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38 Cards in this Set
- Front
- Back
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Learning objectives
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Understand pre-renal, renal, and post renal causes of acute kidney injury
Understand the major causes of acute kidney injury, in regard to diagnosis, etiology, and treatment Know the general diagnostic approach to acute kidney injury, including clinical parameters, urine sediment, urinary indices, radiological studies and renal biopsy Have a general understanding of the approach and management of a patient with acute kidney injury |
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Acute kidney injury: overview
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Comprised of a wide spectrum of clinical syndromes characterized by an abrupt decrease in GFR
Resulting in the accumulation of nitrogenous waste products, including urea and creatinine, as well as other uremic middle molecules and inflammatory components Decline in urine output can be variable Precise correlation between changes in serum creatinine level and GFR do not exist -Relatively small rises in serum creatinine are associated with worse outcomes |
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AKI: Incidence and prevalence
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Reported prevalence (US data) ranges from 1%-7.1% of all hospital admissions
Critically ill-patients: 5–20% will experience an episode of AKI during course of illness (of which 4.9% will receive RRT) Data from the Intensive Care National Audit Research Centre (ICNARC) suggests that AKI accounts for nearly 10 percent of all ICU bed days 8.8x more likely for CKD 3.1x more likely for ESRD 2x more likely to die |
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Confounding factors in BUN and Cr levels
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BUN and Cr
-Insensitive and late markers of renal dysfunction -Can also be affected by other confounding factors Increased BUN: GI bleeding, catabolic states, high protein diet, Amino acid infusion/TPN, tetracycline, steroids Increased Cr: Rhabdomyolysis, cimetidine, trimethoprim, probenacid |
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AKI: definition
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An acute and sustained increase in serum Cr concentration of:
-an increase in serum cr by 0.5mg/dl, if baseline Cr <2.5mg/dl OR -an increase in serum Cr by 20%, if baseline Cr>2.5mg/dl AKIN Criteria: An abrupt (within 48hrs) reduction of kidney function -an absolute increase serum Cr >0.3mg/dl OR -a percentage increase of serum Cr>50% OR -reduction of urine output (<0.5ml/kg/hr for >6hrs) RIFLE Classification -Risk, injury, failure, loss, ESRD -Risk in SCr, drop in GFR |
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Pre-renal AKI: clinical syndrome
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Reduced renal perfusion
Preserved renal parenchymal function Kidneys responding appropriately to reduced perfusion with Na and H2O retention, concentrated urine, low urine Na Main pathophysiological mechanisms -True intravascular hypovolemia -Decreased effective circulatory volume --CHF, cirrhosis -Intrarenal vasoconstriction -Renal artery disease |
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Pre-renal AKI: pathophysiology
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Hypovolemia
-Fall in systemic BP -Activation of sympathetic nervous system, RAAS, and release of ADH -All of these processes act to maintain blood pressure and maintain CO/cerebral perfusion Renal response -Autoregulation of RBF and GFR occurs within narrow limits -When renal perfusion falls, PG/NO vasodilation of afferent arteriole maximize RBF -Increased Na resorption results in decreased Na delivery to macula densa which further potentiates afferent arteriole vasodilation -AgII mediated vasocontriction of efferent arteriole maintain glomerular capillary hydrostatic pressures, thus GFR -Increase ADH and aldosterone restore volume depletion Prolonged or severe hypovolemia -Autoregulatory dilatation of afferent arteriole is maximal at a mean systemic arterial BP 80mmHG -During states of prolonged or severe hypovolemia, the compensatory renal response becomes overwhelmed and intrinsic kidney injury ensues |
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Autoregulation of GFR
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Decreased renal perfusion
-NO and PG vasodilate afferent arteriole which increases Pgc and maintains GFR -Ag vasoconstricts efferent arteriole which increases Pgc and maintains GFR KIDNEY SLIDE |
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Pre-renal AKI: causes
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True Volume Depletion
-Extra-renal: diarrhea, vomiting, GI bleeding, blood loss, burns, third spacing -Renal: diuretic use, diabetes insipidus, osmotic diuresis Low Effective Circulation -CHF, cirrhosis, shock/sepsis Vasoconstriction -Hypercalcemia, contrast dye, cyclosporine/tacrolimus Pharmacological -NSAIDs, ACEs/ARBs Renal artery disease KIDNEY SLIDE |
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Pre-renal AKI: clinical presentation
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Varies depending on cause of reduced perfusion
Nonspecific signs and symptoms of renal failure -Weakness, nausea, vomiting, change in appetite -Changes in UOP and swelling True Volume Depletion -History of extracellular fluid loss from skin, gastrointestinal or renal source -Inquire about recent infections, fever, diarrhea, diuretic use, decrease hydration, orthostatic lightheadedness, thirst -On exam: signs of hypovolemia such as orthostatic hypotension, tachycardia, dry mucous membrane, decrease skin turgor, no axillary moisture, oliguria or concentrated urine Low effective circulation -History of heart failure, low cardiac output, cirrhosis -Inquire about SOB, PND, orthopnea, changes in weight -On exam: edema, third heart sound, JVD, pulmonary crackles/effusion |
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Pre-renal AKI: diagnosis
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Serum chemistry
-Elevated BUN/Cr >20:1 -Low urinary flow in prerenal state allows for increase urea absorption -Monitor for complications of ARF (hyperkalemia, acidosis) Urinalysis -Bland sediment Fractional Excretion of Sodium (FENa) -Percent of filtered Na that is excreted in the urine -FENa= (UNa*PCr)/(UCr*PNa)*100 -FENa <1% Pre-renal azotemia -Difficult to interpret with use of diuretics, therefore use fractional excretion of urea --Use FEurea <35% Pre-renal azotemia Urine Sodium -Increased proximal reabsorption of Na in response to hypovolemia -UNa<20 Pre-renal azotemia KIDNEY SLIDE |
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Pre-renal AKI: treatment
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Expedient treatment: minimizes the risk of progression to intrinsic injury
Key is to normalize the effective blood flow to the kidney Optimize renal perfusion and volume status by giving isotonic fluids, blood products, or pressor agents -Exception: low effective circulation due to heart failure requires diuretic therapy Stop any drugs that may exacerbate the condition Treat underlying disease(s) |
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Intrinsic AKI: overview
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In intrinsic causes of AKI, the primary lesion is in the kidney
The renal parenchyma is not intact -Vascular/Microvascular -Glomerular -Interstitium -Tubules Unlike pre-renal and post renal causes, recovery is not expected to be as dramatic with removal of the culprit |
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Acute tubular necrosis (ATN): history and PE
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Most common type of intrinsic AKI
Nonspecific signs and symptoms of renal failure History: may be similar to prerenal symptoms -Prolonged prerenal symptoms such as recent infections, fever, diarrhea, diuretic use, decrease hydration, orthostatic lightheadedness, thirst. Maybe exhibit symptoms of heart failure -Episodes of hypotension and recent surgeries -Recent contrast administration -Review medications for nephrotoxins Physical Exam: similar to pre-renal -Signs of hypovolemia such as orthostatic hypotension, tachycardia, dry mucous membrane, decrease skin turgor, no axillary moisture, oliguria/concentrated urine -Signs of heart failure |
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Causes of ATN
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Ischemia
-Prolonged hypoperfusion -Crush Injury & trauma -Septic shock -Pancreatitis Endotoxins -Hemoglobin -Myoglobin -Uric acid -Immunoglobulin light chains Exotoxins -Heavy metals (lead) -Ethylene glycol -Contrast dye -Antibiotics (aminoglycosides, amphotericin B) *It is important to remember that pre-renal and ATN are two extremes of the same clinical spectrum KIDNEY SLIDE |
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Pathophysiology of ATN
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Ischemic ATN is a progression of the prerenal state to a point at which compensatory mechanisms decompensate
Ischemia: Overwhelming levels of AII and endothelin-1 cause intense vasoconstriction: further reducing perfusion Increase in inflammatory cytokines potentiates endothelial injury Congestion and obstruction of capillaries Tubular cells: Disruption of actin cytoskeleton leading to a loss of brush border Loss of polarity of epithelial cells results in failure of tight junctions: back leak of tubular fluid, detached BM Apoptosis and necrosis of tubular epithelium |
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Phases of ATN
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Initiation
-Oliguric phase (urine output <400 cc.day) -Inciting event damages tubular epithelial cells causing necrosis: blockage of tubular lumen by necrotic debris: reduction in GFR, vasoconstriction resulting in prolonged ischemia Maintenance -Ongoing renal failure; lasts 7-21days, rarely beyond 4-6wks -Creatinine usually increases 0.5-1.0 mg/dl/day -Conversion from oliguria to non-oliguria does not improve mortality Recovery -Polyuric phase: regeneration of tubular epithelium, but unable to reabsorb H2O and electrolytes -Recovery phase: gradual return of BUN/Cr to baseline or near normal levels KIDNEY SLIDE |
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Diagnosis of ATN
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Serum Chemistry
-Elevated BUN and Cr -BUN/Cr <20:1 Urine -FENa >2% -Urine Na >40 -Urine osmolality <350 Urine Sediment -Classic “Muddy Brown Cast” KIDNEY SLIDE |
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Treatment of ATN
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Largely supportive
-Attempt to improve renal perfusion, maintain SBP>100mmHG -Avoid nephrotoxic agents -Remember to adjust doses of medication for CrCl<10-15 Medical therapy, including dialysis -Correct volume status -Treat electrolyte disturbances -Treat acidosis |
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Contrast induced nephropathy: Pathogenesis, risk factors
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Subset of ATN frequently seen in hospital settings
Pathogenesis -Vasoconstriction renal arteries -Direct tubular injury Risk factors -Underlying renal insufficiency (PCr >1.5; GFR<60ml/min) -Diabetic nephropathy with renal insufficiency -Advanced heart failure or other cause of reduced renal perfusion (such as hypovolemia) -Percutaneous coronary intervention, which also promotes the development of atheroemboli -High total dose of contrast agent KIDNEY SLIDE |
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Contrast induced nephropathy: clinical presentation, diagnosis, differentiate from atheroembolic disease
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Clinical presentation
-Renal failure apparent within the first 12- 24 hours (IMPORTANT) after the contrast study -Non-oliguric with mild decline in renal function -Patients occasionally require dialysis (especially if baseline Cr > 4 mg/dL) Diagnosis -Similar to ATN -History with recent contrast administration & characteristic rise in plasma creatinine concentration beginning with the first 12 -24 hours Differentiate from atheroembolic disease: -Presence of other embolic lesions (as on the toes) or livedo reticularis -Transient eosinophilia and hypocomplementemia -Onset of renal failure that may be delayed for days to weeks after the procedure -Protracted course with frequently little or no recovery of renal function KIDNEY SLIDE |
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Contrast induced nephropathy: prevention, treatment
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Prevention
-Avoid contrast if possible in high risk individuals -Use of nonionic low osmolal agents -Use lower doses of contrast -Avoid repetitive, closely spaced studies (eg, <48 hours apart) -Avoid volume depletion and NSAIDs Treatment -Volume expand, if not contraindicated -Prior to and continued for several hours after contrast administration -Type of fluid isotonic bicarbonate or isotonic saline -Mucomyst, conflicting data --Recommended day prior to and day of procedure KIDNEY SLIDE |
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Atheroembolic disease: overview
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Cholesterol crystal embolization occurs when portions of an atherosclerotic plaque break off and embolize distally
Resulting in partial or total occlusion of multiple small arteries (or glomerular arterioles) Leading to tissue or organ ischemia Seen after manipulation of the aorta or other large arteries during arteriography, angioplasty, or surgery |
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Atheroembolic disease: clinical presentation and renal manifestations
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Clinical presentation
-Blue toe syndrome -CVA -Livedo reticularis -Gastrointestinal manifestations Renal manifestations -Occurs primarily in older patients (mean age 66yrs) -Marked renal impairment with an acute onset, seen within one to two weeks of event -Sub-acute presentation: renal dysfunction occurs in staggered steps, separated by periods of stable kidney function -Not a rare cause of acute renal failure in elderly patients KIDNEY SLIDE |
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Atheroembolic diasese: diagnosis
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Urine:
-Bland urine sediment -Eosinophiluria during the active phase -Proteinuria is usually not a prominent feature; however, nephrotic range proteinuria Eosinophilia Hypocomplementemia Definitive diagnosis: Biopsy -Skin lesion (if present) -Kidney KIDNEY SLIDE |
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Acute interstitial nephritis: definition, common causes
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Defines a pattern of renal injury characterized histopathologically by inflammation and edema of the renal interstitium
Most commonly caused by: -Drugs -Infections -Autoimmune disorders -Idiopathic KIDNEY SLIDE |
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Clinical presentation of acute interstitial nephritis
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Nonspecific symptoms (except for drug induced)
-Malaise, anorexia, or nausea and vomiting -Acute or sub-acute onset -Signs and features of ARF Eosinophilia Urine -White cells, white cell casts, and red cell casts -Urine eosinophils (not always) -<1gm proteinuria Evidence of renal tubular dysfunction -Fanconi’s syndrome: resulting in glucose, phosphorus, amino acids, uric acid in urine |
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Onset and symptoms of drug induced acute interstitial nephritis
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Onset of disorder
-Up to 1-2 weeks after initial exposure -3-5days after second exposure -Latent period variable: 1day, up to 18months Classical Symptoms -Rash (15% at presentation) -Fever (27%) -Eosinophilia (23%) -Triad (10%) KIDNEY SLIDE |
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Acute interstitial nephritis: diagnosis
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Clinical symptoms
ARF improves with removal of offending agent Peripheral eosinophilia Urine eosinophils, sterile pyuria Definitive: renal biopsy |
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Acute interstitial nephritis: treatment
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Drug-induced
Discontinue offending agent -Should expect improvement in renal function in 3-7days -May take several weeks-months Trial of corticosteroids -1mg/kg/day prednisone x 4-6weeks -May hasten recovery of renal function Other causes -Treat underlying disease |
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Post-renal AKI: causes
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Urteral
-Intrinsic: crystals, light chain casts, stones, blood clots, papillary necrosis, fungus balls, edema -Extrinsic: gravida uterus, uterine prolapse, uterine tumors, RP fibrosis, RP tumor, radiation therapy Bladder -Diabetes Mellitus, Multiple Sclerosis, Spinal cord injury, Anticholinergic agents Urethral obstruction -Posterior Urethral Valves, BPH, diverticula, strictures, tumors, obstructed foley catheter |
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Post-renal AKI: clinical presentation
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Pain: Especially with acute obstruction
-Flank pain-upper tract; Suprapubic-lower tract -Colicky pain, radiating down to groin is suggestive of stones Change in UOP -COMPLETE: Anuria with bilateral obstruction or unilateral in solitary kidney obstruction -PARTIAL/INTERMITTENT: polyuria, polyuria alternating with oligoanuria Palpable mass -Increase kidney size due to hydronephrosis/edema -Suprapubic mass may be distended bladder Bladder symptoms : hesitancy, weak stream, dysuria, postvoid dribbling Hypertension: increase renin levels: activate RAAS, increase ECF: impaired Na excretion Recurrent UTIs: obstruction promotes stasis Renal calculi: obstruction promotes infection; urease producing organism: struvite stones Type IV RTA (hyperkalemic, metabolic acidosis): damage tubular cells can not respond to aldosterone Hematuria: stones, tumors |
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Post-renal AKI: diagnosis
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Serum chemistry
-Elevated BUN/Cr -FeNa>2%-4% Urine -Bland sediment -Hematuria --Stones, tumors -Crystals Imaging KIDNEY SLIDE |
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Post-renal AKI: treatment and prognosis
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Relieve obstruction
Extent of recovery after relief of obstruction depends on severity and duration of obstruction -<1week: usually recovers completely -<2weeks: 70% chance; <3weeks: 30% chance ->12weeks: no recovery Post Obstructive Diuresis -Commonly seen after relief of severe bilateral obstruction -Polyuria --Osmotic diuresis caused by retain urea --Volume overload --Tubular concentration defect KIDNEY SLIDE |
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Diagnostic approach to AKI: serum chemistry, urinalysis
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Serum Chemistry
-BUN/Cr >20: 1 prerenal -BUN/Cr <20: 1 intrinsic -BUN/Cr >15 and variable in post renal Urinalysis -Bland sediment: pre-renal, post renal -Epithelial cells and muddy brown casts: ATN -RBC cast: Glomerulonephritis -Eosinophils: AIN KIDNEY SLIDE |
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Renal biopsy: indications, contraindications
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Indications
-Isolated glomerular hematuria with proteinuria or renal insufficiency -Isolated non-nephrotic proteinuria (< 1-2gm/day) -Nephrotic syndrome -Acute nephritic syndrome -Unexplained acute or sub-acute renal failure Contraindications -Uncorrectable bleeding diathesis -Small kidneys, indicative of chronic damage -Severe hypertension -Multiple bilateral cysts -Hydronephrosis -Active renal/peri-renal infection -Uncooperative patient KIDNEY SLIDE |
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Treatment of AKI
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PREVENTION
Identify high risk groups -Pre-existing kidney disease -Diabetics -Solitary kidney -Multiple myeloma Avoid Nephrotoxins -Contrast -Aminoglycosides -NSAIDS KIDNEY SLIDE |
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Indications for dialysis
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AEIOU
Acidosis -Persistent metabolic acidosis with pH<7.2 with bicarbonate therapy Electrolyte Abnormalities -Persistent hyperkalemia ± EKG changes despite medical therapy Intoxications -Drug intoxications Overload -Refractory volume overload despite diuretics Uremia -Signs of uremia (altered mental status, pericardial rub) KIDNEY SLIDE |
