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IM NEPHRO > AKD > Flashcards

AKD Flashcards

1
Q

SEVERITY

A
  • asymptomatic
  • fatal
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2
Q
  • sudden
  • Renal function
  • Retention of nitrogenous wastes
A

AKD

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3
Q

duration of AKD

A
  • acute
  • chronic
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4
Q

Categories of Acute Kidney Injury

  • Hypovolemia
  • Decreased cardiac output
  • Decreased effective circulating vol
    + Congestive heart failure
    + Liver failure
  • Impaired renal autoregulation
    + NSAIDs
    + ACE-VARB
    + Cyclosporine
A

PRERENAL

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5
Q

Categories of Acute Kidney Injury

INTRARENAL

A
  • Glomerular
    + Acute glomerulonephritis
  • tubules and interstitium= sepsis/ infection, ischemia, Nephrotoxins
  • Vascular
    +Vasculitis
    + Malignant hypertension
    + TTP-HUS
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6
Q

Categories of Acute Kidney Injury

POSTRENAL

A
  • Bladder outlet obstruction
  • Bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidney)
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7
Q

Factors that affect the autoregulatory response:

A
  • Atherosclerosis
  • Age
  • long standing hypertension
  • SBP <80 mm Hg
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8
Q

narrowing and
impaired vasodilation

A

Hyalinosis and myointimal
hyperlasia

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9
Q

ecreased perfusion pressure in the presence of NSAIDs

A
  • Decreased vasodilatory prostaglandins
  • increased angiotensisn II
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10
Q

creased perfusion pressure in the presence of ACE-I or ARB

A
  • slightly increased vasodilatory prostaglandins
  • decreased angiotensin II
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11
Q
  • Arterial vasodilation in the splanchnic circulation despite volume overload
  • Reduced systemic vascular resistance
  • Vasoconstriction: Hypovolemia
A

HEPATORENAL SYNDROME

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12
Q

perturbations in the microcirculation
occlusion of small vessels

A

HYPOXIA

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13
Q

directly
generation of free radicals

A

CYTOTOXIC DAMAGE

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14
Q

Nephrotoxins: Antibiotics

Exogenous:
high trough levels

A

Vancomycin

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15
Q

Nephrotoxins: Antibiotics

Exogenous:
both cause tubular necrosis
(vasoconstriction and direct tubular injury)

A

Aminoglycosides & Amphotericin B

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16
Q

Nephrotoxins: Antibiotics

Exogenous:
tubular obstruction

A

Acyclovir

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17
Q

Nephrotoxins: Antibiotics

Endogenous

A
  • intrarenal vasoconstriction,
  • direct proximal tubular toxicity
  • mechanical obstruction
  • Intratubular crystals
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18
Q

Intrinsic: Glomerulonephritis

A
  • glomerular podocytes
  • mesangium
  • endothelial cells
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19
Q

Where is WBC cast found in urinary?

A

Distal

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20
Q

Where is Epithelial cell cast found in urinary?

A

Distal

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21
Q

Where is hyaline cast found in urinary?

A

Loop of Henle

22
Q

History of poor fluid intake or fluid
loss (hemorrhage, diarrhea, vomiting, sequestration into extravascular
space); NSAID/ACE-I/ARB; heart failure;
evidence of volume depletion (tachycardia, absolute or postural hypotension, low jugular Venous pressure,
dry mucous membranes), decreased ffective circulatory volume (cirrhosis,
heart failure)

A

Prerenal azotemia

23
Q
  • BUN/creatinine ratio above 20,
    -FeNa <1%,
  • hyaline casts in urine sediment,
  • urine specific gravity >1.018,
  • urine osmolality >500 mOsm/kg
A

Prerenal azotemia

24
Q

epsis, sepsis syndrome, or septic
shock. Overt hypotension not always
seen in mild to moderate AKI

A

Sepsis-associated AKI

25
Q

Positive culture from normally sterile
body fluid; urine sediment often
contains granular casts, renal tubular epithelial cell casts

A

Sepsis-associated AKI

26
Q

Systemic hypotension, often superimposed upon sepsis and/or reasons for limited renal reserve such as older age, CKD

A

Ischemia-associated AKI

27
Q

Urine sediment often contains granular casts, renal tubular epithelial cell casts FeNa typically >1%

A

Ischemia-associated AKI

28
Q

Nephrotoxin-Associated AKI: Endogenous

  • Traumatic crush injuries, seizures, immobilization
  • Elevated myoglobin, creatine kinase; urine heme positive with few red blood cells
  • FeNa may be low (<1%)
A

Rhabdomyolysis

29
Q

Nephrotoxin-Associated AKI: Endogenous

  • Age >60 years, constitutional symptoms, bone pain
  • Monoclonal spike in urine or serum
    electrophoresis; low anion gap; anemia
  • Bone marrow or renal biopsy can be
    diagnostic
A

Multiple myeloma

30
Q

Nephrotoxin-Associated AKI: Endogenous

  • Recent chemotherapy
  • Hyperphosphatemia, hypocalcemia,
    hyperuricemia
A

Tumor lysis

31
Q

Nephrotoxin-Associated AKI: Endogenous

  • Recent blood transfusion with transfusion reaction
    Recent chemotherapy
  • Anemia, elevated LDH, low haptoglobin
  • FeNa may be low (<19%); evaluation for transfusion reaction
A

Hemolysis

32
Q

Nephrotoxin-Associated AKI: Exogenous

  • Exposure to iodinated contrast
  • Characteristic course is rise in SCr within 1-2 d, peak within 3-5 d, recovery within 7 d
  • FeNa may be low (<1%)
A

Contrast nephropathy

33
Q

Nephrotoxin-Associated AKI: Exogenous

  • Aminoglycoside antibiotics, cisplatin, tenofovir, zoledronate, ethylene glycol,
    aristolochic acid, and melamine
  • Urine sediment often contains granular casts, renal tubular epithelial cell casts. FeNa typically > 19%.
  • Can be oliguric or nonoliguric
A

Tubular injury

34
Q
  • skin rash, arthralgias, sinusitis (AGBM disease) lung hemorrhage, recent skin infection or pharyngitis (poststreptococcal)
  • ANA, ANCA, AGBM antibody, hepatitis
    serologies, cryoglobulins, blood culture, decreased complement levels,
    ASO titer (abnormalities of these tests depending on etiology)
A

Glomerulonephritis/ vasculitis

35
Q
  • Nondrug-related causes include tubulointerstitial nephritis-uveitis (TINU) syndrome, Legionella infection
  • Eosinophilia, sterile pyuria; often
    nonoliguric
  • Urine eosinophils have limited diagnostic accuracy; kidney biopsy may be necessary
A

Interstitial nephritis

36
Q
  • Neurologic abnormalities and/or AKI;
    recent diarrheal illness; use of calcineurin inhibitors; pregnancy or postpartum; spontaneous
  • Schistocytes on peripheral blood
    smear, elevated LDH, anemia, thrombocytopenia
  • Typical HUS
A

TTP/HUS

37
Q
  • Recent manipulation of the aorta or other large vessels; may occur spontaneously or after anticoagulation; retinal plaques, palpable purpura, livedo reticularis, GI bleed
  • Hypocomplementemia, eosinophiluria (variable), variable amounts of
    proteinuria
A

Atheroembolic disease

38
Q
  • History of kidney stones, prostate
    disease, obstructed bladder catheter,
    retroperitoneal or pelvic neoplasm
  • specific findings other than AKI;
    may have pyuria or hematuria
A

Postrenal AKI

39
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

General Issues

A

. Optimization of systemic and renal hemodynamics through volume resuscitation and judicious use of vasopressors
2. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs, aminoglycosides) if possible
3. Initiation of renal replacement therapy when indicated

40
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Hyperkalemia

A

a. Restriction of dietary K intake
b. Discontinuation of K-sparing diuretics, ACE inhibitors, ARBs, NSAIDs
c. Loop diuretics to promote urinary potassium loss
d. Potassium binding ion-exchange resin (sodium polystyrene sulfonate)
e. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry of potassium intracellularly
f. Inhaled beta-agonist therapy to promote entry of potassium intracellularly
g. Calcium gluconate or CaCl (1 g) to stabilize the myocardium

41
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

  1. Hyponatremia
A

a. Restriction of enteral free water intake, minimization of hypotonic intravenous solutions including those containing dextrose
b. Hypertonic saline is rarely necessary in AKI. Vasopressin antagonists are generally not needed.

42
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

  1. Volume overload
A

a. Salt and water restriction
b. Diuretics
c. Ultrafiltration

43
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

  1. Nephrotoxin-specific
    a. Rhabdomyolysis:
    b. Tumor lysis syndrome:
A

a. Rhabdomyolysis: aggressive intravenous fluids; consider forced alkaline
diuresis
b. Tumor lysis syndrome: aggressive intravenous fluids and allopurinol
or rasburicase

44
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Metabolic acidosis

A

a. Sodium bicarbonate (if pH <7.2 to keep serum bicarbonate >15 mmol/L)
b. Administration of other bases, e.g., THAM
c. Renal replacement therapy

45
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Hyperphosphatemia

A

a. Restriction of dietary phosphate intake
b. Phosphate binding agents (calcium acetate, sevelamer hydrochloride,
aluminum hydroxide—taken with meals)

46
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Hypocalcemia

A

Calcium carbonate or calcium gluconate if symptomatic

47
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Hypermagnesemia

A

Discontinue Mg?* containing antacids

48
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Hyperuricemia

A

Acute treatment is usually not required except in the setting of tumor
lysis syndrome

49
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Nutrition

A

Sufficient protein and calorie intake (20-30 kcal/kg per day) to avoid negative nitrogen balance. Nutrition should be provided via the enteral route if possible.

50
Q

MANAGEMENT OF ACUTE KIDNEY INJURY

Drug dosing

A

a. Careful attention to dosages and frequency of administration of
drugs, adjustment for degree of renal failure
b. Note that serum creatinine conc. may overestimate renal function in the non-steady state characteristic of patients with AKI

IM NEPHRO (7 decks)

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