Abstract A 35-year-old woman with a thirteen-year history of substance use disorder and chronic nonhealing skin infections presented with low back pain and was diagnosed with spinal osteomyelitis, psoas and epidural abscesses, urinary incontinence, and left hydronephrosis. Polymicrobial bacteremia was identified. Laboratory evaluation revealed acute kidney injury (creatinine 1.24 mg/dL, baseline 0.7 mg/dL), elevated inflammatory markers (erythrocyte sedimentation rate greater than 130 mm/hr, C-reactive protein 22.4 mg/L), and microcytic anemia. Over 2 months, renal function deteriorated (creatinine 1.75 mg/dL, albumin less than 1.5 g/dL, hemoglobin 5 g/dL), with heavy proteinuria and hematuria. Further testing demonstrated nephrotic-range proteinuria, low serum albumin, elevated urine light chains without a monoclonal spike on serum protein electrophoresis, and low complement component 3 (C3) with normal complement component 4 (C4), findings suggestive of ongoing inflammatory consumption rather than immune complex glomerulonephritis. The patient left the hospital against medical advice, without further evaluation or treatment. A kidney biopsy performed two weeks later revealed renal Amyloid A (AA) amyloidosis. Electron microscopy demonstrated diffuse amyloid deposition in the renal tubules, interstitium, and arterioles, as well as loss of podocyte foot processes. These findings were consistent with inflammation-driven amyloidosis secondary to chronic infection. Following the biopsy, renal function further declined (creatinine 4.63 mg/dL), resulting in a diagnosis of stage 4 chronic kidney disease due to AA amyloidosis. Renin-angiotensin-aldosterone system (RAAS) blockade was avoided due to hyperkalemia, and management prioritized controlling inflammation and volume overload with albumin-assisted diuresis. Within six months, the patient was admitted to the hospital following a motor vehicle accident and was found to have end-stage renal disease (ESRD) requiring hemodialysis. Her hospitalization was complicated by pneumothorax, pneumonia with septic emboli, fractures, abscesses, and sepsis. Subsequently, she developed hypertensive emergencies and posterior reversible encephalopathy syndrome (PRES), reflecting the systemic manifestations of advanced amyloid disease. This case highlights the urgent need for early recognition and intervention in patients with chronic soft-tissue infection and polysubstance use, who are at high risk for rapid progression to ESRD from AA amyloidosis. As recurrent abscesses sustain elevated SAA levels and accelerate amyloid deposition, timely and effective control of the underlying inflammation is critical. Early use of biologic disease-modifying antirheumatic drugs (bDMARDs), particularly tocilizumab, has demonstrated efficacy in reducing proteinuria and preventing progression to ESRD in AA amyloidosis associated with chronic inflammatory diseases. Proactive treatment of at-risk populations could halt or even reverse renal damage, reducing the burden of advanced kidney disease. This abstract is funded by: None
Rudmann et al. (Fri,) studied this question.