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Lysozyme is a protein that hydrolyzes bacterial peptidoglycans and is produced by neutrophils, monocytes, and macrophages. It is filtered through the glomeruli, reabsorbed by proximal tubular cells, and degraded within lysosomes. Lysozyme-induced nephropathy is a kidney disorder caused by proximal tubular injury secondary to excessive lysozyme production in diseases such as myeloid malignancies and sarcoidosis. We present a case of chronic kidney disease initially suspected to be diabetic nephropathy, later identified as lysozyme-induced nephropathy secondary to a myelodysplastic/myeloproliferative neoplasm (MDS/MPN).Treatment for the underlying hematologic malignancy successfully prevented progression to dialysis.
A 75-year-old man had been treated for diabetes mellitus for more than 20 years, under good glycemic control throughout the course. Three years earlier, he developed weight loss and multiple lymphadenopathies and was referred to our hospital. Lymph node and bone marrow biopsies revealed a diagnosis of MDS/MPN, with chronic myelomonocytic leukemia (CMML) being strongly suspected. Because the disease was not considered severe, a conservative management approach was adopted.Kidney function gradually declined to serum creatinine 1.49 mg/dL, and he was referred to our department one year ago. At that time, kidney impairment was attributed to diabetic nephropathy, and conservative therapy was continued. However, kidney function continued to deteriorate, prompting a kidney biopsy.
Urinalysis showed no hematuria, proteinuria of 1.34 g/gCr, and a markedly elevated urinary lysozyme level (1,190 μg/mL; reference range <1.0 μg/mL). Blood tests revealed leukocytosis (14,800/μL, monocytes 54.0%), anemia (Hb 7.0 g/dL), elevated serum creatinine (3.69 mg/dL), and a markedly increased serum lysozyme concentration (265 μg/mL; reference range 4.2〜11.5 μg/mL). Kidney pathology demonstrated hypertrophic and distended proximal tubular epithelial cells with eosinophilic cytoplasm on light microscopy. Immunohistochemistry showed strong lysozyme positivity within the cytoplasm of tubular epithelial cells. Electron microscopy demonstrated numerous enlarged lysosomes containing electron-dense material, consistent with lysozyme accumulation. These findings led to a diagnosis of lysozyme-induced nephropathy. Based on these findings, hydroxycarbamide therapy was initiated for the underlying MDS/MPN, resulting in improved kidney function (serum creatinine decreased from 4.76 to 2.86 mg/dL).
In patients with myeloid neoplasms accompanied by monocytosis who develop kidney dysfunction, lysozyme-induced nephropathy should be considered an important differential diagnosis that must not be overlooked. Early recognition and appropriate treatment of the underlying hematologic disorder may prevent progression to end-stage kidney disease.
