Urinary proteomics before and after extracorporeal circulation in patients with and without acute kidney injury

Aregger, Fabienne; Pilop, Christiane; Uehlinger, Dominik E.; Brunisholz, René A.; Carrel, Thierry; Frey, Felix J.; Frey, Brigitte M.

doi:10.1016/j.jtcvs.2009.11.015

Cited by 26 publications

(19 citation statements)

References 26 publications

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“…It is elevated in urine during energy-demanding conditions (15), but decreases in acute kidney injury (16). However, on individual quantification in the validation set, ZAG levels were similar to those found in patients with FSGS-unrelated proteinuria, thus lacking the specific link to FSGS.…”

Section: Discussionmentioning

confidence: 72%

A Form of Apolipoprotein A-I Is Found Specifically in Relapses of Focal Segmental Glomerulosclerosis Following Transplantation

López-Hellı́n

Cantarell

Jimeno

et al. 2013

American Journal of Transplantation

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Section: Discussionmentioning

confidence: 72%

A Form of Apolipoprotein A-I Is Found Specifically in Relapses of Focal Segmental Glomerulosclerosis Following Transplantation

López-Hellı́n

Cantarell

Jimeno

et al. 2013

American Journal of Transplantation

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“…111 Aregger and collegues examined the urinary proteome of 36 adults undergoing CPB. 112 In the 6 patients that developed AKI, defined by RIFLE criteria, urinary albumin was increased, and zinc-alpha-2-glycoprotein and a fragment of adrenomedullin-binding protein were decreased. Most recently, Heller and colleagues have shown that urinary calprotectin, an activator of the innate immune system, reliably differentiates pre-renal azotemia from intrinsic AKI in a group of hospitalized patients, supporting the predictive role of the urinary proteome even in heterogeneous patient populations.…”

Section: Protein Biomarkers Of Akimentioning

confidence: 96%

Marking renal injury: can we move beyond serum creatinine?

Slocum

Heung

Pennathur

2012

Translational Research

127

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Acute kidney injury (AKI) is a prevalent and devastating condition associated with significant morbidity and mortality. Despite marked improvements in clinical care, the outcomes for subjects with AKI have shown limited improvement in the past 50 years. A major factor inhibiting clinical progress in this field has been inability to accurately predict and diagnose early kidney dysfunction. The current gold-standard clinical and biochemical criteria for diagnosis of AKI, Risk Injury Failure Loss End-stage renal disease (RIFLE), and its modification, Acute Kidney Injury Network (AKIN) criteria, rely on urine output and serum creatinine (SCr) which are insensitive, non-specific, and late markers of disease. The recent development of a variety of analytical mass spectrometry (MS) based platforms have enabled separation, characterization, detection, and quantification of proteins (proteomics) and metabolites (metabolomics). These high-throughput platforms have raised hopes of identifying novel protein and metabolite markers, and recent efforts have led to several promising novel markers of AKI. However, substantial challenges remain including need to systematically evaluate incremental performance of these markers over and beyond current clinical and biochemical criteria for AKI. Here, we discuss the basic issues surrounding AKI biomarker development, highlight the most promising markers currently under development, and discuss the barriers towards wide-spread clinical implementation of these markers.

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“…Although these are small studies, they suggest that the excretion of this protein is decreased during AKI. Further proteomic studies are needed to determine whether a decrease in urinary uromodulin would be a suitable biomarker for AKI 82 . Could the baseline rate of urinary uromodulin excretion be predictive of susceptibility to AKI?…”

Section: Recent Advancesmentioning

confidence: 99%

Uromodulin in Kidney Injury: An Instigator, Bystander, or Protector?

El‐Achkar

2012

American Journal of Kidney Diseases

100

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Uromodulin, also known as Tamm-Horsfall protein, is a glycoprotein expressed exclusively by renal tubular cells lining the thick ascending limb of the loop of Henle. Although the physiologic functions of this protein remain elusive, significant progress has been made over the last decade that highlights the importance of uromodulin in the pathophysiology of various diseases, such as medullary cystic kidney disease, urinary tract infections, and nephrolithiasis. Meanwhile, there is a renewed interest in the role of uromodulin in kidney injury, both acute and chronic. In this article, we review the existing evidence that supports a role for uromodulin in acute kidney injury (AKI), chronic kidney disease (CKD), and renal inflammation. Contrary to the conventional view of uromodulin as an instigator in kidney injury, new data from uromodulin knockout mice reveal a protective role for this protein in AKI, possibly through down-regulating interstitial inflammation. In CKD, uromodulin excretion, when adjusted for kidney function, is increased; the significance of this remains unclear. Although it has been suggested that uromodulin exacerbates progressive kidney injury, we propose that the elevation in uromodulin secretion is instead reactive to injury, and reflects an increase of uromodulin in the renal parenchyma where it slows the injury process.

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Urinary proteomics before and after extracorporeal circulation in patients with and without acute kidney injury

Abstract: Cardiopulmonary bypass leads to increased urinary excretion of inflammatory proteins and markers of tubular injury. Zinc-alpha-2-glycoprotein is a potentially useful predictive marker for acute kidney injury after cardiopulmonary bypass surgery.

Cited by 26 publications

References 26 publications

A Form of Apolipoprotein A-I Is Found Specifically in Relapses of Focal Segmental Glomerulosclerosis Following Transplantation

A Form of Apolipoprotein A-I Is Found Specifically in Relapses of Focal Segmental Glomerulosclerosis Following Transplantation

Marking renal injury: can we move beyond serum creatinine?

Uromodulin in Kidney Injury: An Instigator, Bystander, or Protector?

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