{"id":4900,"date":"2025-11-22T18:08:13","date_gmt":"2025-11-22T23:08:13","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=4900"},"modified":"2025-12-07T23:11:52","modified_gmt":"2025-12-08T04:11:52","slug":"diagnostic-blood-tests-for-kidney-function-and-disease","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/diagnostic-blood-tests-for-kidney-function-and-disease\/","title":{"raw":"8p6 Diagnostic Blood Tests for Kidney Function and Disease","rendered":"8p6 Diagnostic Blood Tests for Kidney Function and Disease"},"content":{"raw":"<strong>Diagnostic Blood Tests for Kidney Function and Disease<\/strong>\r\n<h1><strong>1. Blood Nitrogen Waste Tests:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Blood Urea Nitrogen (BUN):<\/strong>\u00a0Measures nitrogenous waste (urea) in the blood.<\/li>\r\n \t<li><strong>Creatinine:<\/strong>\u00a0A waste product from muscle metabolism.\r\n<ul>\r\n \t<li>Elevated levels indicate\u00a0<strong>kidney dysfunction<\/strong>\u00a0because the kidneys fail to excrete these wastes effectively.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>\r\n<h2><strong>Glomerular Filtration Rate (GFR)<\/strong>:<\/h2>\r\n<ul>\r\n \t<li>defined as: the volume of blood plasma filtered by nephrons\/minute.<\/li>\r\n \t<li>Measuring GFR is the gold-standard for assessing Kidney Function. GFR should be 60 or higher.<\/li>\r\n \t<li>Assessed by comparing <strong>serum<\/strong> levels of\u00a0<strong>urea and creatinine<\/strong>\u00a0with their\u00a0<strong>urine concentrations<\/strong>\u00a0over time.<\/li>\r\n \t<li>A\u00a0<strong>decreased GFR<\/strong>\u00a0signifies impaired kidney filtration (<strong>glomeruli<\/strong> and\/or <strong>nephron<\/strong> are impaired).<\/li>\r\n \t<li>GFR of 15 or lower indicates kidney failure.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>2. Blood pH and Acid-Base Balance:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Metabolic Acidosis:<\/strong>\r\n<ul>\r\n \t<li>Occurs when kidneys\u00a0<strong>fail to excrete excess hydrogen ions<\/strong>.<\/li>\r\n \t<li>Results in <strong>increased<\/strong> <strong>acidity<\/strong> of the blood (pH &lt;7.35).<\/li>\r\n \t<li>Daily metabolism (enzymatic reactions) of the body typically produces acids that need to be excreted). The more acid, the more free H+ ions exist in the blood (typically in the form of carbonic acid and lactate).\u00a0 Kidneys maintain blood pH7.4, by ensuring excess H+ ions are excreted in the form of urine.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>3. Anemia:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Caused by decreased secretion of erythropoietin (EPO):<\/strong>\r\n<ul>\r\n \t<li>Kidneys produce EPO, which stimulates red blood cell production.<\/li>\r\n \t<li>Damage to kidneys leads to\u00a0<strong>reduced EPO<\/strong>, causing\u00a0<strong>less RBC formation<\/strong>.<\/li>\r\n \t<li>Results in\u00a0<strong>anemia<\/strong>, with decreased oxygen-carrying capacity.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>4. Immune and Post-infectious Testing:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Antibody detection:<\/strong>\r\n<ul>\r\n \t<li><strong>Anti-streptolysin O<\/strong>\u00a0and\u00a0<strong>anti-streptokinase<\/strong>\u00a0antibodies indicate recent or ongoing\u00a0<strong>post-streptococcal glomerulonephritis (PSGN)<\/strong>.<\/li>\r\n \t<li>These antibodies were developed to eliminate <strong>Group A beta-hemolytic streptococcal infection <\/strong>and unfortunately cross-react with tissues of the body.\u00a0 These antibodies may cause\u00a0<strong>glomerular damage<\/strong>\u00a0and\u00a0<strong>inflammation<\/strong>, potentially leading to\u00a0<strong>permanent kidney damage<\/strong>\u00a0if untreated.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h2><strong>5. Microbial Cultures:<\/strong><\/h2>\r\n<ul>\r\n \t<li><strong>Bacterial or viral cultures:<\/strong>\u00a0 Used when infection is suspected.\r\n<ul>\r\n \t<li>Identify specific pathogens to guide appropriate\u00a0<strong>antibiotic or antiviral therapy<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>6. Renin Levels:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Elevated serum renin <\/strong>indicates <strong>poor blood flow <\/strong>to the kidney (due to heart disease or other causes of shock).\u00a0 The kidney is very susceptible to ischemia when blood flow is poor as there is no anastomoses (alternative blood vessels), and cells are not able to store oxygen.<\/li>\r\n \t<li><strong>Cause:<\/strong>\r\n<ul>\r\n \t<li>Reduced blood flow to the kidney (e.g., artery occlusion, trauma), triggering excessive\u00a0<strong>renin secretion<\/strong>.<\/li>\r\n \t<li>Renin activates\u00a0<strong>angiotensin II<\/strong>, causing vasoconstriction and stimulating\u00a0<strong>aldosterone<\/strong>\u00a0and\u00a0<strong>ADH<\/strong>\u00a0to increase blood volume and pressure (which unfortunately makes hypertension even worse).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>In cases of Hypertension, elevated serum renin<\/strong>\u00a0suggests the\u00a0<strong>kidney<\/strong>\u00a0is the\u00a0<strong>primary source of hypertension<\/strong>.\r\n<ul>\r\n \t<li>Indicates\u00a0<strong>renal origin of hypertension<\/strong>\u2014a potential target for therapy.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Low levels of renin<\/strong> will occur during kidney failure when kidney cells are no longer able to produce renin.<\/li>\r\n<\/ul>\r\n<strong>\u00a0<\/strong>\r\n<h1><strong>Summary:<\/strong><\/h1>\r\nKidney function tests include serum <strong>BUN<\/strong>, <strong>creatinine levels<\/strong>, and <strong>GFR<\/strong> to evaluate filtration efficiency. Elevated waste products, acid-base disturbances, and anemia suggest kidney damage. Serological tests for <strong>post-streptococcal infections<\/strong> and <strong>renin levels<\/strong> help diagnose specific causes of kidney-related hypertension or damage. Cultures and imaging aid in identifying infectious or structural pathologies, guiding targeted treatment.","rendered":"<p><strong>Diagnostic Blood Tests for Kidney Function and Disease<\/strong><\/p>\n<h1><strong>1. Blood Nitrogen Waste Tests:<\/strong><\/h1>\n<ul>\n<li><strong>Blood Urea Nitrogen (BUN):<\/strong>\u00a0Measures nitrogenous waste (urea) in the blood.<\/li>\n<li><strong>Creatinine:<\/strong>\u00a0A waste product from muscle metabolism.\n<ul>\n<li>Elevated levels indicate\u00a0<strong>kidney dysfunction<\/strong>\u00a0because the kidneys fail to excrete these wastes effectively.<\/li>\n<\/ul>\n<\/li>\n<li>\n<h2><strong>Glomerular Filtration Rate (GFR)<\/strong>:<\/h2>\n<ul>\n<li>defined as: the volume of blood plasma filtered by nephrons\/minute.<\/li>\n<li>Measuring GFR is the gold-standard for assessing Kidney Function. GFR should be 60 or higher.<\/li>\n<li>Assessed by comparing <strong>serum<\/strong> levels of\u00a0<strong>urea and creatinine<\/strong>\u00a0with their\u00a0<strong>urine concentrations<\/strong>\u00a0over time.<\/li>\n<li>A\u00a0<strong>decreased GFR<\/strong>\u00a0signifies impaired kidney filtration (<strong>glomeruli<\/strong> and\/or <strong>nephron<\/strong> are impaired).<\/li>\n<li>GFR of 15 or lower indicates kidney failure.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>2. Blood pH and Acid-Base Balance:<\/strong><\/h1>\n<ul>\n<li><strong>Metabolic Acidosis:<\/strong>\n<ul>\n<li>Occurs when kidneys\u00a0<strong>fail to excrete excess hydrogen ions<\/strong>.<\/li>\n<li>Results in <strong>increased<\/strong> <strong>acidity<\/strong> of the blood (pH &lt;7.35).<\/li>\n<li>Daily metabolism (enzymatic reactions) of the body typically produces acids that need to be excreted). The more acid, the more free H+ ions exist in the blood (typically in the form of carbonic acid and lactate).\u00a0 Kidneys maintain blood pH7.4, by ensuring excess H+ ions are excreted in the form of urine.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>3. Anemia:<\/strong><\/h1>\n<ul>\n<li><strong>Caused by decreased secretion of erythropoietin (EPO):<\/strong>\n<ul>\n<li>Kidneys produce EPO, which stimulates red blood cell production.<\/li>\n<li>Damage to kidneys leads to\u00a0<strong>reduced EPO<\/strong>, causing\u00a0<strong>less RBC formation<\/strong>.<\/li>\n<li>Results in\u00a0<strong>anemia<\/strong>, with decreased oxygen-carrying capacity.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>4. Immune and Post-infectious Testing:<\/strong><\/h1>\n<ul>\n<li><strong>Antibody detection:<\/strong>\n<ul>\n<li><strong>Anti-streptolysin O<\/strong>\u00a0and\u00a0<strong>anti-streptokinase<\/strong>\u00a0antibodies indicate recent or ongoing\u00a0<strong>post-streptococcal glomerulonephritis (PSGN)<\/strong>.<\/li>\n<li>These antibodies were developed to eliminate <strong>Group A beta-hemolytic streptococcal infection <\/strong>and unfortunately cross-react with tissues of the body.\u00a0 These antibodies may cause\u00a0<strong>glomerular damage<\/strong>\u00a0and\u00a0<strong>inflammation<\/strong>, potentially leading to\u00a0<strong>permanent kidney damage<\/strong>\u00a0if untreated.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h2><strong>5. Microbial Cultures:<\/strong><\/h2>\n<ul>\n<li><strong>Bacterial or viral cultures:<\/strong>\u00a0 Used when infection is suspected.\n<ul>\n<li>Identify specific pathogens to guide appropriate\u00a0<strong>antibiotic or antiviral therapy<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>6. Renin Levels:<\/strong><\/h1>\n<ul>\n<li><strong>Elevated serum renin <\/strong>indicates <strong>poor blood flow <\/strong>to the kidney (due to heart disease or other causes of shock).\u00a0 The kidney is very susceptible to ischemia when blood flow is poor as there is no anastomoses (alternative blood vessels), and cells are not able to store oxygen.<\/li>\n<li><strong>Cause:<\/strong>\n<ul>\n<li>Reduced blood flow to the kidney (e.g., artery occlusion, trauma), triggering excessive\u00a0<strong>renin secretion<\/strong>.<\/li>\n<li>Renin activates\u00a0<strong>angiotensin II<\/strong>, causing vasoconstriction and stimulating\u00a0<strong>aldosterone<\/strong>\u00a0and\u00a0<strong>ADH<\/strong>\u00a0to increase blood volume and pressure (which unfortunately makes hypertension even worse).<\/li>\n<\/ul>\n<\/li>\n<li><strong>In cases of Hypertension, elevated serum renin<\/strong>\u00a0suggests the\u00a0<strong>kidney<\/strong>\u00a0is the\u00a0<strong>primary source of hypertension<\/strong>.\n<ul>\n<li>Indicates\u00a0<strong>renal origin of hypertension<\/strong>\u2014a potential target for therapy.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Low levels of renin<\/strong> will occur during kidney failure when kidney cells are no longer able to produce renin.<\/li>\n<\/ul>\n<p><strong>\u00a0<\/strong><\/p>\n<h1><strong>Summary:<\/strong><\/h1>\n<p>Kidney function tests include serum <strong>BUN<\/strong>, <strong>creatinine levels<\/strong>, and <strong>GFR<\/strong> to evaluate filtration efficiency. Elevated waste products, acid-base disturbances, and anemia suggest kidney damage. Serological tests for <strong>post-streptococcal infections<\/strong> and <strong>renin levels<\/strong> help diagnose specific causes of kidney-related hypertension or damage. Cultures and imaging aid in identifying infectious or structural pathologies, guiding targeted treatment.<\/p>\n","protected":false},"author":1370,"menu_order":9,"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-4900","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\/4900","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\/4900\/revisions"}],"predecessor-version":[{"id":5266,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4900\/revisions\/5266"}],"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\/4900\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=4900"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=4900"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=4900"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=4900"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}