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17 Acute Kidney Injury Flashcards

1
Q

Definitions

  • Acute Kidney Injury (AKI)
  • Acute Renal Failure (ARF)
  • Azotemia
  • Uremia
  • Oliguria
  • Anuria
A
  • Acute Kidney Injury (AKI)
    • Loss of renal function, as assessed by GFR, over a period of hours to days
    • Hallmark: retention of nitrogenous waste products in the blood
      • Often, but not always, accompanied by a reduction in urine volume
  • Acute Renal Failure (ARF)
    • Older term for AKI
    • Now, severe AKI requiring renal replacement therapy
  • Azotemia
    • Accumulation of nitrogenous waste products (e.g., urea, creatinine) in the blood
  • Uremia
    • Symptomatic renal failure
    • Symptoms: anorexia, nausea, vomiting, muscle cramps, restless legs, sleep disorders, asterixis, mental status changes, seizures, fluid and electrolyte disturbances, anemia, platelet dysfunction and pericarditis
  • Oliguria
    • Low urine volume
    • 24-hour urine volume < 400 to 500 mL
      • Volume of 400 to 500 mL = min urine volume required to excrete the obligate daily solute load at a max urinary conc
  • Anuria
    • Absence of urine
    • 24-hour urine volume < 100 mL.
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2
Q

Manifestations of AKI

  • Primary clinical manifestations
  • Conc of urea & creatinine in AKI
  • Na & water retention
  • K, H, & phosphate excretion
  • Excretion of meds or their metabolites
A
  • Primary clinical manifestations
    • Accumulation of nitrogenous waste products in the blood
      • Esp urea (BUN) & creatinine
    • Initially: accumulation of substances (azotemia) is asymptomatic
    • W/ time: symptoms of renal failure (uremia)
  • Conc of urea & creatinine in AKI
    • Not necessarily in steady state
    • Not possible to estimate GFR from serum concs of these solutes
  • Na & water retention
    • –> expansion of EC volume & volume overload
    • –> edema & pulm vascular congestion or pulm edema
  • K, H, & phosphate excretion
    • Decreased excretion –> hyperkalemia, metabolic acidosis, & hyperphosphatemia
  • Excretion of meds or their metabolites
    • Decreased excretion of meds or their metabolites –> accumulation & toxicity
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3
Q

Differential diagnosis of azoetmia

  • Azotemia
  • Most common cause of azotemia
  • What causes increased plasma urea conc despite preserved GFR
  • What causes increased creatinine conc in the absence of renal failure
A
  • Azotemia
    • Acute elevations of urea/BUN or creatinine
  • Most common cause of azotemia
    • AKI
  • What causes increased plasma urea conc despite preserved GFR
    • Increased urea generation from protein loading
      • Protein is metabolized to urea
    • GI bleeding
      • Endogenous protein load
    • Catabolic steroids (ex. glucocorticoids)
      • Increase protein catabolism
    • Tetracycline antibiotics
      • Inhibit protein synth
  • What causes increased creatinine conc in the absence of renal failure
    • Inhibition of tubular secretion of creatinine by meds (ex. cimetidien or trimethoprim)
    • Interference w/ colorimetric creatinine assays by meds (ex. cefoxitin, flucytosine, or acetoacetate (ketoic states))
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4
Q

Clinical definition & staging of AKI

  • Consensus definition of AKI
  • Staging of AKI
    • Stage 1
      • Increase in serum creatinine
      • Urine output
    • Stage 2
      • Increase in serum creatinine
      • Urine output
    • Stage 3
      • Increase in serum creatinine
      • Urine output
  • AKI vs. CKD vs. AKD
    • AKI
    • CKD
    • AKD
A
  • Consensus definition of AKI
    • Increased serum creatinine by > 0.3 mg/dL within 48 hrs
    • Increased serum creatinine by > 50% within 7 days
    • Urine volume < 0.5 ml/kg per hour for > 6 hrs
  • Staging of AKI
    • Stage 1
      • Increase in serum creatinine: > 0.3 mg/dl or 1.5-2x baseline
      • Urine output: < 0.5 ml/kg per hour for 6-12 hrs
    • Stage 2
      • Increase in serum creatinine: 2-3x baseline
      • Urine output: < 0.5 ml/kg per hour for > 12 hrs
    • Stage 3
      • Increase in serum creatinine: > 3x baseline or > 4 mg/dl or initiation of renal replacement therapy
      • Urine output: < 0.3 ml/kg per hour for > 24 hrs or anuria for > 12 hrs
  • AKI vs. CKD vs. AKD
    • AKI
      • Increase in serum creatinine by > 50% within 7 days
      • Increase in serum creatinine by > 0.3 mg/dl within 2 days
    • CKD
      • GFR < 60 ml/min per 1.73 m2 for < 3 months
    • AKD
      • AKI
        or
      • GFR < 60 ml/min per 1.73 m2 for < 3 months or decrease in GFR by > 35% or an increase serum creatinine by > 50% for < 3 months
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5
Q

Classification of etiologies of AKI

A
  • Prerenal AKI
    • Prerenal azotemia
      • No structural damage
      • Decrease in kidney function is due to hypoperfusion
  • Intrinsic AKI
    • Acute tubular necrosis (ATN)
    • Acute interstitial nephritis (AIN)
    • Acute glomerulonephritis (AGN)
    • Acute vascular syndromes
    • Intratubular obstruction
  • Postrenal AKI
    • Obstructive uropathy
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6
Q 
Prerenal AKI (prerenal azotemia):
Pathophysiology
  • Occurs when…
  • Key aspect
  • Normal response to decreased perfusion
  • Abnormal response to decreased perfusion
  • Tubular Na & urea reabsorption in states of decreased renal perfusion w/ maintained GFR & prerenal azotemia
A
  • Occurs when…
    • Decreased renal perfusion –> decreased GFR
    • Exaggeration of the normal physoilogic response to reductions in renal perfusion
  • Key aspect
    • Absence of histologic changes in the kidney
    • Reduction in renal function is entirely hemodynamically mediated
  • Normal response to decreased perfusion
    • Mediated by AII –> AffA & EffA vasoconstriction
    • Release of vasodilatory prostaglandins –> inhibits AII effect on AffA
    • Net effect: EffA vasoconstriction w/ minimal/no change in AffA tone
      • Maintains glomerular capillayr pressure depsite decreased renal plasma flow
      • Preserves GFR at the expense of increased FF
  • Abnormal response to decreased perfusion
    • Further decreased renal perfusion –> decreased ability to maintain GFR
    • Decrease glomerular capillary pressure –> decreased GFR despite elevated FF
  • Tubular Na & urea reabsorption in states of decreased renal perfusion w/ maintained GFR & prerenal azotemia
    • Increased Na reabsorption –> decreased urine Na
    • Increased urea reabsroption –> increased plasma urea : creatinine ratio
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7
Q 
Prerenal AKI (prerenal azotemia):
Clinical settings in which prerenal AKI occurs
  • True volume
  • Effective blood volume
  • States of renal vasculature
A
  • True volume depletion
  • Decreased effective blood volume
    • CHF
    • Cirrhosis
    • Nephrotic syndrome
    • Sepsis
  • States of renal vasoconstriction
    • Hypercalcemia
    • NSAIDs
      • Inhibit AffA dilation in opposition to AII’s effect
      • Decrease renal plasma flow & glomerular capillary pressure in states associated w/ increased AII production
    • Hepatorenal syndrome
      • Intense renal vasoconstriction w/ advanced liver disease
      • Resembles other forms of prerenal azotemia but doesn’t reverse w/ IV volume expansion
      • Reversal of the liver disease w/ liver transplant (or kidney transplant into a pt w/o liver disease) restores renal function
      • Poor prognosis w/o liver transplant
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8
Q 
Prerenal AKI (prerenal azotemia):
Clinical presentation
  • History
  • Physical exam
    • Typical
    • True volume depletion
    • CHF
    • Liver disease
  • Lab findings
    • BUN : creatinine
    • Urine output
    • Urine osmolality
    • Renal tubular Na reabsorption
    • Urine sediment
A
  • History
    • Acute volume losses (ex. vomiting, diarrhea, acute blood loss)
    • Decompensated CHF, liver disease, or acute infection
    • Diuretic use
    • Changes in weight
    • Thirst
    • Orthostatic symptoms (ex. lightheadedness on standing)
  • Physical exam
    • Typical: HoTN, tachycardia, orthostatic changes, decreased skin turgor, & dry mucous membranes & axillae
    • True volume depletion: not distended neck veins, clear lung fields, minimal/no peripheral edema
    • CHF: pulm rales, S3 cardiac gallop, peripheral edema
    • Liver disease: ascites, peripheral edema
  • Lab findings
    • BUN : creatinine ratio > 20 : 1
      • Passive urea reabsroption from the tubule due to decreased tubular fluid flow rate
    • Oliguria < 500 ml / 24 hrs
      • May be non-oliguric
    • Concentrated urine
      • Urine osmolality > 700 mmol/L
      • Urine specific gravity > 1.020
      • Reflects hemodynamically mediated vasopressin secretion
    • Increased renal tubular Na reabsorption
      • Urine Na < 20 mmol/L
      • Fractoin excretion of Na < 0.01
    • Bland urine sediment
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9
Q 
Prerenal AKI (prerenal azotemia):
Fractional excretion of Na (FE<sub>Na</sub>)
  • FENa
  • Calculation
  • FENa in prerenal states vs. ATN in pts w/ oliguria & AKI
  • Etiologies of FENa < 0.01
A
  • FENa
    • Index of renal tubular Na reabsorption
    • Differentiates b/n etiologies of AKI
  • Calculation
    • FENa = excreted Na / filtered Na
      • Excreted Na = urine Na (UNa) * urine volume (V)
      • Filtered Na = plasma Na (PNa) * GFR
    • FENa = (UNa * V) / (PNa * GFR)
      • GFR = [urine creatinine (UCr) * V] / plasma creatinine (PCr)
    • FENa = (UNa / PNa) / (UCr / PCr)
  • FENa in prerenal states vs. ATN in pts w/ oliguria & AKI
    • Prerenal FENa​ < 0.01
    • ATN FENa > 0.02
  • Etiologies of FENa < 0.01
    • Normal renal function
    • Prerenal azotemia
    • Hepatorenal syndrome
    • Early obstructive uropathy
    • Contrast nephropathy
    • Rhabdomyolysis
    • Acute glomerulonephritis
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10
Q 
Prerenal AKI (prerenal azotemia):
Treatment
  • Primary treatment
  • Discontinue…
  • In pts w/ underlying heart disease
A
  • Primary treatment
    • Correction of volume deficits via administration of crystalloid soln’s
  • Discontinue…
    • Diuretics
    • Meds that alter intrarenal hemodynamics (NSAIDs, ACE-Is, ARBs)
  • In pts w/ underlying heart disease
    • Optimize cardiac function w/ inotropic support &/or vasodilators
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11
Q 
Postrenal AKI (obstructive uropathy):
Definition
  • Results from…
  • Hallmark
  • Upper vs. lower tract obstruction
  • Unilateral upper tract obstruction
  • For upper tract obstruction to cause AKI…
  • Complete vs. partial obstruction
A
  • Results from…
    • Partial or complete obstruction of hte urinary tract b/n the renal pelvis & urethral meatus
  • Hallmark
    • Hydronephrosis (dilation of the renal collecting system)
  • Upper vs. lower tract obstruction
    • Upper: above the urinary bladder (ex. ureters, renal pelvis)
    • Lower: at the bladder outlet or urethra
  • Unilateral upper tract obstruction
    • Hydronephrosis will be present
    • Serum creatinine ill be normal or minimally elevated due to continued function of hte contralateral kidney
  • For upper tract obstruction to cause AKI…
    • Obstruction must be bilateral
    • Unilateral obstruction will only cause AKI if the contralateral kidney is absent or nonfunction
  • Complete vs. partial obstruction
    • Complete –> anuria
    • Partial –> urine flow that’s normal, decreased (oliguria), increased (polyuria), or fluctuating b/n oliguria & polyuria
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12
Q 
Postrenal AKI (obstructive uropathy):
Pathophysiology
  • Initially
  • Later
A
  • Initially
    • Obstruction in the renal collecting system
    • –> increased intratubular pressure in the nephron
    • –> increased hydrostatic pressure in bowman’s space
    • –> increased renal plasma flow –> increased glomerular capillary pressure
    • –> decreased gradient b/n pressures in the glomerular capillary & bowman’s space –> decreased GFR
    • –> initial increased renal plasma flow decreases –> decreased glomerular capillayr pressure –> decreased GFR
  • Later
    • Intratubular pressure returns to normal
    • –> decreased renal plasma flow –> decreased glomerular capillary pressure & GFR
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13
Q 
Postrenal AKI (obstructive uropathy):
Etiologies
  • Upper tract obstruction
    • Intrinsic obstruction
    • Extrinsic obstruction
  • Lower tract obstruction
A
  • Upper tract obstruction
    • Intrinsic obstruction
      • Nephrolithiasis
      • Papillary necrosis
      • Blood clot
      • Transitional cell carcinoma
    • Extrinsic obstruction
      • Retroperitoneal or pelvic malignancy
      • Retroperitoneal adenopathy
      • Retroperitoneal fibrosis
      • Endometriosis
      • Abdominal aortic aneurysm
  • Lower tract obstruction
    • Benign prostatic hypertrophy
    • Prostate cancer
    • Transitional cell carcinoma
    • Urethral stricture
    • Bladder stones
    • Blood clots
    • Neurogenic bladder
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14
Q 
Postrenal AKI (obstructive uropathy):
Clinical presentation
  • History
    • Frequently
    • May present w/
    • Bladder outlet obstruction
    • Upper tract disease
    • Either upper or lower tract disease
    • Important to elicit
  • Physical exam
  • Lab findings
    • BUN : creatinine
    • Urine sediment
    • Urine chemistries
A
  • Hisotry
    • Frequently: no complaints
    • May present w/: anuria, polyuria, widely fluctuating urine volume
    • Bladder outlet obstruction: urinary frequency, urgency, intermittency, hesitancy, nocturia, incomplete voiding
    • Upper tract disease: flank pain (ureteral colic)
    • Either upper or lower tract disease: hematuria
    • Important to elicit: pelvic malignancy, radiation therapy, prostate disease
  • Physical exam
    • Distended bladder palpable as a suprapubic mass
    • Prostatic enlargmeent
    • Pelvic masses
    • Adenopathy
  • Lab findings
    • BUN : creatinine > 20 : 1 (variable)
    • Urine sediment
      • Often unremarkable
      • Microscopic hematuria (w/o RBC casts) may be present
      • Crystaluria may be seen w/ nephrolithiasis
    • Urine chemistries (variable & non-diagnostic)
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15
Q 
Postrenal AKI (obstructive uropathy):
Diagnostic studies
  • Post-void residual bladder volume
  • Radiologic studies
    • Renal ultrasound
    • CT scan
    • Nuclear medicine excretory renogram
    • Retrograde pyelography
    • Antegrade nephrostogram
A
  • Post-void residual bladder volume (lower tract obstruction)
    • Measured by placing a bladder catheter or using an ultrasound device to measure residual bladder volume after having pt void & completely empty bladder
    • Residual bladder volume > 100 ml –> voiding dysfunction
  • Radiologic studies (upper tract obstruction)
    • Renal ultrasound: initial imaging study
    • CT scan: best initial study for kidney stones
    • Nuclear medicine excretory renogram: functional test, used to define if urinary tract dilatoin is due to obstruction
    • Retrograde pyelography: invasive, may be accompanied by placement of ureteral stent for treatment
    • Antegrade nephrostogram: invasive, usually accompanied by placement of percutaneous nephrostomy for treatment
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16
Q 
Postrenal AKI (obstructive uropathy):
Treatment
  • General
  • Lower tract obstruction
  • Upper tract obstruction
  • Post-obstructive diuresis
A
  • General
    • Mechanical relief of obstruction
    • Relieved within 1-2 weeks –> functional recovery is excellent
    • Obstruction present > 4 weeks –> chronic kidney injury is likely
  • Lower tract obstruction
    • Placement of a bladder catheter
  • Upper tract obstruction
    • Placement of ureteral stents or percutaneous nephrostomies
    • Relief of obstruction on one side may recover renal function, but both kidneys need to be decompressed to provide optimal long-term benefit
  • Post-obstructive diuresis
    • May accompany relief of urinary obstruction
    • Pts need to be monitored closely to not deplete volume
      • Often requires IV fluid
    • May be multifactorial resulting from…
      • Excretion of excess salt & water retained during obstruction
      • Urea diuresis as the azotemia resolves
      • Renal salt wasting caused by tubular injury as a result of the obstruction
      • Nephrogenic diabetes insipidus caused by the obstruction
17
Q

Intrinsic AKI:
Acute tubular necrosis:
Etiologies

  • General
  • Ischemic ATN
  • Nephrotoxic ATN
    • Exogenous toxins
    • Endogenous toxins
A
  • General
    • Most common form of intrinsic AKI (85% of cases)
    • Etiology is frequently multifactorial
  • Ischemic ATN
    • Prolonged prerenal azotemia
    • Hypotension
    • Hypovolemic shock
    • Cardiopulmonary arrest
    • Cardiopulmonary bypass
    • Sepsis
  • Nephrotoxic ATN
    • Exogenous toxins (Drug-induced)
      • Radiocontrast agents
      • Aminoglycoside antibiotics
      • Amphotericin B
      • Cisplatinum
      • Acetaminophen
    • Endogenous toxins (Pigment nephropathy)
      • Hemoglobin (intravascular hemolysis)
      • Myoglobin (rhabdomyolysis)
18
Q

Intrinsic AKI:
Acute tubular necrosis:
Pathophysiology

  • Animal vs. human pathology
  • At the cellular level, nephrotoxic or ischemic injury –>
  • Ultimately…
  • Loss of GFR is due to…
  • Recovery of renal function
A
  • Animal vs. human pathology
    • Animals: widespread cell necrosis
    • Humans: patchy cell necrosis that doesn’t necessarily correlate w/ severity
  • At the cellular level, nephrotoxic or ischemic injury –>
    • Loss of normal tubular epithelial cell morphology
    • –> loss of normal apical brush border
    • –> loss of cellular polarity (differentiation b/n apical & basolateral membrane domains)
      • Migration of transport proteins usually restricted to the basolateral membrane (ex. Na/K ATPase) into the apical membrane or vice versa (ex. Na/H exchanger)
    • Loss of epithelial cell polarity disrupts tubular transports
    • Also renal vasoconstriction & endothelial cell injury
  • Ultimately…
    • Epithelial cel ldeath occurs due to necrosis & apoptosis
    • Viable & dead cells slough into the tubular lumen –> areas of denuded tubular BM
    • Sloughed cells & debris form epithelial cell casts which may obstruct the tubular lumen
  • Loss of GFR is due to…
    • Renal vasoconstriction
    • Tubular obstruction from sloughed debris
    • Back-leak of glomerular ultrafiltrate across teh denuded tubular BM
  • Recovery of renal function
    • Remaining viable epithelial cells dedifferentiate, proliferate, & spread across the denuded BM
    • Re-differentiation & re-establishment of cell polarity
19
Q

Intrinsic AKI:
Acute tubular necrosis:
4 phases of endothelial injury & activation of inflammatory pathways

A
  • Initiation
    • Acute ischemic event
  • Extension
    • Initiating event has resolved
    • Endothelial injury, vasoconstriciton, & activation of inflammatory mediators –> continued tubular injury
  • Maintenance
    • Continued ifnlammation
    • Resolution of endothelial injury
    • Initiation of tubular repair
    • Migration of epitehlial cells over denuded BM
  • Recovery
    • Proliferatoin & re-differentiatoin of epithelial cells
    • Recovery of GFR toward normal
20
Q

Intrinsic AKI:
Acute tubular necrosis:
Clinical presentation

  • History
  • Physical exam
  • Lab adata
    • BUN : creatinine
    • Urine volume
    • Urine osmolality
    • Renal Na
    • Urine sediment
A
  • History
    • Acute illnesses
    • Meds
    • Exposure to other nephrotoxins
    • Episodes of HoTN
  • Physical exam
    • Hemodynamic status
    • Volume status
    • Features of associated illness
  • Lab data
    • BUN : creatinine < 10 : 1
    • Urine volume
      • Oliguric or non-oliguric
    • Isothenuric urine
      • Urien osmolality ≈ 300 mmol/L
      • Specific gravity ≈ 1.010
    • Renal Na wasting
      • Urine Na > 40 mmol/L
      • FENa > 0.02
    • Urine sediment
      • Tubular epithelial cells & epithelial cell casts
      • Granular casts (“muddy” brown casts)
21
Q

Intrinsic AKI:
Acute tubular necrosis:
Treatment & prognosis

  • Treatment
  • Prognosis
    • Non-oliguric
    • Overall
    • Recovery of renal function in survivors
    • Episodes of ATN
A
  • Treatment
    • Supportive
      • No pharmacologic therapy
    • Acute dialysis or hemofiltration may support pts w/ severe renal injury & organ failure
      • Volume overload, metabolic acidosis, hyperkalemia, uremic syndrome (pericarditis, encephalopathy), azotemia
  • Prognosis
    • Non-oliguric: better prognosis than oliguric due to lesser degree of actual cellular injury
    • Overall: mortality ≈50%
    • Recovery of renal function in survivors: 65-90%
      • Not back to prior baseline
      • Recovery occurs within 2-4 weeks of onset
    • Episodes of ATN
      • May contribute to development of progression of CKD
      • Associated w/ development of end-stage kidney disease
22
Q

Intrinsic AKI:
Acute interstitial nephritis:
General & pathology

  • Aka
  • General
  • Classic presentation
  • Pathology
A
  • Aka
    • Allergic interstitial nephritis
  • General
    • Immune mediated form of AKI
    • Lymphocytic infiltration of interstitium
    • Accounts for 5-10% of intrinsic AKI cases
  • Classic presentation (30% of cases)
    • AKI w/ triad of fever, rash, & eosinophilia
  • Pathology
    • Lymphocytic infiltrate
    • Frequently accompanied by eosinophils
23
Q

Intrinsic AKI:
Acute interstitial nephritis:
Etiologies

  • Drug induced
  • Infection-related
  • Systemic diseases
  • Other
A
  • Drug induced (most common)
    • Penicillins
    • Cephalosporins
    • Sulfonamides
    • Rifampin
    • Phenytoin
    • Furosemide
      Proton pump inhibitors
    • NSAIDs (may have atypical presentation with nephrotic range proteinuria and absence of eosinophilia)
  • Infection-related
    • Bacterial
    • Viral
    • Rickettsial
    • Tuberculosis
  • Systemic diseases
    • Systemic lupus erythematosus
    • Sarcoidosis
    • Sjögren’s syndrome
    • Tubulointerstitial nephritis and uveitis (TIN)
  • Other
    • Malignancy
    • Idiopathic
24
Q

Intrinsic AKI:
Acute interstitial nephritis:
Clinical presentation

  • History
  • Physical exam
  • Lab findings
  • Urine findings
A
  • History
    • Preceding illness or drug exposure
  • Physcial exam
    • Fever
    • Rash
  • Lab findings
    • Eosinophilia
  • Urine findings
    • Non-nephrotic proteinuria
    • Hematuria
    • Pyuria
    • WBC casts
    • Eosinophiluria
      • Non-specific finding
        • Don’t need to see them to make the diagnosis
        • Absence doesn’t rule out the diagnosis
      • Positive predictive value of ~ 50%
      • Negative predictive value of > 90%
25
Q

Intrinsic AKI:
Acute interstitial nephritis:
Treatment

  • Key treatment
  • Critical aspect of treatment
  • Value of glucocorticoid treatment
A
  • Key treatment
    • Remove the underlying tirgger for the immune process
  • Critical aspect of treatment
    • Discontinuation of the offending drug
    • Treatment of the underlying infection
    • Treatment of the underlying systemic disease
  • Value of glucocorticoid treatment
    • Uncertain
    • May be used in pts who fail to respond to conservative therapy
26
Q

Intrinsic AKI:
Acute glomerulonephritis

  • General
  • Presentation
  • Exact diagnosis requires…
  • Etiologies
A
  • General
    • Accounts for 5-10% of intrinsic AKI cases
  • Presentation
    • Nephritic urine sediment
    • Hematuria
    • RBC casts
  • Exact diagnosis requires…
    • Kidney biopsy
  • Etiologies
    • Poststreptococcal glomerulonephritis
    • Postinfectious glomerulonephritis
    • Endocarditis-associated glomerulonephritis
    • Systemic vasculitis
    • Thrombotic microangiopathy
      • Hemolytic-uremic syndrome (HUS)
      • Thrombotic thrombocytopenic purpura (TTP)
    • Rapidly progressive glomerulonephritis (RPGN)
27
Q

Intrinsic AKI:
Acute vascular syndromes

  • General
  • Examples –> renal infarction
  • Irreversible AKI
  • Atheroembolic disease
  • Atheroembolism
  • Cutaneous findings
  • Initial shower of emboli
  • Clinical course of kidney disease
  • Pathognomonic finding
  • Atheroembolic disease frequently occurs after…
A
  • General
    • Uncommon forms of AKI
  • Examples –> renal infarction
    • Renal artery thromboembolism
    • Renal artery dissection
    • Renal vein thrombosis
  • Irreversible AKI
    • Bilateral infarction
    • Infarction affects a single functioning kidney
  • Atheroembolic disease
    • Aka cholesterol embolism
    • Results from rupture of atheromatous plaques in the aorta w/ embolization of atheromatous material into distal arterioles
    • May affect many organ systems (ex. GI tract, muscle & skin, kidney)
  • Cutaneous findings
    • Livedo reticularis
    • Micro-infarcts of the digits (blue-toe syndrome)
  • Initial shower of emboli
    • Usually doesn’t result in vascular occlusions
    • Triggers a secondary inflammatory response –> fibrosis
  • Clinical course of kidney disease
    • Frequently sub-acute (days to weeks) rather than acute
  • Pathognomonic finding
    • Biconcave, needle-shaped clefts on histologic exam of blood vessels
    • Result from the dissolutoin of the cholesterol crystals int eh emboli during tissue fixation
  • Atheroembolic disease frequently occurs after…
    • Antiographic procedures
    • Frequently needs to be differentiated fromteh more common radiocontrast-inducted ATN
28
Q

Intrinsic AKI:
Intratubular obstruction

  • General
    • May result from…
A
  • General
    • Uncommon form of AKI
  • May result from…
    • Crystaline material
      • Uric acid in tumor lysis syndrome
      • Ca oxylate following ethylene glycol ingestion or drug crystals (ex. acyclovir)
      • Meds (ex. acyclovir)
    • Proteinaceous material
      • Light chain cast nephropathy in multiple myeloma (ex. Bence-Jones protein deposition)
29
Q

How to get AKI in multiple myeloma

A
  • Light chain cast nephropathy (myeloma kidney)
  • Hypercalcemic nephropathy
  • Acute uric acid nephropathy
  • Plasma cell infiltration fo the kidney
  • Hyperviscosity syndrome
  • AL amyloidosis
  • Light-chain deposition disease
  • Proximal tubular dysfunction (acquired from Fanconi’s syndrome)
30
Q

Diagnostic evaluation of a pt w/ AKI

  • Prerenal AKI
    • BUN : Cr
    • UNa (mmol/L)
    • FENa
    • Urine sediment
  • Postrenal AKI
    • BUN : Cr
    • UNa (mmol/L)
    • FENa
    • Urine sediment
  • Intrinsic AKI
    • ATN
      • BUN : Cr
      • UNa (mmol/L)
      • FENa
      • Urine sediment
    • AIN
      • BUN : Cr
      • UNa (mmol/L)
      • FENa
      • Urine sediment
    • AGN
      • BUN : Cr
      • UNa (mmol/L)
      • FENa
      • Urine sediment
    • Vascular
      • BUN : Cr
      • UNa (mmol/L)
      • FENa
      • Urine sediment
    • Intratubular obstruction
      • BUN : Cr
      • UNa (mmol/L)
      • FENa
      • Urine sediment
A
  • Prerenal AKI
    • BUN : Cr > 20 : 1
    • UNa (mmol/L) < 20
    • FENa < 0.01
    • Urine sediment: normal
  • Postrenal AKI
    • BUN : Cr > 20 : 1
    • UNa (mmol/L) > 20
    • FENa: variable
    • Urine sediment: normal or RBCs
  • Intrinsic AKI
    • ATN
      • BUN : Cr < 10 : 1
      • UNa (mmol/L) > 40
      • FENa > 2%
      • Urine sediment: muddy brown casts, tubular epithelial cells
    • AIN
      • BUN : Cr < 20 : 1
      • UNa (mmol/L) > 20
      • FENa > 1%
      • Urine sediment: WBCs, WBC casts, RBCs, eosinophils
    • AGN
      • BUN : Cr: variable
      • UNa (mmol/L) < 40
      • FENa < 1%
      • Urine sediment: RBCs, RBC casts
    • Vascular
      • BUN : Cr: variable
      • UNa (mmol/L) > 20
      • FENa: variable
      • Urine sediment: normal or RBCs, eosinophils in atheroembolic disease
    • Intratubular obstruction
      • BUN : Cr: variable
      • UNa (mmol/L): variable
      • FENa: variable
      • Urine sediment: crystals or presence of Ig light chains (Bence-Jones proteins) in the urine
31
Q

Management of AKI

  • Prerenal azotemia
  • Obstructive uropathy
  • Intrinsic AKI
    • Since the majority of etiologies have no specific treatment, the major focus of care is on general supportive management, including…
    • Indications for renal replacement therapy in acute kidney injury include…
A
  • Prerenal azotemia (prerenal AKI)
    • Volume repletion
    • Discontinue diuretics
    • Discontinue other offending drugs (NSAIDs, ACEI, ARBs)
    • Inotropic support for cardiac dysfunction
  • Obstructive uropathy (postrenal AKI)
    • Bladder catheterization for lower tract obstruction
    • Percutaneous nephrostomies or ureteral stents for upper tract obstruction
    • Fluid management during post-operative diuresis
  • Intrinsic AKI
    • Since the majority of etiologies have no specific treatment, the major focus of care is on general supportive management, including
      • Fluid management and diuretics to avoid volume overload
      • Diuretics
      • Bicarbonate supplementation to treat metabolic acidosis
      • Potassium restriction to minimize the risk of hyperkalemia
      • Phosphate restriction and phosphate binders to treat hyperphosphatemia
      • Adjustment of drug dosing to prevent toxicity due to decreased clearance
      • Nutrition support
    • Indications for renal replacement therapy (dialysis & hemofiltration) in AKI include
      • Volume overload unresponsive to diuretic therapy
      • Metabolic acidosis unresponsive to alkali replacement
      • Persistent hyperkalemia
      • Overt uremic symptoms such as pericarditis and encephalopathy
      • Severe azotemia (BUN > 80-100 mg/dL) in the absence of uremic symptoms

Renal (24 decks)

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