Abstract: SA-PO140
Lysozyme-Induced AKI: A Case Series
Session Information
- AKI: Epidemiology, Risk Factors, Prevention - III
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Cossey, Larry Nicholas, Arkana Laboratories, Little Rock, Arkansas, United States
- Larsen, Christopher Patrick, Arkana Laboratories, Little Rock, Arkansas, United States
Background
Only rare case reports exist describing increased serum lysozyme with acute kidney injury. This study represents the first case series to describe the clinical and laboratory findings associated with this disease.
Methods
17 kidney biopsy samples displaying lysozyme-induced acute kidney injury and associated clinical histories were prospectively collected from 2012-2019. 40 additional kidney biopsies were utilized as controls to compare morphologic findings. Light microscopy, immunofluorescence, electron microscopy, thioflavin T, Congo red, and lysozyme IHC were performed. Laser microdissection coupled with mass spectrometry was performed on our initial two patients.
Results
82% of patients were male with an average age of 66 years. 94% presented with acute kidney injury and average serum creatinine of 2.95 mg/dL. All patients had proteinuria with an average protein:creatinine ratio of 2.2. Hematuria was present in 42%, however where available, all urine sediments were bland. Serum lysozyme results were available in 10 patients all showing elevated levels. Hematologic disease was present in 71% of patients with chronic myelomonocytic leukemia affecting 31%. Outcome data was limited but showed recovery to near baseline serum creatinine in 4/4 (13 months f/u) who were treated for their underlying disease. Progressive CKD/ESKD was seen in 3/3 (3 months f/u), who did not undergo treatment of their underlying disease. The most helpful histologic features in identifying this disease were the pattern and intensity of lysozyme staining, Congo red reactivity without birefringence, weak Thioflavin T staining, extent of proximal tubule protein resorption droplets, and refractile protein resorption droplets in proximal tubules. Laser microdissection of proximal tubules followed by mass spectrometry showed lysozyme as the most frequent protein hit identified and a >20 fold increase in lysozyme hits compared to controls.
Conclusion
Lysozyme-induced acute kidney injury occurs in the setting of increased serum lysozyme leading to increased lysozyme in the proximal tubules. It is most commonly seen in the context of hematologic malignancy. While subtle, a constellation of morphologic and immunohistochemical findings exist that allow for accurate diagnosis. In our limited outcome data, treatment of the patient's underlying disease is critical for recovery of kidney function and favorable prognosis.