Abstract: PUB207
Transient Nephrotic Proteinuria After Amino Acid Supplementation
Session Information
Category: Pathology and Lab Medicine
- 1700 Pathology and Lab Medicine
Authors
- Perez, Aubriana C., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Gill, Mohammad Danial, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Khayat, Maurice I., VA North Texas Health Care System, Dallas, Texas, United States
Introduction
Abrupt development of nephrotic-range proteinuria often prompts urgent evaluation for glomerular pathology, especially in patients with known autoimmune disease. Non-pathologic glomerular proteinuria can mimic severe intrinsic kidney disease, resulting in an unnecessary renal biopsy. We present a case of transient, nephrotic proteinuria after amino acid (AA) supplementation in a patient with mixed connective tissue disease. (MCTD).
Case Description
A 52-year-old man with MCTD complicated by interstitial lung disease, Raynaud’s syndrome, recent pulmonary emboli on apixaban and CKD 3a was discovered to have new nephrotic-range proteinuria (UPCR 4.6 g/g from UPCR 0.1 g/g in 2024) on screening rheumatologic labs. Notably, he had been lost to follow up and off azathioprine for 18 months.
One week prior he had been admitted for a heart failure exacerbation and was noted to have an increased creatinine from baseline (1.6-1.8 from 1.3-1.4 mg/dL), attributed to initiation of empagliflozin.
His presentation prompted concern for autoimmune glomerular disease, and he was admitted for renal biopsy requiring bridging anticoagulation. Repeat UPCR had decreased to 0.5 g/g (concurrent UACR 0.181 g/g). Urinalysis and renal ultrasound were unremarkable. Screening serologies to include ANCA and anti-dsDNA were negative. A 24-hour urine protein confirmed reduction to 88 mg/day.
Further history revealed use of an expired over-the-counter (OTC) AA supplement immediately prior to initial labs and self-discontinued in the interim. Given his negative work-up, spontaneous improvement and procedural bleeding risk, renal biopsy was deferred.
Discussion
Sudden development of nephrotic-range proteinuria commonly raises concern for glomerular disease, especially in patients with underlying risk factors. However, mimics such as non-pathologic contributors to proteinuria are important to exclude and may drastically change management.
Transient proteinuria has been associated with AA supplementation. In physiologic studies, L-arginine increased urinary albumin excretion through glomerular hyperfiltration and impaired proximal tubular protein reabsorption. Cross-reactivity with AA can also result in overestimation of excretion in some urine protein assays.
This case highlights the importance of evaluation for non-pathologic etiologies of abrupt proteinuria, whose discovery may obviate the need for invasive evaluation.