Authors
Ilker Atay, Erhan Eroz, Zeynep Bayramoğlu, Abdurrahman Çömlekçi, Berfu Korucu
Published in
Journal of nephrology. Sep 26, 2026. Epub Sep 26, 2026.
Abstract
AA amyloidosis is driven by persistently elevated serum amyloid A (SAA) in chronic inflammation. Severe obesity has emerged as a potential inflammatory driver of renal AA amyloidosis. We report a 47-year-old man with prior sleeve gastrectomy who developed progressive kidney dysfunction and proteinuria after substantial weight regain. At presentation, he weighed 126 kg (body mass index, 45.2 kg/m2); serum creatinine was 4.3 mg/dL (estimated glomerular filtration rate, 15 mL/min/1.73 m2) and urine albumin-to-creatinine ratio (UACR) was 3.4 g/g. Kidney biopsy confirmed AA amyloidosis, while extensive evaluation for autoimmune, infectious, hereditary, malignant, and monoclonal causes was unrevealing. SAA was 80 mg/L with persistently elevated inflammatory markers. Semaglutide was initiated as part of a weight-management strategy. Following a 47-kg weight loss, creatinine decreased to 2.34 mg/dL, estimated glomerular filtration rate increased to 32 mL/min/1.73 m2, UACR declined to 1.0 g/g, and SAA fell to <10 mg/L, with improvement in C-reactive protein, erythrocyte sedimentation rate, and HbA1c. In the absence of another identifiable cause, the parallel improvement in SAA, systemic inflammation, proteinuria, and kidney function supports severe obesity as a potential inflammatory contributor to renal AA amyloidosis, although causality cannot be inferred from a single case.
PMID:
42791222
Bibliographic data and abstract were imported from PubMed on 26 Sep 2026.
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