STEPUP Renal and Genitourinary System: Renal Failure Flashcards
What is the definition of acute kidney injury? Can creatinine be normal in acute kidney injury?
1) A rapid decline in renal function, with an increase in serum creatinine level (a relative increase of 50% or an absolute increase of 0.5 to 1.0 mg/dL)
2) The creatinine may be normal despite markedly reduced glomerular filtration rate (GFR) in the early stages of acute kidney injury (AKI) due to the time it takes for creatinine to accumulate in the body
What are the RIFLE criteria of AKI?
1) RISK: 1.5-fold increase in the serum creatinine or GFR decrease by 25% or urine output <0.5mL/kg/hr for 6 hours
2) INJURY: Twofold increase in the serum creatinine or GFR decrease by 50% or urine output <0.5mL/kg/hr for 12 hours
3) FAILURE: Threefold increase in the serum creatinine or GFR decrease by 75% or urine output of <0.5 mL/kg/hr for 24 hours, or anuria for 12 hours
4) LOSS: Complete loss of kidney function (i.e., requiring dialysis) for more than 4 weeks
5) ESRD: Complete loss of kidney function (i.e., requiring dialysis for more than 3 months
What are different levels of urine output in AKI? Can you have severe AKI without reduction in urine output?
1) Nonoliguric, oliguric, or anuric
2) Yes, severe AKI may occur without a reduction in urine output (nonoliguric AKI)
What are the most common findings in patients with AKI? What are these findings due to?
1) Weight gain and edema
2) This is due to a positive water and sodium (Na+) balance
What is AKI characterized by? What is an elevated BUN also seen with aside from AKI? What is an elevated Cr also seen with aside from AKI?
1) Azotemia (elevated BUN and Cr)
2) Elevated BUN is also seen with catabolic drugs (e.g., steroids), GI/soft tissue bleeding, and dietary protein intake
3) Elevated Cr is also seen with increased muscle breakdown and various drugs. The baseline Cr level varies proportionately with muscle mass
What is the prognosis of AKI in most patients? What does the prognosis depend on? How does the prognosis change in an older patient with a more severe insult?
1) More than 80% of patients in whom AKI develops recover completely
2) Prognosis varies widely depending on the severity of renal failure and other comorbidities
3) The older the patient and the more severe the insult, the lower is the likelihood of complete recovery
What is the most common cause of death in AKI patients?
Infection (75% of all deaths) followed by cardiorespiratory complications
What are the three categories/types of AKI?
1) Prerenal AKI - decrease in renal blood flow (60% to 70% of cases)
2) Intrinsic AKI - damage to renal parenchyma (25% to 40% of cases)
3) Postrenal AKI - urinary tract obstruction (5% to 10% of cases)
What type of AKI is the most common? Is it reversible?
1) Prerenal AKI
2) Potentially reversible
What is the cause of prerenal AKI?
1) Decrease in systemic arterial blood volume or renal perfusion
2) Can complicate any disease that causes hypovolemia, low cardiac output, or systemic vasodilation
What are the etiologies of prerenal AKI?
1) Hypovolemia - dehydration, excessive diuretic use, poor fluid intake, vomiting, diarrhea, burns, hemorrhage
2) CHF
3) Hypotension (systolic BP below 90 mm Hg), from sepsis, excessive antihypertensive medications, bleeding, dehydration
4) Renal arterial obstruction (kidney is hypoperfused despite elevated blood pressure)
5) Cirrhosis, hepatorenal syndrome
6) In patients with decreased renal perfusion, NSAIDs (constrict afferent arteriole), ACE inhibitors (cause efferent arteriole vasodilation), and cyclosporin can precipitate prerenal failure
What should you monitor and watch out for in a patient with AKI?
1) Daily weights, intake, and output
2) BP
3) Serum electrolytes
4) Watch Hb and Hct for anemia
5) Watch for infection
What happens to renal blood flow in prerenal failure and how does this affect GFR? What happens to the renal parenchyma and tubular function? Is prerenal renal failure reversible? What can it lead to?
1) Renal blood flow decreases enough to lower the GFR, which leads to decreased clearance of metabolites (BUN, Cr, uremic toxins)
2) Because the renal parenchyma is undamaged, tubular function (and therefore the concentrating ability) is preserved. Therefore, the kidney responds appropriately, conserving as much sodium and water as possible
3) This form of AKI is reversible on restoration of blood flow; but if hypoperfusion persists, ischemia results and can lead to acute tubular necrosis (ATN)
What are clinical features of prerenal kidney failure?
Signs of volume depetion (dry mucous membranes, hypotension, tachycardia, decreased tissue turgor, oliguria/anuria)
What happens to urine output in prerenal failure? BUN-to-serum Cr ratio? Urine osmolality? Urine Na+? Urine-plasma Cr ratio? What type of urine sediment is found?
1) Oliguria - always found in prerenal failure (this is to preserve volume)
2) Increased BUN-to-serum Cr ratio (>20:1 is the classic ratio) - because kidney can reabsorb urea
3) Increased urine osmolality (>500 mOsm/kg H2O) - because the kidney is able to reabsorb water
4) Decreased urine Na+ (<20 mEq/L with fractional excretion of sodium [FENa] <1%) because Na+ is avidly reabsorbed
5) Increased urine-plasma Cr ratio (>40:1) - because much of the filtrate is reabsorbed (but not the creatinine)
6) Bland urine sediment
What is the definition of intrinsic renal failure? Are the kidneys able to concentrate urine?
1) Kidney tissue is damaged such that glomerular filtration and tubular function are significantly impaired
2) The kidneys are unable to concentrate urine effectively
What are causes of intrinsic renal failure?
1) Tubular disease (ATN)
2) Glomerular disease (acute glomerulonephritis [GN])
3) Vascular disease
4) Interstitial disease
What is the cause of acute tubular necrosis?
Can be caused by ischemia (most common cause) and nephrotoxins
What are examples of glomerular disease in intrinsic renal failure?
Goodpasture syndrome, Wegener granulomatosis, poststreptococcal GN, and lupus
What are examples of vascular disease in intrinsic renal failure?
Renal artery occlusion, TTP, and HUS
What is the first thing to do in diagnosis of AKI? What first test should you check? What should you determine next? What are some signs to look for that suggest prerenal etiology? What does an allergic reaction (rash) suggest etiology of? What suggests a postrenal etiology? What other things should be reviewed and what other tests should be done for AKI?
1) History and physical examination
2) The first thing to do is to determine the duration of renal failure. A baseline Cr level provides this information.
3) The second task is to determine whether AKI is due to prerenal, intrarenal, or postrenal causes. This is done via a combination of H&P and laboratory findings
4) Signs of volume depletion and CHF suggest a prerenal etiology
5) Signs of an allergic reaction (rash) suggest acute interstitial nephritis (an intrinsic renal etiology)
6) A suprapubic mass, BPH, or bladder dysfunction
7) Medication review, urinalysis, urine chemistry (FENa, osmolality, urine Na+, urine Cr), renal ultrasound (to rule out obstruction)
How does urinalysis differ in prerenal and intrinsic renal AKI? BUN/Cr ratio? FENa? Urine Osmolality? Urine Sodium?
1) Prerenal:
a) Urinalysis: Hyaline casts
b) BUN/Cr Ratio: >20:1
c) FENa: <1%
d) Urine Osmolality: >500 mOsm
e) Urine Sodium: <20
2) Intrinsic Renal:
a) Urinalysis: Abnormal
b) BUN/Cr Ratio: <20:1
c) FENa: >2%-3%
d) Urine Osmolality: 250-300mOsm
e) Urine Sodium: >40
How do urine osmolarity, urine Na+, FENa, and urine sediment differ in prerenal failure and ATN?
1) Prerenal failiure:
a) Urine osmolarity: >500
b) Urine Na+: <20
c) FENa: <1%
d) Urine sediment: Scant
2) ATN:
a) Urine osmolarity: >350
b) Urine Na+: >40
c) FENa: >1%
d) Urine sediment: Full brownish pigment, granular casts with epithelial casts
What is important to note about prerenal azotemia and ischemic AKI in terms of renal hypoperfusion?
1) Note that prerenal azotemia and ischemia AKI are part of a spectrum of manifestations of renal hypoperfusion
2) The latter differs in that injury to renal tubular cells occurs
What is rhabdomyolysis caused by? What happens in rhabdomyolysis? What laboratory studies are elevated in rhabdo? What is the treatment?
1) Skeletal muscle breakdown caused by trauma, crush injuries, prolonged immobility, seizures, snake bites
2) Release of muscle fiber contents (myoglobin) into bloodstream. Myoglobin is toxic to kidneys, which can lead to AKI
3) Presents with markedly elevated creatine phosphokinase (CPK), hyperkalemia, hypocalcemia, hyperuricemia
4) Treat with IV fluids, mannitol (osmotic diuretic) and bicarbonate (drives K back into cells)
What are two causes of acute tubular necrosis (ATN)?
1) Ischemic AKI
2) Nephrotoxic AKI
What is ischemic AKI caused by? What does it lead to in ATN?
1) Secondary to severe decline in renal blood flow, as in shock, hemorrhage, sepsis, disseminated intravascular coagulation, heart failure
2) Ischemia results in the death of tubular cells
What is nephrotoxic AKI caused by that results in ATN?
1) Injury secondary to substances that directly injure renal parenchyma and result in cell death
2) Causes include antibiotics (aminoglycosides, vancomycin), radiocontrast agents, NSAIDs (especially in the setting of CHF), poisons, myoglobinuria (from muscle damage, rhabdomyolysis, strenuous exercise), hemoglobinuria (from hemolysis), chemotherapeutic drugs (cisplatin), and kappa and gamma light chains produced in multiple myeloma
What do the clinical features of intrinsic renal failure depend on? What symptom is usually present? Is recovery possible?
1) Clinical features depend on the cause
2) Edema is usually present
3) Recovery may be possible but takes longer than in prerenal failure
What are laboratory findings in intrinsic renal failure for BUN-to-serum Cr ratio? Urine Na+? Urine osmolality? Urine-plasma Cr ratio?
1) Decreased BUN-to-serum Cr ratio (<20:1, typically closer to 10:1 ratio) in comparison with prerenal failure. Both BUN and Cr levels are still elevated, but less urea is reabsorbed than in prerenal failure
2) Increased urine Na+ (>40 mEq/L with FENa > 2% to 3%) - because Na+ is poorly reabsorbed
3) Decreased urine osmolality (<350 mOsm/kg H2O) - because renal water reabsorption is impaired
4) Decreased urine-plasma Cr ratio (<20:1) - because filtrate cannot be reabsorbed
How common of a cause of AKI is postrenal failure? What is the etiology of postrenal failure and what must happen for creatinine to rise? What happens to renal function if postrenal failure is treated? If postrenal failure is untreated, what happens? What are causes of postrenal failure?
1) Least common cause of AKI
2) Obstruction of any segment of the urinary tract (with kidney) causes increased tubular pressure (urine produced cannot be excreted), which leads to decreased GFR. Blood supply and renal parenchyma are intact. Note that both kidneys must be obstructed for creatinine to rise
3) Renal function is restored if obstruction is relieved before the kidneys are damaged
4) Postrenal obstruction, if untreated, can lead to ATN
5) Causes:
a) Urethral obstruction secondary to enlarged prostate (BPH) is the most common cause
b) Obstruction of solitary kidney
c) Nephrolithiasis
d) Obstructing neoplasm (bladder, cervix, prostate, and so on)
e) Retroperitoneal fibrosis
f) Ureteral obstruction is an uncommon cause because obstruction must be bilateral to cause renal failure
Describe the course of ATN in phases
1) Onset (insult)
2) Oliguric phase
3) Diuretic phase
4) Recovery phase
Describe the oliguric phase of ATN
1) Azotemia and uremia - average length 10 to 14 days
2) Decreased urine output
Describe the diuretic phase of ATN
1) Begins when urine output is >500mL/day
2) High urine output due to the following: fluid overload (excretion of retained salt, water, other solutes that were 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)
What is urine osmolality? How does dehydration affect urine osmolality? What happens to urine osmolality in ATN and why?
1) Urine osmolality is a measure of urine concentration. The higher the osmolality, the more concentrated the urine
2) Dehydration in a healthy person leads to increase in urine concentration (osmolality) as follows: Dehydration causes low intravascular volume, which triggers ADH release, which stimulates reabsorption of water from kidney to fill the vasculature. Increased water reabsorption leads to more concentrated urine
3) In ATN, the tubule cells are damaged and cannot reabsorb water (or sodium); so the urine cannot be concentrated, which leads to low urine osmolality
What tests can you do to diagnose AKI?
1) Blood tests
2) Urinalysis
3) Urine chemistry
4) Urine culture and sensitivities
5) Renal ultrasound
6) CT scan
7) Renal biopsy
8) Renal arteriography
What blood tests can be used to diagnose AKI?
1) Elevation in BUN and Cr levels
2) Electrolytes (K+, Ca2+, PO43-), albumin levels, CBC with differential
What are two ways in which a urinalysis can be used to diagnose AKI? What do findings on microscopic examination of the urine sediment indicate?
1) A dipstick test positive for protein (3+,4+) suggests intrinsic renal failure due to glomerular insult
2) Microscopic examination of the urine sediment:
a) Hyaline casts are devoid of contents (seen in prerenal failure)
b) RBC casts indicate glomerular disease
c) WBC casts indicate glomerular disease
d) Fatty casts indicate nephrotic syndrome
What are three basic tests for postrenal failure?
1) Physical examination - palpate the bladder
2) Ultrasound - look for obstruction, hydronephrosis
3) Catheter - look for large volume of urine
How is the diagnosis of AKI usually made? Is the patient symptomatic?
1) Diagnosis of AKI is usually made by finding elevated BUN and Cr levels
2) The patient is usually asymptomatic
What tests should you obtain in any patient with AKI?
1) Urinalysis
2) Urine chemistry
3) Serum electrolytes (Na+, K+, BUN, Cr), CBC
4) Bladder catheterization to rule out obstruction (diagnostic and therapeutic)
5) Renal ultrasound to look for obstruction
What urine chemistry tests can be used to distinguish between different forms of AKI? How do you measure/calculate each of these tests? What do values of these tests indicate?
1) Urine Na+, Cr, and osmolality: Urine Na+ depends on dietary intake
2) FENa: collect urine and plasma electrolytes simultaneously = [(UNa)/(PNa)/(UCr)/PCr) x 100], where U = urine and P = plasma
a) Values below 1% suggest prerenal failure
b) Values above 2% to 3% suggest ATN
c) FENa is most useful if oliguria is present
3) Renal failure index 5 (UNa/[UCr/PCr]) x 100)
a) Values below 1% suggest prerenal failure
b) Values above 1% suggest ATN
When do you run urine culture and sensitivities for AKI?
If infection is suspected
Why is a renal ultrasound in AKI useful? Is it frequently ordered in AKI?
1) Useful for evaluating kidney size and for excluding urinary tract obstruction (i.e., postrenal failure) - presence of bilateral hydronephrosis or hydroureter
2) Order for most patients with AKI - unless the cause of the AKI is obvious and is not postrenal
When is a CT scan of the abdomen and pelvis usually done?
It may be helpful in some cases; usually done if renal ultrasound shows an abnormality such as hydronephrosis
When is a renal biopsy done in the setting of AKI?
Useful occasionally if there is suspicion of acute GN or acute allergic interstitial nephritis
When is renal arteriography done for AKI?
To evaluate for possible renal artery occlusion; should be performed only if specific therapy will make a difference
What should first be excluded when evaluating a patient with AKI?
First exclude prerenal and postrenal causes, and then, if necessary, investigate intrinsic renal causes
What are the most common mortal complications in the early phase of AKI?
1) Hyperkalemic cardiac arrest
2) Pulmonary edema
What are 4 categories of complications in AKI?
1) ECF volume expansion and resulting pulmonary edema
2) Metabolic
3) Uremia
4) Infection
How do you treat ECF volume expansion and resulting pulmonary edema in AKI?
Diuretic (furosemide)
What metabolic abnormalities can happen in AKI?
1) Hyperkalemia
2) Metabolic acidosis (with increased anion gap)
2) Hypocalcemia
4) Hyponatremia
5) Hyperphosphatemia
6) Hyperuricemia
