Acute Kidney Failure Flashcards

1
Q

AKF: define:

A
  1. Kidney can’t maintain homeostasis, leading to nitrogenous waste buildup

NOT SAME AS renal insufficiency where kidney function is deranged, but can still support LIFE!!

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2
Q

AKI defined as; define anuria, oliguria, polyuria

A

occurring over hrs/days; lab definition is increase in baseline creatinine by 50% or decrease in clearance by 50%; often a deterioration of renal function which requires dialysis;

anuria: less than 100 mls/24 hr OR no urine output
oliguria: 2.5 L/24hr

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3
Q

Causes of AKI:

A
  1. pre-renal (inadequate perfusion with absolute and relative hypovolemia, reduced CO, renovascular occlusion: check volume status)
  2. Renal (AKI despite perfusion and excretion with ATN, AIN, atheroemboli: check UA, full blood count, autoimmune screen)
  3. Post-renal (blocked outflow with pelvi-calyceal, ureteric, vesicoureteric junction, bladder neck: check bladder, catheter, US)
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4
Q

For ATN, causes?

A
  1. ischemic
  2. nephrotoxic: endogenous toxins (heme pigments like myoglobin and hemoglobin; myeloma light chains) vs exogenous (aminoglycosides, amphotericin B, radiocontrast agents, heavy metals with cis-platinum, mercury, poisons like ethylene glycol) HARP
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5
Q

For AIN, causes? Clinically?

A
  1. allergic IN (drugs)
  2. infections (bacterial, viral)
  3. sarcoidosis; SIA!!!
    fever, rash, arthralgias, eosinophilia, UA (microscopic hematuria, sterile pyuria, eosinophiluria) FU RAE
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6
Q

Contrast-induced AKI: prev? risk factors?

A

Less than 1% in patients with normal renal function;

  1. renal insufficiency
  2. DM
  3. multiple myeloma
  4. high osmolar contrast media (try low-osmolar)
  5. contrast medium volume (try and minimize)

The RM DOVe

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7
Q

clinical characteristics of contrast-induced AKI and pre-procedure prophylaxis?

A

24-48 hrs after exposure, lasts 5-7 days, non-oliguric (majority), dialysis rarely needed, urinary sediment (variable), low fractional excretion of Na;
IV fluid, mucomyst (N-acetylcysteine), bicarb, maybe fenoldopam but the go-to is IV fluid!!

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8
Q

Glomerulonephritis is characterized by

A

inflamm and damage of the glomeruli; allows leak of protein w/w/o blood in urine

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9
Q

Proliferative vs. non-prolif glomerulonephritis examples:

A
  1. Membranoproliferative, post-infectious, IgA nephropathy, rapidly progressive glomerulonephritis (Goodpasture vs. vasculitic disorders like Wegeners and microscopic polyangiitis)
  2. Membranous, minimal change, FSGS
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10
Q

AKI post-renal causes:

A
  1. Intra-renal obstruction: acute uric acid nephropathy, drugs (acyclovir)
  2. extra-renal obstruction (renal pelvis or ureter like stones, clots, papillary necrosis, tumors), bladder (BPH), urethra (stricture)
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11
Q

Bland urinary sediment seen in

A

pre-renal azotemia and urinary outlet obstruction

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12
Q

RBC casts or dysmorphic RBCs seen in

A

acute glomerulonephritis and small vessel vasculitis

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13
Q

WBC’s and WBC casts seen in

A

AIN, acute pyelonephritis

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14
Q

ATN would show _____ in urinary sediment:

A
  1. renal tubular epithelial cells,
  2. RTE cell casts
  3. pigmented granular (muddy brown) casts
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15
Q

FeNa < 1% in; 1-2% in; >2% in

A
  1. prerenal
  2. ATN (unusual)
  3. glomerular or vascular injury;
  4. prerenal
  5. ATN sometimes
  6. AIN: higher FeNa b/c of tubular damage;
  7. ATN
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16
Q

AKI signs and symps:

A

weight gain, peripheral edema, HTN; hyperkalemia, N/V, pulmonary edema, ascites, asterixis, encephalopathy

17
Q

Lab findings in AKI:

A
  1. rising creatinine and urea
  2. rising K
  3. decreasing Hb
  4. Acidosis
  5. Hyponatremia
  6. Hypocalcemia
18
Q

Indications for acute dialysis:

A
  1. Acidosis (metabolic)
  2. electrolytes (hyperkalemia)
  3. ingestion of drugs/ischemia
  4. overload (fluid)
  5. uremia