AKI Flashcards
What does RIFLE stand for?
ased on severity: Risk, Injury, Failure → GFR, sCr, UOP
- Based on outcome: Loss, End-stage → duration of loss
of kidney function and end-stage renal disease
AKI is classified into 3 stages per the Acute Kidney Injury Network (AKIN)
in 2004. What 2 lab parameters are considered in this classification?
Stage Creatinine Criteria UOP Criteria
1 sCr increase of >0.3 mg/dL or <0.5 mL/kg/h for >6 h
sCr increase to ≥ 150%-200% from baseline
2 sCr increase to > 200%-300% from baseline <0.5 mL/kg/h for >12 h
3 sCr increase to >300% from baseline or
sCr ≥ 4 mg/dL with acute rise of ≥0.5 mg/dL <0.3 mL/kg/h for x 24 h or anuria X 12h
How many % of cardiac output
circulates through the kidneys?
20%; filters 1600 L of blood per day
What is the proximal convoluted
tubule and what does it do?
Continuation of epithelium of the Bowman’s capsule; begins the controlled reabsorption of several nutrients:
glucose, amino acids, Na, bicarb, K, Cl, Calcium, Phos, water, and other solutes + produces ammonium
What is the loop of Henle and what
does it do?
Urine is concentrated here via osmotic gradient in
the renal medulla
What is the distal tubule and what
does it do?
Reabsorption of sodium and water; affected by hormones like vasopressin, PTH, calcitonin
What are the major functions of the
kidneys?
- Excretory: urea, uric acid, creatinine, ammonia, excess vitamins/minerals, drug/poison metabolites
- Acid-base balance: bicarbonate/H+, phosphate buffers, citrate, amino acid metabolites
- Endocrine: calcitriol production, EPO
- Fluid-electrolyte balance: ADH/vasopressin, renin (RAAS)
How is AKI diagnosed/described per the
Acute Kidney Injury Network (AKIN) in 2004?
An abrupt (within 48 h) reduction in kidney function defined as:
- An absolute increase in sCr >0.3 mg/dL, or
- A percentage increase of 50%, or
- A reduction in UOP (oliguria of <0.5 mL/kg/h for >6 hours)
What are some causes of prerenal AKI?
Renal hypoperfusion d/t intravascular volume depletion, decreased cardiac output, early sepsis, diuretic abuse, cirrhosis, hepatorenal syndrome Result in reduced UOP, sodium retention, nitrogenous waste accumulation. Occurs in 50-60% of AKI cases
What conditions can cause intravascular
volume depletion in prerenal AKI?
Hemorrhage, vomiting (including during pregnancy), diarrhea, surgical drainage, burns, fever, third-spacing, diuretic use, inadequate volume resuscitation, septic abortion, hypoadrenalism
What are some treatment goals for prerenal AKI?
1) Early diagnosis
2) Restoration of renal perfusion / volume status
Prerenal azotemia should reverse within 1-2 days after, but recovery depends on renal function decline / pre-existing CKD
Limited nutrition needed
What are some diagnostic signs of postrenal
AKI?
Severe sudden onset of oliguria/anuria
Urine osmolality >400 mOsm/kg early and 300 mOsm/kg later with BUN:Cr ratio of 10:1 to 20:1
5-15% of all cases Most commonly affects elderly and young
What are some treatment goals in postrenal AKI?
1) Correcting obstruction
2) Resuming normal hydration
Minimal nutrition intervention needed
How is intrinsic / parenchymal AKI different from pre- and post-renal AKI?
Intrinsic/parenchymal AKI involves tissue damage to the renal parenchyma; while pre-renal and post-renal AKI are the consequence of extra-renal diseases leading to the decreased GFR
Causes of intrinsic/parenchymal AKI can be classified
based on the four compartments of the kidneys. What are
the 4 classifications?
1) Vascular disease
2) Interstitial nephritis
3) Glomerular disease
4) Acute Tubular Necrosis (ATN)
When would renal replacement therapy (RRT)
be initiated in AKI?
- Worsening azotemia
- High K
- Volume overload
- Severe acidosis that is resistant to conservative therapies
- Significant symptoms of uremia present
No consensus: used in 85% oliguric AKI; 30% of nonoliguric AKI
What are the different types of continuous RRT?
- Continuous hemofiltration → clearance through convection
- arteriovenous (CAVH) or venovenous (CVVH) - Continuous hemodialysis → clearance through diffusion
- arteriovenous (CAVHD), venovenous (CVVHD), or sustained low-efficiency dialysis (SLED) - Continuous hemodiafiltration→ clearance through both convection & diffusion
- arteriovenous (CAVHDF) or venovenous (CVVHDF) - Slow continuous ultrafiltration (SCUF)
What nutrients are lost in each HD treatment?
2-5 g of peptides and 2-8 g of free amino acids
What nutrients are lost in each PD treatment?
Average 10 g/day of protein lost, but can rise to 20 g/day or more depending on peritoneal membrane permeability
What nutrients are lost in each CRRT treatment?
Protein loss of 1.5 - 7.2 g/day,
Amino acid losses of 15-30 g/day, directly proportional to
CRRT effluent flow
Glutamine losses of 2-4 g/day (exogenous replacement likely needed)
How should you interpret BUN and serum
creatinine (SCr) in AKI?
- More related to changes in kidney function & nutrition status; less reflective of nutrition status
- SCr reflects creatinine clearance, affected by muscle mass
- BUN:Creatinine ratio evaluates kidney function vs. volume status
- Ratio greater than 10:1 or 20:1 reflects possible hemoconcentration, may need additional hydration or adjustment in diuretic therapy
What factors contribute to hyperkalemia in AKI?
- UOP <1L/day
- Metabolic acidosis exacerbates hyperkalemia d/t intracellular to
extracellular redistribution - Rhabdomyolysis, tumor lysis syndrome, GI bleeding
- Potassium intake from diet, nutrition support, supplements, IV, drugs, ACE inhibitors, potassium sparing diuretics (spironolactone)
How is hyperkalemia in AKI managed?
- Promote intracellular shift of potassium using:
- Insulin & IV glucose
- Correcting acidosis with bicarbonate - Beta-2 agonists
- IV calcium gluconate
- Potassium binding resins (sodium polystyrene sulfonate)
- Diuretics
- Dialysis
What factors contribute to hypokalemia in AKI?
- Extracellular to intracellular shifts with refeeding syndrome in the malnourished
- May occur in the recovery/diuretic phase of AKI
- Aggressive use of diuretic without sufficient K+ replacement
- Magnesium deficiency may cause hypokalemia that is resistant to K+ supplementation
