Acute Kidney Injury Flashcards
Abdominal compartment syndrome
from increased intra-abdominal pressure
(e.g. from intra-abdominal bleeding, ascites, or severe gut edema etc).
Perfusion to the organs can be critically reduced - leading to pre-
renal AKI. Pressure on the ureters etc can result in post-renal AKI.
AKIN criteria
define and classify the severity of acute kidney injury. Uses urine output and serum
creatinine levels as criteria.
Glomerular filtration rate
Compares the amount of creatinine excreted in the urine with the amount in the blood over 24 hours
Intra-renal AKI cause
Intra-renal AKI refers to AKI that affects the nephron function.
Factors contributing to intra-renal AKI include those that result in ischemia, and those that arise from nephrotoxins.
Myoglobinuria
Presence of myoglobulin in the urine; occurs when myoglobulin is released into the blood subsequent to muscle breakdown e.g. during crush injury, extensive trauma etc.
It contributes to intra-renal AKI because it is nephrotoxic
Nephrotoxic
cause damage to the tubular cells in the nephron. They include drugs (aminoglycoside antibiotics), furosemide, contrast
Post-renal AKI cause
occurs from causes ‘beyond’ the kidney
Pre-renal AKI cause
Pre-renal AKI is renal dysfunction that arises from inadequate blood flow to the kidney
Primary Function of the Kidney:7
o Maintain fluid and electrolyte balance
o Remove metabolic waste products
o Maintain acid-base balance
o Maintain endocrine functions
oHelp regulate blood pressure
o Release of erythropoietin for RBC production
o Produces active form of Vitamin D
Juxtaglomerular Cells (Granular Cells)
Located in the smooth muscle cells of the afferent arteriole
They store, produce and secrete renin.
Play critical role in RAAS
Autoregulation of renal blood flow.
RAAS system is a….
RAAS is one of the body’s compensatory mechanisms.
Renal Assessment
Patient history Monitoring volume status -Intake and output , 24 hour balance -Hourly urine output -Daily weights -Color and consistency of urine
Monitoring hemodynamic parameters
- Hourly blood pressure and heart rate
- Frequent CVP (if available)
Monitoring oxygen supply/respiratory parameters (hourly)
Reviewing urine and serum lab values
Urine Volume
- One of the first indicators of decreased renal perfusion
- Subject to other conditions, so trends and full assessment required
- Monitor on hourly basis
Urinalysis
Aids in locating site of damage
Guides management of renal dysfunction
Urine Sodium
Reflects renal perfusion
Decreased perfusion, RAAS, sodium retained, therefore urinary sodium concentration falls.
Urine Osmolality
Measure of the concentration of solutes in the urine (the ratio of urine density compared with water density). Provides information on the kidney’s ability to concentrate urine. It’s included as part of urinalysis
Creatinine
By product of muscle breakdown and cell metabolism
Produced and cleared at a constant rate
Filtered out by glomerulus- NOT reabsorbed
In patients with low perfusion states, a small rise in creatinine might occur as a result of decreased filtering at the glomerular level
May be falsely elevated in hypercatabolism seen in CC patients not properly fed.
Urea
By product of protein metabolism
Not a reliable indicator of renal function on its own (affected by protein intake, digestion of blood from UGIB).
BUN:Cr Ratio
Can help identify etiology of AKI
Urea-filtered out of the blood at glomerulus, significant percentage of it is reabsorbed as the filtrate passes through the renal tubules
Creatinine-filtered out of the blood at the glomerulus but is NOT reabsorbed in the renal tubules (so it’s peed out!)
In low perfusion states: Filtrate flow rate through tubules slows
Tubules still working normally therefore MORE BUN is reabsorbed = increased serum BUN levels
Creatinine not affected by slower flow rate as not reabsorbed = no/minimal increase in creatinine
Creatinine Clearance Test
•Compares the amount of creatinine excreted in the urine in 24 hours against the amount that has been reabsorbed into the blood
.The number that we get then provides us with an accurate GLOMERULAR FILTRATION RATE!
decreased creatinine clearance indicates decreased renal function!
Glomerular Filtration Rate (GFR)
Calculates how much blood passes through the glomerulus per minute
Sodium and water
Responds to Aldosterone
Water
Responds to ADH (vassopressin)
Bicarbonate
Buffer
LOW IN AKI: Renal injury leads to poor reabsorption of HCO3
Contributes to metabolic acidosis
Anion gap
An anion gap refers to the difference between the cations and the anions and is calculated using Na (the most abundant cation in the serum) and Cl & HCO3 (the most abundant anions in serum). The calculation looks like this:
“gap” reflecting all the
unmeasurable ions present in the extracellular fluid (sulfates, ketones & lactate)
Increased anion gap: either an over production of acids or decreased excretion of acids
•In Renal Failure, an increased anion gap reflects
the metabolic acidosis that arises when renal
tubule damage results in retention of acids and
poor reabsorption of bicarbonate
3 Types of AKI
PRERENAL
INTRARENAL
POSTRENAL
Pre renal AKI
Before the kidney, due to hypoperfusion
nephron is intact
Pre Renal Injury = Decreased GFR
•May lead to intra-renal AKI
Intra renal AKI
Damage to renal parenchyma (nephron)
•Ischemic and nephrotoxic causes
Post renal AKI
Any obstruction in the outflow of urine
Results from an obstruction which hinders the flow of urine from beyond the kidney through the remainder of the urinary tract
•May lead to intra-renal AKI
Pre renal AKI LABS
Rise in BUN
CR relatively stable
urine output decreased and increased urine concentration
Pre ranal AKI causes
Poor perfusion to kidneys hypotension/hypovolemia Cardiac dysfunction leading to poor renal perfusion sepsis hemorrhage, post cardiac arrest
•Source of problem is not the kidneys but what happens before the kidneys (tubular function of the nephron is intact)
Drugs that alter renal perfusion
NSAIDS
ACE inhibitors
Subtypes of Intrarenal AKI
Ischemic and Nephrotoxic
Ischemic Intrarenal Injury
- Decreased renal perfusion = decreased oxygen supply to the tubules
- Tubular cells are highly metabolic
- When tubular epithelial cells become hypoxic, ATP production by renal cell mitochondria is impaired and the energy needed for active transport of solutes is not available
- Ischemia compromises normal tubular function –swell and become necrotic
- Necrotic cells slough off and obstruct the tubule lumen and cause “back leak” of tubular fluid which decreases GFR
Nephrotoxic Intrarenal Injury
Is associated with a concentration of a toxin in the tubules which causes cellular necrosis
. Contrast dye, aminoglycosides, amphotericin B, myoglobin
•Cellular dysfunction and death results in loss of normal functions of the nephron (filtration, secretion and reabsorption)
•Cells slough off and cause obstruction of the tubular lumens and decrease GFR
Nephrotoxic Drugs
PCN Cyclosporins Furosemide Corticosteroids Contast dye
Rhabdomylosis
Complication of skeletal muscle injury
- Damaged muscle releases myoglobin into the blood where it gets filtered by the glomerulus and travels to the PCT.
- Blocks PCT and overwhelms tubules ability to reabsorb metabolites resulting in toxic injury.
- Myoglobinuriaresults: Dark, tea coloured urine. Decreased u/o.
Prevention of AKI
•Recognition is key
•Monitor for signs of developing AKI
•Using effective preventative strategiessuch as:
-Early and aggressive IV fluid replacement (.9%NS)
-Maintain adequate MAP
-Limiting exposure to nephrotoxins
-Careful with BiPaP/CPAP-Monitoring for intra abdominal compartment syndrome
Management of AKI
Primary management is alleviating the precipitating causes •Management of issues which arise as a result of AKI ○Fluid balance ○Electrolyte abnormalities ○Acid-base imbalance ○Relevant supportive care •Renal Replacement Therapies ○Hemodialysis ○Peritoneal dialysis ○Continuous dialysis (CRRT)
Difference Between: Ischemic Intra Renal Injury and Nephrotoxic Intra-Renal Injury
In nephrotoxin Injury
•Basement membrane intact
•Necrotic areas usually more localised
•Healing process more rapid
Decreased GFR results in 7
Filtrate travels more slowly through the tubule This causes •Increased urea reabsorption •Increased sodium reabsorption •Increased water reabsorption •Decreased urine volume •Increased concentration of urine •Low urine sodium levels •Small increase in creatinine
Intra renal AKI Causes
- Rhabdo
- nephrotoxic drugs,
- persistent pre-renal AKI
- A condition which produces damage to the site of the nephron itself and may involve the glomeruli and renal tubules.
Post renal AKI causes
trauma to ureters Enlarged prostate kidney stones, abdominal compartment syndrome, tumours, strictures
Abdominal compartment syndrome creates excessive pressure on the ureters blocking out flow of urine
increased anion gap
An increased anion gap
reflects either overproduction of acids or decreased excretion of acids. In renal dysfunction
it reflects a metabolic acidosis that arises when tubules dysfunction results in retention of
acids and poor reabsorption of bicarbonate
Where does the concentration and dilution of the urine occur
In the juxtamedullary nephrons
The function of aldosterone is primarily
Control of sodium and water
After angiotensin I is converted to angiotensin II, the adrenal glands are stimulated to secrete:
Aldosterone
Increased secretion of ADH results in
increased resorption of water in collecting duct
Angiotensin 2 actions
- potent vasoconstrictor (arterioles so increases afterload)
- stimulates the release of aldosterone
- Triggers production of Vassopressin (ADH)
- enhances SNS activity
aldosterone action
reabsorption of sodium and water
increasing circulating volume and preload
Vassopressin
also known as ADH- antidiuretic hormone
increases reabsorption of water in kidneys
increasing circulating volume and preload
