Anushree C., Yale University, New Haven, Connecticut, United States
Introduction
Amyloidosis is characterized by the deposition of misfolded proteins across multiple organ systems, including the kidney. AA amyloidosis, a distinct subtype, arises from the sustained overproduction of serum amyloid A (SAA) protein, an acute-phase reactant synthesized in hepatocytes in response to pro-inflammatory cytokines. In the developing world, most cases are associated with infectious processes and in developed nations pathology such as rheumatoid arthritis or Familial Mediterranean Fever. Here, we present a case of biopsy-proven AA amyloidosis in a patient with longstanding metastatic carcinoid tumor with worsening hepatic metastases, highlighting a rare and clinically important etiology.
Case Description
A 58-year-old male with CKD3a, 19-year history of metastatic carcinoid tumor, complicated by hepatic and biliary metastases, portal vein thrombosis, and prior pulmonary and tricuspid valve replacement in 2014. For his carcinoid tumor, he had been maintained on lanreotide for several years. Nephrology was consulted for evaluation of progressive renal dysfunction. His creatinine had been relatively stable until approximately three months prior to admission, when it increased from a baseline of 1.0–1.1 mg/dL to 1.35 mg/dL, and further to 2.10 mg/dL at the time of presentation. On admission, his urine protein-to-creatinine ratio was 0.73g/g and urine albumin-to-creatinine ratio was 0.64g/g. Serologic was unremarkable. Renal ultrasound showed preserved kidney sizes bilaterally without obstruction. Renal biopsy showed AA amyloidosis in light of positivity with Congo red staining, moderate arterionephrosclerosis and acute tubular injury.
Discussion
In developed nations AA amyloidosis is thought to be in the setting of chronic inflammatory disorders. While it has been seen in some solid organ tumors, its occurrence with carcinoid tumor is exceptionally rare. The abrupt worsening in renal function, coinciding temporally with radiographic worsening of hepatic lesions suggests that increasing tumor burden may have intensified the chronic inflammatory state. This case reinforces the importance of maintaining a high index of suspicion for AA amyloidosis in patients with longstanding carcinoid tumor who develop unexplained or accelerating renal dysfunction, proteinuria, or other systemic features of amyloid deposition.