N-terminal brain natriuretic propeptide levels correlate with procalcitonin and C-reactive protein levels in septic patients

Abstract

The aim of this study was to find the relationship between N-terminal brain natriuretic propeptide (NT-proBNP), procalcitonin (PCT) and C-reactive protein (CRP) plasma concentrations in septic patients. This was a prospective study, performed at Medical University Hospital No. 5 in łódź. Twenty patients with sepsis and severe sepsis were included in the study. N-terminal brain natriuretic propeptide, procalcitonin and C-reactive protein concentrations, and survival were evaluated. In the whole studied group (128 measurements), the mean NT-proBNP, procalcitonin and C-reactive protein concentrations were, respectively: 140.80±84.65 pg/ml, 22.32±97.41 ng/ml, 128.51±79.05 mg/l. The correlations for the NT-proBNP level and procalcitonin and C-reactive protein levels were 0.3273 (p<0.001) and 0.4134 (p<0.001), respectively. NT-proBNP levels correlate with PCT and CRP levels in septic patients. In the survivor subgroup, the mean NT-proBNP plasma concentrations were significantly lower than in the non-survivor subgroup.

The Risk of Heart Failure and Cardiometabolic Complications in Obesity May Be Masked by an Apparent Healthy Status of Normal Blood Glucose

“…In ZFs, the basal levels of 8-isoprostane were significantly elevated ( Figure 2(b) ) but were reduced by hemin, whereas cotreatment of hemin with SnMP nullified the effects. Given that ET-1 and ANP are known to interact reciprocally [ 41 ], we investigated whether the hemin-dependent suppression of ET-1 ( Figure 2(a) ) would be associated with a parallel potentiation of ANP. In ZFs, the basal ANP levels were markedly depressed by 1.7-fold ( Figure 2(c) ) but interestingly were robustly enhanced by hemin by 3.3-fold.…”

“…Since TGF- β mobilizes the extracellular matrix by stimulating fibronectin and collagen causing tissue damage and hypertrophy [ 49 , 57 ], the concomitant reduction of TGF- β , fibronectin, and collagen IV in ZFs may account for reduced cardiac lesions. Another mechanism by which the HO system suppresses extracellular matrix and profibrotic agents like TGF- β and ET-1 may be due to the HO-dependent potentiation of ANP, a substance known to suppress extracellular matrix [ 41 , 58 ]. Generally, ANP and ET-1 have opposing effects [ 59 ].…”

“…Generally, ANP and ET-1 have opposing effects [ 59 ]. For example, ANP reduces fibrosis by inhibiting TGF- β 1 and fibronectin [ 41 ], while ET-1 acts in conjunction with TGF- β 1 to stimulate the synthesis of fibronectin [ 58 ]. Similarly, ANP suppresses inflammation to reduce insulin resistance [ 59 ], while ET-1 stimulates inflammatory/oxidative insults causing insulin resistance [ 60 ].…”

The Heme Oxygenase System Suppresses Perirenal Visceral Adiposity, Abates Renal Inflammation and Ameliorates Diabetic Nephropathy in Zucker Diabetic Fatty Rats

“…The interaction between ET-1 and ANP is well known [48]. For example ANP inhibits ET-1 [70], and interestingly, the hemin-induced increase of ANP was accompanied by a parallel reduction of ET-1. On the other hand, ANP attenuates fibrosis by abating extracellular matrix/profibrotic proteins including fibronectin and TGF-β1 [70], while ET-1 acts in concert with TGF-β1 to stimulate fibronectin synthesis [71].…”

Heme Oxygenase Improves Renal Function by Potentiating Podocyte-Associated Proteins in Nω-Nitro-l-Arginine-Methyl Ester (l-NAME)-Induced Hypertension

“…19,28 Interestingly, the HO system, adiponectin, and ANP have all been shown to increase cGMP. 19,33 Moreover, the potentiation of ANP, a substance that promote natriuresis and vasodilatation and alongside the parallel reduction of ET-1, a substance that stimulates sodium retention and vasoconstriction, 34 together with the suppression of aldosterone may account for the increased sodium excretion and enhanced urinary volume. Alternatively, the increased sodium excretion and enhanced urinary volume observed in HA-treated animals may result from the concomitant enhancement of ANP, and its surrogate marker urinary cGMP.…”