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*MHD Exam 5 > AKI > Flashcards

AKI Flashcards

1
Q

What is the definition of acute kidney injury (AKI)?

A

an abrupt decline in renal function as measured by a rise in serum BUN and creatinine, or a drop in urine output

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2
Q

What are the 3 main etiologies of AKI?

A
  • Pre-renal azotemia: any change in systemic hemodynamics leading to a decrease in effective circulating volume-> reduced flow to kidneys-> reduced GFR
  • Intra-renal: direct injury to the kidney
  • Post-renal azotemia: structural/functional hindrance to urinary flow leading to backup of urine and decreased GFR
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3
Q

What are the diagnostic criteria for AKI?

A

1) Increase in serum creatinine by >0.3 mg/dL within 48 hrs OR increase in serum creatinine to 1.5x baseline within past 7 days
2) Urine volume <0.5 mL/kg/hr for 6 hrs

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4
Q

Is pre-renal azotemia generally reversible or irreversible?

A

reversible with treatment of underlying etiology

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5
Q

What are the pre-renal azotemia etiologies?

A
  • Absolute decrease in ECV (hemorrhage, volume depletion)
  • Relative decrease in ECV (heart failure, cirrhosis)
  • Impaired renal autoregulation with low ECV (NSAIDs, ACEIs/ARBs)
  • Renal vasoconstriction or occlusion (renal artery stenosis, hypercalcemia)
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6
Q

What is the net filtration pressure in the kidney (formula)?

A

NFP= glomerular hydrostatic press. - Bowman’s capsule press. - glomerular oncotic press.

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7
Q

What are urine Na+ and FeNa in pre-renal azotemia?

A
  • Na+: <20 mEq/L (low)
  • FeNa: <1% (low

The kidneys are trying to reabsorb as much Na+ and water as possible to conserve volume.

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8
Q

What is the urine osmolality in pre-renal azotemia?

A

> 500 (high)

Kidneys are reabsorbing sodium AND water, leaving concentrated urine.

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9
Q

What is the BUN:creatinine ratio in pre-renal azotemia?

A

> 20:1 (elevated)

Urea is reabsorbed along with Na+ and water, so serum BUN is high. Creatinine is secreted into the PCT (does NOT get reabsorbed), so serum creatinine is lower while urine creatinine is higher.

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10
Q

What is the most common cause of AKI in hospitalized patients?

A

acute tubular necrosis

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11
Q

What are endogenous substances that may cause ATN?

A

myoglobin (rhabdo), uric acid (tumor lysis syndrome), hemoglobin (massive hemolysis), bilirubin (liver failure)

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12
Q

Which part of the nephron is sensitive to ischemic injury vs. toxic injury?

A
  • ischemic: PCT and TAL (high oxygen req. due to high metabolic rate)
  • Toxic: PCT (first exposed to toxin)
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13
Q

When does the maintenance phase of ATN occur?

A

1-3 weeks (may be prolonged to 3 months in some cases, depending on the injury)

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14
Q

Acute interstitial nephritis is inflammation of:

A

the tissue (interstitium) surrounding the tubules; also known as acute tubulo-interstitial nephritis

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15
Q

What is acute interstitial nephritis most often caused by?

A

medications that act as haptens to induce a hypersensitivity rxn (eosinophils seen in biopsy)

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16
Q

What is the classic triad associated acute interstitial nephritis?

A

fever, rash, peripheral eosinophilia (but urine eosinophils are neither sensitive nor specific)

17
Q

How can acute interstitial nephritis be distinguished from acute glomerulonephritis?

A

AIN involves sterile pyuria (positive WBC with negative urine culture) and protein in urine

18
Q

Which features are pathognomonic for acute glomerulonephritis?

A

dysmorphic RBCs and RBC casts

19
Q

What happens to the tubular epithelium in acute tubular necrosis?

A

loss of the brush border leading to loss of polarity

20
Q

What happens during the maintenance phase of ATN?

A

established renal injury leading to oliguria and muddy brown urine with casts noted in sediment

21
Q

What happens during the recovery phase of ATN?

A
  • Repair and regeneration of tubules with recovery of renal function (decreased BUN:creatinine)
  • Polyuria and risk for hypokalemia and hypernatremia
22
Q

Renal ______ and ______ are vulnerable to ischemic necrosis due to chronically under-perfused state.

A

medulla; papillae

23
Q

Sloughing of renal papillae in renal papillary necrosis leads to:

A

gross hematuria, proteinuria, flank pain

24
Q

Renal papillary necrosis is more common in [men/women] and often [bilateral/unilateral].

A

women; bilateral (although CAN be unilateral)

25
Q

Renal papillary necrosis is typically seen in:

A 
SAAD papa
S=Sickle cell disease
A=Acute pyelonephritis
A=Analgesic nephropathy
D=Diabetes
26
Q

What are the meds that commonly cause acute interstitial nephritis?

A

P’s:

  • Proton pump inhibitors
  • Penicillins (and cephalosporins)
  • Pain meds (NSAIDs)
  • Pee meds (diuretics)
  • RifamPin
27
Q

What are some of the key features of a urinalysis in intrinsic kidney injury?

A
  • (+) WBCs with negative culture (inflammation but no infection)
  • hematuria
  • proteinuria
  • (+) RBCs
28
Q

What are urine Na+ and FeNa in intrinsic kidney injury?

A
  • Na+: >20 mEq/L (high)
  • FeNa: >1% (high)

due to impaired reabsorption of Na+ into serum as tubules are injured

29
Q

What is the serum BUN:creatinine in intrinsic kidney injury?

A

<10:1 (low)

As tubules are injured, urea reabsorption and creatinine secretion are impaired. So, there is not a rise in BUN.

30
Q

What are the indications for dialysis in AKI?

A

AEIOU
A=Acidosis (metabolic)
E=Electrolyte imbalance (hyperkalemia)
I=Intoxications with a dialyzable drug (SLIME- salicylates, lithium, isopropanol, methanol, ethylene glycol)
O=Overload (vol. overload not responsive to diuresis)
U=Uremia (elevated BUN w/ signs of uremia– bleeding, asterixis, encephalopathy, pericarditis)

31
Q

What are the general ways that AKI is managed?

A
  • Treatment of underlying etiology
  • Management of electrolyte disturbances
  • Maintenance of MAP
  • Dosing meds to renal function
  • Lifestyle changes (weight, BP, salt intake)
  • Avoidance of contrast studies and nephrotoxic meds
32
Q

24 hour creatinine is often an [overestimate/underestimate] of true GFR.

A

overestimate, as 10% of urine creatinine is from tubular secretion

33
Q

Why was creatinine chosen to measure GFR?

A

It is freely filtered and not reabsorbed nor secreted (however, we now know that ~10% of creatinine is secreted into tubules).

34
Q

What are potential causes of high BUN?

A
  • pre-renal state
  • high dose steroids
  • hypercatabolic states (high fevers, burns)
  • high cell turnover states
  • high protein diet
  • GI bleeds
35
Q

What are the pitfalls of using creatinine to estimate GFR in AKI patients?

A
  • AKI is NOT a steady state, thus cannot calculate eGFR using ANY of the available formulae
  • serum creatinine lags behind the actual injury (oliguria usually observed first)
  • serum creatinine depends on rate of production, rate of clearance, and volume of distribution (all are changing in AKI)
  • creatinine is produced predominantly by muscle (muscular people may have high creatinine; emaciated people may have low creatinine)
36
Q

What are common causes of upper urinary tract obstruction?

A

bilateral kidney stones, extrinsic compression by tumors/fibrosis –> hydronephrosis

37
Q

What are common causes of lower urinary tract obstruction (bladder and below)?

A

BPH, anticholinergics and sympathomimetics, neurogenic bladder

*MHD Exam 5 (14 decks)

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