Flashcards in Renal Failure Deck (66):
In a nutshell definition of AKI
rapid decline in renal function with increase in creatinine (0.5 - 1.0 increase)
acute renal failure vs AKI
Acute renal failure is the early stage of AKI when creatinine may be normal despite reduced GFR due to time it takes for creatinine to accumulate in body
3 types of AKI
prerenal - due to decreased renal blood flow (MCC)
intrinsic - due to damage to renal parenchyma
postrenal - urinary tract obstruction (least common)
What 3 aspects of kidney function does RIFLE criteria look at?
Creatinine increase, GFR decrease, urine output
What does RIFLE stand for?
used to define AKI
1.5x increase creatinine
25% decrease GFR
<0.5 ml/kg/hr UO for 6 hours
2.0x increase in creatinine
50% decrease GFR
<0.5 ml/kg/hr UO for 12 hours
3.0x increase in creatinine
75% decrease GFR
<0.5 ml/kg/hr UO for 24 hours or anuria 12 hours
complete loss of kidney function (requiring HD) for more than 4 weeks
complete loss of kidney function (requiring HD) for more than 3 months
T/F: AKI always results in oliguria or anuria
FALSE. can present with no oliguria (nonoliguric AKI)
Most common findings in AKI patient
Weight gain and edema due to positive water and sodium balance
What is azotemia?
Elevated BUN and Cr; characterizes AKI
What else causes elevated BUN besides AKI?
catabolic drugs like stereoids
GI/soft tissue bleeding
dietary protein intake
What else causes elevated Cr besides kidney problems?
baseline Cr depends on muscle mass
so any muscle breakdown can increase Cr...drugs can also increase Cr
Prognosis for AKI
80% of patients completely recover...but depends on age of patient and severity of renal failure
Most common causes of death in AKI patients
infection followed by cardiorespiratory problems
What mechanisms cause prerenal failure
ANYTHING THAT DECREASES BLOOD FLOW TO KIDNEYS
- decreased CO
- volume loss / sequestration
ie hypovolemia, excessive diuretic use, poor fluid intake, vomiting, diarrhea, burns, diarrhea, CHF, renal arterial obstruction, cirrhosis/hepatorenal syndrome, patient on NSAIDs, ACE inhibitors, cyclosporin
What do NSAIDs do to kidneys? and ACE inhibitors?
NSAIDs - constrict afferent arterioles
Ace inhibitors - dilate efferent arterioles
Pathophysiology of prerenal AKI
DECREASED RENAL BLOOD FLOW leads to LOWER GFR which leads to decreased clearance of metabolites...
however renal parenchyma isn't damaged so tubular function and CONCENTRATING ABILITY IS PRESERVED.
What clinical features are typically seen in patient with prerenal AKI?
SIGNS OF VOLUME LOSS
dry mucous membranes, hypotension, tachycardia, decreased tissue turgor, oliguria/anuria)
What lab findings are seen in AKI
OLIGURIA ALWAYS (to preserve volume)
urine with HIGH OSMOLALITY (since kidney retains water) (>500)
urine with LOW Na, (FENa <1%)
Increased urine-plasma Cr ration (>40:1) (filtrate is reabsorbed, but not creatinine)
bland urine sediment
intrinsic renal failure
glomerular filtration and tubular function are imparied therefore kidneys CANNOT CONCENTRATE URINE
Causes of intrinsic renal failure
- ATN (Most common - due to ischemia, nephrotoxins
- glomerular disease (i.e. acute glomerulonephritis)
- vascular disesase
What kinds of glomerular diseases can cause intrinsic renal failure
What kinds of vascular disease can cause intrinsic renal failure
renal artery occlusion
How does rhabdomyolysis damage kidneys
When skeletal muscle breaksdown (either from trauma, crush injuries, or snake bites), skeletal muscles release myoglobin which are toxic to kidneys. In addition, you get hyperkalemia, hyperuricemia, hypocalcemia, and elevated CPK. Treat with IV fluids, mannitol (to drain that bad shit out), and bicarb (to get K back into cells)
What causes ischemic AKI
ANYTHING THAT LEADS TO SEVERE DECLINE IN RENAL BLOOD FLOW
heart failure, DIC, shock, hemorrhage, sepsis
What can cause nephrotoxic AKI
any substance that damages renal parenchyma
NSAIDS, antibiotics (aminoglycosides, vanc), radiocontrast agents, NSAIDS (esp in CHF), poisons, myoglobin, hemoglobinuria, chemo (cisplatin), kappa gamma light chains seen in multiple myeloma
What recovery usually takes longer, prerenal or intrinsic renal failure?
Lab findings in intrinsic renal failure
DECREASED urine osmolality (kidney cannot concentrate urine)
Increased urine Na (kidney cannot retain Na)
DECREASED urine plasma Cr ratio (kidney cannot reabsorb filtrate)
Decreased BUN/Cr ratio (although both still elevated, kidney cannot reabsorb urea as well as in prerenal)
post renal failure
least common cause of AKI
obstruction in the urinary tract with intact renal blood supply and parenchyma intact.
Leads to increased GFR (both kidneys must be obstructed for Cr to rise)
causes of post renal
urethral obstruction secondary to BPH (most common cause)
obstructing neoplasm (i.e. bladder, cervical cancer)
How to monitor patient with AKI
- daily weight, Is and Os
- Serum electrolytes
- Hgb/Hct to check for anemia
- monitor for infection
What lab values will usually indicate AKI?
elevated BUN and Cr
What two types of AKI can cause ATN?
ischemic AKI and nephrotoxic AKI (anything that destroys tubular cells)
What 3 tests can you do to rule out postrenal failure?
- physical exam (palpate bladder)
- insert catheter (look for large volume of urine)
- bladder and kidney U/S to check for obstruction and hydronephrosis
What to always obtain in patient with AKI?
bladder catheterization to rule out obstruction
What do muddy brown cast, RBC casts, fatty casts, and WBC casts indicate on U/A
muddy brown casts/renal tubular cells - ATN
RBC casts/ RBCs - glomerular disease
WBC casts/WBCs - pyelonephritis, acute interstitial nephritis
fatty casts - nephrotic syndrome
Where would you see increased protein and blood?
Acute glomerfulonephritis and acute interstitial nephritis
What are some complications of AKI?
ECF volume expansion -> pulmonary edema (treat with furosemide)
What electrolyte disturbances can be seen in AKI?
metabolic acidosis (increased anion gap) - correct with sodium bicarb
hyperphosphatemia -> hypocalcemia
What is a common feared complication of AKI?
infection! (ex: pneumonia, UTI, wound infection, and sepsis)
uremia itself is thought to impair immune function; infxn likely multifactorial
General measures for AKI treatment
- avoid nephrotoxic meds (i.e. NSAIDS, aminoglycosides, radiocontrasts)
- adjust medication doses for renal function
- correct fluid imbalances/electrolyte disturbances
- optimize cardiac output
- dialysis if indicated
Indications for dialysis
intractable metabolic acidosis
urgent symptoms of volume overload
Definition of chronic kidney disease (CKD)
decreased kidney function (GFR<60)
kidney damage (structural/functional abnormalities) for at least 3 months regardless of cause
Causes of CKD
-DM (most common)
- HTN (25% of cases)
- chronic GN
- interstitial nephritis, polycystic kidney disease, obstructive uropathy (any AKI left untreated or prolonged)
CV features of CKD
- CHF (due to volume overload, HTN, and anemia)
- pericarditis (from symptomatic uremia)
Mechanism behind HTN in CKD
decreased GFR stimulates RAAAS system -> BP increase
GI features of CKD
Neurologic features of CKD
lethargy, somnolence, confusion, confusion, peripheral neuropathy, uremic seizures, weakness, asterexis, hyperreflexia, "restless legs"
these come from hypocalcemia
Hematologic features of CKD
normocytic normochromic anemia (secondary to EPO deficiency)
bleeding (secondary to platelet dysfunction due to uremia (platelets can't degranulate in uremic environment)
Endocrine/metabolic features of CKD
- hyperphosphatemia -> hypocalcemia
- can also sometimes have secondary hyperparathyroidism causing hypercalcemia and (calciphylaxis from ppt) and renal osteodystrophy
- low testosterone in men and amenorrhea/infertility/hyperprolacinemia in women
What tests to run to dx CKD
- urinalysis (sediment)
- Cr and GFR
- Renal u/s to rule out obstruction
What diet to recommend in patient with CKD
LOW SALT, LOW PROTEIN
restrict potassium, phosphorus, and magnesium
What BP med recommended for CKD patient
ACE inhibitors (dilate efferent arteriole) shown to reduce risk of progression to ESRD (BUT WATCH OUT FOR HYPERKALEMIA)
How to treat hyperphosphatemia
calcium citrate (phosphate binder)
What supplements to give to prevent secondary hyperparathyroidism
calcium and vit D
What intoxications are indications for dialysis?
ethylene glycol, lithium, aspirin (salicyclic acid), magnesium containing laxatives
Options for HD access?
- central catheter in subclavian or jugular vein
- tunneled catheter (lowers rate of infxn, can use for up to 6 months)
- AV fistula (best form; needs surgery, audible bruit)
Pros and cons to HD
Pro: efficient than PD, can be initiated quickly
Con: less similar to true physiology of kidney, can lead to hypotension during rapid removal and fluid shifts, hypo-osmolality
How does peritoneal dialysis work?
peritoneum is the dialysis membrane, HYPEROSMOLAR HIGH GLUCOSE solution is used as dialysate fluid and infused into peritoneal cavity which draws up water from blood via osmosis...fluid has to be drained and replaced several times a day
Advantages of peritoneal dialysis
patient can perform dialysis on their own, mimics true physiology of kidney
What are dialysis still prone to despite having the filtration function of the kidney
since dialysis only can simulate FILTRATION and NOT SYNTHESIS...patients are still prone to vit D and EPO deficiency
Complications of HD
hypotension, hypo-osmolality (n/v, headache, seizures), anticoag complications, infection of access site, HD associated amyloidosis of b2 microglobulin in bones and joints