Flashcards in Acut kidney injury Deck (50)
RFs for acute kidney injury?
- age: older than 75
- preexisting CKD
- liver failure
- exposure to IV contrast
- cardiac surgery
What is the definition of an acute kidney injury?
- abrupt (w/in 48 hrs) decline in kidney fxn as manifested by:
increase in serum creatinine: greater than 0.3 mg/dL or greater or equal to 1.5x that from baseline
or decrease in urine output of less than 0.5 ml/kg/hr x 6 hr
- or need for dialysis
What is azotemia?
- elevated BUN and/or creatinine
- the build up of abnormally large amts of nitrogenous waste products in the blood
What is oliguria?
- urine output of less than 400 ml/day
- urine output less than 20 cc/hr
What is anuria?
- urine output of less than 100 mL/day
How common is acute kidney injury?
- 7% of hospitalized pts
- 66% of ICU pts
- 2-3 cases/1000 persons
Sxs of acute kidney injury?
- cna be asx but when sxs are present they are secondary to uremia/azotemia:
pericardial effusion, pericardial friction rub, arrhythmias
abd pain, ileus
bleeding secondary to platelet dysfxn
encephalopathic changes including asterixis, confusion, seizures
Where does BUN come from?
- when protein is used for energy the carbon is cleaved from AA and leaves behind a N
- N takes up 2 H+ to form NH3+ = ammonia
-NH3+ is then processed through the liver to become urea
- when the urea enters the blood stream it is called BUN, excreted by kidney
In what situations will there be an increase in BUN?
- when protein is broken down and more NH3+ forms:
When will BUN decrease?
- in liver failure
- if liver is unavailable to convert ammonia to urea then the BUN will decrease and ammonia will increase
How does a GFR lead to an increased BUN?
- 2 ways:
1. decreased flow through glomerulus
2. slower transport time allows more BUN to be resorbed at level of PCT
What is creatinine?
- formed by normal breakdown of muscle
- more muscle = higher creatinine
- lower muscle mass the lower the creatinine
Creatinine levels in reduced GFR?
- decreased GFR leads to increased Cr
- instead of Cr being reabsorbed in tubules like BUN, with a decreased GFR the creatinine is just dumped out
- in DCT creatinine is actively secreted from the body to be eliminated by kidneys
- this active secretion at the DCT can be blocked by drugs such as cimetidine and trimethorpim therefore increasing the serum creatinine
When will creatinine levels increase?
- with muscle breakdown
- blockage at sites in DCT that allow for active secretion
- decreased GFR as there is less creatinine presented at glomerulus to be filtered out
Normal BUN/Cr ratio?
- normal: 10-20:1
- elevated is greater than 20:1
- increased ratio in a low flow (low BP) state
What lab abnormalities will you see in AKI?
- increased BUN, creatinine
- decreased GFR
- platelet dysfunction
- anion gap metabolic acidosis
3 types of AKI?
- prerenal: decreased renal perfusion
- intrinsic: alteration of normal process within the kidney
- post renal: inadequate drainage of urine distal to kidney
What could be the cause of prerenal failure?
- problem: lack of blood flow to glomerulus
low cardiac output (CHF)
Hypotension (shock, sepsis, CHF)
hypovolemia (bleeding, vomiting, diarrhea)
renal artery atheroembolic disease
decreased glomerular perfusion pressure by dilation of efferent arteriole (ACEI and ARBs)
decreased glomerular perfusion pressure by dilation of afferent arteriole by NSAIDs
How does vomiting lead to metabolic alkalosis and hypokalemia?
- vomiting: loss of H+, gain of HCO3-
- decreased renal perfusion pressure which leads to increase in angiotensin II - increase in Na+ reabsorption for H+ exchange of excretion
and also increase in aldosterone which increases H+ secretion, and also K+ secretion
What will urine Na+ and urine osmolality be?
- urine Na+ = low
- urine water content is low which makes it very concentrated = high osmolality, high specific gravity
Abnormalities of prerenal failure?
- BUN/Cr ratio is elevated (greater than 20:1)
- urine Na+ is low (less than 20)
- urine water content is low = elevated SG and osmolality (osmolality going to be greater than 500, and SG is greater than 1.010)
- shouldn't be any sediment in the urine but may see benign or hyaline casts
- FENa less than 1%
What is the tx for prerenal failure?
- tx underlying cause (CHF, septic, meds, vomiting)
- maintain euvolemia
- maintain as near a normal electrolyte status
- avoid nephrotoxic drugs (NSAIDs, glucophage - metformin, diuretics, IV contrast, ACEI, ARB, etc)
- short course of dialysis may be needed
- Most recover over time
What is wrong in postrenal failure?
- least common cause of AKI (5-10%)
- obstruction somewhere in the kidney, ureter, bladder or urethra
- most common cause is prostatic obstruction
What are the causes of postrenal failure (AKI)?
- anticholinergic drugs (cause urinary retention)
- cancers: bladder, prostate, cervical
- neurogenic bladder (spinal cord injury)
- urethral stones or strictures
Signs and sxs of postrenal failure?
- hx is key
- may present with oliguria or anuria
- low back pain or abdominal pain
- flank pain
- enlarged prostate or pelvic mass on exam
- distended bladder
- inability to void
What will a workup of postrenal failure include depending on the hx?
- bladder ultrasound (scan)
- bladder cath (dx and therapeutic)
- CT scan of abdomen and pelvis (renal stones and hydronephrosis)
- US of kidney may show hydronephrosis
lab abnorm noted in postrenal failure?
- BUN/Cr ratio: 10-20:1
- urine Na+ variable depending on degree of obstruction
- urine osmolality may be high in beginning and end up less than 400
- urine sediment may be normal, have RBCs, white cells and possible crystals
Tx of postrenal failure?
- possible may relieve obstruction temporarily by placement of bladder catheter
- refer to urology for definitive tx:
What is intrinsic AKI?
- 50% of all cases
- exclude pre and post renal causes (many are reversible)
- prerenal failure that isn't tx can lead to ischemia and development of intrinsic failure
- renal parenchymal disease: sites of injury include glomerulus, interstitium, tubules or vasculature
What is acute glomerulonephritis? Examples?
- immunologic mechanism triggers inflammation that can result in damage to basement membrane, mesangium, or capillary endothelium
- systemic illness: SLE, wegeners, goodpastures
- red cell casts and sig proteinuria
What are the usual causes of acute interstitial nephritis? Presentation? Lab abnormalities?
- most cases related to med use
- also caused by bacterial, viral or fungal infections of the kidney
presentation- 1/3 of time hx of maculopapular rash, fever, and arthralgias
labs- EOSINOPHILS in urine
What is the most common type of acute intrinsic renal injury? 3 main causes?
- 3 main causes:
ischemia, sepsis, and nephrotoxic drugs
When does ATN occur?
- when tubules fail to fxn
- failure to reabsorb BUN so BUN/Cr ratio should be less than 10:1
- failure to reabsorb Na and water = lead to elevated urine Na+ (greater than 20) and low urine SG and osmolality (less than 450)
- cell sloughing causes urine to be positive for sediment = MUDDY BROWN casts (granular), renal tubular epithelial cells and epithelial cell casts
Why would ATN be secondary to ischemia?
- tubular damage from site of low perfusion
- inadequate GFR (prerenal) but also by decreased renal blood flow to renal cellular fxnl units due to:
prolonged surgery (esp cardiac and major vascular)
How can ATN be secondary to toxins?
- may occur 5-10 days after exposure
- aminoglycosides (up to 25% of pts receiving thes drugs):
gentamicin, amikacin (Most nephrotoxic), streptomycin and tobramycin
- amphotericin B
- ethlyene glycol (anti-freeze)
- sulfonamides, cephalosporins
What is contrast nephropathy?
- form of ATN
- occurs 24-48 hrs post contrast exposure
- risk factors for development: DM, CKD, high contrast load, concurrent use of nephrotoxic drugs, age
- mechanism of injury unclear but likely involves:
direct toxicity of reactive O2 species (free radicals)
contrast induced diuresis
increased urinary viscosity
increased O2 consumption
imbalance of vasoconstriction vs vasodilation
How can we prevent contrast nephropathy?
- min amt of contrast used - talk to radiologist
- hydrate pre and post procedure with NS
- mucomyst (N-Acetylcysteine): 600 mg po BIDx 3 days starting day prior to procedure
- stop metformin (glucophage) the day of contrast load and for 48 hr post (can lead to lactic acidosis)
- Ask yourself: Do you really need this test? any alternatives?
Other causes of ATN?
- blood transfusion rxn, hemolytic anemia
- multiple myeloma
- uric acid
- myoglobin: muscle breakdown, when severe called rhabdomyolysis (CK greater than 16000), crush injuries, muscle necrosis from pressure pts in unconscious pts, seizures, cocaine, and ETOH
What is the FENa used for?
- useful for determining if the casue of AKI is prerenal or ATN
- prerenal if FENa is less than 1%
- intrinsic if FENa is greater than 2%
What are dark granular and epithelial casts indicators of?
- pure ATN
What are crystals an indicator of?
- crystalluric ARF
What are WBCs and WBC casts indicators of?
- acute interstitial nephritis
What are RBCs and RBC casts indicators of?
- proliferative/necrotizing glomerulonephritis
Management of AKI?
- tx underlying cause!!!
- maintain euvolemia
- manage electrolytes
- manage BP
- stop potentially nephrotoxic meds!!!!
- may need temporally dialysis
General work up of AKI?
- assess volume status
- UA: dipstick, microscopic exam, urine Na+, urine Cr
- serum BUN and Creatinine (BMP)
- fractional excretion of NA+
What imaging studies do you want to do in intrinsic AKI?
- renal US
- bladder scan for post void residual
- CT or MRI
- renal bx in certain cases
What test is most impt noninvasive test in dx eval of pts with AKI?
Labs of prerenal AKI?
- urine Na is going to be less than 20
- BUN/Cr ratio will be more than 20:1
- FEna is less than 1
Labs of intrinsic AKI?
- Urine Na will be greater than 20
- BUN/Cr ratio less than 10:1, and FEna is greater than 2