Risk Factors and Outcome of Hospital-Acquired Acute Renal Failure. A Clinical Epidemiologic Study

Shusterman, Neil H.; Strom, Brian L.; Murray, Thomas G.; Morrison, Gail; West, Suzanne L.; Maislin, Greg

doi:10.1016/s0022-5347(17)42463-3

Cited by 76 publications

(105 citation statements)

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“…From 5% to 7% of hospitalized patients are reported to experience AKI (2,3); the estimated annual health care expenditures attributable to hospital-acquired AKI exceed $10 billion (4). Renal ischemia reperfusion injury (IRI) associated with renal transplantation, postcardiopulmonary bypass surgeries, and other major vascular surgeries is the leading cause of AKI; sepsis and nephrotoxic drug injury are other major contributory factors (5,6).…”

Section: Introductionmentioning

confidence: 99%

Cell-specific translational profiling in acute kidney injury

et al. 2014

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Acute kidney injury (AKI) promotes an abrupt loss of kidney function that results in substantial morbidity and mortality. Considerable effort has gone toward identification of diagnostic biomarkers and analysis of AKI-associated molecular events; however, most studies have adopted organ-wide approaches and have not elucidated the interplay among different cell types involved in AKI pathophysiology. To better characterize AKI-associated molecular and cellular events, we developed a mouse line that enables the identification of translational profiles in specific cell types. This strategy relies on CRE recombinase-dependent activation of an EGFP-tagged L10a ribosomal protein subunit, which allows translating ribosome affinity purification (TRAP) of mRNA populations in CRE-expressing cells. Combining this mouse line with cell type-specific CRE-driver lines, we identified distinct cellular responses in an ischemia reperfusion injury (IRI) model of AKI. Twenty-four hours following IRI, distinct translational signatures were identified in the nephron, kidney interstitial cell populations, vascular endothelium, and macrophages/monocytes. Furthermore, TRAP captured known IRI-associated markers, validating this approach. Biological function annotation, canonical pathway analysis, and in situ analysis of identified response genes provided insight into cell-specific injury signatures. Our study provides a deep, cell-based view of early injury-associated molecular events in AKI and documents a versatile, genetic tool to monitor cell-specific and temporal-specific biological processes in disease modeling.

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Section: Introductionmentioning

confidence: 99%

Cell-specific translational profiling in acute kidney injury

et al. 2014

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“…Acute risk factors include volume depletion, exposure to nephrotoxic agents, surgery, and sepsis (5)(6)(7)(8). Chronic risk factors include age, chronic kidney disease (CKD), diabetes, and congestive heart failure (8,9). However, models using these traditional risk factors remain inadequate (5,6,(10)(11)(12).…”

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confidence: 99%

Searching for Genes That Matter in Acute Kidney Injury

Coca

Patel

et al. 2009

Clinical Journal of the American Society of Nephrology

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Background and Objectives: Identifying patients who may develop acute kidney injury (AKI) remains challenging, asclinical determinants explain only a portion of individual risk. Another factor that likely affects risk is intrinsic genetic variability. Therefore, a systematic review of studies was performed that related the development or prognosis of AKI to genetic variation.Design, setting, participants, and measurements: MEDLINE, EMBASE, HuGEnet, SCOPUS, and Web of Science were searched for articles from 1950 to Dec 2007. Two independent researchers screened articles using predetermined criteria. Studies were assessed for methodological quality via an aggregate scoring system. Results: The 16 included studies were of cohort or case-cohort design and investigated 35 polymorphisms in 21 genes in association with AKI. Fifteen gene-gene interactions were also investigated in four separate studies. Study populations were primarily premature infants or adults who were critically ill or postcardiac bypass patients. Among the studies, five different definitions of AKI were used. Only one polymorphism, APO E e2/e3/e4, had greater than one study showing a significant impact (P < 0.05) on AKI incidence. The mean quality score of 5.8/10 (range four to nine), heterogeneity in the studies, and the dearth of studies precluded additional meta-analysis of the results.Conclusions: Current association studies are unable to provide definitive evidence linking genetic variation to AKI. Future success will require a narrow consensus definition of AKI, rigorous epidemiologic techniques, and a shift from a priori hypothesis-driven to genome-wide association studies.

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“…Contrast medium (CM) was the next most common cause, accounting for 12% of cases of AKI, and was associated with an in-hospital mortality of 6%. In 1987, Shusterman et al (5) demonstrated that CM was one of four major factors contributing to hospital acquired AKI (the others being volume depletion, congestive heart failure, and aminoglycosides).…”

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confidence: 99%

Contrast-Induced Nephropathy

Rudnick

Goldfarb

Tumlin

2008

Clinical Journal of the American Society of Nephrology

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A lthough the clinical features of contrast-induced nephropathy (CIN) have been well described for some time (1,2), during the past 15 yr, interest among physicians on the subject of CIN has dramatically increased. A PubMed search of the phrase "contrast-induced nephropathy" between 1990 and 2007 produced 347 citations. During the past 5 yr alone, there were 290 citations, 159 of which appeared since 2006 (3).Intravascular administration of contrast is widely known to be a common cause of hospital-acquired acute kidney injury (AKI). In 1983, Hou et al. (4) prospectively evaluated 2216 patients with hospital-acquired AKI and found decreased renal perfusion and major surgery to be the leading causes of AKI. Contrast medium (CM) was the next most common cause, accounting for 12% of cases of AKI, and was associated with an in-hospital mortality of 6%. In 1987, Shusterman et al. (5) demonstrated that CM was one of four major factors contributing to hospital acquired AKI (the others being volume depletion, congestive heart failure, and aminoglycosides).The exact risk for CIN is difficult to determine. It is widely known that in patients with normal renal function, even in the presence of diabetes, the risk for CIN is Յ1 to 2% (1). In patients with chronic kidney disease (CKD), it is also well accepted that the risk for CIN is significantly increased and rises in proportion to the severity of underlying renal impairment (1,6,7). Another established observation is that the coupling of CKD and diabetes dramatically increases the risk for CIN compared with that observed for CKD alone (6). Recent studies on CIN in "high-risk" patients have demonstrated a wide range of incidences from 1 to 45% (8,9). Reasons for this wide variation in CIN risk include study differences in the number and severity of underlying risk factors, definition of CIN used, prospective or retrospective collection of data, exclusion or nonexclusion of patients with other AKI etiologies, timing of the baseline serum creatinine (SCr) relative to hydration administration, type and amount of CM used, type and amount of hydration, and presence or absence of other prophylactic measures. Unfortunately, the consequence of these multiple factors makes it difficult to state with reasonable accuracy the clinical risk for CIN in a "high-risk" patient. Additional problems caused by the apparently observed wide range of CIN incidences are methodologically inadequate comparisons of studies for the value of procedural or prophylactic strategies to minimize CIN risk and prospective, randomized, controlled trials that are underpowered to answer the question for which they were designed.Despite the uncertainty of the incidence of CIN in "high-risk" patients, there are a number of reasons to believe that CIN will be an increasing cause of hospital-and outpatient-acquired AKI. Use of intravascular contrast is widespread and continues to expand. In 2003, 80 million doses of CM were administered worldwide (10,11). As of 2004, 3.3 million coronary angiograms, 25.7 million c...

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Risk Factors and Outcome of Hospital-Acquired Acute Renal Failure. A Clinical Epidemiologic Study

Cited by 76 publications

References 0 publications

Cell-specific translational profiling in acute kidney injury

Cell-specific translational profiling in acute kidney injury

Searching for Genes That Matter in Acute Kidney Injury

Contrast-Induced Nephropathy

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