Primary and secondary hyperoxaluria: Understanding the enigma

Bhasin, Bhavna; Ürekli, Hatice Melda; Atta, Mohamed G.

doi:10.5527/wjn.v4.i2.235

Cited by 151 publications

(166 citation statements)

References 95 publications

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“…104 Clinical trials testing whether IL-1 blockade can also improve outcomes in diseases such as GN, vasculitis, or AKI are still awaited. 105 Timing is probably an issue, because the diagnosis of AKI, based on its current definition, is not recognized before the kidney is largely destroyed. Therefore, IL-1 blockade might be more feasible in chronic disorders for which some experimental evidence exists such as primary hyperoxaluria or diabetes.…”

Section: Il-1-related Drugs and Clinical Datamentioning

confidence: 99%

Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease

Anders

2016

JASN

204

152

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Kidney injury implies danger signaling and a response by the immune system. The inflammasome is a central danger recognition platform that triggers local and systemic inflammation. In immune cells, inflammasome activation causes the release of mature IL-1b and of the alarmin IL-1a. Dying cells release IL-1a also, independently of the inflammasome. Both IL-1a and IL-1b ligate the same IL-1 receptor (IL-1R) that is present on nearly all cells inside and outside the kidney, further amplifying cytokine and chemokine release. Thus, the inflammasome-IL-1a/IL-b-IL-1R system is a central element of kidney inflammation and the systemic consequences. Seminal discoveries of recent years have expanded this central paradigm of inflammation. This review gives an overview of arising concepts of inflammasome and IL-1a/b regulation in renal cells and in experimental kidney disease models. There is a pipeline of compounds that can interfere with the inflammasome-IL-1a/IL-b-IL-1R system, ranging from recently described small molecule inhibitors of NLRP3, a component of the inflammasome complex, to regulatory agency-approved IL-1-neutralizing biologic drugs. Based on strong theoretic and experimental rationale, the potential therapeutic benefits of using such compounds to block the inflammasome-IL-1a/IL-b-IL-1R system in kidney disease should be further explored.

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Section: Il-1-related Drugs and Clinical Datamentioning

confidence: 99%

Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease

Anders

2016

JASN

204

152

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“…Primary hyperoxaluria results from an inherited defect in oxalate metabolism that results in increased endogenous production of oxalate (Box 2). 2,3 Secondary hyperoxaluria may result from either dietary excess, enteric hyperabsorption (Figure 2), or enhanced endogeneous production resulting from exposure to its precursors (ascorbic acid) or from pyridoxine deficiency. The absorption of oxalate in the gastrointestinal tract is influenced by many factors, including gut health and function, 4 oxalate intake or oxalate content of food 5 (Appendix 2, available at www.cmaj.ca/lookup/suppl/ doi:10.1503/cmaj.151327/-/DC1) and, most importantly, the intake of other nutrients such as calcium, magnesium and fat.…”

Section: Pathogenesis Of Hyperoxaluriamentioning

confidence: 99%

Oxalate nephropathy from cashew nut intake

Bernardino¹,

Parmar

2016

CMAJ

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“…42 Oksalatın barsaklardan absorpsiyonu diyet kalsiyumu ile ters orantılıdır. Kalsiyumdan fakir diyet oksalat absorpsiyonunu artırarak hiperokzalüriye neden olmaktadır.…”

Section: Sekonder Hiperokzalüriunclassified