Flashcards in Acute Kidney Injury Deck (53)
Risk factors for acute kidney injury
1. Age > 75
3. Preexisting chronic kidney disease
5. Liver failure
7. Exposure to IV contrast
8. Cardiac surgery
Acute kidney injury definition
Abrupt (within 48 hours) decline in kidney function as manifested by
1. Increase in serum creatinine
≥ 0.3 mg/dL or ≥ 1.5 times that from baseline
2. OR decrease in urine output of less than 0.5 mL/kg/hr X 6h
3. OR need for dialysis
What is azotemia? 2
What is Oliguria?
What is Anuria?
-Elevated BUN and/or creatinine
-The build up of abnormally large amounts of nitrogenous waste products in the blood
2. Urine output less than 400 mL/day
Urine output less than 20 cc/hr
3. Urine output less than 100 mL/day
Can be asymptomatic but when symptoms are present they are secondary to what?
What are the symtpoms of acute renal injury?
1. Nausea, vomiting
3. Altered sensorium
5. Pericardial effusion, pericardial friction rub, arrhythmias
6. Pulmonary edema
7. Abdominal pain, ileus
8. Bleeding secondary to platelet dysfunction
9. Encephalopathic changes including asterixis, confusion, seizures
Where does BUN come from?
1. When protein is used for energy the carbon is cleaved from the amino acid and leaves behind a Nitrogren.
2. The N takes up 3 H+ to form NH3+ which is ammonia.
3. The ammonia (NH3+) is then processed through the liver to become urea.
4. When the urea enters the blood stream it is called the blood urea nitrogren (BUN).
5. The blood urea nitrogren is then excreted by the kidney
1. Why does BUN increase?
2. What causes elevated BUN levels? 6
1. when protein is broken down and more ammonia forms
When wil BUN decrease?
Liver failure- If the liver is unavailable to convert ammonia to urea then the BUN will decrease and the ammonia increases
Decreased GFR (glomerular filtration rate) leads to increased BUN in 2 ways
1. Decreased flow through the glomerulus
2. Slower transport time allows more BUN to be resorbed at the level of the PCT
What is Creatinine:
1. How is it formed?
2. How does muscle mass affect the creatinine?
3. How does age affect the creatinine?
1. Creatinine is formed from the normal breakdown of muscle
2. The more muscle mass the higher the creatinine
3. The lower the muscle mass the lower the creatinine (therefore normal reduction in creatinine as a person ages and loses muscle mass)
1. Decreased GFR leads to what?
2. How is creatinine handled differently by the kidney?
3. What happens to it in the DCT?
4. What drugs will block this from happening in the DCT? 2
1. Decreased GFR also leads to increased creatinine
2. Instead of the creatinine being reabsorbed in the tubules like BUN…. with a decreased GFR the creatinine is just dumped out
3. In the DCT creatinine is actively secreted from the body to be eliminated by the kidneys
1. cimetidine and
2. trimethoprim therefore increasing the serum creatinine
Causes of Increased BUN?
1. Decreased GFR
2. Less BUN presented at the glomerulus to be removed from the blood
3. Slower transport time through 4. PCT allows more reabsorption
Increased protein breakdown
1. Increased with muscle breakdown
2. Blockage at the sites in the DCT that allow for active secretion
3. Decreased GFR as there is less creatinine presented at the glomerulus to be filtered out
(not reabsorbed in the PCT like BUN)
Normal BUN/creatinine levels?
What kind of state does it occur in?
Normal is 10-20:1
Elevated is > 20:1
Increased ratio in a low flow (low blood pressure) state
Laboratory abnormalities with AKI
1. Increased BUN, Creatinine
2. Decreased GFR
7, Platelet dysfunction
8. Anion gap metabolic acidosis
Classification of acute kidney injury is based on where the problem lies.
1. Prerenal (decreased renal perfusion)
2. Intrinsic (alteration of normal process within the kidney)
3. Post renal (inadequate drainage of urine distal to the kidney)
The problem with prerenal failure is what?
lack of blood flow to the glomerulus
Prerenal failure can occur with the following disease processes?
1. Low cardiac output (CHF)
2. Hypotension (shock, sepsis, CHF)
3. Hypovolemia (bleeding, vomiting, diarrhea, etc)
4. Renal artery stenosis
5. Renal artery atheroembolic disease
6. Decreased glomerular perfusion pressure by dilation of the efferent arteriole (ACEI and ARBs)
7. Decreased glomerular perfusion pressure by dilation of the afferent arteriole by NSAIDs
In an attempt to increase
Volume in a low flow state
Na is reabsorbed. How?
1. Decreased renal perfusion
2. leads to increase in Angio II and Aldosterone
3. HCO3 reabsorbtion, H+ secretion and K+ secretion
1. What does the increased K+ secretion lead to?
2. What does the increased HCO3 reabsorption and H+ secretion lead to?
2. Metabolic alkalosis (maintance)
1. Because of low perfusion pressures in prerenal failure the kidney increases what?
2. What is this an attempt to do?
3. If this is the case, what would the urine sodium and
4. urine osmolality (and SG?) be in prerenal failure?
1. Na+ reabsorption
2. Increase volume
3. Urine sodium is low
Urine water content is low which makes it very concentrated =
4. high osmolality, high specific gravity
Summary of prerenal failure abnormalities
1-2. What is elevated?
3-4. What is low?
5. What may we see in the urine?
6. What is the FENa?
1. BUN/creatinine ratio is elevated (>20:1)
2. elevated SG and osmolality (osmolality > 500; SG > 1.010)
3. Urine sodium is low (
Treatment of prerenal failure
Whats the prognosis?
1. Treat underlying cause
2. Maintain euvolemia
3. Maintain as near a normal electrolyte status
4. Avoid nephrotoxic drugs (NSAIDs, glucophage, diuretics, IV contrast, ACEI, ARB, etc)
5. Short course of dialysis may be needed
The good news…..most recover over time
1. Is it reversible?
2. How common is it?
3. What is the cause? 4
4. What is the most common cause?
2. Least common cause of acute kidney injury (5-10%)
3. Obstruction somewhere in the -kidney,
4. Most common cause is prostatic obstruction
Specific disease processes/meds that cause postrenal failure
1. BPH (benign prostatic hypertrophy)
2. Anticholinergic drugs (cause urinary retention)
3. Cancers (bladder, prostate, cervical)
4. Neurogenic bladder (spinal cord injury)
5. Urethral stones or strictures
Postrenal signs and symptoms
1. History is key
2. May present with oliguria or anuria
3. Low back pain or abdominal pain
4. Flank pain
5. Enlarged prostate or pelvic mass on exam
6. Distended bladder
7. Inability to void
Depending on history, work up may include:
1. Bladder ultrasound
2. Bladder catheterization (diagnostic and therapeutic)
3. CT scan of the abdomen and pelvis (renal stones and hydronephrosis)
4. Ultrasound of the kidney may show hydronephrosis
Abnormalities noted in postrenal failure
1. BUN/Creatinine ratio?
2. Urine sodium?
3. Urine osmolality?
4. Urin sediment? 4
1. BUN/creatinine ratio 10-20:1
2. Urine sodium variable depending on the degree of obstruction
3. Urine osmolality may be high in the beginning and end up less than 400
4. Urine sediment may be
-white cells and
Treatment of postrenal failure
1. Possibly may relieve obstruction temporarily by what?
2. Refer to urology for definitive treatment. What are our options here?
1. placement of a bladder catheter