Obesity-induced AA amyloidosis: A diagnosis of exclusion
2020
A 47-year-old woman with morbid obesity (body mass index: 41 kg/m2) and a history of
hypertension, pulmonary embolism and successfully treated gout (one year ago) presented with
nephrotic syndrome (15 g/24 h) and loss of kidney function (endogenous creatinine clearance 27
ml/min/1.73 m2). A kidney biopsy revealed AA amyloid. An extensive investigation was performed
to detect an underlying inflammatory disease process by testing blood and urine, imaging and
genetic testing for autoinflammatory diseases. Serum levels of C-reactive protein (CRP) and
serum amyloid A protein (SAA) were continuously elevated. Serum amyloid P component (SAP)-
scintigraphy showed intense uptake in a massively enlarged liver and in the spleen. This extensive
investigation did not reveal an underlying inflammatory process. Her gout became asymptomatic
almost immediately after start of treatment. Therefore, we concluded that morbid obesity was the
most probable cause of her AA amyloidosis. Treatment with colchicine and prednisolone did not
substantially reduce the SAA and CRP levels. Also, treatment with anakinra (interleukin-1 receptor
antagonist) and tocilizumab (interleukin-6 receptor antagonist) failed. The downhill course of the
disease progressed to complete renal failure within three years and dialysis was started. This case
indicates that the long-standing low-grade inflammation seen in morbid obesity may be a potential
cause of systemic AA amyloidosis and may be difficult to treat. However, it is essentially a diagnosis
of exclusion, since known underlying inflammatory conditions should be excluded first.
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