{"id":4941,"date":"2025-11-22T19:03:48","date_gmt":"2025-11-23T00:03:48","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=4941"},"modified":"2025-12-07T23:15:07","modified_gmt":"2025-12-08T04:15:07","slug":"acute-kidney-injury-aki","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/acute-kidney-injury-aki\/","title":{"raw":"8p14 Acute Kidney Injury (AKI)","rendered":"8p14 Acute Kidney Injury (AKI)"},"content":{"raw":"<strong> Acute Kidney Injury (AKI):<\/strong>\r\n<h1><strong>Definition:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Sudden, severe decline in kidney function occurring\u00a0<strong>within 48 hours<\/strong>. Often reversible if treated. (Formerly called Acute Kidney Failure)<\/li>\r\n<\/ul>\r\n<h1><strong>Features:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Rapid reduction in\u00a0<strong>glomerular filtration rate (GFR)<\/strong>.<\/li>\r\n \t<li>Leads to\u00a0<strong>accumulation of nitrogenous wastes<\/strong>\u00a0(urea, creatinine, ammonia, uric acid) in the blood (<strong>azotemia<\/strong>).<\/li>\r\n \t<li>Disrupts\u00a0<strong>fluid and electrolyte balance<\/strong>.<\/li>\r\n \t<li>Causes\u00a0<strong>metabolic acidosis<\/strong>\u00a0due to retention of acids.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Effects on the Body:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Toxic wastes impair\u00a0<strong>cell function<\/strong>\u00a0in organs like the\u00a0<strong>heart<\/strong>,\u00a0<strong>brain<\/strong>, and\u00a0<strong>skeletal muscles<\/strong>.<\/li>\r\n \t<li>Imbalance of\u00a0<strong>pH<\/strong>\u00a0and\u00a0<strong>electrolytes<\/strong>\u00a0significantly influences\u00a0<strong>heart rhythm<\/strong>\u00a0and\u00a0<strong>muscle function<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Causes of Acute Renal Injury:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Severe shock or circulatory failure:<\/strong>\r\n<ul>\r\n \t<li>Sudden\u00a0<strong>decreased blood flow,<\/strong>\u00a0e.g., any form of prolonged\/untreated <strong>shock<\/strong> such as:\r\n<ul>\r\n \t<li><strong>hypovolemic shock<\/strong> due to burns\/injuries\/hemorrhaging,<\/li>\r\n \t<li><strong>septic shock<\/strong> due to serious infections,<\/li>\r\n \t<li><strong>cardiogenic shock<\/strong> due to myocardial infarction.<\/li>\r\n \t<li><strong>Pathogenesis: <\/strong>\r\n<ul>\r\n \t<li>Drops blood flow significantly, causing\u00a0<strong>ischemia<\/strong>.<\/li>\r\n \t<li>Results in\u00a0<strong>necrosis<\/strong>\u00a0of the nephron cells.<\/li>\r\n \t<li>Inflammation and\u00a0<strong>white blood cell infiltration<\/strong>\u00a0can cause obstruction.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Primary Lesions: <\/strong>\r\n<ul>\r\n \t<li><strong>Trauma or infection<\/strong>\u00a0causing inflammation and necrosis.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Nephrotoxins:<\/strong>\r\n<ul>\r\n \t<li>Drugs like\u00a0<strong>NSAIDs<\/strong>,\u00a0<strong>acetaminophen<\/strong>, and\u00a0<strong>aspirin<\/strong>\u00a0in overdose can\u00a0<strong>damage<\/strong>\u00a0renal nephrons.<\/li>\r\n \t<li>Results in\u00a0<strong>necrosis<\/strong>, inflammation, and\u00a0<strong>obstruction<\/strong>\u00a0of filtrate flow, reducing urine output.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Obstructions: Back pressure<\/strong>\u00a0from obstructive stones or tumors.\r\n<ul>\r\n \t<li>Can be caused by\u00a0<strong>blood clots<\/strong>,\u00a0<strong>kidney<\/strong> <strong>stones<\/strong>,\u00a0<strong>tumors<\/strong>, or\u00a0<strong>scarring<\/strong>.<\/li>\r\n \t<li>Blockage increases\u00a0<strong>pressure<\/strong>, damages nephrons in a\u00a0<strong>backward (retrograde)<\/strong>\u00a0manner.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Secondary to rhabdomyolysis:<\/strong> Damage to skeletal muscles results in myoglobinemia, myoglobin accumulation damages nephron tubules and leads to myoglobinuria and brown-tinged urine<\/li>\r\n \t<li><strong>Secondary to Post-streptococcal Glomerulonephritis (PSGN):<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Upper respiratory infection (\u201cStrep Throat\u201d) with <strong>Group A beta-hemolytic Streptococcus<\/strong>\u00a0can trigger\u00a0<strong>glomerulonephritis<\/strong><\/li>\r\n \t<li><strong>PSGN<\/strong>:\u00a0 damage and inflammation to glomeruli due to accumulation of antibody complexes, causing inflammation and damage.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Pathological Features:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Necrosis:<\/strong>\u00a0Death of nephron cells reduces filtration capacity.<\/li>\r\n \t<li><strong>Inflammation:<\/strong>\u00a0White blood cells and edema further impair nephron function.<\/li>\r\n \t<li><strong>Obstruction of tubules:<\/strong>\u00a0Increases backpressure, reduces urine output (<strong>oliguria<\/strong>).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Symptoms &amp; Signs:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Oliguria:<\/strong>\u00a0Reduced urine output (common in critically ill).<\/li>\r\n \t<li>Accumulation of waste products (<strong>azotemia<\/strong>): elevated\u00a0<strong>urea<\/strong>\u00a0and\u00a0<strong>creatinine<\/strong>.<\/li>\r\n \t<li><strong>Electrolyte imbalances<\/strong>,\u00a0<strong>acid-base disturbances<\/strong>:\r\n<ul>\r\n \t<li><strong>Metabolic acidosis:<\/strong>\u00a0due to impaired hydrogen ion secretion.<\/li>\r\n \t<li><strong>Hyperkalemia:<\/strong>\u00a0excess potassium in blood.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Toxic accumulation:<\/strong>\u00a0Systemic effects including\u00a0<strong>confusion<\/strong>,\u00a0<strong>weakness<\/strong>,\u00a0<strong>arrhythmias<\/strong>,\u00a0<strong>respiratory issues<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Reversibility:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Often\u00a0<strong>recoverable<\/strong>\u00a0if the underlying cause is promptly treated.<\/li>\r\n \t<li>Damage can be\u00a0<strong>prevented or minimized<\/strong>\u00a0if managed early.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Summary:<\/strong><\/h1>\r\nAcute kidney injury (AKI) occurs suddenly due to <strong>blood flow reduction (ischemia), infection, inflammation, toxin exposure,<\/strong> or <strong>obstruction,<\/strong> leading to <strong>nephron dysfunction, nephron death and kidney failure<\/strong>.\u00a0 Signs and symptoms relate to the <strong>rapid accumulation of wastes<\/strong> and<strong> electrolyte imbalance in the bloodstream<\/strong>.\u00a0 Prompt diagnosis and management are essential to prevent permanent damage.\u00a0 Recognizing the causes and early signs allows prompt treatment\u2014such as removing offending agents and supporting kidney function\u2014to prevent irreversible damage.\u00a0 Acute and toxic kidney injuries impair fluid, electrolyte, and waste balance, threatening life if not managed urgently.\r\n\r\n&nbsp;","rendered":"<p><strong> Acute Kidney Injury (AKI):<\/strong><\/p>\n<h1><strong>Definition:<\/strong><\/h1>\n<ul>\n<li>Sudden, severe decline in kidney function occurring\u00a0<strong>within 48 hours<\/strong>. Often reversible if treated. (Formerly called Acute Kidney Failure)<\/li>\n<\/ul>\n<h1><strong>Features:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Rapid reduction in\u00a0<strong>glomerular filtration rate (GFR)<\/strong>.<\/li>\n<li>Leads to\u00a0<strong>accumulation of nitrogenous wastes<\/strong>\u00a0(urea, creatinine, ammonia, uric acid) in the blood (<strong>azotemia<\/strong>).<\/li>\n<li>Disrupts\u00a0<strong>fluid and electrolyte balance<\/strong>.<\/li>\n<li>Causes\u00a0<strong>metabolic acidosis<\/strong>\u00a0due to retention of acids.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Effects on the Body:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Toxic wastes impair\u00a0<strong>cell function<\/strong>\u00a0in organs like the\u00a0<strong>heart<\/strong>,\u00a0<strong>brain<\/strong>, and\u00a0<strong>skeletal muscles<\/strong>.<\/li>\n<li>Imbalance of\u00a0<strong>pH<\/strong>\u00a0and\u00a0<strong>electrolytes<\/strong>\u00a0significantly influences\u00a0<strong>heart rhythm<\/strong>\u00a0and\u00a0<strong>muscle function<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Causes of Acute Renal Injury:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Severe shock or circulatory failure:<\/strong>\n<ul>\n<li>Sudden\u00a0<strong>decreased blood flow,<\/strong>\u00a0e.g., any form of prolonged\/untreated <strong>shock<\/strong> such as:\n<ul>\n<li><strong>hypovolemic shock<\/strong> due to burns\/injuries\/hemorrhaging,<\/li>\n<li><strong>septic shock<\/strong> due to serious infections,<\/li>\n<li><strong>cardiogenic shock<\/strong> due to myocardial infarction.<\/li>\n<li><strong>Pathogenesis: <\/strong>\n<ul>\n<li>Drops blood flow significantly, causing\u00a0<strong>ischemia<\/strong>.<\/li>\n<li>Results in\u00a0<strong>necrosis<\/strong>\u00a0of the nephron cells.<\/li>\n<li>Inflammation and\u00a0<strong>white blood cell infiltration<\/strong>\u00a0can cause obstruction.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<li><strong>Primary Lesions: <\/strong>\n<ul>\n<li><strong>Trauma or infection<\/strong>\u00a0causing inflammation and necrosis.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Nephrotoxins:<\/strong>\n<ul>\n<li>Drugs like\u00a0<strong>NSAIDs<\/strong>,\u00a0<strong>acetaminophen<\/strong>, and\u00a0<strong>aspirin<\/strong>\u00a0in overdose can\u00a0<strong>damage<\/strong>\u00a0renal nephrons.<\/li>\n<li>Results in\u00a0<strong>necrosis<\/strong>, inflammation, and\u00a0<strong>obstruction<\/strong>\u00a0of filtrate flow, reducing urine output.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Obstructions: Back pressure<\/strong>\u00a0from obstructive stones or tumors.\n<ul>\n<li>Can be caused by\u00a0<strong>blood clots<\/strong>,\u00a0<strong>kidney<\/strong> <strong>stones<\/strong>,\u00a0<strong>tumors<\/strong>, or\u00a0<strong>scarring<\/strong>.<\/li>\n<li>Blockage increases\u00a0<strong>pressure<\/strong>, damages nephrons in a\u00a0<strong>backward (retrograde)<\/strong>\u00a0manner.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Secondary to rhabdomyolysis:<\/strong> Damage to skeletal muscles results in myoglobinemia, myoglobin accumulation damages nephron tubules and leads to myoglobinuria and brown-tinged urine<\/li>\n<li><strong>Secondary to Post-streptococcal Glomerulonephritis (PSGN):<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Upper respiratory infection (\u201cStrep Throat\u201d) with <strong>Group A beta-hemolytic Streptococcus<\/strong>\u00a0can trigger\u00a0<strong>glomerulonephritis<\/strong><\/li>\n<li><strong>PSGN<\/strong>:\u00a0 damage and inflammation to glomeruli due to accumulation of antibody complexes, causing inflammation and damage.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Pathological Features:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Necrosis:<\/strong>\u00a0Death of nephron cells reduces filtration capacity.<\/li>\n<li><strong>Inflammation:<\/strong>\u00a0White blood cells and edema further impair nephron function.<\/li>\n<li><strong>Obstruction of tubules:<\/strong>\u00a0Increases backpressure, reduces urine output (<strong>oliguria<\/strong>).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Symptoms &amp; Signs:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Oliguria:<\/strong>\u00a0Reduced urine output (common in critically ill).<\/li>\n<li>Accumulation of waste products (<strong>azotemia<\/strong>): elevated\u00a0<strong>urea<\/strong>\u00a0and\u00a0<strong>creatinine<\/strong>.<\/li>\n<li><strong>Electrolyte imbalances<\/strong>,\u00a0<strong>acid-base disturbances<\/strong>:\n<ul>\n<li><strong>Metabolic acidosis:<\/strong>\u00a0due to impaired hydrogen ion secretion.<\/li>\n<li><strong>Hyperkalemia:<\/strong>\u00a0excess potassium in blood.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Toxic accumulation:<\/strong>\u00a0Systemic effects including\u00a0<strong>confusion<\/strong>,\u00a0<strong>weakness<\/strong>,\u00a0<strong>arrhythmias<\/strong>,\u00a0<strong>respiratory issues<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Reversibility:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Often\u00a0<strong>recoverable<\/strong>\u00a0if the underlying cause is promptly treated.<\/li>\n<li>Damage can be\u00a0<strong>prevented or minimized<\/strong>\u00a0if managed early.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Summary:<\/strong><\/h1>\n<p>Acute kidney injury (AKI) occurs suddenly due to <strong>blood flow reduction (ischemia), infection, inflammation, toxin exposure,<\/strong> or <strong>obstruction,<\/strong> leading to <strong>nephron dysfunction, nephron death and kidney failure<\/strong>.\u00a0 Signs and symptoms relate to the <strong>rapid accumulation of wastes<\/strong> and<strong> electrolyte imbalance in the bloodstream<\/strong>.\u00a0 Prompt diagnosis and management are essential to prevent permanent damage.\u00a0 Recognizing the causes and early signs allows prompt treatment\u2014such as removing offending agents and supporting kidney function\u2014to prevent irreversible damage.\u00a0 Acute and toxic kidney injuries impair fluid, electrolyte, and waste balance, threatening life if not managed urgently.<\/p>\n<p>&nbsp;<\/p>\n","protected":false},"author":1370,"menu_order":17,"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-4941","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\/4941","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\/4941\/revisions"}],"predecessor-version":[{"id":5275,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4941\/revisions\/5275"}],"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\/4941\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=4941"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=4941"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=4941"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=4941"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}