AKI - Acute Kidney Injury Flashcards
What is the best method of assessing kidney function. What is the normal range
GFR or eGFR: Normal = 100-120
State the causes of Pre-renal AKI (10)
Reduced blood flow
Absolute: Diarrhea, vomiting, severe burns, major hemorrhage, dehydration
Relative: Distributive shock (sepsis), Adrenal insufficiency, CCF, ACE inhibitors, renal artery stenosis, embolus
What is azotemia?
increased nitrogen products in the blood => increased urea
What is the normal urine output range?
What is considered reduced or oliguria?
What is considered severe?
Normal = 0.5-2ml/kg/hr
Oliguria = <0.5ml/kg/hr
Severe <0.3ml/kg/hr
Define AKI
reduced renal function leading to increased serum creatinine and/or reduced urine output (<0.5ml/kg/hr)
Urea may deposit in the skin causing skin discoloration. What color is it? In severe uremia what does it become?
Grey-yellow colour
Severe = Uremic frost (white flakes)
State the signs and symptoms of uremia
Nausea, dizziness, anorexia
Encephalopathy: Asterixes, confusion, disturbed sleep
Pruritis with scratch marks
Skin discoloration (grey-yellow discoloration)
Pericarditis - Pericardial rub
Uremia may eventually lead to pericarditis. What finding would support this? Describe the finding
Pericardial rub. scratchy creaky sounds like rubbing leather.
Heard loudest over left sternal border (2-3 intercostal space)
Rash in the setting of oliguria. What are your differentials
HUS - hemolytic uremic syndrome
HSP (IgA vasculitis)
SLE
Sepsis
What are the risk factors for an AKI?
5 on your HANDS Mneumonic
Hypertension
Age
Nephrotoxins - Aminoglycosides, heavy metals (Lead), ethylene glycol, myoglobin (increased CPK in rhabdomyolysis), uric acid (tumor lysis syndrome), tetracycline, IV contrast, ACE inhibitors
Diabetes
Systolic BP<90 (hypotension)
What is tumor lysis syndrome and with relation to the kidney what may it cause?
What other acute condition may it cause? How is it treated?
Tumor lysis syndrome is caused by the quick turnover of cells typically occurring in chemotherapy. This leads to the release of high amounts of uric acid leading to Acute tubular necrosis.
High serum uric acid levels may also cause gout. This is treated acutely with Colchicine + hydration and chronically (preventative) with Allopurinol + hydration
Give 5 causes of intra-renal AKI
Acute Tubular Necrosis
Glomerulonephritis
Acute interstitial nephritis
Hepatorenal syndrome
HUS - Hemolytic uremic syndrome
TTP - Thrombotic Thrombocytopenic Purpura
How would you differentiate between a Pre-renal cause and Acute Tubular Necrosis?
We use serum BUN and urinalysis with sedimentation examination
Pre-renal vs ATN
BUN or urea creatinine ratio in serum: >20:1 vs Normal or <15
FeNA: <1% vs >2%
Urine Na: <20 vs >35 mEq/L
Urine osmolality: >500 vs <350 mosm/kg
Casts: None vs Brown, muddy cell casts (epithelia)
Acute Tubular Necrosis:
What are the causes?
Explain the pathophysiology
Causes:
Ischemia => any pre-renal cause
Nephrotoxins => Aminoglycosides, heavy metals (lead), myoglobin, Uric acid, Ethylene glycol
Pathophysiology:
Dead tubular cells (from ischemia or nephrotoxins) slough off and plug the tubule causing an obstruction which can produce brown cellular casts in urine. This leads to increased tubular pressure causing:
reduced GFR => Oliguria and Azotemia
reduced gradient of diffusion => Hyperkalemia and metabolic acidosis
Intrarenal damage => reduced reabsorption => increased elimination of Na, urea, and water
Explain the pathophysiology of glomerulonephritis in the context of AKI
How would you SCREEN for GN?
Antibody deposition leads to the activation of the complement system (C3/C4) which recruits macrophages to attack the podocytes leading to increased permeability => Hematuria (micro) and Proteinura (<3.5g/day). This leads to
hypoalbuminemia => Oedema and HTN
reduced gradient => reduced GFR => Oliguria and azotemia
C3/C4, electrophoresis, ASOT