Page 66 of 76 RENAL DECOMPENSATION Acute Renal Failure ARF What is acute renal

Page 66 of 76 renal decompensation acute renal

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Page 66 of 76 RENAL DECOMPENSATION Acute Renal Failure (ARF) What is acute renal failure (ARF)? Sudden loss of kidney function Altered fluid and electrolytes What are the risk factors for ARF? Volume depletion: dehydration Nephrotoxic ABX and other nephrotoxic agents Frequent bouts or sustained hypotension (kidneys aren’t being perfused) Sepsis, SIRS (decreased BF to kidneys) CV failure, heart failure, MI How is ARF classified? Prerenal : conditions decrease blood flow to kidneys (anything that prevents BF to kidneys) Intrarenal : conditions affecting internal (parenchymal) structures (swelling, calculi, glomerulonephritis) o Acute tubular necrosis (ATN) : Toxin OR Ischemia damages Postrenal : conditions obstruction urine outflow WHAT ARE CAUSES OF PRERENAL FAILURE? Hypotension/Hypo profusion, dehydration (Usually a volume issue= decreased BF to kidneys) Decreased cardiac output: MI, CHF, dysrythmias, sepsis (need blood and O2 to do work) Renal artery disorder: embolus, or thrombus, stenosis, trauma (kidneys need O2 to work) WHAT ARE CAUSES INTRARENAL FAILURE? Vascular disease Acute glomerulonephritis Acute tubercular necrosis (ATN) o Prolonged ischemia o Nephrotoxins-drug** major cause Acute Tubercular Necrosis (ATN) Ischemic acute tubular necrosis (ATN) results from prolonged hypoperfusion. A sequence of pathophysiological processes results in the sloughing off of necrotic cells that block the tubular lumen. o Toxic ATN occurs when a nephrotoxin becomes concentrated in the renal tubular cells and causes necrosis. The necrotic cells slough off and obstruct the tubular lumen, similar to ischemic ATN. o In toxic ATN, the basement membrane of the renal cells usually remains intact, and the necrotic areas are more localized. Types of ATN o Ischemic ATN – continuum of prerenal conditions
Page 67 of 76 o Nephrotoxic ATN – caused by drugs—(aminoglycosides) May not occur for 7-10 days o Prevention- Dose dependent – lower dose Risk factors: Volume-depletion-hydrate and advanced age
Page 68 of 76 What is the clinical course of ATN? There are 4 phases o Onset (initiating) Phase: Find and treat cause, Prevent damage o Oliguric or Non-Oliguric Phase (UOP=urinary output) Oliguric = UOP < 400 ml/day (7-14 days) Non-oliguric = UOP > 400 ml/day (5-8 days) o Diuretic Phase – UOP > 4-5,000 ML/day! (1-2 weeks) o Recovery Phase--months – 1 year Contract- Induced Nephropathy (CIN) o Begins w/in 48 hours of receiving,peaks in 3-5 days, returns 3-5 days Nonoliguric , transient, reversible Diabetics at greatest risk Prevention: AGGRESSIVE HYDRATION before, during, after procedure Postrenal Caused by obstruction Backflow of urine causes congestion of nephron Requires blockage of both kidneys Causes: stricture, tumors, stones, trauma, blood clots, BPH (causes obstruction) Relief of blockage: o PROFOUND diuresis (5-8 L/DAY) follows relief of obstruction!

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