Acute Kidney Injury + B&B

Question 1

what are 2 ways to identify a decrease in GFR, such as that which occurs with acute kidney injury?

Answer 1

1. increase in BUN and creatinine - note creatinine is more specific (but only valid when creatinine concentration is stable)
2. decrease in urine output - only useful when it is really low (<0.5 ml/kg over 6 hour period)

Question 2

what should you be sure to rule out when treating a suspected post-renal azotemia?

Answer 2

obstruction - common and reversible cause of post-renal azotemia (only if BOTH kidneys are obstructed)

associated with ureter/urethra and bladder issues and hydronephrosis

obstruction can be identified with ultrasound or CT scan

Question 3

hydronephrosis

Answer 3

dilation/distention of the renal collecting system of one or both kidneys due to obstruction of urine outflow distal to renal pelvis (ureter, urinary bladder, urethra)

Question 4

what is the cause of pre-renal azotemia (acute kidney injury)?

Answer 4

kidney hypoperfusion, either due to true hypovolemia or selective renal ischemia (such as bilateral renal artery stenosis or drug-induced)

prerenal AKI reverses rapidly if renal perfusion is restored because the integrity of the renal parenchyma remains intact

Question 5

what are 4 general causes of intrarenal azotemia/ acute kidney injury?

Answer 5

1. vascular injury - embolus/thrombus, vasculitis
2. glomerular injury - nephrotic or nephritic syndrome
3. interstitial nephritis - meds #1 cause (eosinophilia, WBC casts)
4. acute tubular necrosis - ischemic or toxic injury (muddy brown casts)

Question 6

what are the common toxins that cause intra-renal acute kidney injury (via acute tubular necrosis)? (3 major categories)

Answer 6

1. medications: aminoglycosides, vancomycin
2. contrast dye (iodinated)
3. pigments: hemoglobin, myoglobin

—> “muddy brown” casts in urine

Question 7

what is a normal BUN:creatinine ratio and how does it change with pre-renal vs intra-renal acute kidney injury?

Answer 7

normal BUN:Cr = 10-15 : 1
this is because urea is filtered + reabsorbed, while creatinine is filtered + secreted

BUN:Cr ratio remains normal with acute tubular necrosis (intra-renal)

BUN:Cr ratio RISES with pre-renal azotemia, >20:1
this is because increased Na+/H2O reabsorption will increase urea reabsorption as well

*therefore, BUN:Cr ratio is a good way to tell if pre-renal AKI has progressed to intra-renal AKI

Question 8

how can urinary [Na+] be used to distinguish if pre-renal azotemia has progressed to intra-renal azotemia?

Answer 8

Na+ retention occurs in response to decreased renal perfusion - low urinary Na+ suggests pre-renal (low perfusion) cause of azotemia

in intra-renal azotemia (acute tubular necrosis), Na+ reabsorption is impaired - increase in urinary Na+ / fraction of excreted Na+

Question 9

how can urinary osmolarity be used to distinguish if pre-renal azotemia has progressed to intra-renal azotemia?

Answer 9

hypoperfusion (pre-renal AKI) stimulates ADH release —> concentrated urine

however in acute tubular necrosis (intra-renal AKI), urine concentrating ability is impaired —> urine osmolarity is lower, close to that of plasma (300-350mOsm/kg)

Question 10

what would urinalysis of post-renal (obstructive) azotemia show?

Answer 10

high pressure in tubules prevents filtration and disrupts reabsorption

—> increased BUN and Cr
—> high BUN:Cr ratio
—> high urine Na+ and fractional excretion of Na+
—> low urine osmolarity

Question 11

what are the 2 most common causes of chronic renal failure (aka chronic kidney disease)?

Answer 11

1. diabetes —> diabetic nephropathy
2. HTN —> hypertensive nephrosclerosis

Question 12

secondary vs tertiary hyperparathyroidism

Answer 12

secondary: PTH stimulation in renal failure

tertiary: PTH becomes autonomous from constant stimulation, leading to VERY high PTH levels (—> HIGH Ca2+) - often requires parathyroidectomy

Question 13

what are 3 ways by which rhabdomyolysis can develop?

Answer 13

1. intense physical exercise, esp. if dehydrated
2. crush injuries (trauma)
3. drugs (statins, fibrates)

Question 14

elevated levels of what are hallmark of rhabdomyolysis?

Answer 14

creatinine kinase - usually VERY high (>1,000)

will also see elevated aldolase, lactate dehydrogenase, AST/ALT, potassium, phosphate, purines (hyperuricemia), myoglobin

Question 15

why is hyperuricemia seen in rhabdomyolysis?

Answer 15

muscle contents spilled everywhere, including purines

purines are metabolized to uric acid in liver —> hyperuricemia

Question 16

how is myoglobin toxic to the kidneys? (such as what occurs with rhabdomyolysis)

Answer 16

obstructs tubules, toxic to proximal tubule cells, induces vasoconstriction (especially in medulla) —> renal hypoxia

myoglobin makes urine appear dark

renal failure and subsequent death is the feared outcome of rhabdomyolysis!

Question 17

Pt is a 78yo M presenting to the ED after being found on their kitchen floor. Pt describes muscle pain and weakness. Dark urine is noted and positive for heme dipstick, but there is no evidence of RBC in the urine on microscopy. Labs show hypocalcemia. What is likely going on? How will you treat him?

Answer 17

rhabdomyolysis following crush injury (fall in kitchen)

dark urine and positive heme dipstick due to myoglobin (toxic to kidneys), initial phase of rhabdo. presents with hypocalcemia due to calcium depositing in damaged myocytes

treat with IV fluids, electrolytes, potentially dialysis (depending on severity)

Question 18

Pt is a 58yo M presenting to the ED with complaints of muscle pain and weakness. Dark urine is noted, and blood shows high levels of creatinine kinase and hyperuricemia. Patient is taking a fibrate. What is going on?

Answer 18

rhabdomyolysis - can be caused by intense physical exercise (esp. if dehydrated), crush injuries (trauma), or drugs - statins, fibrates

Question 19

which 2 classes of drugs are known to cause rhabdomyolysis?

Answer 19

1. statins
2. fibrates