{"id":8113,"date":"2021-11-15T22:59:47","date_gmt":"2021-11-15T20:59:47","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/nephrology\/acute-kidney-injuries-recognition-prevention-prerenal-and-postrenal-renal-failure\/"},"modified":"2022-01-18T13:59:51","modified_gmt":"2022-01-18T11:59:51","slug":"acute-kidney-injuries-recognition-prevention-prerenal-and-postrenal-renal-failure","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/nephrology\/acute-kidney-injuries-recognition-prevention-prerenal-and-postrenal-renal-failure\/","title":{"rendered":"Acute kidney injuries, recognition, prevention, prerenal and postrenal renal failure"},"content":{"rendered":"\n<p class=\"wp-block-paragraph\">AKI describes a rapid decline in renal function (days to weeks) leading to <strong>azotemia <\/strong>with\/without <strong>oliguria<\/strong>.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">It is used interchangeably with acute renal failure.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">The clinical definition is an <strong>increase in<\/strong> <strong>Scr <\/strong>and a <strong>decrease in urine output<\/strong> for a period of fewer than 3 months.<\/p>\n\n\n<span class=\"block-heading\" id=\"header_1\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Classification<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<ul class=\"wp-block-list\"><li>&nbsp;AKI is classified according to what is the source of the problem, i.e. is it:<ul><li><strong>Prerenal<\/strong> (reduced perfusion)<\/li><li><strong>Intrarenal<\/strong> (intrinsic kidney disease)<\/li><li><strong>Postrenal <\/strong>(obstruction).<\/li><\/ul><\/li><li>Pre-renal and intrarenal are divided into oliguric renal failure (worse) and non-oliguric renal failure.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Prerenal failure<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<ul class=\"wp-block-list\"><li><strong>Most common cause of AKI. <\/strong>There&#8217;s no structural damage to the kidney, but rather just loss of perfusion.<\/li><li>CHF and liver cirrhosis can sometimes hide hypovolemia.<\/li><li>Causes include:<ul><li><strong>Hypovolemia <\/strong>(dehydration)<\/li><li><strong>Decrease in effective circulatory volume<\/strong> (cirrhosis, PAH, HF, shock)<\/li><li><strong>Drugs with vascular disease<\/strong> (ACEi\/ARBs with renal artery stenoses, NSAIDs and renal hypoperfusion).<\/li><\/ul><\/li><li>Hyperosmolar urine with low sodium.<\/li><li>Increased sodium resorption (low urinary sodium).<\/li><li>Increased BUN\/sCr due to an increase in urea reabsorption.<\/li><li>Typically reversible (if treated quickly).<ul><li>Restore fluids (hypovolemia), vasopressors (HF, shock), diuretics (cirrhosis, PAH).<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Intrarenal failure<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<ul class=\"wp-block-list\"><li><strong>Causes:<\/strong><ul><li><strong>Most frequent cause is ATN<\/strong> &#8211; due to renal ischemia and toxins; <strong>hypoperfusion<\/strong> is common in patients with shock\/requiring reanimation, and <strong>drugs<\/strong> such as aminoglycosides, diclofenac, contrast material, but also in rhabdomyolysis, severe hemolysis<\/li><li>Glomerular diseases (GN, RPGN [crescentic GN])<\/li><li>Vascular disease (vasculitides [WG, microscopic polyangiitis], cholesterol embolism [spontaneous, after catheter intervention, anticoagulant-mediated], HUS, malignant hypertension, scleroderma)<\/li><li>Tubulo-interstitial diseases (ATN, tubulo-interstitial nephritis [antibiotics, NSAIDs], bilateral pyelonephritis)<\/li><li>Intratubular obstruction (tumor lysis syndrome -&gt; urate crystals, MM)<\/li><\/ul><\/li><li>Hyposmolar urine with high sodium.<\/li><li>Decreased BUN\/sCr ratio due to decreased urea reabsorption.<\/li><li>Treatment:<ul><li>ATN. remove the offending agent<\/li><li>GN. ACEi\/ARBs<\/li><li>Vasculitides, tubulo-interstitial nephritis. Steroids<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Post-renal<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<ul class=\"wp-block-list\"><li>Causes:<ul><li>BPH\/carcinoma<\/li><li>Urolithiasis (single kidney? Bilateral?)<\/li><li>Bladder dysfunction (neurogenic bladder)<\/li><li>Retroperitoneal fibrosis<\/li><\/ul><\/li><li>Hyposmolar urine with high sodium.<\/li><li>Normal BUN\/sCr ratio.<\/li><li>Treatment is catheter and surgery.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Recognition<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<ul class=\"wp-block-list\"><li>Clinically: <strong>hypotension<\/strong>, reduced urine output and a rise in serum creatinine and BUN.<\/li><li>Initial weight gain and peripheral edema.<\/li><li>Later,<strong> symptoms of uremia <\/strong>(anorexia, nausea, vomiting, myoclonic jerks, seizures, asterixis, coma).<\/li><li><strong>Tests:<\/strong><ul><li>sCr, BUN<\/li><li>Urinalysis<\/li><li>US and x-ray (calculi)<\/li><li>ANA tests (lupus nephritis)<\/li><li>Biopsy<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Prevention<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<ul class=\"wp-block-list\"><li>Monitor BP in patients with trauma\/burns\/hemorrhage<\/li><li>Maintain adequate fluids and blood volume<\/li><li>Minimize contrast agent usage, use low-osmolar agents, avoid NSAIDs<\/li><li>Increase fluid intake in chemotherapy (prevent tumor lysis syndrome)<\/li><li><strong>Endothelin receptor antagonists<\/strong><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Staging systems<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<ul class=\"wp-block-list\"><li>The <strong>RIFLE (Risk, Injury, Failure, Loss, ESRD)<\/strong> classification defines and stratifies the risk of AKI based on the increase in<strong> serum creatinine<\/strong>,<strong> decrease in GFR<\/strong>, and<strong> need of dialysis <\/strong>allowing the monitoring of the severity and outcome of AKI.<\/li><li><strong>AKIN<\/strong> is an updated, modified version of RIFLE, where the increase in Src is based on 48 hours (compared to 7 days with RIFLE).<\/li><li>Patients who had AKI are at high risk for developing <strong>CKD <\/strong>later in life.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_8\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">BUN\/sCr ratio<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_8\">\n\n\n<p class=\"wp-block-paragraph\">Urea reabsorbed by the tubules can be regulated (increased or decreased) whereas creatinine reabsorption remains the same (minimal reabsorption).<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Normal BUN<\/strong> is 6-24mg\/dL;<strong> normal sCr<\/strong> is 0.7-1.3mg\/dL (and slightly lower for women).<\/li><li><strong>Normal BUN\/sCr ratio<\/strong> is 12-20. AKI with normal ratio can mean postrenal failure.<\/li><li><strong>Elevated BUN\/sCr<\/strong> is seen in prerenal AKI, due to increased urea reabsorption.<\/li><li><strong>Decreased BUN\/sCr <\/strong>is seen in intrarenal AKI, due to decreased urea reabsorption, or due to advanced liver disease\/malnutrition.&nbsp;<\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Hepatorenal syndrome<\/strong>. Involves development of renal failure in patients with severe liver disease. The hallmark of the disease is advanced liver damage (cirrhosis) causes renal vasoconstriction and decrease in renal function.<\/p>\n\n\n<\/span><span class=\"block-heading\" id=\"header_9\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Misc<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_9\">\n\n\n<ul class=\"wp-block-list\"><li>Metformin + contrast material (which causes ARF) will lead to lactic acidosis. Therefore, metformin has to be stopped 48 hours prior<\/li><li>Post-catheter intervention cholesterol embolism can cause ARF, presenting in days, with &#8220;marbled&#8221; blue-reddish skin marks and digit necrosis.<\/li><li>Also\u2026during the cath. Intervention, contrast material is used, so that can also be the cause of ARF<\/li><li>In rhabdomyolysis, CK and aldolase are increased<\/li><li>In massive hemolysis, hGB decreases and LDH increases<\/li><\/ul>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Classification<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Prerenal failure<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Intrarenal failure<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Post-renal<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Recognition<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Prevention<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Staging systems<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">BUN\/sCr ratio<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Misc<\/h3><\/div>","protected":false},"excerpt":{"rendered":"<p>AKI describes a rapid decline in renal function (days to weeks) leading to azotemia with\/without oliguria. It is used interchangeably with acute renal failure. The clinical definition is an increase in Scr and a decrease in urine output for a period of fewer than 3 months. Classification &nbsp;AKI is classified according to what is the [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":685,"menu_order":13,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-8113","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.9 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Acute kidney injuries, recognition, prevention, prerenal and postrenal renal failure &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/nephrology\/acute-kidney-injuries-recognition-prevention-prerenal-and-postrenal-renal-failure\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"3 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/nephrology\\\/acute-kidney-injuries-recognition-prevention-prerenal-and-postrenal-renal-failure\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/nephrology\\\/acute-kidney-injuries-recognition-prevention-prerenal-and-postrenal-renal-failure\\\/\",\"name\":\"Acute kidney injuries, recognition, prevention, prerenal and postrenal renal failure &#8211; 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