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Int J Mol Sci. 2019 Apr 23;20(8). pii: E1997. doi: 10.3390/ijms20081997.

Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis.

Giuliani KTK1,2,3, Kassianos AJ4,5,6,7, Healy H8,9,10, Gois PHF11,12,13.

Author information

1
Kidney Health Service, Royal Brisbane and Women's Hospital, Brisbane, QLD 4029, Australia. Kurt.Giuliani@uqconnect.edu.au.
2
Conjoint Kidney Research Laboratory, Chemical Pathology-Pathology Queensland, Brisbane, QLD 4029, Australia. Kurt.Giuliani@uqconnect.edu.au.
3
Faculty of Medicine, University of Queensland, Brisbane, QLD 4006, Australia. Kurt.Giuliani@uqconnect.edu.au.
4
Kidney Health Service, Royal Brisbane and Women's Hospital, Brisbane, QLD 4029, Australia. Andrew.Kassianos@qimrberghofer.edu.au.
5
Conjoint Kidney Research Laboratory, Chemical Pathology-Pathology Queensland, Brisbane, QLD 4029, Australia. Andrew.Kassianos@qimrberghofer.edu.au.
6
Faculty of Medicine, University of Queensland, Brisbane, QLD 4006, Australia. Andrew.Kassianos@qimrberghofer.edu.au.
7
Institute of Health and Biomedical Innovation/School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD 4059, Australia. Andrew.Kassianos@qimrberghofer.edu.au.
8
Kidney Health Service, Royal Brisbane and Women's Hospital, Brisbane, QLD 4029, Australia. Helen.Healy@health.qld.gov.au.
9
Conjoint Kidney Research Laboratory, Chemical Pathology-Pathology Queensland, Brisbane, QLD 4029, Australia. Helen.Healy@health.qld.gov.au.
10
Faculty of Medicine, University of Queensland, Brisbane, QLD 4006, Australia. Helen.Healy@health.qld.gov.au.
11
Kidney Health Service, Royal Brisbane and Women's Hospital, Brisbane, QLD 4029, Australia. Pedro.FrancaGois@health.qld.gov.au.
12
Conjoint Kidney Research Laboratory, Chemical Pathology-Pathology Queensland, Brisbane, QLD 4029, Australia. Pedro.FrancaGois@health.qld.gov.au.
13
Faculty of Medicine, University of Queensland, Brisbane, QLD 4006, Australia. Pedro.FrancaGois@health.qld.gov.au.

Abstract

Pigment nephropathy is an acute decline in renal function following the deposition of endogenous haem-containing proteins in the kidneys. Haem pigments such as myoglobin and haemoglobin are filtered by glomeruli and absorbed by the proximal tubules. They cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. Haem is associated with inflammation in sterile and infectious conditions, contributing to the pathogenesis of many disorders such as rhabdomyolysis and haemolytic diseases. In fact, haem appears to be a signalling molecule that is able to activate the inflammasome pathway. Recent studies highlight a pathogenic function for haem in triggering inflammatory responses through the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. Among the inflammasome multiprotein complexes, the NLRP3 inflammasome has been the most widely characterized as a trigger of inflammatory caspases and the maturation of interleukin-18 and -1β. In the present review, we discuss the latest evidence on the importance of inflammasome-mediated inflammation in pigment nephropathy. Finally, we highlight the potential role of inflammasome inhibitors in the prophylaxis and treatment of pigment nephropathy.

KEYWORDS:

NLRP3 inflammasome; acute kidney injury; haem; pigment nephropathy; rhabdomyolysis

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