Ischemic acute kidney injury induces a distant organ functional and genomic response distinguishable from bilateral nephrectomy

Hassoun, Heitham T.; Grigoryev, Dmitry N.; Lie, Mihaela L.; Liu, Manchang; Cheadle, Chris; Tuder, Rubin M.; Rabb, Hamid

doi:10.1152/ajprenal.00023.2007

Cited by 184 publications

(176 citation statements)

References 39 publications

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“…Proinflammatory cytokines such as IL-6, IL-8 and TNF-α are increased in patients with AKI, 16 and increased levels of IL-6 and IL-8 predicted prolonged mechanical ventilation in patients with AKI. 15 The inflammatory nature of AKI and the resultant effect on the lungs is highlighted by studies in animal models demonstrating that inflammatory genes are up-regulated in the kidney and lung 32 and that anti-inflammatory treatment with IL-6 inhibition, 33 α-MSH 34 or a p38 MAP kinase inhibitor 35 protect against lung injury in animal models of AKI. Because ESRD is generally regarded as an immune-deficient state, 21 it is possible that the proinflammatory cytokine production may be dampened in patients with ESRD.…”

Section: Discussionmentioning

confidence: 99%

In Critically Ill Patients Requiring CRRT, AKI Is Associated with Increased Respiratory Failure and Death Versus ESRD

et al. 2011

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Background/aims: To compare outcomes of critically ill patients with acute kidney injury (AKI) requiring continuous renal replacement therapy (CRRT) versus those with pre-existing end-stage renal disease (ESRD) requiring CRRT to identify factors that contribute to the increased mortality seen in AKI patients. Methods: Retrospective cohort of 257 intensive care unit (ICU) patients who received CRRT. AKI is defined as requiring CRRT with an admission serum creatinine ≤1 mg/dL; ESRD is defined as chronic dialysis dependence. Primary outcome was hospital mortality. Multivariate logistic regression was performed to determine the impact of APACHE II score, intubation, vasopressors, infection, diabetes, hypertension, gender, and race on mortality. Results: Of 257 patients requiring CRRT, 28 had ESRD and 108 had AKI. Hospital mortality was higher in patients with AKI versus ESRD (69% vs. 39%, p = 0.0032). Severity of illness using APACHE II was similar in AKI and ESRD. Patients with AKI were more likely to require mechanical ventilation (89% vs. 57%, p = 0.0003). After multivariate analysis, the requirement for mechanical ventilation was the single factor associated with increased hospital mortality [odds ratio (OR): 3.1]. Conclusions: In ICU patients requiring CRRT, patients with AKI have a higher mortality than patients with ESRD due to an increased need for mechanical ventilation.

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Section: Discussionmentioning

confidence: 99%

In Critically Ill Patients Requiring CRRT, AKI Is Associated with Increased Respiratory Failure and Death Versus ESRD

et al. 2011

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“…5,9,[12][13][14] Even relatively small changes in renal function after administration of contrast medium are associated with substantial increases in mortality rates 14 ; this finding suggests that renal insufficiency is a sensitive marker of poor outcomes for patients at risk or perhaps that transient episodes of renal ischemia may produce secondary hemodynamic or vascular changes in other organs. 15 The materials cited in this review include recent guidelines and published reports of clinical trials of contrastinduced AKI and its prevention. These materials were retrieved by a PubMed search covering the period January 1990 through January 2008.…”

Section: Contrast-inducedmentioning

confidence: 99%

Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology

Goldfarb

McCullough

McDermott

et al. 2009

Mayo Clinic Proceedings

135

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Contrast-induced acute kidney injury (AKI) (also known as contrast-induced nephropathy) is an abrupt deterioration in renal function that can be associated with use of iodinated contrast medium. Although the increase in serum creatinine concentration is transient in most cases, contrast-induced AKI may lead to increased morbidity and mortality rates in selected at-risk populations. This review summarizes the findings of a multidisciplinary panel composed of computed tomography radiologists, interventional radiologists, cardiologists, and nephrologists convened to address the specialty-specific issues associated with minimizing the incidence of contrast-induced AKI. As part of this initiative, the panel developed specialty-specific protocols for preventing contrast-induced AKI, taking into account, for example, the variations in patient risk profile, inpatient or outpatient status, and staffing resources that characterize various clinical settings. The 3 protocols, each reflecting a consensus of expert opinion, address the prevention of contrast-induced AKI in interventional radiology, diagnostic computed tomography radiology, and interventional cardiology settings. The protocols are presented in the context of a review of recent guidelines and published reports of trials that discuss contrast-induced AKI and its prevention. © 2009 Mayo Foundation for Medical Education and ResearchA cute kidney injury (AKI) is a heterogeneous disorder with multiple etiologies, risk factors, and clinical presentations. Although patients with AKI are ultimately cared for by nephrologists, AKI occurs in various clinical settings and is associated with a specific etiology in each. The term contrast-induced AKI refers to the disorder as it occurs after exposure to iodinated contrast media, a disorder that has been more commonly known as contrastinduced nephropathy (CIN). The Acute Kidney Injury Network, recognizing the need for improving outcomes associated with the various forms of AKI, recently proposed using the following standardized diagnostic definition in all cases: an abrupt (within 48 hours) reduction in kidney function, evidenced by an increase in the serum creatinine concentration of at least 0.3 mg/dL (to convert to µmol/L, multiply by 88.4) or at least 50% from baseline or a reduction in urine output (documented oliguria of <0.5 mL/kg/h for >6 hours).1,2 The criterion of oliguria does not apply for many cases of contrast-induced AKI because patients are treated with intravenous fluids before and after the procedure with the goal of increasing periprocedural urine output. The most commonly used definition of CIN is an increase from the baseline serum creatinine concentration of at least 0.5 mg/dL or at least 25% within 48 to 72 hours after exposure to contrast media. [3][4][5] Because the medical community is moving to adopt the concept and terminology of the American College of Radiology (ACR) in reference to studies of contrast-induced renal dysfunction and its prevention, 6 this report will do the same. However, we rec...

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“…The reliability of detected transcriptional changes was ensured using the 50 th percentile of the most variable hybridization signals from controls (n=5) as described previously (14). The resulting standard deviation (σ = 0.416) was submitted to the microarray sample size identifying formula proposed by Wei et al (15), imposing 90% of detecting power (1-β) and accepting a 1% or 5% false discovery rate (significance level α = 0.01 or 0.05) for cross-(n=5-10) and intra-group (n=3-4) analyses, respectively.…”

Section: Power Prediction Analysis For Significance Of Transcriptionamentioning

confidence: 99%

Identification of candidate genes in scleroderma-related pulmonary arterial hypertension

Grigoryev

Mathai

Fisher

et al. 2008

Translational Research

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We hypothesize that pulmonary arterial hypertension (PAH)-associated genes identified by expression profiling of peripheral blood mononuclear cells (PBMCs) from patients with idiopathic pulmonary arterial hypertension (IPAH) can also be identified in PBMCs from scleroderma patients with PAH (PAH-SSc). Gene expression profiles of PBMCs collected from IPAH (n=9), PAH-SSc (n=10) patients and healthy controls (n=5) were generated using HG_U133A_2.0 GeneChips and processed by RMA/GCOS_1.4/SAM_1.21 data analysis pipeline. Disease severity in consecutive patients was assessed by functional status and hemodynamic measurements. The expression profiles were analyzed using PAH severity-stratification, and identified candidate genes were validated with real time PCR (rtPCR). Transcriptomics of PBMCs from IPAH patients was highly comparable with that of PMBCs from PAH-SSc patients. The PBMC gene expression patterns significantly correlate with right atrium pressure (RA) and cardiac index (CI), known predictors of survival in PAH. Array stratification by RA and CI identified 364 PAH-associated candidate genes. Gene ontology analysis revealed significant (Z score > 1.96) alterations in angiogenesis genes according to PAH severity: MMP9 and VEGF were significantly upregulated in mild as compared to severe PAH and healthy controls, as confirmed by rtPCR. These data demonstrate that PBMCs from patients with PAH-SSc carry distinct transcriptional expression. Furthermore, our findings suggest an association between angiogenesis-related gene expression and severity of PAH in PAH-SSc patients. Deciphering the role of genes involved in vascular remodeling and PAH development may reveal new treatment targets for this devastating disorder.

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Ischemic acute kidney injury induces a distant organ functional and genomic response distinguishable from bilateral nephrectomy

Cited by 184 publications

References 39 publications

In Critically Ill Patients Requiring CRRT, AKI Is Associated with Increased Respiratory Failure and Death Versus ESRD

In Critically Ill Patients Requiring CRRT, AKI Is Associated with Increased Respiratory Failure and Death Versus ESRD

Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology

Identification of candidate genes in scleroderma-related pulmonary arterial hypertension

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