Acute Kidney Injury Flashcards
functions of kidney
- maintain fluid and electrolyte balance
- remove metabolic waste products
- maintain acid-base balance
- maintain endocrine function (BP, helps w/ RBC prod., activates vitamin D)
location of kidneys on body
bilaterally below diaphragm
cortex
outer area, highly vascular, houses nephrons, blood vessels, secretes EPO, produces urine
flow pattern
cortex -> pyramid -> renal papilla -> minor calyx -> major calyx -> renal pelvis -> hilium -> ureter -> bladder -> urethra
what is important to note about urea?
urea can diffuse back into blood or be actively transported into filtrate
what is important to note about creatinine?
filtered by glomerulus, should never be reabsorbed
what does ADH work on?
collecting duct and distal convoluted tubule
aldosterone affects the reabsorption of ____ at the ____
sodium, distal convoluted tubule
glomerulus function
filters fluids and solutes from blood
proximal tubule
- resorbs Na, K, Cl, HCO3, urea, glucose, and amino acids
- filtrate leaves isosmotic
loop of henle function
- resorbs Na, K, Cl
- blocks resorption of H2O from ascending limb
- countercurrent mechanism dilutes or concentrates urine
- filtrate leaves hypoosmotic
distal tubule function
- Na, K, Ca, Phosph selectively resorbed
- H2O resorbed in the presence of ADH
- Na resorbed in the presence of aldosterone
- filtrate leaves hypoosmotic
collecting duct function
- resorption similar to that in distal tubule
- H2O resorbed in presence of ADH
- HCO3 and H resorbed or secreted to acidify urine
- filtrate leaves hyperosmotic or hypoosmotic depending on body needs
urine is produce through
filtration, secretion, reabsorption
passive transport
gradient high to low (diffusion), no ATP
active transport
- uses ATP, against concentration gradient
- rate of movement depends on availability and saturation of carriers and ATP availability
renal BP regulation
maintains renal blood flow, GFR and BP
intrinsic renal BP regulation
– internal kidney compensation mechanisms
1) Arteriole Myogenic mechanism
2) Tubuloglomerular feedback mechanism:
- Juxtaglomerular Apparatus = Juxtaglomerular cells, Macula Densa cells and Extraglomerular Mesangial cells
- Adjust blood flow into glomerulus and stimulates RAAS/SNS
- Responsible for hormonal regulation of body’s BP, kidney’s blood flow and GFR
extrinsic BP regulation
- global compensation mechanisms (affect GFR but primary role is to increase BP)
- SNS
- RAAS
flow of blood
afferent to efferent
juxtaglomerular cells location and function
location: smooth muscle cells of the afferent arteriole
function: act as baroreceptors that detect changes of pressure in the afferent arteriole.
- they produce, store, and secrete renin, which is released in low BP states
- play critical role in RAAS
- autoregulation of renal blood flow
- Low BP → JG cells sense this → stimulate renin release → RAAS
macula densa
location: in the wall of the distal tubule where it comes into contact with the glomerulus
function: Detect changes in NaCl levels in DCT
Low BP → low GFR → increased NaCl
reabsorption time in PCT → less NaCl gets to DCT → Macula densa senses low NaCl and releases Prostaglandins → PG stimulates JG cells to release renin ( for RAAS), and stimulates afferent arteriole to vasodilate → increases GFR
High BP → high GFR → increased NaCl in tubules b/c too fast to absorb it in PCT –> increase in NaCl at DCT → macula densa senses high NaCl → stimulates afferent arteriole to vasoconstrict → decrease GFR
AKI
- refers to anything from mild impairment to acute renal failure
- characterized by a sharp increase in Cr and a decline in urine output
- more than 50% of critical care patients will develop an AKI
- AKI increases mortality by 10-50%
pre-renal AKI
- arises from inadequate blood flow to the kidney
- due to prolonged hypoTN (sepsis, vasodilation), prolonged low CO (heart failure, cardiogenic shock), prolonged volume depletion (dehydration, hemorrhage), renal vasculature thrombo-emboli
- reversible if treated early
pre-renal AKI patho
decreased filtrate volume means filtrate travels slower through tubule= more time for reabsorption
- Increased urea/Na/H20 reabsorption
- Increased urine concentration/osmolarity, decreased urine Na, decrease u/o, increased serum BUN
pre-renal AKI lab changes
BUN increased = increased reabsorption time
Cr slightly increased = d/t decrease in GFR
pre-renal AKI body’s response to decreased kidney perfusion
activate renal autoregulation systems
intrinsic: myogenic and tubuloglomerular apparatus
extrinsic: SNS, RAAS
drugs that can contribute to pre-renal AKI
- ACE inhibitors
- NSAIDs
- diuretics
intrarenal AKI
- any condition that produces damage to the site of the nephron itself and may involve the glomeruli and renal tubules
- often a continuation of pre-renal if low perfusion is not corrected
ischemic intra-renal failure
- decreased renal perfusion→ decreased O2 → decreased ATP production → cells become anaerobic/no active transport → cell swelling→ cell death
- dead tubular epithelial cells slough off, clump together and obstruct tubule lumen ( “casts”)
- cells sloughing leaves gaps in tubule epithelium/low ATP disrupts tight junctions in basement membrane = creates “holes”, allowing filtrate to back leak out
- back leak increases pressure back towards the glomerulus = decreases GFR
- Macula densa sense high Na d/t to decreased re-absorption–> stimulates JG to vasoconstrict afferent arteriole –> further decrease in GFR (BAD!)
end result of ischemic intra-renal failure
tubular function impairment & disruption of normal reabsorption/secretion, decreased GFR
ischemic intrarenal failure lab work
- urine casts
- Cr/BUN up proportionately
- urine sodium up
- urine osmolality down/urine [ ] down
- u/o varies
BUN/ CR= Cr/Bun both up proportionately because less blood is getting to kidneys to be filtered (so build up in blood), and tubules have decreased function. BUN is not getting filtered back into blood like it would in a working kidney, so BUN and CR getting excreted the same
causes of intrarenal failure
- nephrotoxic drugs (contrast, certain abx, furosemide, corticosteroids, some anesthetic agents)
- endogenous endotoxins (myoglobinuria)
- infectious/inflammatory cause (acute glomerulonephritis d/t diabetes, HTN, lupus, viral or bacterial reasons; interstitial nephritis from allergies, autoimmune, side effect of abx, diuretics)
nephrotoxic intrarenal failure
- Basement membrane intact
- Necrotic areas usually more localized
- Healing process more rapid
- Risk of this type of injury increased with: advanced age, volume depletion, hepatic dysfunction, concurrent use of multiple nephrotoxic drugs
ischemic intrarenal failure
- Damage to the entire nephron, decreased oxygen affects all cells in nephron
- low perfusion = ischemic renal failure
*<25 min = mild and reversible
*>60-90 mins = permanent damage
post renal failure
- not very common
- d/t obstruction (tumor, prostate, blocked catheter, kidney stones, abdominal compartment syndrome)
intra-abdominal compartment syndrome
- increased pressure in abdominal cavity that causes decreased perfusion to organs and/ or the outflow of urine from the kidneys
- Common causes: retroperitoneal hemorrhage, inflmtn (ischemic gut), ascites, bowel obstruction
- Tx: Alleviate the pressure!
components of renal assessment
- pt history
- physical assessment
- volume status
- hemodynamic parameters
- resp assessment
- lab work (urine, blood)
T or F: No single lab value measure’s renal
function, but there are many that give an indication of renal function and dysfunction
true
urine tests
1) Urine Volume/Output
2) Urinalysis
3) Urine Sodium
4) Urine osmolality
urine volume/output
one of the first indicators of decreased renal perfusion; subject to other conditions so check trends and ax; monitor on hourly basis; normal >0.5ml/kg/hr
urinalysis
aids in locating site of damage; ax chemical/physical and microscopic elements; guides management of renal dysfx
urine sodium
reflects renal perfusion, decreased renal perfusion activates RAAS which causes aldosterone release and sodium retention = urinary sodium [ ] decreases; low sodium urine can be indicative of hypovolemia
urine osmolality
measure of concentration of dissolved particles in urine. Provides info on the kidney’s ability to concentrate or dilute urine. It’s included as part of urinalysis
BUN
- 2-8mmol
- produced, filtered, reabsorbed
- Not a reliable indicator of renal function on its own (affected by protein intake, liver disease, tissue breakdown, digestion of blood from UGIB, kidney functions)
creatinine
- 40-120umol
- produced, excreted
- not reabsorbed
- May be falsely elevated in hypercatabolism seen in CC pts not properly fed
- In patients with low perfusion states, a small rise in creatinine might occur as a result of decreased filtering at the glomerular level
BUN: Cr Ratio
- helps identify etiology of AKI
- when ratio is increased >20:1 = BUN is increasing more than Cr, suspect renal hypoperfusion (prerenal)
- when ratio is decreased <10:1, BUN and Cr increasing proportionally together, suspect intrarenal injury
creatinine clearance test
- 24hr collection test
- most accurate renal function test
- compares amount of creatinine excreted in the urine in 24 hrs against the amount that has been reabsorbed into the blood
- gives us GFR
- decreased = decreased renal function
estimated GFR
- estimates how much blood passes through the glomerulus per minute
- calculated considering age, weight, sex and serum creatinine
- Lower the eGFR= potential sign of kidney issue
- EGFR decreases with age, but may not be indicative of kidney damage
preventing AKI
- monitor for signs of it developing
- early and aggressive IV fluid replacement
- maintain adequate MAP
- limiting exposure to nephrotoxins
- monitoring for intra-abdominal compartment syndrome
- diuretics for fluid overload (lasix challenge)
managing AKI
- alleviate precipitating cause
- management of issues which arise as a result of AKI
- RRT (hemodialysis, peritoneal dialysis, CRRT)
- nutrition - limit protein to prevent increased BUN; fluid, Na, K and Phosph restrictions
does dopamine have a role in prevention of AKI when using low doses?
no
who is at risk for AKI?
- sepsis pts
- pts receiving nephrotoxic drugs (-mycin/sporin, penicillin, corticosteroids, lasix, contrast, anesthetic)
- pts getting NSAIDS or ACE-i
- pts who develop rhabdo (myoglobinuria)
- intraabdominal compression
