A Case of Lysozyme Nephropathy During the Treatment of Prostate Cancer

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A Case of Lysozyme Nephropathy During the Treatment of Prostate Cancer

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Co-author 1

Shoji Saito saito13@med.nagoya-u.ac.jp Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan *

Co-author 2

Ririka Jinno ririkaringo@icloud.com Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 3

Yuto Tazawa ytazawa.chukyo@gmail.com Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 4

Yui Fukuda imokempifukuda@gmail.com Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 5

Azusa Kobayashi azusa.0121@gmail.com Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 6

Marie Tanaka robinmari@gmail.com Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 7

Hibiki Shinjo shinjo14@nagoya2.jrc.or.jp Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 8

Asami Takeda asamitakeda@hotmail.co.jp Japanese Red Cross Hospital Aichi Medical Center Nagoya Dai-ni Hospital Nephrology Nagoya Japan -

Co-author 9

Co-author 10

Co-author 11

Co-author 12

Co-author 13

Co-author 14

Co-author 15

Introduction

Lysozyme nephropathy is a rare cause of acute tubular injury observed in patients with hematologic malignancies, especially chronic myelomonocytic leukemia (CMML) and acute myelomonocytic leukemia. Excess lysozyme production associated with malignancy can lead to acute kidney injury and proteinuria. Lysozyme freely filters through the glomerulus and is reabsorbed by the proximal tubular epithelium. While this occurs at physiologically low levels, excessive reabsorption of lysozyme causes toxic acute tubular injury.

Methods

Results

A man in his 80s was diagnosed with prostate cancer in year X-3 and started treatment by using abiraterone and prednisolone.Year X-1, he was consulted to hematology due to leukocytosis and thrombocytosis, and was monitored for suspected chronic myelomonocytic leukemia (CMML). Year X-2month, he was admitted to the ER due to an altered mental status and hospitalized urgently. After admission, the patient experienced ventricular tachycardia (VT) leading to temporary cardiac arrest. He was diagnosed with Torsades de Pointes (TdP) due to hypokalemia and hypomagnesemia. Hypokalemia was also considered a potential effect of abiraterone, leading to discontinuation of oral medication. Prednisolone was also tapered off and discontinued. Year X-1month, the patient was referred to nephrology due to AKI. Renal biopsy was performed and renal pathology showed interstitial nephritis.

Conclusion

Cellular infiltration is observed throughout nearly the whole interstitium, with extensive atrophic tubules. Numerous granular deposits are seen primarily in the proximal tubules, distributed relatively uniformly within the cytoplasm. Based on the distribution pattern of granules observed in the renal tubules and the patient's medical history, we diagnosed the patient with lysozyme nephropathy. Steroid treatment was initiated, and the patient’s kidney function improved rapidly. The lysozyme nephropathy is thought to become apparent after the steroids are discontinued.

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