Renal/GU Flashcards
Define acute kidney injury.
a rapid decline in renal function, with an increase in serum creatine level (relative increase of 50% or absolute increase of 0.5-1.0 mg/dL)
What are the RIFLE criteria?
a method for stratifying varying degrees of renal dysfunction
- Risk: 1.5 fold increase in serum creatinine, GFR decrease by 25%, or UOP less than 0.5 mL/kg/hr for 6 hours
- Injury: 2-fold increase in serum creatinine, GFR decrease by 50%, or UOP less than 0.5 mL/kg/hr for 12 hours
- Failure: 3-fold increase in serum creatinine, GFR decrease by 75%, or UOP less than 0.5 mL/kg/hr for 24 hours
- Loss: of kidney function requiring dialysis for more than 4 weeks
- ESRD: loss of kidney function requiring dialysis for more than 3 months
What would cause an elevated BUN or creatinine apart from AKI?
- BUN may be elevated by catabolic drugs such as steroids, GI/soft tissue bleeding, or dietary protein intake
- creatinine may be elevated with increased muscle breakdown and various drugs
What is the most common cause of death in those with AKI?
infection
What happens to BUN/Cr, FENa, and urine osmolality in someone with pre-renal azotemia?
- when RBF decreases, BUN reabsorption is enhanced and the BUN/Cr increases > 15
- since tubular function is intact, FENa is normal (<1%) and urine osmolarity is normal (>500 mOsm/kg)
What happens to BUN/Cr, FENa, and urine osmolality in someone with post-renal azotemia?
- in the early stage, increased tubular pressure enhances BUN reabsorption, and the BUN/Cr increases > 15
- in the early stage, tubular function is also normal with FENa < 1% and urine osmolarity > 500mOsm/kg
- with long-standing obstruction, tubular damage ensues and the BUN/Cr falls, FENa rises, and there is an inability to concentrate urine
How is fractional excretion of a solute calculated?
FE = (solute excreted)/(solute filtered) = (urine solute)(urine flow rate)/(GFR x plasma solute) = (plasma creatinine x urine solute)/(urine creatinine x plasma solute)
Pre-Renal Failure
- causes
- pathogenesis
- presentation
- lab findings
- the most common cause of AKI
- due to decreased systemic arterial blood volume or renal perfusion as in hypovolemia, CHF, hypotension, renal arterial obstruction, hepatorenal syndrome, and NSAIDs, ACE inhibitors, and cyclosporin
- in these situations renal blood flow decreases, lowering GFR, which leads to decreased clearance of metabolites like BUN, Cr, and uremic toxins; tubular function is preserved so the kidney conserves sodium and water
- presents with signs of volume depletion
- labs demonstrate oliguria, an increased BUN/Cr ratio greater than 20, increased urine osmolality, and decreased urine sodium with a FENa less than 1%
- UA is likely to demonstrate hyaline casts
Name three drugs that may precipitate prerenal failure and through what mechanism they do.
- NSAIDs constrict afferent arterioles
- ACE inhibitors cause efferent arteriole vasodilation
- cyclosporin
How can labs help you differentiate between prerenal and intrinsic renal failure?
- prerenal is likely to have a BUN/Cr ratio greater than 20, FENa less than 1%, high urine osmolality, and low urine sodium
- intrinsic is likely to have a BUN/Cr ratio less than 20, FENa of 1-2%, low urine osmolality, and high urine sodium
Intrarenal Failure
- pathogenesis
- causes
- presentation
- laboratory findings
- damaged renal parenchyma such that GFR and tubular function are significantly impaired
- may be caused by acute tubular necrosis, glomerular disease, vascular diseases like TTP or HUS, interstitial nephritis
- presentation varies depending on the cause
- lab findings include BUN/Cr ratio less than 20 although both are still elevated in serum, increased urine sodium and decreased urine osmolality
Describe how rhabdomyolysis affects the kidneys and how it appears on labs.
- skeletal muscle breakdown caused by trauma, crush injuries, prolonged immbolity, snake bites, etc.
- leads to myoglobin released into the blood stream, which is toxic to the kidneys, leading to intrinsic AKI
- presents with elevated creatine phosphokinase, hyperkalemia, hypocalcemia, and hyperuricemia
- treat with IV fluids, mannitol for diuresis, and bicarbonate
Postrenal Failure
- the least common cause of AKI
- due to an obstruction of any segment of the urinary tract; however, both kidneys must be obstructed for creatinine to rise
- this is most commonly due to BPH; other causes include obstruction of a solitary kidney, nephrolithiasis, obstructing neoplasm
Why is post renal failure uncommon?
because both kidneys must be obstructed for the creatinine to rise
Acute Tubular Necrosis
- the most common cause of acute renal failure
- due to ischemia or nephrotoxicity in the form of aminoglycosides, vancomycin, heavy metals, myoglobinuria as in crush injury, ethylene glycol, radio contrast dye, or urate from tumor lysis syndrome, cisplatin, amphotericin, kappa and gamma light chains in multiple myeloma
- injury results in necrosis of tubular epithelial cells, which form brown, granular casts and diminish GFR
- tubular dysfunction leads to elevated BUN and Cr, though the BUN/Cr is < 15, FENa 1-2%, and Osm < 500
- UA likely to find muddy brown casts with trace protein and no blood
- clinical features include oliguria as well as hyperkalemia and acidosis due to the inability to secrete these cations
- reversible but requires supportive dialysis since electrolyte imbalances can be fatal
- recovery takes 2-3 weeks as tubular cells are stable and take time to re-enter the cell cycle
What is the workup like for a patient with AKI?
- urinalysis
- urine chemistry
- serum electrolytes
- bladder catheterization to rule out obstruction
- renal ultrasound to rule out obstruction
What do each of the following suggest when found on urinalysis:
- hyaline casts
- RBC casts
- WBC casts
- fatty casts
- hyaline: prerenal failure
- RBC casts: glomerular disease
- WBC casts: renal parenchymal inflammation
- fatty casts: nephrotic syndrome
What are the most common mortal complications seen in the early phases of AKI?
hyperkalemic cardiac arrest and pulmonary edema
What are the possible complications of AKI?
- volume expansion resulting in pulmonary edema
- hyperkalemia due to decreased excretion of potassium and the movement of potassium from the ICF to ECF due to tissue destruction and acidosis
- metabolic acidosis with anion gap due to decreased excretion of hydrogen ions
- hypocalcemia due to an inability for form active vitamin D
- hyponatremia if water intake is greater than body losses
- hyperphosphatemia
- hyperuricemia
- uremia
- infection due to impaired immune function secondary to azotemia
Acute Kidney Injury
- a rapid decline in renal function with an increase in serum creatinine
- can be prerenal (most common), intrarenal, or postrenal (least common)
- prerenal is caused by hypovolemia, low cardiac output, systemic vasodilation, hepatorenal syndrome, or renal artery obstruction; intrarenal by acute tubular necrosis, glomerular disease, or interstitial disease; post renal by an obstruction of both kidneys
- weight gain and edema are the most common presenting symptoms; others include uremia and changes in urine volume
- prerenal shows an elevated BUN/Cr ratio, high urine osmolality, low urine sodium, and low FENa; intrarenal shows lower BUN/Cr, low urine osmolality, high urine sodium, and high FENa
- hyaline casts suggest prerenal failure, muddy brown casts suggest ATN, RBC casts indicate glomerular disease, WBC casts indicate parenchymal inflammation, and fatty casts indicate nephrotic syndrome
- may be complicated by volume expansion and pulmonary edema, hyperkalemia, metabolic acidosis, hypocalcemia, hyponatremia, hyperphosphatemia, hyperuricemia, uremia, and infection
- treat by adjusting medication regimen, stabilizing fluid levels with IVF or diuretics, and correcting electrolyte disturbances
- order dialysis for severe and intractable complications
Why does radiographic contrast lead to ATN? How does this affect it’s practical administration?
it causes a spasm of the afferent arteriole, which we can prevent with saline hydration before the contrast
What is the difference between azotemia and uremia?
- azotemia refers to an elevation of BUN
- uremia refers to the signs and symptoms associated with accumulation of nitrogenous wastes due to impaired renal function (usually when BUN is greater than 60)
At what point does azotemia typically become symptomatic as uremia?
once BUN is greater than 60
How is ESRD defined?
- not by either BUN or creatinine
- but rather as a loss of kidney function that leads to laboratory and clinical findings of uremia
Chronic Kidney Disease
- decreased kidney function (GFR < 60) or kidney damage for at least 3 months
- most commonly caused by diabetes or hypertension; other causes include chronic glomerulonephritis, interstitial nephritis, PKD, and AKI
- presets with hypertension, CHF, volume overload, uremia, normocytic anemia, platelet dysfunction and bleeding, immune dysfunction, hyperphosphatemia causing hypocalcemia and a secondary hyperparathyroidism complicated by renal osteodystrophy and calciphylaxis, hyperkalemia, hypermagnesemia, and metabolic acidosis
- diagnose with a CMP, estimation of GFR, CBC, and renal ultrasound
- symptomatic volume overload and severe hyperkalemia are the complications that require the most urgent treatment
- management involves a low protein diet (0.7-0.8 g/kg); restriction of sodium, magnesium, potassium, and phosphate; ACE inhibitors; glycemic control; calcium citrate as a phosphate binder; oral calcium and vitamin D supplementation; EPO; and dialysis or transplantation
Describe the presentation of chronic kidney disease
- hypertension secondary to salt and water retention
- CHF due to volume overload, HTN, and anemia
- uremia: pericarditis, n/v, loss of appetite, restless legs, asterixis, hyperreflexia, altered mental status
- normocytic normochromic anemia secondary to EPO deficiency
- bleeding due to platelet dysfunction as a result of uremia, which prevents platelet degranulation
- hyperphosphatemia due to reduced clearance, decreases 1,25-OH vitamin D production, leads to hypocalcemia, causing secondary hyperparathyroidism, manifesting as renal osteodystrophy, and fractures
- calciphylaxis as calcium and phosphate precipitate causing vascular calcifications and then necrotic skin lesions
- decreased testosterone in men; amenorrhea, infertility, and hyperprolacitinemia in women
- volume overload with pulmonary edema
- hyperkalemia, hypermagnesemia, metabolic acidosis
- immune dysfunction
What is renal insufficiency?
a term used when a patient’s renal function is irreversibly compromised by not failed
Why are ACE inhibitors important in the treatment of chronic kidney disease?
- because it dilates the efferent arteriole of the glomerulus, slowing the progression of proteinuria
- it also helps control blood pressure, which slows disease progression
What are the indications for dialysis?
AEIOU
- Acidosis (intractable)
- Electrolytes (severe, persistent hyperkalemia)
- Intoxications (with methanol, ethylene glycol, lithium, or aspirin)
- Overload (volume not manageable with other means)
- Uremia (severe)
Describe the process of and the pros and cons related to hemodialysis as opposed to peritoneal dialysis.
- patient’s blood is heparinized and then passed through the dialyzer for 3-5 hours, 3 days per week
- access is obtained with a central catheter, tunnel catheter, AV fistula, or implantable graft
- more efficient and can be initiated more quickly than peritoneal dialysis
- however, it is less similar to the normal physiology of the kidney so there is a greater risk of hypotension or hypoosmolality during the process
What is the advantage of continuous arteriovenous hemodialysis and continuous venovenous hemodialysis?
they use lower flower rates than traditional hemodialysis, which minimizes any rapid shifts in volume or osmolality, making it a good option for hemodynamically unstable patients
Describe the process of and the pros and cons related to peritoneal dialysis as opposed to hemodialysis.
- the peritoneum serves as the dialysis membrane with a dialysate fluid infused into the peritoneal cavity
- the fluid must be drained and replaced every hour in an acute setting but once every 4-8 hours thereafter
- advantageous in that patients can learn to do it on their own
- the dialysate fluid has a high glucose load which can contribute to hyperglycemia, it is a risk factor for peritonitis, it increases intraabdominal pressure posing a risk for inguinal or abdominal hernia, it increases abdominal girth so it has some cosmetic disadvantages
How do we define proteinuria?
as urinary excretion of more than 150mg protein/day
How do glomerular, tubular, and overflow proteinuria compare with one another in cause ?
- glomerular is due to increased glomerular permeability to proteins and protein loss tends to be more severe
- tubular is due to decreased tubular reabsorption of the smaller proteins which are normally filtered through the glomerulus due to sickle cell disease, urinary tract obstruction, or interstitial nephritis
- overflow proteinuria is caused by increased production of small proteins which overwhelm the tubules’ ability to reabsorb them (i.e. Bence Jones protein in multiple myeloma)
Describe nephrotic syndrome.
- defined by urine protein excretion greater than 3.5g/day
- presents with hypoalbuminemia and resulting edema
- hyperlipidemia in the form of elevated LDL and VLDL as the liver attempts to increase albumin synthesis
- increased risk fo infection as immunoglobulins are lost
- hypercoagulable state as antithrombin III is lost
Describe nephritic syndrome.
changes due to inflammation of the glomeruli
- proteinuria is limited (< 3.5 g/day)
- oliguria and azotemia, signs of AKI
- salt retention with periorbital edema and hypertension
- RBC casts
Urine dipstick is capable of detecting what types and amounts of protein?
- detects concentrations 30mg/dL or higher (won’t detect microalbuminuria)
- more sensitive to albumin than immunoglobulins
How should microalbuminuria be diagnosed?
- defined as albumin excretion of 30-300mg/day, which is below the sensitivity of a dipstick
- special dipsticks are required to screen for microalbuminuria and should then be confirmed with a radioimmunoassay
