SU2M - Renal Failure Flashcards
RIFLE Criteria for AKI
- RISK: 1.5 fold increase in serum creatinine or GFR decreased by 25% or urine output <0.5 mL/kg/hr for 6 hrs
- INJURY: Twofold increase in the serum creatinine or GFR decrease by 50% or urine output <0.5 mL/kg/hr for 12 hrs
- FAILURE: Three fold increase in serum creatinine or GFR decreased by 75% or urine output <0.5 mL/kg/hr for 24 hours, or anuria for 12 hrs
- LOSS: Complete loss of kidney function (requiring dialysis) for more than 4 wks
- ESRD: Complete loss of kidney function for more than 3 mnths
Acute Renal Failure: definition?
- AKA Acute Kindey Injury (AKI)
- rapid decline in renal function
- with an increase in serum creatinine
- at first the creatinine can be normal, despite the low GFR, bc it takes time for the creatinine to accumulate in the body
Most common clinical findings in AKI?
- Weight gain
- Edema
* *due to water and sodium retention
Azotemia: definition?
-elevated BUN and Creatinine
What are 3 non-kidney causes of an elevated BUN?
- Catabolic drugs (ex. Steroids)
- GI/soft tissue bleeding
- Dietary protein intake
2 non-kidney causes of elevated creatinine?
- Increased muscle breakdown –> baseline creatinine varies proportionately with muscle mass
- Some drugs
3 Categories of AKI?
- Prerenal
- Intrinsic renal failure
- Postrenal failure
2 Ssx of prerenal failure?
- Signs of volume depletion
2. Signs of CHF
Signs of acute interstitial nephritis?
- aka intrinsic renal failure
- signs of an allergic rxn, ex. Rash
3 ssx that suggest post renal failure etiology?
- Suprapubic mass
- BPH
- Bladder dysfunction
Pathophysiology of prerenal AKI?
- renal blood flow decreases enough (by whatever cause, CHF, hypovolemia, etc.) to lower GFR –> decreased clearance of metabolites (ex. BUN, creatinine)
- kidney conserves as much sodium and water as possible –> renal parenchyma is undamaged, tubular function & concentrating ability is preserved!
- *reversible if blood flow is restored before extensive damage from ischemia occurs
8 Things to monitor in AKI?
- Daily weights
- Intake
- Output
- BP
- Serum electrolytes
- Hb –> watch for anemia
- Hct –> watch for anemia
- Watch for infection
Urine osmolarity: prerenal failure v. ATN?
- prerenal: > 500 –> kidney is still able to resorb water!
- ATN: 250-300mOsm –>water reabsorption is impaired
Urine Na+: prerenal failure v. ATN?
- prerenal failure = < 20 –> because kidney can still resorb Na!
- ATN = > 40 –> Na is poorly absorbed
Fractional excretion of Na: prerenal failure v. ATN?
- prerenal = <1%
- ATN = > 2-3%
Urine sediment: prerenal failure v. ATN?
- prerenal = scant
- ATN = full brownish pigment, granular casts w/ epithelial casts
BUN/Cr ratio: prerenal v. ATN?
- prerenal = > 20:1 –> kidney can still resorb urea!
- ATN = < 20:1 –> less urea can be absorbed
Intrinsic renal failure: definition?
- kidney tissue is damaged
- glomerular filtration and tubular function are significantly impaired
- kidneys are unable to concentrate urine effectively
4 causes of intrinsic renal failure?
- Tubular disease = ATN, can be caused by ischemia or nephrotoxins
- Glomerular disease = acute glomerular nephritis, ex. Goodpastures, Wegener’s, poststreptococcal GN, lupus
- Vascular disease –> ex. Renal artery stenosis, etc
- Interstitial disease –> ex. Allergic interstitial nephritis (often due to hypersensitivity rxn to a medication)
Rhabdomyolysis: 5 causes
- skeletal muscle breakdown, caused by:
1. Trauma
2. Crush injuries
3. Prolonged immobility
4. Seizures
5. Snake bites
Rhabdomyolysis: pathophysiology?
- release of muscle fiber contents (myoglobin) into the blood stream
- myoglobin is toxic to the kidneys
- can lead to AKI
Rhabdomyolysis: lab findings?
- markedly elevated creatinine phosphokinase (CPK)
- hyperkalemia
- hypocalcemia
- hyperuricemia
Rhabdomyolysis: tx?
- IV fluids
- Mannitol = osmotic diuretic
- Bicarbonate = drives K back into the cells
Ischemic AKI
- cause of ATN
- secondary to severe decline in renal blood flow –> shock, hemorrhage, sepsis, DIC, heart failure
- ischemia ==> death of tubular cells
Nephrotoxic AKI
- cause of ATN
- kidney injury secondary to substances that directly injure renal parenchyma ==> death of cells
- causes: antibiotics, radiocontrast, NSAIDs (esp w/ CHF), poisons, myoglobinuria (ex from rhabdo), hemoglobinuria, chemotx, and kappa and gamma light chains produced in multiple myeloma
Post renal failure: definition
- obstruction of any segment of the urinary tract (with intact kidneys) –> increased tubular pressure bc the urine produced cant be excreted –> decreased GFR
- blood supply and renal parencyma are intact
- *both kidneys must be obstructed for creatinine to rise
- renal fctn can be restored if obstruction is relieved before the kidneys are damaged
- can lead to ATN if untreated
6 common causes of postrenal failure?
- Obstruction due to enlarged prostate –> most common cause
- Obstruction of one kidney
- Nephrolithiasis
- Obstructing neoplasm
- Retroperitoneal fibrosis
- Urethral obstruction –> uncommon, bc must be bilateral to cause renal failure
3 basic tests for postrenal failure?
- Palpate the bladder
- Ultrasound –> look for obstruction or hydronephrosis
- Catheter –> look for large volume of urine
3 phases of ATN?
- Oliguric phase:
- azotemia and uremia
- usually lasts 10-14 days
- urine output <400-500 mL/day - Diuretic phase:
- begins when urine outflow is >500 mL/day
- high urine output due to: fluid overload (excess retained during oliguric phase) osmotic diuresis (due to retained solutes during oliguric phase), tubular cell damage (delayed recovery of epithelial cell function relative to GFR) - Recovery phase:
- recovery of tubular function
What are hyaline casts seen in?
-prerenal failure
RBC casts seen in?
-glomerular disease
WBC casts indicate?
-indicate renal parenchymal inflammation
What do fatty casts indicate?
-nephrotic syndrome
In early phase of AKI, what are the 2 most deadly complications?
- Hyperkalemic cardiac arrest
2. Pulmonary edema
4 possible complications of Acute Kidney Injuries?
- ECF volume expansion –> pulmonary edema
- Metabolic disturbances –> hyperkalemia (decreased excretion, and K is moving from ICF –> ECF) metabolic acidosis (decreased excretion of H+), hypoCa, hypoNa, hyperphos, hyperuricemia
- Uremia –> toxic end products from metabolism accumulate
- Infection –> occurs in 50-60% of cases (possibly bc uremia impairs immune fctn)
3 tx for prerenal failure?
- Tx underlying disorder
- Give normal saline to maintain euvolemia and restore BP –> do not give with edema or ascites though!
- Eliminate any offending agents (ex. ACEi or NSAIDs)
3 Tx for intrinsic renal failure?
- Supportive
- Eliminate causal/offending agent
- If oliguric –> furosemide to increase urine flow
Postrenal tx?
- Bladder catheter
Chronic kidney disease: definition?
-decreased kidney function (GFR <60mL/min) or kidney damage (structural or functional) for at least 3 months, regardless of cause
5 Causes of Chronic kidney disease?
- Diabetes –> MOST common! (30%)
- HTN –> second most common! (25%)
- Chronic glomerular nephritis (15%)
- Interstitial nephritis, polycystic kidney disease, obstructive uropathy
- Any cause of AKI can lead to CKD
At what BUN does uremia typically occur?
- > 60
Chronic renal insufficiency?
- when a pts renal function os irreversibly compromised, but NOT failed
- chronic elevation of serum creatinine to 1.5-3.0mg/dL
What is the major cause of mortality in pts with CKD?
- infection
- have increased susceptibility –> uremia inhibits cellular and humoral immunity
Why can CKD lead to fragile bones and fractures?
- kidney cant clear phosphate as well –> hyperphosphetemia –> decreased production of 1,25-dihydroxy vitamin D –> hypocalcemia –> hyperparathyroidism –> removes Ca from bones –> bones become weak
- this is called renal osteodystrophy!
Calciphylaxis and CKD
- CKD causes hyperphosphetemia bc the kidney can get rid of phosphate as well
- hyperphosphetemia can cause phosphate and calcium to precipitate –> vascular calcifications –>necrotic skin leasions
In CKD what are the 2 most common complications that require urgent intervention?
- Symptomatic volume overload
2. Severe hyperkalemia
3 life-threatening complications in CKD?
- Hyperkalemia –> get EKG (but can have hyperK without EKG changes)
- Pulmonary edema –> secondary to volume overload, monitor weight
- Infection –> ex pneumonia, UTI, sepsis
What are the preferred meds in CKD? What should you be cautious about when using them?
- ACEi
- can cause hyperK
What can be used to correct hyperphosphetemia? MOA?
- calcium citrate
- MOA: binds phosphate
Dialysate
- artificial solution that resembles human plasma used in all forms of dialysis
- diffusion of fluid and solutes occurs through a semipermieable membrane between the blood and the solution
3 Situation in which dialysis can be used?
- CKD –> to bridge until renal transplant, or as a permanent tx when transplant is not an option
- AKI –> until the kidneys heal & renal fctn improves
- Overdose if medications or the ingestion of some substances cleared by the kidneys –> some, but not all can be dialyzed
5 Absolute indications for dialysis?
- Acidosis –> significant metabolic acidosis
- Electrolytes –> severe, persistent hyperkalemia
- Intoxication –> of methanol, ethylene glycol, lithium, aspirin
- Overload –> hypervolemia that is not managed by other means
- Uremia –> severe, based on CLINICAL presentation, not by labs (**uremic pericarditis is an absolute indication for dialysis!!)
* *Think “A-E-I-O-U”
4 Dialyzable substance?
- Salicyclic acid
- Lithium
- Ethylene glycol
- Magnesium-containing laxatives
What is the usual frequency of hemodyalisis?
-3-5 hrs of dialysis for 3 days a week
Which arteries are used to make an AV fistula for dialysis? What clinical sign indicates that it is patent?
- radial or brachial arteries are connected to veins in the forearm
- an audible bruit indicates that the fistula is patent
What are 2 advantages to hemodialysis?
- More efficient than peritoneal dialysis –> high flow rates and efficient dialyzers = shorter time required for dialysis
- Can be initiated more quickly in the emergency setting
2 Disadvantages to hemodialysis?
- Less similar to the physiology of the natural kidney than peritoneal dialysis, so the pt is predisposed to:
a) hypotension - bc of rapid removal of intravascular volume –> rapid fluid shifts from extravascular space into cells
b) hypo-osmolality - due to solute removal - Requires vascular access
Frequency of peritoneal dialysis?
- dialysis fluid is drained and replaced every hour in acute peritoneal dialysis
- but only needs to be drained and replaced every hour in CAPD ( = continuous ambulatory peritoneal dialysis)
2 Advantages of peritoneal dialysis?
- Patient can learn to perform dialysis on their own
2. Mimics the physiology of the normal kidney more closely than hemodialysis
4 Disadvantages to peritoneal dialysis?
- High glucose load in the solution can lead to hyperglycemia and hypertriglyceridemia
- Peritonitis is a significant potential complication
- Patient must be highly motivated to self-administer
- Cosmetic = the dialysate fluid will increase their abdominal girth
Limitations to both forms of dialysis?
-dialysis cannot replace the kidneys synthetic functions –> pts are often epo and vit D deficiency
6 Complications of hemodialysis?
- Hypotension - can cause myocardial ischemia, fatigue, etc
- Hypo-osmolality - relative to the brain, can cause nausea, vomiting, headache, seizures, or coma
- “First-use syndrome” = chest pain, back pain, & anaphylaxis (rare) - can occur immediately after the use of a new machine
- Anticoagulation complications - bleeding
- Infection of vascular site - can lead to sepsis
- Amyloidosis of beta2 microglobulin in bones and joints
4 Complications associated with peritoneal dialysis?
- Peritonitis - ssx: fever and abdominal pain
- Abdominal/inguinal hernia - risk is increased bc of increased abdominal P
- Hyperglycemia - esp in diabetics
- Protein malnutrition
