IntroductionAcute kidney injury (AKI) is a common complication among hospitalized patients. The aim of this study was to evaluate the utility of blood neutrophil gelatinase-associated lipocalin (NGAL) assessment as an aid in the early risk evaluation for AKI development in admitted patients.MethodsThis is a multicenter Italian prospective emergency department (ED) cohort study in which we enrolled 665 patients admitted to hospital from the ED.ResultsBlood NGAL and serum creatinine (sCr) were determined at ED presentation (T0), and at: 6 (T6), 12 (T12), 24 (T24) and 72 (T72) hours after hospitalization. A preliminary assessment of AKI by the treating ED physician occurred in 218 out of 665 patients (33%), while RIFLE AKI by expert nephrologists was confirmed in 49 out of 665 patients (7%). The ED physician's initial judgement lacked sensitivity and specificity, overpredicting the diagnosis of AKI in 27% of the cohort, while missing 20% of those with AKI as a final diagnosis.The area under the receiver operating characteristic curve (AUC), obtained at T0, for blood NGAL alone in the AKI group was 0.80. When NGAL at T0 was added to the ED physician's initial clinical judgment the AUC was increased to 0.90, significantly greater when compared to the AUC of the T0 estimated glomerular filtration rate (eGFR) obtained either by modification of diet in renal disease (MDRD) equation (0.78) or Cockroft-Gault formula (0.78) (P = 0.022 and P = 0.020 respectively). The model obtained by combining NGAL with the ED physician's initial clinical judgement compared to the model combining sCr with the ED physician's initial clinical judgement, resulted in a net reclassification index of 32.4 percentage points. Serial assessment of T0 and T6 hours NGAL provided a high negative predictive value (NPV) (98%) in ruling out the diagnosis of AKI within 6 hours of patients' ED arrival. NGAL (T0) showed the strongest predictive value for in-hospital patient's mortality at a cutoff of 400 ng/ml.ConclusionsOur study demonstrated that assessment of a patient's initial blood NGAL when admitted to hospital from the ED improved the initial clinical diagnosis of AKI and predicted in-hospital mortality. Blood NGAL assessment coupled with the ED physician's clinical judgment may prove useful in deciding the appropriate strategies for patients at risk for the development of AKI.See related commentary by Legrand et al., http://ccforum.com/content/17/2/132

The neutrophil-to-lymphocyte ratio (NLR) is an inflammatory marker predicting the prognosis of several diseases. We aimed to assess its role as a predictor of mortality or admission to the intensive care unit in COVID-19 patients. We retrospectively evaluated a cohort of 411 patients with COVID-19 infection. The neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and C-reactive protein (CRP) of patients with COVID-19 were compared. The median age of our sample was 72 years (interquartile range: 70–75); 237 were males. Hypertension, diabetes and ischemic heart disease were the most common comorbidities. The study population was subdivided into three groups according to NLR tertiles. Third-tertile patients were older, showing significantly higher levels of inflammatory markers; 133 patients (32%) died during hospitalization, 81 of whom belonged to the third tertile; 79 patients (19%) were admitted to ICU. NLR showed the largest area under the curve (0.772), with the highest specificity (71.9%) and sensitivity (72.9%), whereas CRP showed lower sensitivity (60.2%) but slightly higher specificity (72.3%). Comparisons between NLR and CRP ROC curves were significantly different (p = 0.0173). Cox regression models showed that the association between NLR and death was not weakened after adjustment for confounders. Comparisons of ROC curves showed no significant differences between NLR, PLR, and CRP. Cox regression analysis showed that NLR predicted the risk of admission to ICU independently of demographic characteristics and comorbidities (HR: 3.9597, p < 0.0001). These findings provide evidence that NLR is an independent predictor of mortality and a worse outcome in COVID-19 patients and may help identify high-risk individuals with COVID-19 infection at admission.

. Lack of activation of molecular forms of the BNP system in human grade 1 hypertension and relationship to cardiac hypertrophy. Am J Physiol Heart Circ Physiol 291: H1529 -H1535, 2006. First published April 28, 2006 doi:10.1152/ajpheart.00107.2006.-We evaluated relationships among two circulating molecular forms of brain natriuretic peptide (BNP32 and NT-proBNP), severity of hypertension (HTN), and cardiac hypertrophy in subjects with mild, moderate, and severe HTN. We prospectively studied 78 patients (43 males; mean age 51.4 Ϯ 11 yr) with essential HTN and 28 age-and sex-matched controls. BNP32 and NT-proBNP were measured by radioimmunoassay. In grade 1 HTN, BNP32 was not elevated and NT-proBNP was reduced (P ϭ 0.030) compared with controls. However, log-transformed values of BNP32 and NT-proBNP were both increased with severity of HTN from grade 1 to 3 (P Ͻ0.0001 and P ϭ 0.003, respectively). By multivariate analysis, log BNP32 was independently predicted by age (␤ ϭ 0.210, P ϭ 0.026) and HTN grade (␤ ϭ 0.274, P ϭ 0.004), whereas log NT-proBNP was independently predicted by sex (␤ ϭ 0.235, P ϭ 0.012) and HTN grade (␤ ϭ 0.218, P ϭ 0.0023). Two forms of BNP were measured in normal subjects and patients with essential HTN. In grade 1 HTN, BNP32 was unchanged and NTproBNP was significantly reduced compared with controls. As severity increased in humans with grade 1 to 3 HTN, both BNP32 and NT-proBNP levels were increased while not being affected by the presence of left ventricular hypertrophy. The lack of activation of BNP32 together with the reduction of NT-proBNP in grade 1 HTN may represent an impaired response of the BNP system in the early phase of HTN. The later activation of both forms of BNP may be a late compensatory effect, because it correlates with severity of HTN rather than cardiac hypertrophy/remodeling. natriuretic peptide; brain natriuretic peptide; amino-terminal pro-brain natriuretic peptide; left ventricular hypertrophy BRAIN NATRIURETIC PEPTIDE (BNP) is synthesized in cardiac myocytes as the precursor proBNP, a 108-amino acid peptide (4, 27, 33), and is converted to biologically active peptide BNP32 via a proteolytic cleavage by corin, a type II transmembrane cardiac serine protease (22,38,39). BNP is present in the circulation in two different forms, the biologically active BNP32 that elicits different beneficial cardiorenal and hormonal actions (1,5,8,11,25,26,40) and the amino-terminal portion of BNP (NT-proBNP) that consists of 76 amino acids.In congestive heart failure (CHF) as well as in hypertension (HTN), ventricular cardiomyocytes are progressively recruited to synthesize BNP (24). Whereas initially a successful defensive endocrine response by the heart to preserve cardiorenal homeostasis might occur, a hyporesponsiveness to cardiac peptides, which might contribute in turn to the progression of hypertension, could follow later. Although BNP32 has emerged as an important diagnostic and prognostic biomarker of CHF (1, 12, 37), its levels are markedly variable in HTN. Therefore, its b...

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