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7. Comparative toxicity of citalopram and the newer antidepressants after overdose

Author

Kelly, C.A., Dhaun, N., Laing, W.J., Strachan, F.E., Good, A.M., and Bateman, D.N.

Subjects
Venlafaxine -- Risk factors, Venlafaxine -- Comparative analysis, Serotonin uptake inhibitors -- Adverse and side effects, Citalopram -- Risk factors, Citalopram -- Comparative analysis, Antidepressants -- Adverse and side effects, Antidepressants -- Research, Environmental issues, Health, Pharmaceuticals and cosmetics industries
Abstract

Objective: To compare the toxicity of citalopram, venlafaxine, mirtazapine, and nefazadone after overdose. Methods: Two-year retrospective review of consecutive patients admitted to the toxicology unit of Edinburgh Royal Infirmary. Outcome measure included physiological variables, ECG recordings, peak creatine kinase, development of arrhythmias, seizure, tremor or agitation, and the need for admission to a critical care facility. Results: A total of 225 patients were studied. Venlafaxine was associated with a significantly higher pulse rate (p Key Words: Citalopram; Venlafaxine; Nefazadone; Mirtazapine; Poisoning., INTRODUCTION Over the last few years there has been a reduction in the use of tricyclic antidepressants with a simultaneous increase in prescriptions for selective serotonin reuptake inhibitors (SSRIs) and [...]

Published
2004

8. P1578Outcomes in patients with renal impairment and myocardial injury or infarction identified by high-sensitivity cardiac troponin testing: a secondary analysis of the High-STEACS trial

Author

Gallacher, P J, primary, Miller-Hodges, E, additional, Shah, A, additional, Anand, A, additional, Lee, K K, additional, Chapman, A R, additional, Farrah, T, additional, Halbesma, N, additional, Blackmur, J, additional, Newby, D E, additional, Mills, N L, additional, and Dhaun, N, additional

Published
2019
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11. Smooth Muscle Endothelin B Receptors Regulate Blood Pressure but Not Vascular Function or Neointimal Remodeling

Author

Miller, E, Czopek, A, Duthie, KM, Kirkby, NS, van de Putte, EEF, Christen, S, Kimmitt, RA, Moorhouse, R, Castellan, RFP, Kotelevtsev, YV, Kuc, RE, Davenport, AP, Dhaun, N, Webb, DJ, Hadoke, PWF, Davenport, Anthony [0000-0002-2096-3117], and Apollo - University of Cambridge Repository

Subjects
EXPRESSION, Science & Technology, BALLOON ANGIOPLASTY, NITRIC-OXIDE, hypertension, RADIOLIGAND BINDING, 1103 Clinical Sciences, respiratory system, neointima, musculoskeletal system, 1102 Cardiovascular Medicine And Haematology, autoradiography, Peripheral Vascular Disease, ORGAN-CULTURE, Cardiovascular System & Hematology, CELLS, endothelin-1, cardiovascular system, Cardiovascular System & Cardiology, ET(B) RECEPTORS, vasoconstriction, CAROTID-ARTERY, Life Sciences & Biomedicine, KNOCKOUT MICE, circulatory and respiratory physiology
Abstract

The role of smooth muscle endothelin$_{B}$ (ET$_{B}$) receptors in regulating vascular function, blood pressure (BP), and neointimal remodeling has not been established. Selective knockout mice were generated to address the hypothesis that loss of smooth muscle ET$_{B}$ receptors would reduce BP, alter vascular contractility, and inhibit neointimal remodeling. ET$_{B}$ receptors were selectively deleted from smooth muscle by crossing floxed ET$_{B}$ mice with those expressing cre-recombinase controlled by the transgelin promoter. Functional consequences of ET$_{B}$ deletion were assessed using myography. BP was measured by telemetry, and neointimal lesion formation induced by femoral artery injury. Lesion size and composition (day 28) were analyzed using optical projection tomography, histology, and immunohistochemistry. Selective deletion of ET$_{B}$ was confirmed by genotyping, autoradiography, polymerase chain reaction, and immunohistochemistry. ET$_{B}$-mediated contraction was reduced in trachea, but abolished from mesenteric veins, of knockout mice. Induction of ET$_{B}$-mediated contraction in mesenteric arteries was also abolished in these mice. Femoral artery function was unaltered, and baseline BP modestly elevated in smooth muscle ET$_{B}$ knockout compared with controls (+4.2±0.2 mm Hg; $\textit{P}$

Published
2017
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20. Markers for work disability in anti-neutrophil cytoplasmic antibody-associated vasculitis

Author

Basu, N., primary, McClean, A., additional, Harper, L., additional, Amft, E. N., additional, Dhaun, N., additional, Luqmani, R. A., additional, Little, M. A., additional, Jayne, D. R. W., additional, Flossmann, O., additional, McLaren, J., additional, Kumar, V., additional, Erwig, L. P., additional, Reid, D. M., additional, Macfarlane, G. J., additional, and Jones, G. T., additional

Published
2014
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21. Urinary endothelin-1 in chronic kidney disease and as a marker of disease activity in lupus nephritis.

Author

Dhaun, N., Lilitkarntakul, P., Macintyre, I.M., Muilwijk, E.W., Johnston, N.R., Kluth, D.C., Webb, D.J., Goddard, J., Dhaun, N., Lilitkarntakul, P., Macintyre, I.M., Muilwijk, E.W., Johnston, N.R., Kluth, D.C., Webb, D.J., and Goddard, J.

Abstract

Item does not contain fulltext, Chronic inflammation contributes to the development and progression of chronic kidney disease (CKD). Identifying renal inflammation early is important. There are currently no specific markers of renal inflammation. Endothelin-1 (ET-1) is implicated in the pathogenesis of CKD. Thus, we investigated the impact of progressive renal dysfunction and renal inflammation on plasma and urinary ET-1 concentrations. In a prospective study, plasma and urinary ET-1 were measured in 132 subjects with CKD stages 1 to 5, and fractional excretion of ET-1 (FeET-1) was calculated. FeET-1, serum C-reactive protein (CRP), urinary ET-1:creatinine ratio, and urinary albumin:creatinine ratio were also measured in 29 healthy volunteers, 85 subjects with different degrees of inflammatory renal disease but normal renal function, and in 10 subjects with rheumatoid arthritis without renal involvement (RA). In subjects with nephritis associated with systemic lupus erythematosus (SLE), measurements were done before and after 6 mo of treatment. In subjects with CKD, plasma ET-1 increased linearly as renal function declined, whereas FeET-1 rose exponentially. In subjects with normal renal function, FeET-1 and urinary ET-1:creatinine ratio were higher in SLE subjects than in other groups (7.7 +/- 2.7%, 10.0 +/- 3.0 pg/mumol, both P < 0.001), and correlated with CRP, and significantly higher than in RA subjects (both P < 0.01) with similar CRP concentrations. In SLE patients, following treatment, FeET-1 fell to 3.6 +/- 1.4% (P < 0.01). Renal ET-1 production increases as renal function declines. In subjects with SLE, urinary ET-1 may be a useful measure of renal inflammatory disease activity while measured renal function is still normal.

Published
2009

22. Explaining fatigue in ANCA-associated vasculitis

Author

Basu, N., primary, McClean, A., additional, Harper, L., additional, Amft, E. N., additional, Dhaun, N., additional, Luqmani, R. A., additional, Little, M. A., additional, Jayne, D. R. W., additional, Flossmann, O., additional, McLaren, J., additional, Kumar, V., additional, Erwig, L. P., additional, Reid, D. M., additional, Macfarlane, G. J., additional, and Jones, G. T., additional

Published
2013
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23. OP0124 Contextualising quality of life in ANCA associated vasculitis (AAV)

Author

Basu, N., primary, McClean, A., additional, Luqmani, R., additional, Harper, L., additional, Flossmann, O., additional, Jayne, D., additional, Little, M., additional, Amft, E.N., additional, Dhaun, N., additional, McLaren, J., additional, Kumar, V., additional, Erwig, L., additional, Jones, G., additional, Reid, D., additional, and Macfarlane, G., additional

Published
2013
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26. Markers for work disability in ANCA-associated vasculitis

Author

Basu, N., primary, Mcclean, A., additional, Harper, L., additional, Little, M., additional, Luqmani, R., additional, Flossmann, O., additional, Jayne, D., additional, Dhaun, N., additional, Kumar, V., additional, Mclaren, J., additional, Amft, E., additional, Erwig, L., additional, Macfarlane, G., additional, Reid, D., additional, and Jones, G., additional

Published
2013
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27. Basic Science * 208. Stem Cell Factor Expression is Increased in the Skin of Patients with Systemic Sclerosis and Promotes Proliferation and Migration of Fibroblasts in vitro

Author

Karrar, S., primary, Shiwen, X., additional, Nikotorowicz-Buniak, J., additional, Abraham, D. J., additional, Denton, C., additional, Stratton, R., additional, Bayley, R., additional, Kite, K. A., additional, Clay, E., additional, Smith, J. P., additional, Kitas, G. D., additional, Buckley, C., additional, Young, S. P., additional, Ye, L., additional, Zhang, L., additional, Goodall, J., additional, Gaston, H., additional, Xu, H., additional, Lutalo, P. M., additional, Zhao, Y., additional, Meng Choong, L., additional, Sangle, S., additional, Spencer, J., additional, D'Cruz, D., additional, Rysnik, O. J., additional, McHugh, K., additional, Bowness, P., additional, Rump-Goodrich, L., additional, Mattey, D., additional, Kehoe, O., additional, Middleton, J., additional, Cartwright, A., additional, Schmutz, C., additional, Askari, A., additional, Gardner, D. H., additional, Jeffery, L. E., additional, Raza, K., additional, Sansom, D. M., additional, Fitzpatrick, M., additional, Wallace, G., additional, Young, S., additional, Shaw, J., additional, Hatano, H., additional, Cauli, A., additional, Giles, J. L., additional, Mathieu, A., additional, Kollnberger, S., additional, Webster, S., additional, Ellis, L., additional, O'Brien, L. M., additional, Fitzmaurice, T. J., additional, Nazeer Moideen, A., additional, Evans, L., additional, Osgood, L., additional, Williams, A., additional, Jones, S., additional, Thomas, C., additional, O'Donnell, V., additional, Nowell, M., additional, Ouboussad, L., additional, Savic, S., additional, Dickie, L. J., additional, Hintze, J., additional, Wong, C. H., additional, Cook, G. P., additional, Buch, M., additional, Emery, P., additional, McDermott, M. F., additional, Hardcastle, S. A., additional, Gregson, C. L., additional, Deere, K., additional, Davey Smith, G., additional, Dieppe, P., additional, Tobias, J. H., additional, Dennison, E., additional, Edwards, M., additional, Bennett, J., additional, Coggon, D., additional, Palmer, K., additional, Cooper, C., additional, McWilliams, D., additional, Young, A., additional, Kiely, P. D., additional, Walsh, D., additional, Taylor, H. J., additional, Harding, I., additional, Hutchinson, J., additional, Nelson, I., additional, Blom, A., additional, Tobias, J., additional, Clark, E., additional, Parker, J., additional, Bukhari, M., additional, Jayakumar, K., additional, Kiely, P., additional, Diffin, J., additional, Lunt, M., additional, Marshall, T., additional, Chipping, J., additional, Symmons, D., additional, Verstappen, S., additional, Bluett, J., additional, Bowes, J., additional, Ho, P., additional, McHugh, N., additional, Buden, D., additional, Fitzgerald, O., additional, Barton, A., additional, Glossop, J. R., additional, Nixon, N. B., additional, Emes, R. D., additional, Dawes, P. T., additional, Farrell, W. E., additional, Mattey, D. L., additional, Scott, I. C., additional, Steer, S., additional, Seegobin, S., additional, Hinks, A. M., additional, Eyre, S., additional, Morgan, A., additional, Wilson, A. G., additional, Hocking, L., additional, Wordsworth, P., additional, Worthington, J., additional, Cope, A., additional, Lewis, C. M., additional, Guerra, S., additional, Ahmed, B. A., additional, Abraham, D., additional, Fonseca, C., additional, Robinson, J., additional, Taylor, J., additional, Haroon Rashid, L., additional, Flynn, E., additional, Isaacs, J., additional, Barrett, J. H., additional, Kingston, B., additional, Ahmed, M., additional, Kirwan, J. R., additional, Marshall, R., additional, Chapman, K., additional, Pearson, R., additional, Heycock, C., additional, Kelly, C., additional, Rynne, M., additional, Saravanan, V., additional, Hamilton, J., additional, Saeed, A., additional, Coughlan, R., additional, Carey, J. J., additional, Farah, Z., additional, Matthews, W., additional, Bell, C., additional, Petford, S., additional, Tibbetts, L.-M., additional, Douglas, K. M. J., additional, Holden, W., additional, Ledingham, J., additional, Fletcher, M., additional, Winfield, R., additional, Price, Z., additional, Mackay, K., additional, Dixon, C., additional, Oppong, R., additional, Jowett, S., additional, Nicholls, E., additional, Whitehurst, D., additional, Hill, S., additional, Hammond, A., additional, Hay, E., additional, Dziedzic, K., additional, Righetti, C., additional, Lebmeier, M., additional, Manning, V. L., additional, Hurley, M., additional, Scott, D. L., additional, Choy, E., additional, Bearne, L., additional, Nikiphorou, E., additional, Morris, S., additional, James, D., additional, Wong, E. C., additional, Long, J., additional, Fletcher, A., additional, Holmes, S., additional, Hockey, P., additional, Abbas, M., additional, Chattopadhyay, C., additional, Flint, J., additional, Gayed, M., additional, Schreiber, K., additional, Arthanari, S., additional, Nisar, M., additional, Khamashta, M., additional, Gordon, C., additional, Giles, I., additional, Robson, J., additional, Kiran, A., additional, Maskell, J., additional, Arden, N., additional, Hutchings, A., additional, Emin, A., additional, Culliford, D., additional, Dasgupta, B., additional, Hamilton, W., additional, Luqmani, R., additional, Jethwa, H., additional, Rowczenio, D., additional, Trojer, H., additional, Russell, T., additional, Loeffler, J., additional, Hawkins, P., additional, Lachmann, H., additional, Verma, I., additional, Syngle, A., additional, Krishan, P., additional, Garg, N., additional, McGowan, S. P., additional, Gerrard, D. T., additional, Chinoy, H., additional, Ollier, W. E., additional, Cooper, R. G., additional, Lamb, J. A., additional, Taborda, L., additional, Correia Azevedo, P., additional, Isenberg, D., additional, Leyland, K. M., additional, Judge, A., additional, Hunter, D., additional, Hart, D., additional, Javaid, M. K., additional, Edwards, M. H., additional, Litwic, A. E., additional, Jameson, K. A., additional, Deeg, D., additional, Cushnaghan, J., additional, Aihie Sayer, A., additional, Jagannath, D., additional, Parsons, C., additional, Stoppiello, L., additional, Mapp, P., additional, Ashraf, S., additional, Wilson, D., additional, Hill, R., additional, Scammell, B., additional, Wenham, C., additional, Shore, P., additional, Hodgson, R., additional, Grainger, A., additional, Aaron, J., additional, Hordon, L., additional, Conaghan, P., additional, Bar-Ziv, Y., additional, Beer, Y., additional, Ran, Y., additional, Benedict, S., additional, Halperin, N., additional, Drexler, M., additional, Mor, A., additional, Segal, G., additional, Lahad, A., additional, Haim, A., additional, Rath, U., additional, Morgensteren, D. M., additional, Salai, M., additional, Elbaz, A., additional, Vasishta, V. G., additional, Derrett-Smith, E., additional, Hoyles, R., additional, Khan, K., additional, Ezeonyeji, A., additional, Takhar, G., additional, Ong, V., additional, Loughrey, L., additional, Bissell, L.-A., additional, Hensor, E., additional, Abignano, G., additional, Redmond, A., additional, Del Galdo, F., additional, Hall, F. C., additional, Malaviya, A., additional, Baker, S., additional, Furlong, A., additional, Mitchell, A., additional, Godfrey, A. L., additional, Ruddlesden, M., additional, Hadjinicolaou, A., additional, Hughes, M., additional, Moore, T., additional, O'Leary, N., additional, Tracey, A., additional, Ennis, H., additional, Dinsdale, G., additional, Roberts, C., additional, Herrick, A., additional, Denton, C. P., additional, Guillevin, L., additional, Hunsche, E., additional, Rosenberg, D., additional, Schwierin, B., additional, Scott, M., additional, Krieg, T., additional, Anderson, M., additional, Matucci-Cerinic, M., additional, Alade, R., additional, Xu, S., additional, Nihtyanova, S., additional, Clark, K. E., additional, Tam, F. W. K., additional, Unwin, R., additional, Stratton, R. J., additional, Schreiber, B., additional, Seng Edwin Lim, C., additional, Corsiero, E., additional, Sutcliffe, N., additional, Wardemann, H., additional, Pitzalis, C., additional, Bombardieri, M., additional, Tahir, H., additional, Donnelly, S., additional, Greenwood, M., additional, Smith, T. O., additional, Easton, V., additional, Bacon, H., additional, Jerman, E., additional, Armon, K., additional, Poland, F., additional, Macgregor, A., additional, van der Heijde, D., additional, Sieper, J., additional, Elewaut, D., additional, Pangan, A. L., additional, Nguyen, D., additional, Badenhorst, C., additional, Kirby, S., additional, White, D., additional, Harrison, A., additional, Garcia, J. A., additional, Stebbings, S., additional, MacKay, J. W., additional, Aboelmagd, S., additional, Gaffney, K., additional, Deodhar, A., additional, Braun, J., additional, Mack, M., additional, Hsu, B., additional, Gathany, T., additional, Han, C., additional, Inman, R. D., additional, Cooper-Moss, N., additional, Packham, J., additional, Strauss, V., additional, Freeston, J. E., additional, Coates, L., additional, Nam, J., additional, Moverley, A. R., additional, Helliwell, P., additional, Wakefield, R., additional, Mease, P., additional, Fleischmann, R., additional, Wollenhaupt, J., additional, Kielar, D., additional, Woltering, F., additional, Stach, C., additional, Hoepken, B., additional, Arledge, T., additional, Gladman, D., additional, Coteur, G., additional, Kavanaugh, A., additional, Purcaru, O., additional, McInnes, I., additional, Gottlieb, A. B., additional, Puig, L., additional, Rahman, P., additional, Ritchlin, C., additional, Li, S., additional, Wang, Y., additional, Mendelsohn, A., additional, Doyle, M., additional, Tillett, W., additional, Jadon, D., additional, Shaddick, G., additional, Cavill, C., additional, Robinson, G., additional, Sengupta, R., additional, Korendowych, E., additional, de Vries, C., additional, Thomas, R. C., additional, Shuto, T., additional, Busquets-Perez, N., additional, Marzo-Ortega, H., additional, McGonagle, D., additional, Richards, G., additional, Bingham, S., additional, John Hamlin, P., additional, Adshead, R., additional, Cambridge, S., additional, Suppiah, P., additional, Cullinan, M., additional, Nolan, A., additional, Thompson, W. M., additional, Mathieson, H. R., additional, Mackie, S. L., additional, Bryer, D., additional, Krutikov, M., additional, Gray, L., additional, Bruce, E., additional, Keat, A., additional, Innes, W., additional, Pandit, R., additional, Kay, L., additional, Lapshina, S., additional, Myasoutova, L., additional, Erdes, S., additional, Wallis, D., additional, Waldron, N., additional, Thorne, I., additional, Harris, C., additional, Vohra, K., additional, Khinchi, D., additional, Kaur, L., additional, Jones, A., additional, Harrison, N., additional, Harris, D., additional, Jones, T., additional, Rees, J., additional, Bennett, A., additional, Fazal, S., additional, Tugnet, N., additional, Barkham, N., additional, Basu, N., additional, McClean, A., additional, Harper, L., additional, Amft, E. N., additional, Dhaun, N., additional, Luqmani, R. A., additional, Little, M. A., additional, Jayne, D. R., additional, Flossmann, O., additional, McLaren, J., additional, Kumar, V., additional, Reid, D. M., additional, Macfarlane, G. J., additional, Jones, G., additional, Yates, M., additional, Watts, R. A., additional, Igali, L., additional, Mukhtyar, C., additional, Doll, H., additional, Yew, S., additional, Suppiah, R., additional, Hoglund, P., additional, Jayne, D., additional, Westman, K., additional, Win Maw, W., additional, Patil, P., additional, Williams, M., additional, Adizie, T., additional, Christidis, D., additional, Borg, F., additional, Robertson, A., additional, Croft, A. P., additional, Smith, S., additional, Carr, S., additional, Youssouf, S., additional, Salama, A., additional, Pusey, C., additional, and Morgan, M., additional

Published
2013
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28. BMJ

Author

Dhaun, N., primary, Montgomery, L., additional, Whitworth, C., additional, Hughes, J., additional, and Harper, J., additional

Published
2011
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29. BMJ

Author

Ford, T., primary, Whitworth, C., additional, and Dhaun, N., additional

Published
2010
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35. Endothelin-1 and the kidney--beyond BP.

Author

Dhaun N, Webb DJ, Kluth DC, Dhaun, Neeraj, Webb, David J, and Kluth, David C

Abstract

Since its discovery over 20 years ago endothelin-1 (ET-1) has been implicated in a number of physiological and pathophysiological processes. Its role in the development and progression of chronic kidney disease (CKD) is well established and is an area of ongoing intense research. There are now available a number of ET receptor antagonists many of which have been used in trials with CKD patients and shown to reduce BP and proteinuria. However, ET-1 has a number of BP-independent effects. Importantly, and in relation to the kidney, ET-1 has clear roles to play in cell proliferation, podocyte dysfunction, inflammation and fibrosis, and arguably, these actions of ET-1 may be more significant in the progression of CKD than its prohypertensive actions. This review will focus on the potential role of ET-1 in renal disease with an emphasis on its BP-independent actions. [ABSTRACT FROM AUTHOR]

Published
2012
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36. Risk factors for metabolic syndrome independently predict arterial stiffness and endothelial dysfunction in patients with chronic kidney disease and minimal comorbidity.

Author

Lilitkarntakul P, Dhaun N, Melville V, Kerr D, Webb DJ, Goddard J, Lilitkarntakul, Pajaree, Dhaun, Neeraj, Melville, Vanessa, Kerr, Debbie, Webb, David J, and Goddard, Jane

Abstract

Objective: Metabolic syndrome (MS) is common in patients with chronic kidney disease (CKD), but its contribution to arterial stiffness and endothelial dysfunction in CKD is not well defined. We hypothesized that risk factors for MS would independently predict arterial stiffness and endothelial dysfunction in CKD patients.Research Design and Methods: Risk factors for MS, carotid-femoral pulse wave velocity (CF-PWV) and flow-mediated dilation (FMD) as measures of arterial stiffness and endothelial dysfunction, respectively, were assessed in 113 minimally comorbid CKD patients and in 23 matched control subjects.Results: CF-PWV correlated with systolic blood pressure (SBP), waist circumference, and plasma glucose (r(2) = 0.25, 0.09, and 0.09; P < 0.01 for all). FMD correlated with SBP (r(2) = 0.09; P < 0.01) and waist circumference (r(2) = 0.03; P < 0.05). CF-PWV increased progressively (r(2) = 0.07; P < 0.01) with increasing number of risk factors for MS. In multiple linear regression, SBP and waist circumference were independent determinants of CF-PWV, whereas only SBP predicted FMD.Conclusions: The number of MS risk factors is an important determinant of arterial stiffness in CKD patients irrespective of the degree of renal impairment. Although BP remains the major determinant of arterial stiffness and endothelial dysfunction, waist circumference independently predicts arterial stiffness. MS risk factors, particularly abdominal girth, are potential targets for future interventional studies in patients with CKD. [ABSTRACT FROM AUTHOR]

Published
2012
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37. Endothelin receptor antagonism and renin inhibition as treatment options for scleroderma kidney.

Author

Dhaun N, MacIntyre IM, Bellamy CO, Kluth DC, Dhaun, Neeraj, MacIntyre, Iain M, Bellamy, Christopher O C, and Kluth, David C

Abstract

Scleroderma renal crisis (SRC) is an important complication of scleroderma associated with significant morbidity and mortality. Current treatment of patients with SRC focuses on renin-angiotensin-aldosterone system (RAAS) blockade, ideally using angiotensin-converting enzyme inhibitors. We present a case of SRC in a patient established on maximal tolerable RAAS-blocking treatment. Introduction of a selective endothelin-A receptor antagonist followed by a direct renin inhibitor provided excellent blood pressure control and complete abrogation of heavy proteinuria. This was associated with a decrease in kidney function, with serum creatinine level increasing by approximately 30%. This increase is considered acceptable after the introduction of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, is regarded as an indicator of drug efficacy, and confers longer term renal protection. Both endothelin receptor antagonism and direct renin inhibition offer alternate novel therapies for patients with SRC. Their ability to preserve or improve kidney function is unclear. [ABSTRACT FROM AUTHOR]

Published
2009
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48. Apelin levels in patients with polyuria-polydipsia syndrome upon copeptin stimulation tests.

Author

Bizzozero CA, Monnerat S, Chapman FA, Dhaun N, Refardt J, and Christ-Crain M

Abstract

Objective: Differentiating between arginine vasopressin deficiency (AVP-D) and primary polydipsia (PP) requires a copeptin-stimulation test. We aimed to characterize changes in apelin, an endogenous hormone antagonising AVP, upon copeptin-stimulation tests., Design: Post-hoc secondary analysis of a multicentric cross-over diagnostic study (NCT03572166)., Methods: Apelin levels were measured in patients included at the University Hospital Basel. The primary outcome was the absolute difference in apelin between baseline and peak of copeptin-stimulation tests with hypertonic saline and arginine infusion. Secondary objectives included the diagnostic ability of apelin., Results: Thirty-eight patients were analysed, 23 (60%) had PP and 15 (40%) had AVP-D. No difference was seen between baseline median [IQR] apelin levels in PP and AVP-D (1079 [912, 1225] and 910 [756, 1039] pmol/l, respectively). Upon hypertonic saline, apelin decreased by -241 [-326, -124] pmol/l in PP and -47.2 [-198, 5.86] pmol/l in AVP-D (p=0.022). The area under the curve (AUC) to differentiate PP from AVP-D was 97.1% (95%CI: 90.5, 100) for copeptin and 49.3% (95%CI: 30.4, 68.1) for apelin (p<.001). Upon arginine, apelin decreased by -39.2 [-96.4, 39.8] pmol/l in PP and increased by 25.8 [2.8, 113.0] pmol/l in AVP-D (p=0.1). The AUC was 97.1% [95%CI: 79.6, 98.0] for copeptin and 60.5% [95%CI: 39.8, 80.0] for apelin (p=0.007)., Conclusions: Our findings suggest that apelin decreases to a greater extent in PP compared to AVP-D upon copeptin-stimulation tests. However, copeptin remains the best marker to differentiate AVP-D from PP., (© The Author(s) 2024. Published by Oxford University Press on behalf of European Society of Endocrinology.)

Published
2024
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49. Cardiovascular and renal effects of apelin in chronic kidney disease: a randomised, double-blind, placebo-controlled, crossover study.

Author

Chapman FA, Melville V, Godden E, Morrison B, Bruce L, Maguire JJ, Davenport AP, Newby DE, and Dhaun N

Subjects
Humans, Male, Female, Double-Blind Method, Middle Aged, Adult, Blood Pressure drug effects, Kidney drug effects, Kidney physiopathology, Kidney metabolism, Aged, Vascular Resistance drug effects, Renal Circulation drug effects, Natriuresis drug effects, Hemodynamics drug effects, Cardiac Output drug effects, Renal Insufficiency, Chronic drug therapy, Renal Insufficiency, Chronic physiopathology, Cross-Over Studies, Glomerular Filtration Rate drug effects, Intercellular Signaling Peptides and Proteins, Apelin
Abstract

Chronic kidney disease (CKD) affects ~10% of the population and cardiovascular disease is its commonest complication. Despite treatment, patient outcomes remain poor and newer therapies are urgently needed. Here, we investigated the systemic and renal effects of apelin in CKD. In a randomized, double-blind, placebo-controlled, crossover study, 24 subjects (12 patients with CKD and 12 matched healthy subjects) received pyroglutamated apelin-13 ([Pyr 1 ]apelin-13, 1 nmol/min and 30 nmol/min) or matched placebo on two separate visits. Systemic and renal hemodynamics were monitored throughout. The co-primary endpoints were change in systemic vascular resistance index and renal blood flow. Secondary endpoints were change in blood pressure, cardiac output, pulse wave velocity, glomerular filtration rate, natriuresis, free water clearance and urinary protein excretion. In both health and CKD, 30 nmol/min [Pyr 1 ]apelin-13 reduced mean arterial pressure by ~4%, systemic vascular resistance by ~12%, and increased cardiac index by ~10%, compared to placebo (p < 0.05 for all). Both doses of [Pyr 1 ]apelin-13 increased renal blood flow by ~15%, natriuresis by ~20% and free water clearance by ~10%, compared to placebo (p < 0.05 for all). In patients with chronic kidney disease only, glomerular filtration rate fell by ~10%, effective filtration fraction by ~5% and proteinuria by ~25% (p < 0.01 for all). Apelin has short-term cardiovascular and renal benefits in CKD. If maintained longer-term, these should improve patient outcomes. Clinical trials of long-acting oral apelin agonists are justified in CKD and other conditions with impaired salt and water balance. Registration number at www.clinicalTrials.gov : NCT03956576. Funded by Kidney Research UK., (© 2024. The Author(s).)

Published
2024
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50. Effects of Zibotentan Alone and in Combination with Dapagliflozin on Fluid Retention in Patients with CKD.

Author

Smeijer JD, Wasehuus VS, Dhaun N, Górriz JL, Soler MJ, Åstrand M, Mercier AK, Greasley PJ, Ambery P, and Heerspink HJL

Subjects
Humans, Male, Female, Aged, Middle Aged, Endothelin Receptor Antagonists therapeutic use, Endothelin Receptor Antagonists administration & dosage, Endothelin A Receptor Antagonists therapeutic use, Endothelin A Receptor Antagonists administration & dosage, Benzhydryl Compounds therapeutic use, Benzhydryl Compounds administration & dosage, Glucosides therapeutic use, Glucosides administration & dosage, Renal Insufficiency, Chronic complications, Renal Insufficiency, Chronic drug therapy, Drug Therapy, Combination, Sodium-Glucose Transporter 2 Inhibitors therapeutic use, Sodium-Glucose Transporter 2 Inhibitors administration & dosage
Published
2024
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