A 48-year-old Maghrebian woman sought opinion for persistent kidney dysfunction for the last 5 years. Her past medical history is remarkable for a sleeve gastrectomy for morbid obesity followed by a drop in body mass index from 58.6 to 40.2 kg/m2 8 years ago. Our patient had visceral type obesity with a gynoid phenotype. She took ibuprofen pills intermittently for mechanical joint pains related to obesity, on an average 1 - 2 tablets a week for the past 10 years. There was no history of recurrent chronic infections, chronic inflammatory disease, or malignancy. 
The patient was aware of her kidney dysfunction for the last 5 years with her serum creatinine values ~ 1.5 mg/dL. At the most recent visit, her serum creatinine was 1.47 mg/dL. She had low-grade proteinuria (urine protein-creatinine ratio of 0.4), microscopic hematuria (5 - 6 per high power field) and aseptic leukocyturia (6 - 8 per high power field). Her blood pressure was 110/75 mmHg. Serum protein electrophoresis and immunoelectrophoresis were normal. Immunological tests including serum anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, serum anti-double stranded DNA antibody, HLA-B27, anti-saccharomyces cerevisiae antibody, and anti-cyclic citrullinated peptide antibody were negative. Serum complement (C3 and C4) levels were within normal range. Serum free light chain kappa-lambda ratio (0.9) was normal. Infectious work-up including hepatitis B surface antigen, hepatitis C core antibody, human immunodeficiency virus, and QuantiFERON-Gold TB were all negative. Her C-reactive protein (CRP) was 19.4 mg/L (normal range: < 10 mg/L), and serum haptoglobin was 2.24 g/L (normal range: 0.41 - 1.65 g/L). 
While the clinical picture (low-grade proteinuria, stable chronic kidney disease) raised the possibility of chronic involvement of the tubulo-interstitial compartment, likely secondary to chronic non-steroidal anti-inflammatory drug use, the background morbid obesity and inflammatory state in this young person could suggest other possibilities such as obesity-related glomerulopathy and immune-mediated glomerular diseases. A kidney biopsy was performed using the trans-jugular approach in view of anticipated technical challenges of accessing the kidneys in morbid obesity. Eight out of the total 13 glomeruli were sclerosed. The rest of the glomeruli had accentuated mesangium without any necrosis or proliferation. Interstitial fibrosis was noted to involve 10 - 15% of the cortex with a scattered mononuclear infiltrate. Discrete arteriolosclerosis was prominent. Congo red staining highlighted mainly arteriolar and arterial amyloid deposits with few deposits in the mesangium (Figure 1A), and apple-green birefringence of these deposits was noted under polarized light (Figure 1B). Direct immunofluorescence did not show significant staining. The deposits stained strongly with anti-SAA antibody (Figure 1C) but not with anti-kappa and anti-lambda antiserum (not shown). Further workup showed serum SAA levels of 26 mg/L (normal < 6 mg/L). Genetic study for SAA gene polymorphism was negative. Sequencing of familial Mediterranean fever gene (MEFV) exon 10 by Sanger sequencing did not show any pathogenic mutation. The patient was on a nutritional care program aiming at weight loss, however, her BMI had stabilized at ~ 40 kg/m2. The patient was started on anakinra (interleukin-1 receptor antagonist) and dapagliflozin. Within the next 6 months, there was improvement of inflammatory markers with SAA decreasing to < 10 mg/L at the 6th month (Table 1). We plan to continue treatment for a total of 12 months duration. We will continue to (i) monitor SAA, CRP, kidney function test and (ii) implement nutritional care at subsequent visits. Her serum creatinine and proteinuria has been stable during the follow-up.