Term
| What is Acute Kidney Injury? |
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Definition
- Rapid decline in glomerular function
- Disruption of fluid, electrolyte, and acid-base homeostasis
- Accumulation of nitrogenous wastes (Azotemia)
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Term
| What is the acronym standing for the classification of AKI, and what is do the letters stand for? |
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Definition
RIFLE
- Risk
- Injury
- Failure
- Loss of kidney
- End-stage kidney disease |
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Term
| What are the RIFLE categories with corresponding Serum Creatinine and Urine Output Criteria? |
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Definition
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RIFLE Category
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Serum Creatinine (Scr) Criteria
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Urine Output Criteria
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Risk
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Increase in Scr by 50% or GFR decrease by 25%
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Urine output < 0.5 mL/kg/hr x 6 hrs
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Injury
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Increased in Scr by 100% or GFR decrease by 50%
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Urine output < 0.5 mL/kg/hr x 12 hrs
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Failure
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Increase in Scr by 100% or GFR decrease by 75% OR Scr > 4 mg/dL
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Urine output > 0.3 mL/kg/ hr x 24 hrs OR anuria (no urine output < 12 hrs
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Loss
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Persistent AKI > 4 weeks
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End-stage Kidney Disease
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Persistent AKI > 3 months
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Term
| What is significant regarding AKI? |
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Definition
- Complicates 30% of admissions to ICU
- Generally diagnosed by rise in serum creatinine (SCr) in routine laboratory work
- Approximately one-half of patients with AKI will have significant reduction in urine output (oliguria) |
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Term
| What are the three classifications of AKI? |
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Definition
- Prerenal - Decreased blood flow to kidneys - 70% of cases
- Postrenal - Due to obstruction of urinary flow - 5%
- Intrinsic - Damage or disease of renal tissue - 24% |
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Term
| What are the causes of community and nosocomial AKI? |
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Definition
•Community acquired:
–Common causes: dehydration, obstruction
–Low mortality
•Nosocomial:
–Common causes: hypotension, sepsis, trauma
–Commonly associated with multi-system organ failure
–High mortality (> 80%) risk increases with age, concomitant nephrotoxic agents and hemodynamic instability
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Term
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Definition
| Biochemical abnormality that refers to increased blood urea nitrogen (BUN) and serum creatinine (Scr) |
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Term
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Definition
Azotemia that is associated with clinical signs and symptoms including:
- Nausea and Vomiting
- Decreased platelet aggregation (Uremic bleeding)
- Encephalopathy
- Pericardial effusion |
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Term
| What is the definition of renal failure? |
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Definition
- Progressive deterioration in renal function as evidenced by:
- Increased BUN and Scr
- Decreased creatinine clearance
- Development of uremic symptoms |
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Term
| What are some causes of prerenal failure? |
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Definition
Intravascular Volume Depletion: Hemorrhage, decrease effective perfusion volume (nephrotic syndrome, cirrhosis), vasodilation (sepsis), Diuretics
Vascular Obstruction: Bilateral renal artery occlusion and ACE inhibitors
Decreased Cardiac Output: Congestive Heart Failure, Myocardial Infarction, Pulmonary Embolism |
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Term
| What are the clinical presentations of prerenal failure? |
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Definition
Volume Depletion: Thirst, Hypotension, Tachycardia
Evidence of decreased effective perfusion volume: Ascites, Edema
Severe Infection: Fever, hypotension, positive blood culture
History of therapy with drugs that may alter renal perfusion (NSAIDS, ACEI, Diuretics) |
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Term
| What part of the nephron do ACEi's have an effect on, and what happens? |
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Definition
- Angiotensin II normally constricts the efferent arteriole
- ACEi's will inhibit this, which decreases GCP (Glomerular Capillary Pressure), affecting renal perfusion |
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Term
| What kind of lab values can we expect to see in a patient with prerenal failure? |
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Definition
- Normal urine sediment, no casts
- Urine osmolality: serum osmolality >1.5
- BUN:Scr > 20
- Low fractional excretion of sodium (FeNa). Prerenal failure <1%, normally 1-2%
*FeNa = UNa x Scr x 100/Ucr x SNa*
UNa = Urine Sodium
Ucr = Urine Creatinine
Scr = Serum Creatinine
SNa = Serum Sodium |
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Term
| How do we go about the management of prerenal failure? |
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Definition
Hemorrhage è Packed red blood cells (PRBCs)
Plasma Losses (burns) è Normal Saline-titrate based on urine output
Improve Cardiac output è Positive inotropes, intraaortic balloon pump
**Therapy is directed at restoring renal blood flow by increasing intravascular volume. Generally rapidly reversible if volume can be restored**
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Term
| What are the causes of intrinsic renal failure? |
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Definition
Acute tubular necrosis (ATN)
- post-prerenal ischemic insult if not correct within 2 days --> 90 of cases (surgery, trauma, sepsis)
- Nephrotoxins (Radiocontrast dyes, Aminoglycosides, many many more)
- Rhabdomyolysis: statins
- Hemolysis: Carbidopa
- Tumor Lysis syndrome: Chemotherapy induced
- Ethylene glycol or methanol ingestion
- Glomerulonephritis: NSAIDS
- Hemolytic Uremic Syndrome/thrombotic-thrombocytopenic purpura (Clopidogrel)
- Allergic Interstitial Nephritis (Antibiotics) |
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Term
| What is the pathophysiology of Post Ischemic ATN? How does this present in a clinical setting? |
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Definition
- Prolonged ischemia results in damage to the renal parenchyma (tissue)
- Severe renal hypoperfusion may result in necrosis of renal tissue and irreversible renal function
- Features similar to prerenal failure
- Does NOT resolve with fluid repletion and restoration of renal blood flow
- Usually charaterized by three phases: Oliguric, Diuretic, Recovery |
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Term
| Name the three phases of ATN |
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Definition
- Oliguric
- Diuretic
- Recovery
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Term
| What is Oliguric phase of ATN? |
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Definition
- 1-2 weeks duration
- Diminished urine output --> <400ml/24h
- Accumulation of metabolic waste products
- Fluid, electrolyte, and acid-base abnormalities appear
- May progress to anuria: urine output < 50ml/24h |
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Term
| What is Diuretic phase of ATN? |
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Definition
- Variable duration
- Indicates initial recovery of the kidneye
- Characterized by increase in urine ouput
- Glomerular filtration gradually increases
- The ability of the tubule to reabsorb sodium and concentrate urine follows |
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Term
| What is Recovery phase of ATN? |
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Definition
- Azotemia resolves 5-60 days after the onset of the diuretic phase
- Ability to maximally concentrate urine will return within several months
- GFR will return to 90-95% of baseline over 1-2 years
- Patiens with worse baseline RF, more severe renal insult may only return to 50% of baseline RF |
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Term
| What kind of laboratory results can we expect from a patient with Post Ischemic ATN? |
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Definition
- Muddy brown appearance from RBC and WBC casts
- Granular or epithelial cell casts
- Urine: serum osmolality <1.3
- BUN: Scr = 1.5
- FeNa > 2%
- May also see: High urine Mg2+ and tubular enzymes (ie N-acetylglucosaminidase NAG) |
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Term
| What are the goals of Post Ischemic ATN management? |
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Definition
Goals
- Improve urine output
- Restore renal function
- Decrease the need for renal replacement therapy (ie hemodialysis)
- Improve survival |
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Term
| What could Renal (low) Dose Dopamine be used for? |
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Definition
– Post Ischemic ATN
- 0.5-2 mcg/kg/min
–Low doses of dopamine (LDD) selectively dilate renal vasculature and theoretically may increase renal blood flow and GFR
–Potential adverse effects of DA include: tachyarrythmias, MI, gut ischemia, ¯ respiratory drive
•Several small clinical trials have demonstrated increases in urine output but inconsistent effects on:
–GFR
–Renal blood flow
No Effect on:
–Need for dialysis
–MORTALITY
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