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      Plasma N‐Terminal Probrain Natriuretic Peptide, Vascular Endothelial Growth Factor, and Cardiac Troponin I as Novel Biomarkers of Hypertensive Disease and Target Organ Damage in Cats

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          Abstract

          Background

          In the absence of ocular target organ damage (ocular‐ TOD), diagnosis of hypertension is challenging in cats. Biomarkers would provide additional support for the diagnosis of hypertension.

          Hypothesis

          Vascular endothelial growth factor ( VEGF), N‐terminal probrain natriuretic peptide ( NT‐pro BNP), cardiac troponin I ( cTnI), and urine protein‐to‐creatinine ratio ( UPC) are predictors of systemic hypertension, will be increased in cats with hypertension with or without ocular‐ TOD, and will decrease with antihypertensive treatment.

          Methods

          Plasma VEGF, NT‐pro BNP, and cTnI concentrations and UPC were determined in healthy geriatric cats, normotensive cats with chronic kidney disease ( CKD), hypertensive cats with evidence of hypertensive retinopathy ( HT‐ocular‐ TOD), and hypertensive cats without hypertensive ocular‐ TOD ( HT‐no TOD). Comparisons among groups were performed. Multivariable binary logistic regression models were built to identify independent biomarkers of hypertension and ocular‐ TOD. Receiver operator characteristic ( ROC) curves were drawn to assess clinical use.

          Results

          Cats with HT‐ocular‐ TOD had significantly higher VEGF than all other groups ( P < .05) and significantly higher NT‐pro BNP than healthy cats ( P < .001). Healthy cats had significantly lower cTnI than all other groups ( P < .05). No differences were found among groups for UPC ( P = .08). Cardiac troponin I and VEGF were independent predictors of hypertension ( P < .05), but none of the biomarkers were independent predictors of ocular‐ TOD. N‐terminal probrain natriuretic peptide concentrations decreased with antihypertensive treatment ( P < .001). The ROC curves indicated that none of the biomarkers met the criteria to function as diagnostic tests for the diagnosis of hypertension or associated ocular‐TOD.

          Conclusions and Clinical Significance

          Despite statistical significance and changes with ocular‐ TOD, antihypertensive treatment, or both, VEGF, NT‐pro BNP, and cTnI did not function as useful diagnostic tests for hypertension. Persistently increased systolic blood pressure ( SBP) measurements in combination with fundoscopy remains the preferred method for diagnosis of feline hypertension.

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          Cardiac troponin I. A marker with high specificity for cardiac injury.

          Laurinda Jaffe, F S Apple, J Ladenson … (1993)
          Levels of MBCK can be increased in patients with skeletal muscle injury or renal failure in the absence of myocardial injury, causing diagnostic confusion. This study was designed to determine whether measurement of cardiac troponin I (cTnI), a myocardial regulatory protein with comparable sensitivity to MBCK, has sufficient specificity to clarify the etiology of MBCK elevations in patients with acute or chronic skeletal muscle disease or renal failure. Of the patients (n = 215) studied, 37 had acute skeletal muscle injury, 10 had chronic muscle disease, nine were marathon runners, and 159 were chronic dialysis patients. Patients were evaluated clinically, by ECG, and by two-dimensional echocardiography. Total creatine kinase (normal, < 170 IU/L) was determined spectrophotometrically, and cTnI (normal, < 3.1 ng/mL) and MBCK (normal, < 6.7 ng/mL) were determined with specific monoclonal antibodies. Values above the upper reference limit were considered "elevated." Elevations of total creatine kinase were common, and elevations of MBCK occurred in 59% of patients with acute muscle injury, 78% of patients with chronic muscle disease and marathon runners, and 3.8% of patients with chronic renal failure. Some of the patients were critically ill; five patients were found to have had myocardial infarctions and one had a myocardial contusion. cTnI was elevated only in these patients. Elevations of cTnI are highly specific for myocardial injury. Use of cTnI should facilitate distinguishing whether elevations of MBCK are due to myocardial or skeletal muscle injury.
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            The role of vascular endothelial growth factor (VEGF) in renal pathophysiology.

            Bieke F. Schrijvers, Allan Flyvbjerg, An S De Vriese (2004)
            Vascular endothelial growth factor (VEGF) is an endothelial-specific growth factor that promotes endothelial cell proliferation, differentiation and survival, mediates endothelium-dependent vasodilatation, induces microvascular hyperpermeability and participates in interstitial matrix remodeling. In the kidney, VEGF expression is most prominent in glomerular podocytes and in tubular epithelial cells, while VEGF receptors are mainly found on preglomerular, glomerular, and peritubular endothelial cells. The role of VEGF in normal renal physiology is essentially unknown. The absence of prominent effects of VEGF blockade in normal experimental animals suggests a limited function during homeostasis, although a role in the formation and maintenance of glomerular capillary endothelial fenestrations has been suggested. VEGF and its receptors are up-regulated in experimental animals and humans with type 1 and type 2 diabetes. Inhibition of VEGF has beneficial effects on diabetes-induced functional and structural alterations, suggesting a deleterious role for VEGF in the pathophysiology of diabetic nephropathy. VEGF is required for glomerular and tubular hypertrophy and proliferation in response to nephron reduction, and loss of VEGF is associated with the development of glomerulosclerosis and tubulointerstitial fibrosis in the remnant kidney. No firm conclusions on the role of VEGF in minimal change or membranous glomerulonephritis can be drawn. VEGF may be an essential mediator of glomerular recovery in proliferative glomerulonephritis. Glomerular and tubulointerstitial repair in thrombotic microangiopathy and cyclosporin nephrotoxicity may also be VEGF-dependent. In conclusion, VEGF is required for growth and proliferation of glomerular and peritubular endothelial cells. While deleterious in some, it may contribute to recovery in other forms of renal diseases.
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              Role of shear-stress-induced VEGF expression in endothelial cell survival.

              Magali Saint-Geniez, N Paz, Patricia D’Amore … (2012)
              Vascular endothelial growth factor (VEGF) plays a crucial role in developmental and pathological angiogenesis. Expression of VEGF in quiescent adult tissue suggests a potential role in the maintenance of mature blood vessels. We demonstrate, using a Vegf-lacZ reporter mouse model, that VEGF is expressed by arterial but not by venous or capillary endothelial cells (ECs) in vivo. Using an in vitro model, we show that arterial shear stress of human umbilical vein ECs (HUVECs) decreases apoptosis and increases VEGF expression, which is mediated by the induction of Krüppel-like factor 2 (KLF2). Additionally, shear stress stimulates the expression of VEGF receptor 2 (VEGFR2) and is associated with its activation. Knockdown of VEGF in shear stressed HUVECs blocks the protective effect of shear stress, resulting in EC apoptosis equivalent to that in control ECs cultured under static conditions. Similarly, treatment of ECs subjected to arterial shear stress with the VEGF receptor tyrosine kinase inhibitor SU1498, or VEGFR2 neutralizing antiserum, led to increased apoptosis, demonstrating that the mechanoprotection from increased shear is mediated by VEGFR2. Taken together, these studies suggest that arterial flow induces VEGF-VEGFR2 autocrine-juxtacrine signaling, which is a previously unidentified mechanism for vascular EC survival in adult arterial blood vessels.
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                Author and article information

                Contributors
                E.S. Bijsmans: ebijsmans@rvc.ac.uk
                Journal
                Journal ID (nlm-ta): J Vet Intern Med
                Journal ID (iso-abbrev): J. Vet. Intern. Med
                Journal ID (doi): 10.1111/(ISSN)1939-1676
                Journal ID (publisher-id): JVIM
                Title: Journal of Veterinary Internal Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0891-6640
                ISSN (Electronic): 1939-1676
                Publication date (Electronic): 07 April 2017
                Publication date (Print): May-Jun 2017
                Volume: 31
                Issue: 3 ( doiID: 10.1111/jvim.2017.31.issue-3 )
                Pages: 650-660
                Affiliations
                [ 1 ] Department of Comparative Biomedical SciencesRoyal Veterinary College LondonUK
                [ 2 ] Department of Clinical Science and ServicesRoyal Veterinary College Hatfield HertfordshireUK
                Author notes
                [*] [* ]Corresponding author: E.S. Bijsmans, Department of Comparative Biomedical Sciences, Royal Veterinary College, Royal College Street, London, NW1 0TU UK; e‐mail: ebijsmans@ 123456rvc.ac.uk .
                Article
                Publisher ID: JVIM14655
                DOI: 10.1111/jvim.14655
                PMC ID: 5435049
                PubMed ID: 28387019
                SO-VID: 333f03b1-85ef-4cf6-9afc-e686436516bd
                Copyright © Copyright © 2017 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.
                License:

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date received : 20 June 2016
                Date revision received : 06 October 2016
                Date accepted : 12 December 2016
                Page count
                Figures: 5, Tables: 5, Pages: 11, Words: 9509
                Funding
                Funded by: Zoetis Ltd
                Categories
                Subject: Standard Article
                Subject: SMALL ANIMAL
                Subject: Standard Articles
                Subject: Cardiology
                Custom metadata
                source-schema-version-number 2.0
                component-id jvim14655
                cover-date May/June 2017
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.0.9 mode:remove_FC converted:17.05.2017

                ScienceOpen disciplines: Veterinary medicine
                Keywords: chronic kidney disease,hypertension
                Data availability:
                ScienceOpen disciplines: Veterinary medicine
                Keywords: chronic kidney disease, hypertension

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