Relevant bibliographies by topics / Renovascular disease

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Renovascular disease'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Renovascular disease"

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Kalra, Philip A. "Renovascular Disease." Medicine 31, no. 7 (July 2003): 116–18. http://dx.doi.org/10.1383/medc.31.7.116.28477.

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Kalra, Philip A. "Renovascular disease." Medicine 35, no. 7 (July 2007): 406–9. http://dx.doi.org/10.1016/j.mpmed.2007.04.003.

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Kalra, Philip A. "Renovascular disease." Medicine 39, no. 6 (June 2011): 364–68. http://dx.doi.org/10.1016/j.mpmed.2011.03.007.

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Vassallo, Diana, and Philip A. Kalra. "Renovascular disease." Medicine 43, no. 7 (July 2015): 419–24. http://dx.doi.org/10.1016/j.mpmed.2015.04.008.

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Vassallo, Diana, and Philip A. Kalra. "Renovascular disease." Medicine 47, no. 8 (August 2019): 526–32. http://dx.doi.org/10.1016/j.mpmed.2019.05.008.

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RANKIN, SHEILA C., ANDREW J. S. SAUNDERS, GARY J. R. COOK, and JOHN E. SCOBLE. "Renovascular Disease." Clinical Radiology 55, no. 1 (January 2000): 1–12. http://dx.doi.org/10.1053/crad.1999.0338.

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Matsumoto, Alan H. "Renovascular Disease." Journal of Vascular and Interventional Radiology 14, no. 2 (February 2003): P60—P61. http://dx.doi.org/10.1016/s1051-0443(03)70089-x.

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Libertino, John A. "Renovascular disease." Current Opinion in Urology 3, no. 2 (April 1993): 107–9. http://dx.doi.org/10.1097/00042307-199304000-00010.

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Hamilton, George. "Renovascular disease." Current Opinion in Urology 4, no. 2 (March 1994): U49. http://dx.doi.org/10.1097/00042307-199403000-00011.

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Olin, Jeffrey W. "Atherosclerotic renovascular disease." Current Opinion in Cardiology 5, no. 5 (October 1990): 659–65. http://dx.doi.org/10.1097/00001573-199010000-00016.

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Dissertations / Theses on the topic "Renovascular disease"

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Vassallo, Diana. "Atherosclerotic renovascular disease : risk prediction and selection for revascularization." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/atherosclerotic-renovascular-disease-risk-prediction-and-selection-for-revascularization(ff841ec0-ae14-40a1-9865-dc014f977a77).html.

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Recent large randomized controlled trials (RCTs) have shown that renal revascularization does not confer added benefit to unselected patients with atherosclerotic renovascular disease (ARVD) treated with multi-targeted medical therapy. Results suggest that contemporary medical vascular protection therapy has contributed to improved clinical outcomes in ARVD. However, patients with †̃high-riskâ€TM clinical features have largely been excluded from RCTs and there is consistent observational evidence that this specific patient subgroup may gain benefit from revascularization. Timely identification of these patients through risk stratification and prediction of outcomes post-revascularization remain important challenges. The main aims of this epidemiological research project were to explore how treatment and clinical end-points in ARVD have evolved over the past three decades, to identify the determinants of long-term end-points in ARVD, to investigate the effect of revascularization in a selected †̃high-riskâ€TM subgroup, to investigate novel biomarker association of key end-points and finally to develop a clinical risk prediction model that can aid risk stratification and patient selection for revascularization. These individual studies were all based on a local database that includes details of demographic and clinical data for patients with ARVD referred to our tertiary renal centre between 1986 and 2014. Primary end-point measures included death, progression to end-stage kidney disease, cardiovascular events and a composite end-point composed of the first of any of the above events. Management of ARVD has been influenced by RCT results, leading to a decline in the number of revascularization procedures performed. Traditional cardiovascular risk factors together with baseline renal function and proteinuria are the most important determinants of adverse events in ARVD thus advocating the use of multi-targeted medical therapy and aggressive risk factor control in all patients with ARVD. Nonetheless ARVD is a heterogenous condition and results of this research project show that revascularization can be of benefit in patients with rapidly deteriorating renal function, bilateral severe ARVD and/or < 1g/day baseline proteinuria. A panel of novel biomarkers may have incremental risk predictive value when used in conjunction with more traditional risk factors, and NT-proBNP levels may aid patient selection for revascularization. A simple clinical risk-prediction score based on easily obtainable variables may be used as a bedside tool to help risk stratification and facilitate patient selection for revascularization, thus encouraging a more patient-specific therapeutic approach.
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Shurrab, Alaa Eldeen. "Relationship of parenchymal disease to renal dysfunction in patients with atherosclerotic renovascular disease." Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492719.

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Ritchie, James. "Epidemiology of atherosclerotic renovascular disease : clinical presentations, prognosis and treatment." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/epidemiology-of-atherosclerotic-renovascular-disease-clinical-presentations-prognosis-and-treatment(c86ec7c6-a636-48b7-9f3e-c086b8cc4905).html.

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Atherosclerotic renovascular disease (ARVD) is a significant cause of chronic kidney disease (CKD) and is associated with an increased risk for cardiovascular morbidity and mortality. Randomised controlled trials, representing over 2100 patients, have failed to demonstrate any prognostic benefit of percutaneous renal revascularisation when utilised in addition to standard medical therapy. This negative finding has been interpreted in three ways. Firstly, that ARVD may be an association of CKD and not a specific disease process. Secondly, that published studies have recruited low-risk patients who are least likely to benefit from revascularisation. Thirdly, that the focus of treatment for patients with ARVD should be optimal medical therapy, not renal revascularisation. This research project had a series of linked aims. These were investigated in two large patient cohorts that had been accumulated at this centre over the last decade. These cohorts comprised > 900 patients with ARVD, the Salford Renovascular Database (SRVD), and > 2500 patients with all-cause CKD, the Chronic Renal Insufficiency Standards Implementation Study (CRISIS). The first aim was to consider whether ARVD should be considered as a specific cause of CKD. Here risks for death and progression to renal replacement therapy were compared between patients having ARVD as their primary cause of renal failure and patients with other coded causes of CKD. In this analysis, patients with ARVD had a greater risk for death and a lesser risk for RRT than patients with other forms of CKD.The second aim of this thesis was to consider if specific patient sub-groups of ARVD could be identified. Patients in the SRVD with currently accepted high- risk clinical presentations were selected and outcomes compared to patients without a high-risk presentation. In this analysis, presentation with flash pulmonary oedema (but with not refractory hypertension or rapidly declining renal function) was associated with an increased risk for death and cardiovascular event. When the effects of revascularisation were considered in patients with high-risk presentations, a mortality benefit was observed in patients with flash pulmonary oedema and in patients presenting with rapidly declining renal function and refractory hypertension in combination. A separate analysis was performed in the SRVD to consider if a high-risk sub-group of ARVD patients could be identified using laboratory measurements. Here, a classification tree methodology was employed to identify ARVD patients with the greatest risk for progression to end stage kidney disease. The results of this analysis were converted into a practically applicable clinical scoring system incorporating renal function, proteinuria, medications, smoking history and renal artery occlusion. The final aim of this thesis was to describe how the majority of ARVD patients should be treated. In this analysis of the SRVD effects of treatment with anti- platelet and beta-blocker therapy were considered, and shown to be associated with reduced risks for cardiovascular events and death.
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Cheung, Ching-Mei. "Evaluation of Renal Morphology, Function and Outcome in Atherosclerotic Renovascular Disease." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509057.

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Macêdo, Thiago Andrade de. "Estudo dos determinantes de doença arterial coronária grave em pacientes hipertensos com indicação de arteriografia renal por suspeita de estenose de artéria rena." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11072012-094212/.

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INTRODUÇÃO: Em pacientes hipertensos com suspeita de doença arterial coronária (DAC), indicações para a realização de arteriografia renal no mesmo procedimento da cinecoronariografia estão bem estabelecidas. Entretanto, em hipertensos com suspeita de estenose de artéria renal (EAR) com indicação de arteriografia renal, não estão bem definidos os determinantes da presença de DAC grave. OBJETIVOS: Avaliar a prevalência e os determinantes de DAC grave em pacientes hipertensos com indicação de arteriografia renal por suspeita de EAR. METODOLOGIA: Oitenta e dois pacientes com suspeita clínica de EAR foram submetidos à cinecoronariografia e arteriografia renal no mesmo procedimento. Lesão arterial significativa em artérias renal e/ou coronária foi definida por obstrução luminal maior ou igual a 70%. RESULTADOS: Obstrução luminal significativa, tanto em artéria coronária quanto em renal, foi encontrada em 39% dos pacientes. Os pacientes com DAC grave apresentaram idade mais avançada (63±12 vs. 56±13 anos; p=0,03), maior prevalência de angina (41 vs. 16%; p=0,013), maior diâmetro do átrio esquerdo (44,7 vs. 40,6mm; p=0,005) e maior velocidade de onda de pulso (12,6 vs. 10,7 m/s, p=0,02), comparados com os pacientes sem DAC grave. A presença de EAR significativa esteve associada a uma maior prevalência de DAC grave comparada a pacientes sem a lesão (66% vs. 22%; p<0,001). A análise multivariada demonstrou que EAR70% esteve associada com DAC grave de maneira independente (OR: 11,48; 95%CI 3,2-40,2; p<0,001), mesmo em pacientes sem angina (OR: 13,48; 95%CI 2,6-12,1; p<0,001). CONCLUSÃO: Há elevada prevalência de doença coronária grave em pacientes hipertensos com estenose de artéria renal significativa. A presença de estenose maior ou igual a 70%, verificada em arteriografia renal, é preditor forte e independente para a presença de DAC grave, mesmo na ausência de angina
INTRODUCTION: In patients with suspected coronary artery disease (CAD), indications for performing coronary and renal angiography at the same setting are well established. However, in hypertensive patients with suspected renal artery stenosis (RAS) with indication for renal angiography, it is not well defined the determinants of the presence of severe CAD. OBJECTIVES: We aimed to evaluate the prevalence and determinants of severe CAD in hypertensive patients referred to renal angiography for the diagnosis of RAS. METHODS: Eighty-two consecutive patients with high clinical risk for RAS systematically underwent renal angiography and coronary angiography at the same procedure. Significant RAS and CAD were defined as arterial luminal obstruction 70%. RESULTS: Either significant RAS or significant CAD were present in 32/82 patients (39%). Patients with severe CAD were older (63±12 vs. 56±13 years, p=0.03), had more angina (41 vs. 16%; p=0.013), higher left atrial diameter (44.7 vs. 40,6mm; p=0.005), and higher pulse wave velocity (12.6 vs. 10.7 m/s); p=0.02) compared to patients without significant CAD. Significant RAS was associated with an increased prevalence of severe CAD compared to patients without the lesion (66% vs. 22%, respectively; p<0.001). Binary logistic regression analysis showed that RAS 70% was independently associated with severe CAD (OR: 11.48; 95%CI 3.2-40.2; p<0.001), even in patients without angina (OR: 13.48; 95%CI 2.6-12.1; p<0.001). CONCLUSION: The prevalence of severe CAD in hypertensive patients with significant RAS is high. The presence of RAS 70%, diagnosed by renal angiography, is a strong and useful predictor to identify severe CAD, independently of the presence of angina
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Ramos, Filho Antonio Celso S. "Avaliação morfofuncional e molecular do detrusor isolado de ratos hipertensos renovasculares." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308915.

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Orientador: Edson Antunes
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-17T00:06:55Z (GMT). No. of bitstreams: 1 RamosFilho_AntonioCelsoS._M.pdf: 1693116 bytes, checksum: 4526088a65a406983163ece45558e71c (MD5) Previous issue date: 2010
Resumo: A hipertensão renovascular é uma forma secundária da hipertensão arterial, que corresponde de 1-5% dos casos de hipertensão. A associação entre hipertensão arterial e disfunções miccionais foi observada no modelo experimental de ratos espontaneamente hipertensos (SHR). Até o momento nenhum estudo avaliou as disfunções miccionais em animais hipertensos renovasculares. Dessa forma, neste estudo, caracterizamos a disfunção miccional em ratos hipertensos renovasculares através do modelo de dois rins, um clip (2K-1C). Em ratos Wistar (200-220 g) colocou-se um clip em torno da artéria renal. Depois de oito semanas, os ratos foram utilizados. Realizou-se estudo cistométrico em ratos anestesiados, assim como curvas concentração-resposta para agentes contráteis e relaxantes em detrusor isolado (DSM). Foram também realizados estudos histomorfométricos e da expressão de RNAm dos receptores muscarínicos M3 e M2 em DSM isolado. Os resultados histomorfométricos mostraram aumentos significantes na espessura da parede da bexiga, no volume intravesical, na densidade de musculatura lisa e na densidade de fibras neurais no grupo 2K-1C em comparação ao SHAM. O agonista muscarínico, carbacol, produziu contrações concentração-dependentes do DSM, as quais foram significantemente maiores no grupo 2K-1C. O inibidor da Rho-quinase, Y27-632 (10 µM), reduziu significantemente a contração induzida pelo carbacol nos ratos SHAM e 2K-1C; porém, no grupo 2K-1C, o DSM continuou hiperativo na presença do Y27-632. A estimulação elétrica (1 - 32 Hz) produziu contração freqüência-dependente do DSM as quais foram maiores no grupo 2K-1C. O agonista purinérgico P2X, ?,?-metileno-ATP (1 - 100 µM), o KCl (1 - 300 µM) e o Ca2+ extracelular (0,01-100 µM) produziram contrações concentração-dependente; porém, não observamos diferenças entre o grupo SHAM e 2K-1C. O agonista não seletivo ?-adrenérgico, isoproterenol, o agonista seletivo ?2-adrenérgico, metaproterenol, e o agonista seletivo ?3-adrenérgico, BRL37-344, produziram relaxamentos menores do DSM nos ratos 2K-1C, e também redução nos níveis intracelulares de AMPc nos detrusores. O efeito relaxante ao nitroprussiato de sódio e BAY41-2272 mantiveram-se iguais nos animais SHAM e 2K-1C. A expressão do RNAm do receptor muscarínico M3 (mas não do M2) no DSM foi significantemente maior nos ratos 2K-1C em comparação ao grupo controle. Os tratamentos crônicos com losartan e captopril normalizaram a pressão arterial sistólica dos animais 2K-1C, normalizaram a função miccional, e reduziram a hipercontratilidade do detrusor induzida pela estimulação elétrica e pelo carbacol, assim como restabeleceram o relaxamento induzido pelo isoproterenol ao nível do grupo SHAM. Concluimos que os ratos hipertensos renovasculares apresentam hiperatividade do detrusor, a qual envolve remodelamento tecidual e aumento da contração via receptor muscarínico M3 associado à redução no relaxamento ?-adrenérgico com redução da sinalização intracelular e produção de AMPc. Os tratamentos com losartan e captopril restauram a função miccional dos animais 2K-1C
Abstract: Renovascular hypertension is a secondary form of arterial hypertension, accounting for 1-5% of cases in unselected population. Association between arterial hypertension and urinary bladder dysfunction has been reported in spontaneously hypertensive rats, but no study evaluated the bladder dysfunction in renovascular hypertensive animals. Therefore, in this study, we explored the bladder dysfunction in renovascular hypertensive rats, using the two-kidney one-clip (2K-1C) model. A silver clip was placed around the renal artery of male Wistar Kyoto rats (200-220 g). After eight weeks, rats were used. Cystometric study in anesthetized rats, along with concentration-response curves to both contractile and relaxant agents in isolated detrusor smooth muscle (DSM) were performed. Histomorphometry and mRNA expression of muscarinic M3 and M2 receptors in DSM were also determined. The histomorphometric data showed significant increases in bladder wall thickness, intravesical volume and density of smooth muscle, as well as density of neural fibers in the 2K-1C group compared with SHAM. The muscarinic agonist carbachol produced concentration-dependent DSM contractions, which were markedly greater in 2K-1C rats. The Rho-kinase inhibitor Y27-632 (10 µM) significantly reduced the carbachol-induced contractions in sham and 2K-1C rats, but DSM in 2K-1C rats remained overactive in the presence of Y27632. Electrical-field stimulation (EFS; 1-32 Hz) produced frequency-dependent DSM contractions that were also greater in 2K-1C group. The P2X receptor agonist ?,?-methylene ATP (1-100 µM), KCl (1-300 mM) and extracellular Ca2+ (0.01-100 M) produced concentration-dependent DSM contractions, but no changes among sham and 2K-1C rats were seen. In 2K-1C rats, the non-selective ?-adrenoceptor agonist isoproterenol, the ?2-adrenoceptor agonist metaproterenol and the ?3-adrenoceptor agonist BRL 37-344 produced lower DSM relaxations, as well as decreased cAMP levels. The relaxant responses to sodium nitroprusside and BAY 41-2272 remained unchanged in 2K-1C rats. Expression of mRNA of muscarinic M3 (but not of M2) receptors in DSM was significantly increased in 2K-1C rats. The chronic treatment with losartan and captopril normalized the blood systolic pressure of 2K-1C animals, improved their urinary function by reducing DSM hypercontractility to EFS and carbacol stimulation, and restored the relaxation induced by the ?-adrenergic agonist isoproterenol to the level of SHAM group. In conclusion, renovascular hypertensive rats exhibit overactive DSM that involves tissue remodeling and enhanced muscarinic M3-mediated contractions associated with reduced ?-adrenoceptor-mediated signal transduction. The treatments with losartan and captopril improved urinary function of 2K-1C animals
Mestrado
Mestre em Farmacologia
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Chen, Ying-Hsiang, and 陳瀅翔. "The Therapeutic and Preventive Effects of Sodium Thiosulfate in Chronic Kidney Disease and Renovascular Hypertension in Rats." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/a44r5x.

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FAVA, Cristiano. "Metabolites of arachidonic acid via CYP450 in human hypertension." Doctoral thesis, 2008. http://hdl.handle.net/11562/337636.

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Background: In the last years there has been considerable interest in exploring the role of 20- hydroxyeicosatetraenoic acid (20-HETE) and 5,6-, 8,9-, 11,12- and 14,15 epoxyeicosatrienoic acids (EETs), metabolites of arachidonic acid via cythochrome P450 (CYP), in hypertension, given the importance of this pathway in the regulation of renal and peripheral vascular tone and the renal handling of sodium. The CYP4A11 and the CYP4F2 are responsible for renal production of 20-HETE. The CYP4A11 F434S and CYP4F2 V433M polymorphisms reduce 20- HETE production, in vitro. Aims: The aim of the first study was to investigate whether activation of the renin angiotensin system in renovascular disease affects the CYP ω-ω-1 hydroxylase (20-HETE) and epoxygenase (EETs) pathways of arachidonic acid metabolism in vivo, each of which interacts with Angiotnsin II (study 1). The aim of the second study was to evaluate the effect of the mentioned polymorphisms on blood pressure (BP) levels, hypertension prevalence and cardiovascular events in a large cohort of middle-aged Swedes (study 2). Methods: Plasma concentration and urinary excretion of 20-HETE, and EETs and their metabolites, dihydroxyeicosatrienoic acids (DHETs), were measured in urine and plasma by mass spectrometry in 10 subjects with renovascular disease, 10 with essential hypertension, and 10 healthy normotensive subjects (controls), pair-matched for gender and age. Vascular and renal function was evaluated in all subjects (study 1). The polymorphisms were genotyped in the cardiovascular cohort of the Malmö Diet and Cancer (MDC-CVA) study. The incidence of fatal and non-fatal cardiovascular events (coronary events, n= 268, and ischemic stroke, n =194) was monitored over 10 years of follow-up. The analysis of blood pressure levels was performed twice: excluding subjects under antihypertensive treatment and including them (study 2). Results: Plasma 20-HETE was highest in subjects with renovascular disease [1.20 (0.42-1.92) ng/mL, median and range] compared to essential hypertensives [0.90 ng/mL (0.40-2.1)] and Metabolites of arachidonic acid via CYP450 in human hypertension controls [0.45 ng/mL (0.14-1.7), P<0.05]. Plasma 20- HETE significantly correlated with plasma renin activity (PRA) in renovascular disease (rs=0.67, n=10, P<0.05). The urinary excretion of 20-HETE was significantly lower in subjects with renovascular disease [12.9, (4.4-24.9) μg/g creatinine] than in controls [31.0 (11.9-102.8) μg/g creatinine, P<0.01)] and essential hypertensives [35.9 (14-72.5) μg/g creatinine, P<0.05]. Total plasma EETs were lowest as was the ratio of plasma EETs to plasma DHETs, an index of epoxide hydrolase activity, in renovascular disease [ratio 2.4 (1.2-6.1)], compared to essential hypertension [3.4 (1.5-5.6)] and controls [6.8 (1.4-18.8), P<0.01] (study 1). In the whole population, CYP4A11 S434S homozygotes had higher adjusted (for number of antihypertensive drugs) and non-adjusted systolic BP and higher prevalence of hypertension respect to F434 carriers. Male but not female CYP4F2 M433 carriers had significantly higher adjusted and non-adjusted systolic and diastolic BP and a trend toward higher hypertension prevalence (p=0.06) respect to V433V homozygotes. After adjustment for major cardiovascular risk factors, the hazard ratio (HR) for ischemic stroke in male CYP4F2 M433 carriers was significantly higher respect to V433V homozygotes (HR 1.69; 95%C.I. 1.1-2.6) even when BP levels and hypertension prevalence were included in the COX proportional-hazard model (study 2). Conclusion: circulating levels of 20-HETE are increased and those of EETs are decreased in RVD, while the urinary excretion of 20-HETE is reduced. Altered CYP 450 arachidonic acid metabolism may contribute to the vascular and tubular abnormalities of RVD (study 1). A common V433M polymorphism of the CYP4F2 might increase the risk of incident ischemic stroke in males but only partially through its elevating effect on BP. Further studies are needed to confirm these data (study 2).
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Books on the topic "Renovascular disease"

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Renal Vascular Disease. W.B. Saunders Company, 1996.

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Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Secondary hypertension. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199685288.003.0502_update_002.

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The causes of secondary hypertension and their therapy are discussed. Considered conditions are secondary hypertension, renovascular hypertension, renal parenchymal disease, primary aldosteronism, phaeochromocytoma, adrenal incidentaloma, and other causes of secondary hypertension.
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Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0213.

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Renovascular disease refers to a narrowing of a main or branch renal artery. Consequences include loss of functional renal tissue and renovascular hypertension, with other manifestations depending on the underlying cause. Worldwide the most common cause is atherosclerotic narrowing, with other causal pathologies including fibromuscular disease (FMD) and inflammatory conditions. FMD occurs much more frequently in women than in men, and is associated with smoking but genetic predisposing factors are also suspected. In South East Asia, Takayasu arteritis is an important cause.Takayasu disease often presents in a non-specific syndromic manner with fatigue and malaise. FMD often presents with early-onset hypertension. Atherosclerotic renal artery stenosis is often clinically silent with suspicion raised due to the existence of other cardiovascular pathology with the more dramatic presentations of acute decompensated heart failure or acute kidney injury less common. Clinical criteria can identify patients at risk.
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Alderson, Helen, Constantina Chrysochou, James Ritchie, and Philip A. Kalra. Ischaemic nephropathy. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0212.

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Ischaemic nephropathy describes loss of renal function or renal parenchyma due to stenosis or occlusion of the renal artery or its branches. In the Western world, this is usually the result of atherosclerotic renovascular disease, but other aetiologies include arteritis, embolic disease, dissection, and fibromuscular disease.Chronic kidney disease is the most common manifestation of ischaemic nephropathy, but hypertension, flash pulmonary oedema, sensitivity to angiotensin blockade, and sensitivity of glomerular filtration rate to blood pressure reduction are all possible manifestations of occlusive diseases of the renal artery or its branches. Proteinuria may also occur.This chapter describes these clinical features and the outcomes of ischaemic nephropathy. It goes on to discuss the haemodynamics and mechanisms and what we understand of the pathophysiology of the condition.
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Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Renal medicine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0017.

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Chapter 17 covers the basic science and clinical topics relating to ophthalmology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers renal basic science, pathophysiology of renal disease, the kidney as an 'endocrine' organ, renal investigations, acute kidney injury, chronic kidney disease/renal failure, renal replacement therapy, renal transplantation, haemodialysis, peritoneal dialysis, nephrotic syndrome, primary glomerular causes of nephrotic syndrome/proteinuria, rapidly progressive glomerulonephritis, IgA nephropathy, mesangiocapillary glomerulonephritis, tubulointerstitial nephritis, renal tubular disorders, urinary tract obstruction, renal stone disease, urinary tract infection in adults, renovascular disease, renal tumours, inherited renal disease, and renal disease and pregnancy.
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Salama, Alan D. The patient with vasculitis. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0159_update_001.

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Primary systemic vasculitis frequently leads to renal involvement and is responsible for significant numbers of patients progressing to end-stage renal disease. Frequently this is due to small vessel vasculitis, in association with antineutrophil cytoplasm antibody, which requires prompt recognition and timely therapeutic intervention to optimize renal and patient outcomes. Other organ systems are often affected. Relapses occur in about 50%.Less commonly medium or larger vessel vasculitis may involve the kidneys and through ischaemia lead to impaired renal function and renovascular hypertension, as in Takayasu’s or Kawasaki disease, and polyarteritis nodosa (PAN).
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Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0215.

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In fibromuscular disease (FMD), renal artery occlusion seems to be rare. Balloon angioplasty appears moderately successful in the medium term in controlling hypertension, at least in younger patients. In more complicated circumstances, medical therapy may be preferred. Similar approaches have been used in Takayasu disease but with less information about lasting outcomes.In atherosclerotic renal disease, the risk of renal artery occlusion and loss of renal function seems higher, but so are the complications of invasive management. Randomized clinical studies have not shown better blood pressure control or renal outcomes between medical therapy and percutaneous revascularization. As a consequence, modern management of atherosclerotic renovascular disease is primarily pharmacological, with interventional techniques reserved for selected presentations such as rapidly declining therapy, acute occlusion, or characteristic ‘flash’ pulmonary oedema.Whilst this approach is widely accepted, long-term outcome data are scant and there is ongoing research interest into specific disease phenotypes, refined interventional techniques, and novel treatment strategies aimed at preserving the renal microcirculation.
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8

Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0214.

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Modern practice typically utilizes indirect angiography by computed tomography or magnetic resonance imaging as the first-line diagnostic tool for renal artery stenosis, with no established screening tool able to meaningfully impact the pre-test probability of a positive finding. Neither can any current imaging technique reliably predict patient, blood pressure, or renal outcome following renal artery revascularization, although promising developments have been made in recent years.A major mechanism of hypertension in renovascular hypertension is overproduction of renin in response to hypoperfusion. While renin levels can be useful in investigating patients likely to have secondary hypertension, in the setting of renal impairment renin levels are not particularly useful in distinguishing treatable renal artery stenosis from other causes of renal disease.
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9

Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
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Book chapters on the topic "Renovascular disease"

1

Findlay, Mark, and Christopher Isles. "Renovascular Disease." In Clinical Companion in Nephrology, 119–22. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14868-7_23.

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2

Kirksey, Lee. "Renovascular Disease." In Cleveland Clinic Manual of Vascular Surgery, 69–78. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1631-3_6.

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3

Bien, Christian G., Christian E. Elger, Ali R. Afzal, Sirajedin Natah, Ritva Häyrinen-Immonen, Yrjö Konttinen, George S. Zubenko, et al. "Renovascular Disease." In Encyclopedia of Molecular Mechanisms of Disease, 1830. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6710.

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4

de Leeuw, Peter W., and Costas Tsioufis. "Atherosclerotic Renovascular Disease." In Secondary Hypertension, 21–32. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45562-0_2.

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5

Bien, Christian G., Christian E. Elger, Ali R. Afzal, Sirajedin Natah, Ritva Häyrinen-Immonen, Yrjö Konttinen, George S. Zubenko, et al. "Renovascular Hypertension." In Encyclopedia of Molecular Mechanisms of Disease, 1830. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6712.

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6

Zhang, Xin, and Alfonso Eirin. "Models of Renovascular Disease." In Renal Vascular Disease, 105–16. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2810-6_6.

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7

Vaughan, E. Darracott, Thomas G. Pickering, David B. Case, Thomas A. Sos, and John H. Laragh. "Hypertension in Renovascular Disease." In Hypertension in Kidney Disease, 77–98. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4271-4_4.

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8

Canzanello, Vincent J. "Medical Management of Renovascular Disease." In Renal Vascular Disease, 305–16. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2810-6_19.

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9

Nagaratnam, Nages, Kujan Nagaratnam, and Gary Cheuk. "Renovascular Disease in the Elderly." In Geriatric Diseases, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-32700-6_35-1.

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10

Nagaratnam, Nages, Kujan Nagaratnam, and Gary Cheuk. "Renovascular Disease in the Elderly." In Geriatric Diseases, 273–76. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-33434-9_35.

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