Lysozyme-Induced Nephropathy: A Diagnosis Not to Forget

Paulo, Núria; Baptista, Pedro V.; Nogueira, Fernando; Pereira, Catarina; Ramos-Cerqueira, Ana Teresa de Abreu; Rocha, Ana Regina

doi:10.7759/cureus.34344

Cited by 3 publications

(3 citation statements)

References 14 publications

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“…In total, he survived 11 months beyond his LyN diagnosis which although not directly terminal, contributed notable morbidity via frailty and functional decline. The broader literature suggests variable prognoses [10] of LyN ranging from recovery of kidney function [12,13] to continued dialysis dependency and eventual palliation [6] .…”

Section: Discussionmentioning

confidence: 99%

A case of chronic myelomonocytic related lysozyme-induced nephropathy

Kansal,

Peiris,

Ramnarain

et al. 2024

Preprint

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Background Lysozyme-induced nephropathy (LyN) is a rare cause of acute kidney injury (AKI) in patients with chronic myelomonocytic leukemia (CMML). Diagnosing LyN is challenging due to the numerous potential and concurrent aetiologies. Previous case reports have demonstrated the diagnostic utility of serum and urinary lysozyme measurements, which may correlate with renal dysfunction; however, the role of renal imaging remains unclear and renal biopsy remains essential for diagnosis.Case presentation An independent 80-year-old male presented to an Australian tertiary hospital with stage 3 AKI on a background of CMML previously treated with thioguanine and hydroxycarbamide. Renal tract ultrasound revealed expansile, non-vascular material bilaterally in renal collecting systems which was confirmed by renal biopsy to be lysozyme-induced nephropathy causing renal dysfunction. Despite escalated anti-leukaemic treatment he progressed to stage 4 chronic kidney disease contributing to increasing frailty and eventually pursued voluntary assisted dying after a fall with terminal traumatic injuries.Conclusions LyN is a rare cause of acute kidney injury amongst patients with chronic myelomonocytic leukaemia. This case highlights a rare instance of LyN and illustrates potential radiological markers that may aid in diagnosis. It also emphasizes the complexity of managing LyN in the context of underlying haematological malignancies.

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Section: Discussionmentioning

confidence: 99%

A case of chronic myelomonocytic related lysozyme-induced nephropathy

Kansal,

Peiris,

Ramnarain

et al. 2024

Preprint

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“…4,6,7 Once the lysosomal burden is high enough in so that it surpasses the absorptive capacity of the proximal tubules, resulting tubular injury occurs, which can manifest as tubular necrosis, tubular atrophy, or interstitial fibrosis. 7,8 CMML and hematological malignancies with myelomonocytic differentiation are the most commonly recognized causes of lysozyme nephropathy. 6 Theoretically, this is due to a clonal monocytic proliferation, which in turn is responsible for an abundance of lysozyme production that becomes toxic to the proximal tubular cells.…”

Section: Discussionmentioning

confidence: 99%

“…In the aforementioned case, a renal biopsy demonstrated the presence of an excess of lysozymes inside the proximal tubule epithelial cells in the setting of concomitant chronic hypertensive ischemic renal disease. Lysozyme, also referred to as muramidase, is a cationic protein that is only approximately 15 kilodaltons in size and is freely filtered by the glomerulus and subsequently reabsorbed by the proximal convoluted tubule via endocytosis, and then degraded in phagolysosomes 4,6,7 . Once the lysosomal burden is high enough in so that it surpasses the absorptive capacity of the proximal tubules, resulting tubular injury occurs, which can manifest as tubular necrosis, tubular atrophy, or interstitial fibrosis 7,8 …”

Section: Discussionmentioning

confidence: 99%

Lysozyme‐induced nephropathy due to systemic granulomatous disease

Ashraf,

Uczkowski,

Stuart

2023

Clinical Case Reports

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Key Clinical MessageLysozyme‐induced nephropathy is a rare form of acute tubular injury that has almost exclusively been reported in patients with monocytic malignancies. Typically, patients will present in acute renal failure A renal biopsy is necessary to confirm the diagnosis and will demonstrate proximal tubular cells with hypereosinophilic granules, which are periodic acid‐Schiff and Jones methenamine silver‐positive. Immunohistochemical staining for lysozyme will also be present. The following rare case will describe a case of lysozyme nephropathy in a patient without any underlying hematological malignancy, but instead with systemic granulomatous disease.

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Comparative proteomic analysis of renal tissue of normotensive and hypertensive rats

Buneeva,

Fedchenko,

Kaloshina

et al. 2024

BIOMED KHIM

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Comparative proteomic analysis of kidney tissue from normotensive (WKY) and spontaneously hypertensive (SHR) rats revealed quantitative and qualitative changes in renal proteins. The number of renal proteins specific for WKY rats (blood pressure 110–120 mm Hg) was 13–16. There were 20–24 renal proteins specific for SHR (blood pressure 180 mm Hg and more). The total number of identified renal proteins common for both rat strains included 972–975 proteins. A pairwise comparison of all possible (SHR-WKY) variants identified 8 proteins specific only for normotensive (WKY) animals, and 7 proteins specific only for hypertensive ones (SHR). Taking into consideration their biological roles, the lack of some enzyme proteins in hypertensive rats (for example, biliverdin reductase A) reduces the production of molecules exhibiting antihypertensive properties, while the appearance of others (e.g. betaine-homocysteine S-methyltransferase 2, septin 2, etc.) can be interpreted as a compensatory reaction. Renal proteins with altered relative content (with more than 2.5-fold change) accounted for no more than 5% of all identified proteins. Among the proteins with an increased relative content in hypertensive animals, the largest group consisted of proteins involved in the processes of energy generation and carbohydrate metabolism, as well as antioxidant and protective proteins. In the context of the development of hypertension, the identified relative changes can apparently be considered compensatory. Among the proteins with the most pronounced decrease in the relative content in hypertensive rats, the dramatic reduction in acyl-CoA medium-chain synthetase-3 (ACSM3) appears to make an important contribution to the development of renal pathology in these animals.

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Lysozyme-Induced Nephropathy: A Diagnosis Not to Forget

Cited by 3 publications

References 14 publications

A case of chronic myelomonocytic related lysozyme-induced nephropathy

A case of chronic myelomonocytic related lysozyme-induced nephropathy

Lysozyme‐induced nephropathy due to systemic granulomatous disease

Comparative proteomic analysis of renal tissue of normotensive and hypertensive rats

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