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Flashcards in Acut kidney injury Deck (50)
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RFs for acute kidney injury?

- age: older than 75
- DM
- preexisting CKD
- liver failure
- sepsis
- 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:
altered sensorium
pericardial effusion, pericardial friction rub, arrhythmias
Pulmonary edema
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:
catabolic state
GI bleeding


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
- hyperkalemia
- hypocalcemia
- hyperphosphatemia
- anemia
- 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

- causes:
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?

- reversible
- 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:
ureteral stent
urethral stent
nephrostomy tube
prostate resection


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