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Samuel Morgan. Ilan Merdler. Moshe Shtark.
Ilana Goldiner. Shmuel Banai. Yacov Shacham. All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
Patients were assessed for the occurrence of in-hospital adverse outcomes. The multivariate regression model demonstrated that subclinical AKI was independently associated with in-hospital adverse outcomes OR 3. Keywords: neutrophil gelatinase-associated lipocalin; ST-segment elevation myocardial infarction; renal injury neutrophil gelatinase-associated lipocalin ; ST-segment elevation myocardial infarction ; renal injury.
Introduction According to consensus criteria, identification of acute kidney injury AKI is based on serum creatinine sCr changes. However, changes in sCr merely reflect functional changes and do not incorporate parameters that directly indicate tubular damage. Furthermore, an acute change in glomerular function after a renal insult does not result in an abrupt increase in sCr due to the time needed for creatinine to accumulate in the body [ 12 ], and it usually takes 24—36 h after a renal insult to reach a new steady state [ 3 ].
Over the past decade, several novel biomarkers have been introduced, allowing earlier detection of Text lonely local singles 64239 and glomerular injury when compared to sCr [ 45 ]. Neutrophil gelatinase-associated lipocalin NGAL is a glycoprotein stored in granules of mature neutrophils in complex with gelatinase. It is reabsorbed by proximal tubules and released by damaged distal tubules in cases of acute tubular damage and may be detected within a few hours of the tubular insult and even in the absence of functional AKI [ 789101112 ].
A large proportion of patients admitted to hospital have various degrees of heart and kidney dysfunction. Bidirectional interactions exist between the heart and kidneys, defined as various types of cardiorenal syndrome CRSwhere a primary disorder of one of these organs often in secondary dysfunction or injury to the other [ 13 ]. A prospective, observational, open-label trial was performed in the Tel Aviv Sourasky medical center. Diagnosis of STEMI was established by a typical history of chest pain, diagnostic electrocardiographic changes, and serial elevation of serum cardiac biomarkers [ 14 ].
The contrast medium used in procedures was iodixanol Visipaque, GE healthcare, Ireland. Following coronary interventional procedures, physiologic 0. In patients with overt heart failure, the hydration rate was reduced at the discretion of the attending physician. All patients underwent a screening echocardiographic examination within three days of admission to assess left ventricular LV ejection fraction. Patient records were evaluated for the in-hospital course and occurrence of adverse outcomes.
These included the development of heart failure episodes defined as the occurrence of both clinical and radiological s of congestion treated conservatively, respiratory failure with the need for mechanical ventilation, new onset atrial fibrillation episodes, as well as in-hospital mortality. These complications were united to form a composite outcome of major adverse in-hospital cardiac events.
Informed consent was obtained from all individual participants included in the study. The study protocol was approved by the local institutional ethics committee Institutional Board Review no. We applied the term subclinical AKI to indicate the absence or presence of tubular injury, in the absence of functional AKI, manifested as sCr elevation [ 1 ].
The sCr was determined upon hospital admission, prior to PCI, and at least once a day throughout hospitalization and was available for all analyzed patients. Quantitative CRP analysis was performed by the Bayer wide-range assay. Patients were stratified into two groups based on Text lonely local singles 64239 presence of subclinical AKI. For post hoc analysis, two continuous variables were compared using the independent sample t -test for normally distributed data and the Mann—Whitney U test for non-normally distributed variables.
Categorial variables were compared using the Chi square or Fisher exact test. The utilization of any and subclinical AKI to assess the risk for adverse in-hospital outcomes was evaluated using a multivariate logistic regression adjusted for all parameters found ificant in the univariate analysis. All statistical analysis was performed using R statistical software version 4. Table 2 presents the key in-hospital adverse outcomes of patients with vs.
The multivariate regression model Table 3 demonstrated that, in addition to any AKI, subclinical AKI was independently associated with in-hospital adverse outcomes OR 3.
Other factors associated with in-hospital adverse outcomes included peak CRP and left ventricular ejection fraction. Our study demonstrated that among STEMI patients treated with primary PCI, the presence of subclinical AKI tubular damage biomarker positivity without loss of function was common and associated with adverse in-hospital outcomes.
Clinical AKI is diagnosed when renal damage and dysfunction reach a threshold sufficient to make sCr rise above 0. An acute change in GFR after a renal insult does not result in an abrupt increase in sCr due to the time needed for creatinine to accumulate in the body [ 2 ], and it usually takes 24—36 h after a renal insult to reach a new steady state [ 3 ].
The delayed increase in sCr after a decline in GFR is seen especially in patients who simultaneously become fluid overloaded. Similarly, sCr does not immediately decrease when GFR improves [ 18 ]. Lack of renal functional deterioration may also reflect the absence of subtle chronic kidney disease, with an intact renal functional reserve that compensates for a transient subtle injury [ 19 ].
Recent data suggest that early diagnosis of AKI can be made by using a single structural or functional biomarker or a combination thereof capable of detecting kidney injury almost in real time [ 6 ].Text lonely local singles 64239
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