{"id":4939,"date":"2025-11-22T19:02:49","date_gmt":"2025-11-23T00:02:49","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=4939"},"modified":"2025-12-07T23:14:53","modified_gmt":"2025-12-08T04:14:53","slug":"vascular-disorders-affecting-the-kidneys-and-development-of-chronic-renal-failure","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/vascular-disorders-affecting-the-kidneys-and-development-of-chronic-renal-failure\/","title":{"raw":"8p13 Vascular Disorders Affecting the Kidneys and Development of Chronic Renal Failure","rendered":"8p13 Vascular Disorders Affecting the Kidneys and Development of Chronic Renal Failure"},"content":{"raw":"<strong> Vasculature: <\/strong>Kidneys rely on constant supply of <strong>oxygenated blood <\/strong>in order to function properly and survive.\r\n\r\n&nbsp;\r\n<h1><strong>A) Lesion-Related Vascular Changes:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Kidney perfusion<\/strong> could be negatively affected by <strong>renal<\/strong> <strong>cancer<\/strong>, <strong>infection<\/strong>, or <strong>trauma<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong>B) Age-Related Vascular Changes:<\/strong><\/h1>\r\n<ul>\r\n \t<li>The kidneys are\u00a0<strong>highly vascularized<\/strong>, making them vulnerable to\u00a0<strong>vascular damage<\/strong>\u00a0with aging.<\/li>\r\n \t<li>Common change:\u00a0<strong>Arteriosclerosis<\/strong> (loss of elasticity) leading to\u00a0<strong>narrowed blood vessels<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong>C) Disease- and Lifestyle-Related Vascular Changes<\/strong><\/h1>\r\n<ul>\r\n \t<li>Other Risk Factors for vascular changes:\u00a0 <strong>Atherosclerosis<\/strong> (build up of fatty plaques) also leads to <strong>narrowed blood vessels<\/strong> and can contribute to increased blood pressure, which can lead to further development of atherosclerosis and narrowing of blood vessels.<\/li>\r\n \t<li>Risk Factors for the development of atherosclerosis include: <strong>Type I and II diabetes mellitus, hypertension, sedentary behaviour, smoking, diet high in fats and\/or sugars, genetics, biological sex, <\/strong>and<strong> age<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong> Impact of Narrowed Blood Vessels:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Reduced blood supply<\/strong>\u00a0causes\u00a0<strong>ischemia<\/strong>\u00a0in the kidney tissue.<\/li>\r\n \t<li>Kidneys\u00a0<strong>do not have a backup blood supply<\/strong>, making them quite susceptible to ischemia.<\/li>\r\n \t<li><strong>Consequences:<\/strong>\r\n<ul>\r\n \t<li>Rapid\u00a0<strong>damage<\/strong>\u00a0to renal tissue, leading to <strong>decline in kidney function<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong> Kidney\u2019s Response to Decreased Blood Flow:<\/strong><\/h1>\r\n<ol>\r\n \t<li><strong>Kidneys<\/strong>\u00a0secrete\u00a0<strong>renin<\/strong> in response to low perfusion. (Memory Trick:\u00a0 Low Blood Flow stimulates RAAAS <span style=\"text-decoration: underline\">R<\/span>enin-<span style=\"text-decoration: underline\">A<\/span>ngiotensin II-<span style=\"text-decoration: underline\">A<\/span>DH-<span style=\"text-decoration: underline\">A<\/span>ldosterone-<span style=\"text-decoration: underline\">S<\/span>ympathetic).<\/li>\r\n \t<li>Increased\u00a0<strong>renin<\/strong>\u00a0activates\u00a0<strong>angiotensin II<\/strong>, which:\r\n<ul>\r\n \t<li><strong>Causes vasoconstriction<\/strong>, raising blood pressure, and<\/li>\r\n \t<li>Stimulates\u00a0<strong>aldosterone<\/strong>\u00a0and\u00a0<strong>ADH<\/strong>\u00a0release from <strong>adrenal gland cortex<\/strong> and <strong>pituitary gland <\/strong>respectively.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Actions of aldosterone and ADH (anti-diuretic hormone):<\/strong>\r\n<ul>\r\n \t<li>Promote\u00a0<strong>salt and water retention by nephrons<\/strong>, reducing salt and water in urine.<\/li>\r\n \t<li>Increase\u00a0<strong>blood volume<\/strong>, further elevating Blood Pressure (BP).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>This creates a\u00a0<strong>vicious cycle<\/strong>:\r\n<ul>\r\n \t<li><strong>Hypertension<\/strong> worsens vessel narrowing (due to reflexive constriction of afferent arteriole as well as development of systemic atherosclerosis).<\/li>\r\n \t<li>Further reduces blood flow, causing more damage.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<h1><strong> Progression to Chronic Kidney Damage:<\/strong><\/h1>\r\n<ol>\r\n \t<li>Persistent high blood pressure damages\u00a0<strong>vessel walls<\/strong>\u00a0in the kidney.<\/li>\r\n \t<li><strong>Nephrosclerosis<\/strong> develops (thickening and hardening of the walls of <strong>renal arterioles<\/strong> and <strong>small arteries)<\/strong>, narrowing blood vessel lumens contributing to ischemia.<\/li>\r\n \t<li><strong>Vascular injury<\/strong>\u00a0also contributes to development of\u00a0<strong>atherosclerosis<\/strong>\u00a0and\u00a0<strong>arteriosclerosis<\/strong>.<\/li>\r\n \t<li><strong>Narrowed lumens<\/strong>\u00a0reduce\u00a0<strong>renal blood flow<\/strong>, leading to <strong>nephron loss<\/strong>,\u00a0<strong>fibrosis<\/strong>, and\u00a0<strong>scarring<\/strong>.<\/li>\r\n \t<li><strong>Atrophy:<\/strong>\u00a0The kidney\u00a0<strong>shrinks<\/strong>\u00a0over time with\u00a0<strong>fibrotic tissue replacing healthy tissue<\/strong>.<\/li>\r\n \t<li><strong>Loss of nephron function:<\/strong> can lead to <strong>Chronic Kidney Failure <\/strong>if not treated\r\n<ul>\r\n \t<li>Kidneys\u00a0<strong>fail to filter blood waste<\/strong>\u00a0effectively.<\/li>\r\n \t<li>Accumulation of\u00a0<strong>waste products<\/strong>\u00a0in blood causes\u00a0<strong>uremia<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<h1><strong> Treatments:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Control hypertension:\u00a0 <\/strong>Using\u00a0<strong>antihypertensive drugs<\/strong>\u00a0(e.g., diuretics, beta-blockers).<\/li>\r\n \t<li><strong>Manage underlying conditions:<\/strong>\u00a0 e.g. Proper <strong>diabetes control<\/strong><\/li>\r\n \t<li><strong>Lifestyle modifications: <\/strong>\r\n<ul>\r\n \t<li>Reduced\u00a0<strong>sodium intake<\/strong>.<\/li>\r\n \t<li><strong>Healthy diet<\/strong> and regular\u00a0<strong>exercise<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Summary:<\/strong><\/h1>\r\nChronic vascular damage from hypertension and atherosclerosis leads to <strong>renal ischemia, nephron loss, fibrosis,<\/strong> and <strong>kidney atrophy<\/strong>. Without intervention, progressive damage results in <strong>end-stage renal failure<\/strong>, characterized by accumulation of waste products, with dialysis or transplant as potential treatments. Preventing vascular damage through blood pressure control and lifestyle changes is essential.","rendered":"<p><strong> Vasculature: <\/strong>Kidneys rely on constant supply of <strong>oxygenated blood <\/strong>in order to function properly and survive.<\/p>\n<p>&nbsp;<\/p>\n<h1><strong>A) Lesion-Related Vascular Changes:<\/strong><\/h1>\n<ul>\n<li><strong>Kidney perfusion<\/strong> could be negatively affected by <strong>renal<\/strong> <strong>cancer<\/strong>, <strong>infection<\/strong>, or <strong>trauma<\/strong>.<\/li>\n<\/ul>\n<h1><strong>B) Age-Related Vascular Changes:<\/strong><\/h1>\n<ul>\n<li>The kidneys are\u00a0<strong>highly vascularized<\/strong>, making them vulnerable to\u00a0<strong>vascular damage<\/strong>\u00a0with aging.<\/li>\n<li>Common change:\u00a0<strong>Arteriosclerosis<\/strong> (loss of elasticity) leading to\u00a0<strong>narrowed blood vessels<\/strong>.<\/li>\n<\/ul>\n<h1><strong>C) Disease- and Lifestyle-Related Vascular Changes<\/strong><\/h1>\n<ul>\n<li>Other Risk Factors for vascular changes:\u00a0 <strong>Atherosclerosis<\/strong> (build up of fatty plaques) also leads to <strong>narrowed blood vessels<\/strong> and can contribute to increased blood pressure, which can lead to further development of atherosclerosis and narrowing of blood vessels.<\/li>\n<li>Risk Factors for the development of atherosclerosis include: <strong>Type I and II diabetes mellitus, hypertension, sedentary behaviour, smoking, diet high in fats and\/or sugars, genetics, biological sex, <\/strong>and<strong> age<\/strong>.<\/li>\n<\/ul>\n<h1><strong> Impact of Narrowed Blood Vessels:<\/strong><\/h1>\n<ul>\n<li><strong>Reduced blood supply<\/strong>\u00a0causes\u00a0<strong>ischemia<\/strong>\u00a0in the kidney tissue.<\/li>\n<li>Kidneys\u00a0<strong>do not have a backup blood supply<\/strong>, making them quite susceptible to ischemia.<\/li>\n<li><strong>Consequences:<\/strong>\n<ul>\n<li>Rapid\u00a0<strong>damage<\/strong>\u00a0to renal tissue, leading to <strong>decline in kidney function<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong> Kidney\u2019s Response to Decreased Blood Flow:<\/strong><\/h1>\n<ol>\n<li><strong>Kidneys<\/strong>\u00a0secrete\u00a0<strong>renin<\/strong> in response to low perfusion. (Memory Trick:\u00a0 Low Blood Flow stimulates RAAAS <span style=\"text-decoration: underline\">R<\/span>enin-<span style=\"text-decoration: underline\">A<\/span>ngiotensin II-<span style=\"text-decoration: underline\">A<\/span>DH-<span style=\"text-decoration: underline\">A<\/span>ldosterone-<span style=\"text-decoration: underline\">S<\/span>ympathetic).<\/li>\n<li>Increased\u00a0<strong>renin<\/strong>\u00a0activates\u00a0<strong>angiotensin II<\/strong>, which:\n<ul>\n<li><strong>Causes vasoconstriction<\/strong>, raising blood pressure, and<\/li>\n<li>Stimulates\u00a0<strong>aldosterone<\/strong>\u00a0and\u00a0<strong>ADH<\/strong>\u00a0release from <strong>adrenal gland cortex<\/strong> and <strong>pituitary gland <\/strong>respectively.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Actions of aldosterone and ADH (anti-diuretic hormone):<\/strong>\n<ul>\n<li>Promote\u00a0<strong>salt and water retention by nephrons<\/strong>, reducing salt and water in urine.<\/li>\n<li>Increase\u00a0<strong>blood volume<\/strong>, further elevating Blood Pressure (BP).<\/li>\n<\/ul>\n<\/li>\n<li>This creates a\u00a0<strong>vicious cycle<\/strong>:\n<ul>\n<li><strong>Hypertension<\/strong> worsens vessel narrowing (due to reflexive constriction of afferent arteriole as well as development of systemic atherosclerosis).<\/li>\n<li>Further reduces blood flow, causing more damage.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<h1><strong> Progression to Chronic Kidney Damage:<\/strong><\/h1>\n<ol>\n<li>Persistent high blood pressure damages\u00a0<strong>vessel walls<\/strong>\u00a0in the kidney.<\/li>\n<li><strong>Nephrosclerosis<\/strong> develops (thickening and hardening of the walls of <strong>renal arterioles<\/strong> and <strong>small arteries)<\/strong>, narrowing blood vessel lumens contributing to ischemia.<\/li>\n<li><strong>Vascular injury<\/strong>\u00a0also contributes to development of\u00a0<strong>atherosclerosis<\/strong>\u00a0and\u00a0<strong>arteriosclerosis<\/strong>.<\/li>\n<li><strong>Narrowed lumens<\/strong>\u00a0reduce\u00a0<strong>renal blood flow<\/strong>, leading to <strong>nephron loss<\/strong>,\u00a0<strong>fibrosis<\/strong>, and\u00a0<strong>scarring<\/strong>.<\/li>\n<li><strong>Atrophy:<\/strong>\u00a0The kidney\u00a0<strong>shrinks<\/strong>\u00a0over time with\u00a0<strong>fibrotic tissue replacing healthy tissue<\/strong>.<\/li>\n<li><strong>Loss of nephron function:<\/strong> can lead to <strong>Chronic Kidney Failure <\/strong>if not treated\n<ul>\n<li>Kidneys\u00a0<strong>fail to filter blood waste<\/strong>\u00a0effectively.<\/li>\n<li>Accumulation of\u00a0<strong>waste products<\/strong>\u00a0in blood causes\u00a0<strong>uremia<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<h1><strong> Treatments:<\/strong><\/h1>\n<ul>\n<li><strong>Control hypertension:\u00a0 <\/strong>Using\u00a0<strong>antihypertensive drugs<\/strong>\u00a0(e.g., diuretics, beta-blockers).<\/li>\n<li><strong>Manage underlying conditions:<\/strong>\u00a0 e.g. Proper <strong>diabetes control<\/strong><\/li>\n<li><strong>Lifestyle modifications: <\/strong>\n<ul>\n<li>Reduced\u00a0<strong>sodium intake<\/strong>.<\/li>\n<li><strong>Healthy diet<\/strong> and regular\u00a0<strong>exercise<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Summary:<\/strong><\/h1>\n<p>Chronic vascular damage from hypertension and atherosclerosis leads to <strong>renal ischemia, nephron loss, fibrosis,<\/strong> and <strong>kidney atrophy<\/strong>. Without intervention, progressive damage results in <strong>end-stage renal failure<\/strong>, characterized by accumulation of waste products, with dialysis or transplant as potential treatments. Preventing vascular damage through blood pressure control and lifestyle changes is essential.<\/p>\n","protected":false},"author":1370,"menu_order":16,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-4939","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":59,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4939","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":4,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4939\/revisions"}],"predecessor-version":[{"id":5274,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4939\/revisions\/5274"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/59"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4939\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=4939"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=4939"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=4939"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=4939"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}