Indoxyl sulphate and kidney disease: causes, consequences and interventions

Ellis, Robert J., Small, David M., Vesey, David A., Johnson, David W., Francis, Ross, Vitetta, Luis, Gobe, Glenda C. and Morais, Christudas (2016) Indoxyl sulphate and kidney disease: causes, consequences and interventions. Nephrology, 21 3: 170-177. doi:10.1111/nep.12580


Author Ellis, Robert J.
Small, David M.
Vesey, David A.
Johnson, David W.
Francis, Ross
Vitetta, Luis
Gobe, Glenda C.
Morais, Christudas
Title Indoxyl sulphate and kidney disease: causes, consequences and interventions
Journal name Nephrology   Check publisher's open access policy
ISSN 1440-1797
1320-5358
Publication date 2016-03-01
Year available 2016
Sub-type Article (original research)
DOI 10.1111/nep.12580
Open Access Status Not Open Access
Volume 21
Issue 3
Start page 170
End page 177
Total pages 8
Place of publication Richmond, VIC Australia
Publisher Wiley-Blackwell Publishing Asia
Collection year 2017
Language eng
Formatted abstract
In the last decade, chronic kidney disease (CKD), defined as reduced renal function (glomerular filtration rate (GFR) < 60 mL/min per 1.73 m2) and/or evidence of kidney damage (typically manifested as albuminuria) for at least 3 months, has become one of the fastest-growing public health concerns worldwide. CKD is characterized by reduced clearance and increased serum accumulation of metabolic waste products (uremic retention solutes). At least 152 uremic retention solutes have been reported. This review focuses on indoxyl sulphate (IS), a protein-bound, tryptophan-derived metabolite that is generated by intestinal micro-organisms (microbiota). Animal studies have demonstrated an association between IS accumulation and increased fibrosis, and oxidative stress. This has been mirrored by in vitro studies, many of which report cytotoxic effects in kidney proximal tubular cells following IS exposure. Clinical studies have associated IS accumulation with deleterious effects, such as kidney functional decline and adverse cardiovascular events, although causality has not been conclusively established. The aims of this review are to: (i) establish factors associated with increased serum accumulation of IS; (ii) report effects of IS accumulation in clinical studies; (iii) critique the reported effects of IS in the kidney, when administered both in vivo and in vitro; and (iv) summarize both established and hypothetical therapeutic options for reducing serum IS or antagonizing its reported downstream effects in the kidney.
Keyword End-stage kidney disease
GFR
Indoxyl sulphate
Oxidative stress
Uremic toxin
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
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