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3. Development of the Kidney

Author

Smyth, Ian M., primary, Cullen-McEwen, Luise A., additional, Caruana, Georgina, additional, Black, M. Jane, additional, and Bertram, John F., additional

Published
2017
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4. Contributors

Author

Abbasi, Soraya, primary, Abbey, James, additional, Adzick, N. Scott, additional, Ahn, Sun-Young, additional, Albertine, Kurt H., additional, Allegaert, Karel, additional, Alper, Seth L., additional, Altit, Gabriel, additional, Altschuler, Steven M., additional, Alvaro, Ruben E., additional, Amorosa, Jennifer M.H., additional, Anbuhl, Kelsey L., additional, Andersen, Claus Yding, additional, Anderson, Richard A., additional, Askenazi, David J., additional, Auten, Richard Lambert, additional, Autmizguine, Julie, additional, Azhibekov, Timur, additional, Back, Stephen A., additional, Badaut, Jérôme, additional, Baker, Peter Russell, additional, Ballard, Philip L., additional, Bancalari, Eduardo H., additional, Barichello, Tatiana, additional, Battaglia, Frederick, additional, Baum, Michel, additional, Beggs, Simon, additional, Bell, Edward F., additional, Benchimol, Corinne, additional, Benders, Manon J.N.L., additional, Bennet, Laura, additional, Bennett, Phillip R., additional, Berger, Melvin, additional, Bernhard, Wolfgang, additional, Bertram, John F., additional, Bhosle, Vikrant K., additional, Bhutani, Vinod K., additional, Black, M. Jane, additional, Bliss, Joseph M., additional, Bolender, David L., additional, Brandenburg, Joline E., additional, Broussard, Delma L., additional, Brown, Laura Davidson, additional, Burrin, Douglas G., additional, Cannon, Barbara, additional, Caplan, Michael, additional, Carlson, Susan E., additional, Carlton, David P., additional, Caruana, Georgina, additional, Cashore, William J., additional, Chaemsaithong, Piya, additional, Chaiyasit, Noppadol, additional, Charlton, Jennifer R., additional, Cheatham, Carol L., additional, Chemtob, Sylvain, additional, Chen, Yi-Yung, additional, Chevalier, Robert L., additional, Chheda, Sadhana, additional, Childs, Andrew J., additional, Christensen, Robert D., additional, Chu, Alison, additional, Chu, David H., additional, Cilio, Maria Roberta, additional, Clark, David A., additional, Cleary-Goldman, Jane, additional, Clemente, Ethel G., additional, Clements, John A., additional, Clyman, Ronald I., additional, Cohen, Susan S., additional, Colombo, John, additional, Cowett, Richard M., additional, Crawford, Peter A., additional, Crowe, James E., additional, Cullen-McEwen, Luise A., additional, Cutfield, Wayne S., additional, D'Alton, Mary E., additional, Danzer, Enrico, additional, Delacourt, Christophe, additional, Devaskar, Sherin U., additional, Diacovo, Thomas G., additional, Docheva, Nikolina, additional, Dormans, John P., additional, Dysart, Kevin, additional, El-Khuffash, Afif, additional, Ellis, Peter James, additional, Empey, Kerry McGarr, additional, Ercal, Baris, additional, Erdős, Melinda, additional, Erickson, Robert P., additional, Fahim, Mohamed A., additional, Faksh, Arij, additional, Frank, Hans-Georg, additional, Friedlich, Philippe S., additional, Friedman, Jed, additional, Gao, Yuansheng, additional, Garland, Marianne, additional, Geddes, Donna, additional, Georgieff, Michael K., additional, Gien, Jason, additional, Giussani, Dino A., additional, Goldman, Armond S., additional, González, Efrén, additional, Good, Misty, additional, Grant, Denis M., additional, Green, Lucy R., additional, Grigoriou, Emmanouil, additional, Grimberg, Adda, additional, Gross, Ian, additional, Grunau, Ruth E., additional, Guignard, Jean-Pierre, additional, Gunn, Alistair Jan, additional, Gurtunca, Nursen, additional, Hadchouel, Alice, additional, Haddad, Gabriel G., additional, Hagberg, Henrik, additional, Hale, Thomas, additional, Hambidge, K. Michael, additional, Hammerman, Cathy, additional, Hansen, Thor Willy Ruud, additional, Hanson, Mark A., additional, Harding, Richard, additional, Harris, Mary Catherine, additional, Hartmann, Peter, additional, Hassiotou, Foteini, additional, Haugen, Guttorm, additional, Hawkes, Colin P., additional, Hay, William W., additional, Hayward, Christina E., additional, Heine, Vivi M., additional, Hellström, Ann, additional, Helmrath, Michael A., additional, Hendricks-Muñoz, Karen D., additional, Herrera, Emilio, additional, Hiatt, Michael J., additional, Hoath, Steven B., additional, Hooper, Stuart B., additional, Huang, Stephen A., additional, Iacobellli, Silvia, additional, Inder, Terrie E., additional, Iruela-Arispe, M. Luisa, additional, Jadcherla, Sudarshan R., additional, Jain, Deepak, additional, Jansson, Thomas, additional, Jefferies, John Lynn, additional, Jetton, Jennifer G., additional, Jobe, Alan H., additional, Johnson, Lois H., additional, Johnston, Richard B., additional, Jones, Rebecca Lee, additional, Jose, Pedro A., additional, Kalhan, Satish C., additional, Kallapur, Suhas G., additional, Kaplan, Michael, additional, Kaplan, Stanley, additional, Karpen, Heidi Eigenrauch, additional, Karpen, Saul J., additional, Karumanchi, S. Ananth, additional, Kaskel, Frederick J., additional, Katheria, Anup C., additional, Katz, Lorraine E. Levitt, additional, Keeney, Susan E., additional, Kern, Steven E., additional, Khanjani, Shirin, additional, Kilpatrick, Laurie E., additional, Kim, Chang-Ryul, additional, Kinsella, John P., additional, Kiserud, Torvid, additional, Koenig, Joyce M., additional, Kollmann, Tobias R., additional, Kolls, Jay K., additional, Krebs, Nancy F., additional, Kulik, Thomas J., additional, Kutikov, Jessica Katz, additional, Lakshminrusimha, Satyan, additional, Lamola, Angelo A., additional, Lasunción, Miguel Angel, additional, Lavoie, Pascal M., additional, LeBien, Tucker W., additional, Lee, Mary M., additional, Lee, Matthew K., additional, Lee, Yvonne K., additional, Leibel, Sandra, additional, Levine, Fred, additional, Levy, Ofer, additional, Liu, Yang, additional, Lobritto, Steven, additional, Loomis, Cynthia A., additional, Lopez, Colleen A., additional, MacIntyre, David A., additional, Mahe, Maxime M., additional, Maheshwari, Akhil, additional, Mankouski, Anastasiya, additional, Mantilla, Carlos B., additional, Marchant, Arnaud, additional, Margolis, Kara Gross, additional, Mariscalco, M. Michele, additional, Maródi, László, additional, Maršál, Karel, additional, Martin, Richard J., additional, Matsell, Douglas G., additional, Matthews, Dwight E., additional, McArdle, Harry J., additional, McManaman, James L., additional, McNamara, Patrick J., additional, McQuillen, Patrick S., additional, McQuinn, Tim C., additional, Mercer, Judith S., additional, Meschia, Giacomo, additional, Miller, Steven P., additional, Minoo, Parviz, additional, Monagle, Paul, additional, Mortola, Jacopo P., additional, Muglia, Louis J., additional, Munshi, Upender K., additional, Namgung, Ran, additional, Narasimhan, Sumana, additional, Nedergaard, Jan, additional, Neu, Josef, additional, Nigam, Sanjay K., additional, Nogee, Lawrence M., additional, Noori, Shahab, additional, O'Brien, Barbara M., additional, Ohls, Robin K., additional, Ortega-Senovilla, Henar, additional, O'Sullivan, Justin M., additional, Owusu, Sarah A., additional, Pal, Abhijeet, additional, Panitch, Howard B., additional, Penn, Anna A., additional, Penn, Raymond B., additional, Pernia, Cameron, additional, Philipps, Anthony F., additional, Picoraro, Joseph A., additional, Pisani, Francesco, additional, Pleasure, David, additional, Pleasure, Jeanette R., additional, Pleasure, Samuel J., additional, Pomeroy, Scott L., additional, Post, Martin, additional, Prakash, Y.S., additional, Prozialeck, Joshua D., additional, Pysher, Theodore J., additional, Quigley, Raymond, additional, Rabinovitch, Marlene, additional, Raffay, Thomas M., additional, Raj, J. Usha, additional, Ramsey, Haley, additional, Rana, Sarosh, additional, Randis, Tara Marie, additional, Ranger, Manon, additional, Ratner, Adam J., additional, Regnault, Timothy R.H., additional, Rigatto, Henrique, additional, Rintoul, Natalie E., additional, Romero, Roberto, additional, Rose, James C., additional, Rosenfeld, Charles R., additional, Ross, A. Catharine, additional, Rozycki, Henry J., additional, Ryan, Thomas D., additional, Sahni, Rakesh, additional, Sajti, Eniko, additional, Sarnat, Harvey B., additional, Satlin, Lisa M., additional, Saugstad, Ola Didrik, additional, Schierding, William, additional, Schmalstieg, Frank C., additional, Schwartz, George J., additional, Schwartz, Jeffrey, additional, Segar, Jeffrey L., additional, Selewski, David T., additional, Seri, Istvan, additional, Shaffer, Thomas H., additional, Shah, Kara N., additional, Shearer, Martin J., additional, Shojaie, Sharareh, additional, Shroyer, Noah F., additional, Sibley, Colin P., additional, Sieck, Gary C., additional, Simmons, Rebecca A., additional, Sivieri, Emidio M., additional, Smith, Francine G., additional, Smith, Lois E.H., additional, Smyth, Ian M., additional, Snarr, Brian S., additional, Snyder, Evan Y., additional, Sola-Visner, Martha, additional, Solhaug, Michael J., additional, Sperling, Mark A., additional, Srinivasan, Lakshmi, additional, Stahl, Andreas, additional, Stanley, Charles A., additional, Steinhorn, Robin H., additional, Stonestreet, Barbara S., additional, Strasburger, Janette F., additional, Styne, Dennis M., additional, Sussel, Lori, additional, Tam, Emily W.Y., additional, Tan, Libo, additional, Thornton, Claire, additional, Tollin, Daniel J., additional, Tóth, Beáta, additional, Towbin, Jeffrey A., additional, Trocle, Ashley, additional, Truog, William E., additional, Tsang, Reginald C., additional, Uhler, Kristin M., additional, Van Den Anker, John N., additional, van Goudoever, Johannes (Hans) B., additional, Vannucci, Susan J., additional, Vickers, Mark H., additional, Virgintino, Daniela, additional, Volpe, Joseph J., additional, Vora, Neeta L., additional, Vyas, Neha V., additional, Wacker-Gussmann, Annette, additional, Wallace, Megan J., additional, Walsh, Brian H., additional, Wang, Alice M., additional, Warburton, David, additional, Ward, Robert M., additional, Watterberg, Kristi L., additional, Werner, Lynne A., additional, Wershil, Barry K., additional, Wert, Susan E., additional, Wessels, Andy, additional, Whitsett, Jeffrey A., additional, Wise, Michael, additional, Wolf, Matthias T., additional, Wolfson, Marla R., additional, Wong, Hector R., additional, Wynn, James L., additional, Yeo, Lami, additional, Yip, Stephen, additional, Yoder, Bradley A, additional, Yoder, Mervin C., additional, Yoshimoto, Momoko, additional, Yuskaitis, Christopher J., additional, Zhou, Dan, additional, and Zovein, Ann, additional

Published
2017
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6. The Human Kidney

Author

Cullen-McEwen, Luise, primary, Sutherland, Megan R., additional, and Black, M. Jane, additional

Published
2016
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7. Contributors

Author

Al-Awqati, Qais, primary, Arts, H.H., additional, Atala, Anthony, additional, Barnes, Felicity J., additional, Benigni, Ariela, additional, Bertram, John F., additional, Black, M. Jane, additional, Bonventre, Joseph V., additional, Buffington, Deborah A., additional, Bush, Kevin T., additional, Cao, Qi, additional, Carroll, Thomas, additional, Cosgrove, Melanie, additional, Costantini, Frank, additional, Cullen-McEwen, Luise, additional, Davidson, Alan J., additional, Dekel, Benjamin, additional, Dodd, Rachel C., additional, Dressler, Gregory R., additional, Duffield, Jeremy S., additional, Dziedzic, Klaudyna, additional, Ferenbach, David A., additional, Finkelstein, Julia B., additional, Goodyer, Paul, additional, Guay-Woodford, L.M., additional, Hammerman, Marc R., additional, Harris, David C.H., additional, Hiatt, Michael J., additional, Hoy, Wendy E., additional, Hughson, Michael D., additional, Huling, Jennifer C., additional, Humes, H. David, additional, Humphreys, Benjamin D., additional, Ilagan, Roger, additional, Knoers, Nine V.A.M., additional, Kopan, Raphael, additional, Kreidberg, Jordan A., additional, Kwartler, Callie S., additional, Lasagni, Laura, additional, Lazzeri, Elena, additional, Little, Melissa H., additional, Lu, Weining, additional, Macconi, Daniela, additional, Matsell, Douglas G., additional, McMahon, Andrew P., additional, Mendelsohn, Cathy, additional, Moeller, Marcus J., additional, Moritz, Karen M., additional, Nigam, Sanjay K., additional, Nishinakamura, Ryuichi, additional, O’Connor, A.K., additional, Oliver, Juan A., additional, Osafune, Kenji, additional, Oxburgh, Leif, additional, Park, Joo-Seop, additional, Peired, Anna, additional, Pino, Christopher J., additional, Pleniceanu, Oren, additional, Presnell, Sharon, additional, Puelles, Victor G., additional, Quaggin, Susan E., additional, Rabelink, Ton J., additional, Ranghini, Egon, additional, Rapoport, Scott, additional, Reinders, Marlies E.J., additional, Remuzzi, Giuseppe, additional, Ricardo, Sharon D., additional, Romagnani, Paola, additional, Scott, Rizaldy P., additional, Sequeira Lopez, Maria Luisa S., additional, Shepherd, Benjamin, additional, Short, Kieran M., additional, Smyth, Ian M., additional, Susztak, Katalin, additional, Sutherland, Megan R., additional, Taguchi, Atsuhiro, additional, Wang, Yiping, additional, Weber, Stefanie, additional, Westover, Angela J., additional, Yokoo, Takashi, additional, Yoo, James J., additional, and Yu, Jing, additional

Published
2016
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8. Podocyte endowment and the impact of adult body size on kidney health

Author

Cullen-McEwen, Luise A., primary, van der Wolde, James, additional, Haruhara, Kotaro, additional, Tribolet, Leon, additional, Dowling, John P., additional, Bertram, Michael G., additional, de Matteo, Robert, additional, Haas, Fabian, additional, Czogalla, Jan, additional, Okabayashi, Yusuke, additional, Armitage, James A., additional, Black, M. Jane, additional, Hoy, Wendy E., additional, Puelles, Victor G., additional, and Bertram, John F., additional

Published
2021
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12. Is nephrogenesis affected by preterm birth? Studies in a non-human primate model

Author

Gubhaju, Lina, Sutherland, Megan R., Yoder, Bradley A., Zulli, Anthony, Bertram, John F., and Black, M. Jane

Subjects
Immunohistochemistry -- Analysis, Corticosteroids -- Health aspects, Corticosteroids -- Research, Diagnostic immunohistochemistry -- Usage, Neurogenesis -- Research, Premature labor -- Risk factors, Premature labor -- Research, Biological sciences
Abstract

Gubhaju L, Sutherland MR, Yoder BA, Zulli A, Bertram JF, Black MJ. Is nephrogenesis affected by preterm birth? Studies in a non-human primate model. Am J Physiol Renal Physiol 297: F1668-F1677, 2009. First published September 16, 2009; doi: 10.1152/ajprenal.00163.2009.--Nephrogenesis occurs predominantly in late gestation at a time when preterm infants are already delivered. The aims of this study were to assess the effect of preterm birth and the effect of antenatal glucocorticoid treatment on nephrogenesis. Preterm baboons, which were delivered at 125 days gestation and ventilated for up to 21 days postnatally, were compared with gestational controls. A cohort of preterm baboons that had been exposed to antenatal glucocorticoids were compared with unexposed preterm baboons. The number of glomerular generations was estimated using a medullary ray glomerular-counting method, and glomerular number was estimated using unbiased stereology. CD31 and WT-1 localization was examined using immunohistochemistry and VEGF was localized using in situ hybridization. The number of glomerular generations was not affected by preterm birth, and total glomerular numbers were within the normal range. Kidneys were significantly enlarged in preterm baboons with a significant decrease in glomerular density (number of glomeruli per gram of kidney) in the preterm kidney compared with gestational controls. Neonates exposed to antenatal steroids had an increased kidney-to-body weight ratio and also more developed glomeruli compared with unexposed controls. Abnormal glomeruli, with a cystic Bowman's space and shrunken glomerular tuft, were often present in the superficial renal cortex of both the steroid-exposed and unexposed preterm kidneys; steroid exposure had no significant effect on the proportion of abnormal glomeruli. The proportion of abnormal glomeruli in the preterm kidneys ranged from 0.2 to 18%. In conclusion, although nephrogenesis is ongoing in the extrauterine environment, our findings demonstrate that preterm birth, independent of steroid exposure, is associated with a high proportion of abnormal glomeruli in some, but not all neonatal kidneys. Whether final nephron endowment is affected in those kidneys exhibiting a high proportion of abnormal glomeruli is yet to be confirmed. baboon; kidney; glomerulogenesis doi: 10.1152/ajprenal.00163.2009

Published
2009

16. Nephrogenesis and the renal renin-angiotensin system in fetal sheep: effects of intrauterine growth restriction during late gestation

Author

Zohdi, Vladislava, Moritz, Karen M., Bubb, Kristen J., Cock, Megan L., Wreford, Nigel, Harding, Richard, and Black, M. Jane

Subjects
Kidney tubules -- Research, Kidney tubules -- Growth, Kidneys -- Growth, Renin-angiotensin system -- Research, Epithelial cells -- Research, Fetus -- Growth, Fetus -- Research, Company growth, Biological sciences
Abstract

Previous studies have shown that intrauterine growth restriction (IUGR) can impair nephrogenesis, but uncertainties remain about the importance of the gestational timing of the insult and the effects on the renal renin-angiotensin system (RAS). We therefore hypothesized that induction of IUGR during late gestation alters the RAS, and this is associated with a decrease in nephron endowment. Our aims were to determine the effects of IUGR induced during the later stages of nephrogenesis on 1) nephron number; 2) mRNA expression of angiotensin A[T.sub.1] and A[T.sub.2] receptors, angiotensinogen, and renin genes in the kidney; and 3) the size of maculae densae. IUGR was induced in fetal sheep (n = 7) by umbilical-placental embolization from 110 to 130 days of the ~147-day gestation; saline-infused fetuses served as controls (n = 7). Samples of cortex from the left kidney were frozen, and the right kidney was perfusion fixed. Total kidney volume, nephron number, renal corpuscle volume, total maculae densae volume, and the volume of macula densa per glomerulus were stereologically estimated, mRNA expression of A[T.sub.1] and A[T.sub.2] receptors, angiotensinogen, and renin in the renal cortex was determined. In IUGR fetuses at 130 days, body and kidney weights were significantly reduced and nephron number was reduced by 24%. There was no difference in renin, angiotensinogen, or A[T.sub.1] and A[T.sub.2] receptor mRNA expression levels in the IUGR kidneys compared with controls. We conclude that fetal growth restriction late in nephrogenesis can lead to a marked reduction in nephron endowment but does not affect renal corpuscle or macula densa size, or renal RAS gene expression. kidney; nephron endowment; macula densa; stereology

Published
2007

21. Early impact of moderate preterm birth on the structure, function and gene expression of conduit arteries

Author

Lombardo, Paul, primary, Nguyen, Vivian B., additional, Flores, Tracey J., additional, Sutherland, Megan R., additional, Nitsos, Ilias, additional, Allison, Beth J., additional, Parkington, Helena, additional, Tare, Marianne, additional, Harding, Richard, additional, De Matteo, Robert, additional, Schneider, Michal, additional, Polglase, Graeme R., additional, and Black, M. Jane, additional

Published
2020
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25. Podocyte endowment and the impact of adult body size on kidney health.

Author

Cullen-McEwen, Luise A., van der Wolde, James, Kotaro Haruhara, Tribolet, Leon, Dowling, John P., Bertram, Michael G., de Matteo, Robert, Haas, Fabian, Czogalla, Jan, Yusuke Okabayashi, Armitage, James A., Black, M. Jane, Hoy, Wendy E., Puelles, Victor G., and Bertram, John F.

Subjects
LOW birth weight, BODY size, ADIPOSE tissues, ADULTS, LOW-protein diet, DIABETIC nephropathies
Abstract

Low birth weight is a risk factor for chronic kidney disease, whereas adult podocyte depletion is a key event in the pathogenesis of glomerulosclerosis. However, whether low birth weight due to poor maternal nutrition is associated with low podocyte endowment and glomerulosclerosis in later life is not known. Female Sprague-Dawley rats were fed a normal-protein diet (NPD; 20%) or low-protein diet (LPD; 8%), to induce low birth weight, from 3 wk before mating until postnatal day 21 (PN21), when kidneys from some male offspring were taken for quantitation of podocyte number and density in whole glomeruli using immunolabeling, tissue clearing, and confocal microscopy. The remaining offspring were fed a normal- or high-fat diet until 6 mo to induce catchup growth and excessive weight gain, respectively. At PN21, podocyte number per glomerulus was 15% lower in low birth weight (LPD) than normal birth weight (NPD) offspring, with this deficit greater in outer glomeruli. Surprisingly, podocyte number in LPD offspring increased in outer glomeruli between PN21 and 6 mo, although an overall 9% podocyte deficit persisted. Postnatal fat feeding to LPD offspring did not alter podometric indexes or result in glomerular pathology at 6mo, whereas fat feeding in NPD offspring was associated with far greater body and fat mass as well as podocyte loss, reduced podocyte density, albuminuria, and glomerulosclerosis. This is the first report that maternal diet can influence podocyte endowment. Our findings provide new insights into the impact of low birth weight, podocyte endowment, and postnatal weight on podometrics and kidney health in adulthood. [ABSTRACT FROM AUTHOR]

Published
2021
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29. Effect of perindopril on cardiovascular hypertrophy of the SHR: respective roles of reduced blood pressure and reduced angiotensin II levels

Author

Black, M. Jane, Campbell, Julie, and Campbell, Gordon R.

Subjects
ACE inhibitors -- Physiological aspects, Heart enlargement, Blood pressure, Angiotensin -- Physiological aspects, Health
Abstract

The aim was to determine cardiovascular hypertrophy in primary hypertension in the spontaneously hypertensive rat (SHR) is induced by increased levels of angiotensin II or by increased blood pressure. SHR were treated from 7 to 15 weeks of age with perindopril to block an in vivo production of A II and concomitantly infused with either a pressor dose of norepinephrine or angiotensin II. At the end of the treatment period, there was no significant difference in the systolic blood pressure in the norepinephrine or angiotensin II-treated groups (201 [+ or -] 9 and 208 [+ or -] 8 mm Hg, respectively). However, there was a significant increase (p < 0.01) in left ventricle-plus-septum /body weigh ratio in angiotensin II compared with norepinephrine-infused SHR (3.72 [+ or -] 0.25 and 2.34 [+ or -] 0.04 mg/g, respectively) and in aortic medial cross-sectional area (0.55 [+ or -] 0.05 and 0.38 [+ or -] 0.01 m[m.sup.2], respectively). Using an unbiased optical dissector/fractionator technique, the number of smooth muscle cells in the descending thoracic aorta of the angiotensin II-infused SHR was not different from norepinephrine-infused rats (5.02 [+ or -] 0.30; x [10.sup.6] and 4.71 [+ or -] 0.42 x [10.sup.6] cells, respectively), and no difference in size of enzyme-isolated cells was observed (mode: 1,326 [+ or -] 127 [mu][m.sup.3] compared with 1,186 [+ or -] 82 [mu][m.sup.3]). The results indicate that angiotensin II directly stimulates cardiac and aortic hypertrophy through a mechanism unrelated to its effect on blood pressure. The aortic hypertropy is not due to an increase in smooth muscle cell size or number and thus must be related to an increase in the extracellular compartment. (Am J Cardiol 1993;71:17E - 21E)

Published
1993

30. Moderate preterm birth affects right ventricular structure and function and pulmonary artery blood flow in adult sheep

Author

Mrocki, Marshall M., Nguyen, Vivian B., Lombardo, Paul, Sutherland, Megan R., Bensley, Jonathan G., Nitsos, Ilias, Allison, Beth J., Harding, Richard, De Matteo, Robert, Schneider, Michal, Polglase, Graeme R., and Black, M. Jane

Subjects
Male, Sheep, Ventricular Remodeling, Heart Ventricles, Infant, Newborn, Parturition, preterm birth, Blood Pressure, cardiomyocytes, heart development, Pulmonary Artery, right ventricle, Research Papers, Translational Perspectives, Animals, Newborn, Heart Rate, Pregnancy, Ventricular Function, Right, Humans, Premature Birth, Animals, Female
Abstract

KEY POINTS: Preterm birth occurs when the heart muscle is immature and ill‐prepared for the changes in heart and lung function at birth. MRI imaging studies show differences in the growth and function of the heart of young adults born preterm, with the effects more pronounced in the right ventricle. The findings of this study, conducted in sheep, showed that following moderate preterm birth the right ventricular wall was thinner in adulthood, with a reduction in the number and size of the heart muscle cells; in addition, there was impaired blood flow in the main artery leading from the right ventricle to the lungs. The findings indicate that being born only a few weeks early adversely affects the cellular structure of the right ventricle and blood flow to the lungs in adulthood. The reduced number of heart muscle cells has the potential to deleteriously affect right ventricular growth potential and function. ABSTRACT: Preterm birth prematurely exposes the immature heart to the haemodynamic transition at birth, which has the potential to induce abnormal cardiac remodelling. Magnetic resonance imaging studies in young adults born preterm have shown abnormalities in the gross structure of the ventricles (particularly the right ventricle; RV), but the cellular basis of these alterations is unknown. The aim of this study, conducted in sheep, was to determine the effect of moderate preterm birth on RV cellular structure and function in early adulthood. Male singleton lambs were delivered moderately preterm (132 ± 1 days; n = 7) or at term (147 ± 1 days; n = 7). At 14.5 months of age, intra‐arterial blood pressure and heart rate were measured. Pulmonary artery diameter and peak systolic blood flow were determined using ultrasound imaging, and RV stroke volume and output calculated. Cardiomyocyte number, size, nuclearity and levels of cardiac fibrosis were subsequently assessed in perfusion‐fixed hearts using image analysis and stereological methods. Blood pressure (systolic, diastolic and mean), heart rate, levels of myocardial fibrosis and RV stroke volume and output were not different between groups. There was, however, a significant reduction in RV wall thickness in preterm sheep, and this was accompanied by a significant reduction in peak systolic blood flow in the pulmonary artery and in RV cardiomyocyte number. Cellular changes in the RV wall and reduced pulmonary artery blood flow following preterm birth have the potential to adversely affect cardiac and respiratory haemodynamics, especially when the cardiovascular system is physiologically or pathologically challenged.

Published
2017

32. Moderate preterm birth affects right ventricular structure and function and pulmonary artery blood flow in adult sheep

Author

Mrocki, Marshall M., primary, Nguyen, Vivian B., additional, Lombardo, Paul, additional, Sutherland, Megan R., additional, Bensley, Jonathan G., additional, Nitsos, Ilias, additional, Allison, Beth J., additional, Harding, Richard, additional, De Matteo, Robert, additional, Schneider, Michal, additional, Polglase, Graeme R., additional, and Black, M. Jane, additional

Published
2018
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34. The Consequences of Chorioamnionitis: Preterm Birth and Effects on Development

Author

Galinsky, Robert, Polglase, Graeme R., Hooper, Stuart B., Black, M. Jane, and Moss, Timothy J. M.

Subjects
Article Subject
Abstract

Preterm birth is a major cause of perinatal mortality and long-term morbidity. Chorioamnionitis is a common cause of preterm birth. Clinical chorioamnionitis, characterised by maternal fever, leukocytosis, tachycardia, uterine tenderness, and preterm rupture of membranes, is less common than subclinical/histologic chorioamnionitis, which is asymptomatic and defined by inflammation of the chorion, amnion, and placenta. Chorioamnionitis is often associated with a fetal inflammatory response. The fetal inflammatory response syndrome (FIRS) is defined by increased systemic inflammatory cytokine concentrations, funisitis, and fetal vasculitis. Clinical and epidemiological studies have demonstrated that FIRS leads to poor cardiorespiratory, neurological, and renal outcomes. These observations are further supported by experimental studies that have improved our understanding of the mechanisms responsible for these outcomes. This paper outlines clinical and experimental studies that have improved our current understanding of the mechanisms responsible for chorioamnionitis-induced preterm birth and explores the cellular and physiological mechanisms underlying poor cardiorespiratory, neural, retinal, and renal outcomes observed in preterm infants exposed to chorioamnionitis.

Published
2013
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35. Low Birth Weight due to Intrauterine Growth Restriction and/or Preterm Birth: Effects on Nephron Number and Long-Term Renal Health

Author

Zohdi, Vladislava, Sutherland, Megan R., Lim, Kyungjoon, Gubhaju, Lina, Zimanyi, Monika A., and Black, M. Jane

Subjects
Article Subject, urologic and male genital diseases
Abstract

Epidemiological studies have clearly demonstrated a strong association between low birth weight and long-term renal disease. A potential mediator of this long-term risk is a reduction in nephron endowment in the low birth weight infant at the beginning of life. Importantly, nephrons are only formed early in life; during normal gestation, nephrogenesis is complete by about 32–36 weeks, with no new nephrons formed after this time during the lifetime of the individual. Hence, given that a loss of a critical number of nephrons is the hallmark of renal disease, an increased severity and acceleration of renal disease is likely when the number of nephrons is already reduced prior to disease onset. Low birth weight can result from intrauterine growth restriction (IUGR) or preterm birth; a high proportion of babies born prematurely also exhibit IUGR. In this paper, we describe how IUGR and preterm birth adversely impact on nephrogenesis and how a subsequent reduced nephron endowment at the beginning of life may lead to long-term risk of renal disease, but not necessarily hypertension.

Published
2012
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38. Assessment of renal functional maturation and injury in preterm neonates during the first month of life

Author

Gubhaju, Lina, Sutherland, Megan R., Horne, Rosemary S.C., Medhurst, Alison, Kent, Alison L., Ramsden, Andrew, Moore, Lynette, Singh, Gurmeet, Hoy, Wendy E., Black, M. Jane, Gubhaju, Lina, Sutherland, Megan R., Horne, Rosemary S.C., Medhurst, Alison, Kent, Alison L., Ramsden, Andrew, Moore, Lynette, Singh, Gurmeet, Hoy, Wendy E., and Black, M. Jane

Abstract

Worldwide, approximately 10% of neonates are born preterm. The majority of preterm neonates are born when the kidneys are still developing; therefore, during the early postnatal period renal function is likely reflective of renal immaturity and/or injury. This study evaluated glomerular and tubular function and urinary neutrophil gelatinase-associated lipocalin (NGAL; a marker of renal injury) in preterm neonates during the first month of life. Preterm and term infants were recruited from Monash Newborn (neonatal intensive care unit at Monash Medical Centre) and Jesse McPherson Private Hospital, respectively. Infants were grouped according to gestational age at birth: ≤28 wk (n = 33), 29–31 wk (n = 44), 32–36 wk (n = 32), and term (≥37 wk (n = 22)). Measures of glomerular and tubular function were assessed on postnatal days 3–7, 14, 21, and 28. Glomerular and tubular function was significantly affected by gestational age at birth, as well as by postnatal age. By postnatal day 28, creatinine clearance remained significantly lower among preterm neonates compared with term infants; however, sodium excretion was not significantly different. Pathological proteinuria and high urinary NGAL levels were observed in a number of neonates, which may be indicative of renal injury; however, there was no correlation between the two markers. Findings suggest that neonatal renal function is predominantly influenced by renal maturity, and there was high capacity for postnatal tubular maturation among preterm neonates. There is insufficient evidence to suggest that urinary NGAL is a useful marker of renal injury in the preterm neonate.

Published
2014

39. Long-Term Renal Consequences of Preterm Birth

Author

Sutherland, Megan R., Ryan, Dana, Black, M. Jane, Kent, Alison, Sutherland, Megan R., Ryan, Dana, Black, M. Jane, and Kent, Alison

Abstract

The normal development of the kidney may be affected by several factors, including abnormalities in placental function, resulting in fetal growth restriction, exposure to maternal disease states, including hypertension and diabetes, antenatal steroids, chorioamnionitis, and preterm delivery. After preterm birth, several further insults may occur that may influence nephrogenesis and renal health, including exposure to nephrotoxic medications, postnatal growth failure, and obesity after growth restriction. In this review article, common clinical neonatal scenarios are used to highlight these renal risk factors, and the animal and human evidence on which these risk factors are based are discussed.

Published
2014

40. Assessment of renal functional maturation and injury in preterm neonates during the first month of life

Author

Gubhaju, L, Sutherland, Megan R., Horne, Rosemary S. C., Medhurst, Alison, Kent, Alison, Ramsden, Andrew, Moore, Lynette, Singh, Gurmeet, Hoy, Wendy E., Black, M. Jane, Gubhaju, L, Sutherland, Megan R., Horne, Rosemary S. C., Medhurst, Alison, Kent, Alison, Ramsden, Andrew, Moore, Lynette, Singh, Gurmeet, Hoy, Wendy E., and Black, M. Jane

Abstract

Worldwide, approximately 10% of neonates are born preterm. The majority of preterm neonates are born when the kidneys are still developing; therefore, during the early postnatal period renal function is likely reflective of renal immaturity and/or injury. This study evaluated glomerular and tubular function and urinary neutrophil gelatinase-associated lipocalin (NGAL; a marker of renal injury) in preterm neonates during the first month of life. Preterm and term infants were recruited from Monash Newborn (neonatal intensive care unit at Monash Medical Centre) and Jesse McPherson Private Hospital, respectively. Infants were grouped according to gestational age at birth: ≤28 wk (n = 33), 29-31 wk (n = 44), 32-36 wk (n = 32), and term (≥37 wk (n = 22)). Measures of glomerular and tubular function were assessed on postnatal days 3-7, 14, 21, and 28. Glomerular and tubular function was significantly affected by gestational age at birth, as well as by postnatal age. By postnatal day 28, creatinine clearance remained significantly lower among preterm neonates compared with term infants; however, sodium excretion was not significantly different. Pathological proteinuria and high urinary NGAL levels were observed in a number of neonates, which may be indicative of renal injury; however, there was no correlation between the two markers. Findings suggest that neonatal renal function is predominantly influenced by renal maturity, and there was high capacity for postnatal tubular maturation among preterm neonates. There is insufficient evidence to suggest that urinary NGAL is a useful marker of renal injury in the preterm neonate.

Published
2014

41. Embryonic stem cells markers are present within rabbit atherosclerotic plaques

Author

Zulli, Anthony, Buxton, Brian F., Black, M. Jane, and Hare, David L.

Subjects
Cholesterol, 616.1 - Patología del sistema circulatorio, de los vasos sanguíneos. Transtornos cardiovasculares, embryonic structures, Atherosclerosis, reproductive and urinary physiology
Abstract

Recent evidence suggests that smooth muscle cells within atherosclerotic plaques originate from vascular progenitor cells. We have previously shown that smooth muscle cells and macrophages present within rabbit atherosclerotic plaques are positive for factors of the renin angiotensin and nitric oxide systems as well as the hematopoietic stem-cell marker CD34 and the panleukocyte marker CD45. To explore the idea that these cells are of primitive types, immunohistochemistry was used to identify pluripotent embryonic stem cells (ESC) markers (Oct-4, SSEA1,3,4, TRA1-60, 81) in these plaques and to compare these to intimal thickening. Objective: To immunolocalise ESC markers in rabbit aortic intimal thickening and atherosclerotic plaques. Design: New Zealand White rabbits were fed either a control (Con) diet, 0.5% cholesterol (Chol) or 1% methionine (Meth) for 12 weeks. Animals were perfusion fixed, aortae excised and processed for paraffin. Immunohistochemistry was performed by standard techniques. Results: Oct-4, SSEA 1, 3 and 4, TRA-1-60 and TRA-1-81 were all present within in atherosclerotic plaques. However, some cells were not positive for TRA-1-60 and TRA-1-81. In fact, positive TRA-1-81 macrophages were uncommon, and positive TRA-1-81 smooth muscle cells were rare. Intimal thickening in Meth did not show any TRA-1-81 positive cells Conclusions: Macrophages and smooth muscle cells within atherosclerotic plaques express markers of ESC. These results suggest that cells within these plaques are primitive and might differentiate into other types of cells.

Published
2008

42. Intrauterine growth restriction delays cardiomyocyte maturation and alters coronary artery function in the fetal sheep

Author

Bubb, Kristen J, Cock, Megan L, Black, M Jane, Dodic, Miodrag, Boon, Wee-Ming, Parkington, Helena C, Harding, Richard, and Tare, Marianne

Subjects
Fetal Growth Retardation, Sheep, Angiotensin II, Vasodilator Agents, Cell Differentiation, Heart, Bradykinin, Coronary Vessels, Muscle, Smooth, Vascular, Pregnancy, 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid, embryonic structures, Integrative, Animals, Vasoconstrictor Agents, Female, Myocytes, Cardiac, Endothelium, Vascular, reproductive and urinary physiology
Abstract

There is now extensive evidence suggesting that intrauterine perturbations are linked with an increased risk of developing cardiovascular disease. Human epidemiological studies, supported by animal models, have demonstrated an association between low birth weight, a marker of intrauterine growth restriction (IUGR), and adult cardiovascular disease. However, little is known of the early influence of IUGR on the fetal heart and vessels. The aim of this study was to determine the effects of late gestational IUGR on coronary artery function and cardiomyocyte maturation in the fetus. IUGR was induced by placental embolization in fetal sheep from 110 to 130 days of pregnancy (D110-130); term approximately D147; control fetuses received saline. At necropsy (D130), wire and pressure myography was used to test endothelial and smooth muscle function, and passive mechanical wall properties, respectively, in small branches of left descending coronary arteries. Myocardium was dissociated for histological analysis of cardiomyocytes. At D130, IUGR fetuses (2.7 +/- 0.1 kg) were 28% lighter than controls (3.7 +/- 0.3 kg; P = 0.02). Coronary arteries from IUGR fetuses had enhanced responsiveness to the vasoconstrictors, angiotensin II and the thromboxane analogue U46619, than controls (P0.01). Endothelium-dependent and -independent relaxations were not different between groups. Coronary arteries of IUGR fetuses were more compliant (P = 0.02) than those of controls. The incidence of cardiomyocyte binucleation was lower in the left ventricles of IUGR fetuses (P = 0.02), suggestive of retarded cardiomyocyte maturation. We conclude that late gestational IUGR alters the reactivity and mechanical wall properties of coronary arteries and cardiomyocyte maturation in fetal sheep, which could have lifelong implications for cardiovascular function.

Published
2006

46. Exposure to intrauterine inflammation leads to impaired function and altered structure in the preterm heart of fetal sheep

Author

Tare, Marianne, primary, Bensley, Jonathan G., additional, Moss, Timothy J. M., additional, Lingwood, Barbara E., additional, Kim, Min Y., additional, Barton, Samantha K., additional, Kluckow, Martin, additional, Gill, Andrew W., additional, De Matteo, Robert, additional, Harding, Richard, additional, Black, M. Jane, additional, Parkington, Helena C., additional, and Polglase, Graeme R., additional

Published
2014
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48. Accelerated Maturation and Abnormal Morphology in the Preterm Neonatal Kidney

Author

Sutherland, Megan R, Gubhaju, Lina, Moore, Lynette, Kent, Alison, Dahlstrom, Jane, Horne, Rosemary S. C., Hoy, Wendy E., Bertram, John, Black, M. Jane, Sutherland, Megan R, Gubhaju, Lina, Moore, Lynette, Kent, Alison, Dahlstrom, Jane, Horne, Rosemary S. C., Hoy, Wendy E., Bertram, John, and Black, M. Jane

Abstract

Nephrogenesis is ongoing at the time of birth for the majority of preterm infants, but whether postnatal renal development follows a similar trajectory to normal in utero growth is unknown. Here, we examined tissue collected at autopsy from 28 kidneys from preterm neonates, whose postnatal survival ranged from 2 to 68 days, including 6 that had restricted intrauterine growth. In addition, we examined kidneys from 32 still-born gestational controls. We assessed the width of the nephrogenic zone, number of glomerular generations, cross-sectional area of the renal corpuscle, and glomerular maturity and morphology. Renal maturation accelerated after preterm birth, with an increased number of glomerular generations and a decreased width of the nephrogenic zone in the kidneys of preterm neonates. Of particular concern, compared with gestational controls, preterm kidneys had a greater percentage of morphologically abnormal glomeruli and a significantly larger cross-sectional area of the renal corpuscle, suggestive of renal hyperfiltration. These observations suggest that the preterm kidney may have fewer functional nephrons, thereby increasing vulnerability to impaired renal function in both the early postnatal period and later in life.

Published
2011

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