Transcript Acute Kidney Injury

Acute Kidney Injury
SUSAN BUDNICK, MD
What is an Acute Kidney Injury?
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AKI is a heterogeneous group of conditions that are all characterized by
an acute impairment of renal function, causing an increase in waste
products normally filtered by the kidneys
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All of these conditions are associated with rise in serum creatinine, BUN
and (sometimes) decreased urine output (UOP).
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Divided into 3 broad categories: Prerenal, intrinsic renal and postrenal
Why do AKIs matter?
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AKI is associated with increased risk of mortality, both while in-hospital and
long term.
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Patients with AKI are more likely to die prematurely after hospitalization, even if
renal function returns to baseline.
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AKI is associated with longer hospital stays and increased cost of stay

Patients with severe AKI, requiring CRRT or HD are at a high risk of
developing progressive CKD and 10% eventually developed ESRD
requiring HD.
How is AKI defined?
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A rise in serum creatinine of at least 0.3mg.dL within 4 hours or 50%
increase from baseline within 1 week
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OR
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A decrease in UOP to <0.5ml/kg lasting longer than 6 hours
The RIFLE criteria for kidney injury
The RIFLE criteria for kidney injury
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The RIFLE classification is based on Creatinine and UOP.
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It includes 3 classes of AKI severity (Risk, Injury and Failure) and 2 classes of
post-AKI outcomes (loss of function and ESRD).
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If UOP and creatinine differ in AKI severity, use the criteria that gives the
most severe diagnosis/prognosis.
Etiologies of AKI
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Generally divided into 3 categories:
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Prerenal: The most common form
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Intrinsic renal: Either due to direct damage by nephrotoxins or secondary to
ATN, ischemia or sepsis (etc.)
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Postrenal/Obstructive: Obstruction causing increased retrograde hydrostatic
pressure that interferes with GFR.
Prerenal Azotemia
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Decreased renal blood flow which causes insufficient hydrostatic pressure
for normal GFR
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Can be due to hypotension, decreased cardiac output and medications
that interfere with autoregulation of glomerular blood flow.
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Can be rapidly reversed with improvement in RBF
Prerenal Azotemia
Remember this?
Common medications
(NSAIDs, ACEi/ARBs)
can affect RBF by
decreasing
autoregulatory functions
Intrinsic Renal Parenchymal Disease

Causes are numerous…

TTP/HUS

ATN (ischemic or toxic)
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HTN
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Sepsis
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Ischemia- can progress from
prerenal azotemia
Endogenous toxins (Hb, myoglobin,
uric acid, light chain proteins)
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Nephrotoxic agents
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DIC
Postrenal Obstruction
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Can occur anywhere from the renal pelvis to the tip of the urethra
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AKI occurs when either both of the kidneys are obstructed or the
unobstructed kidney is dysfunctional.
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Causes are numerous: BPH, neurogenic bladder, anticholinergics,
intraluminal calculi and clots, and compression/damage to normal
structures.
Diagnostic evaluation
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Don’t forget your History and Physical! It can give important clues to the
etiology of AKI.
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Hypotension?
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History of vomiting and diarrhea?
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New medications?
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Dry mucous membranes?
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Do they appear septic?
Patterns of Creatinine Rise
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Contrast induced Nephropathy: Rise in SCr within 24-48 hrs. Peak within 3-5
days and back to baseline in 5-7 days.
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Prerenal azotemia: A rise in creatinine that downtrend when volume status
is corrected.
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Atheroembolic disease: Typically a subacute rise in SCr (Can be rapid rise
and severe in some cases).
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Nephrotoxic agents like aminoglycosides, carboplatins: Rise in SCr delayed
3-14 days after exposure
Diagnostic workup?
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BUN:Creatinine greater than 20:1 suggest prerenal etiology
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Urine electrolytes:
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𝑈𝑁𝑎 𝑥𝑃𝐶𝑟
𝐹𝑒𝑁𝑎 = 𝑃𝑁𝑎 𝑥 𝑈𝐶𝑟
<1% prerenal, >2-3% intrinsic damage, >4% obstructive
Urine sodium is the poor man’s FeNa. If <25, likely retaining sodium due to hypovolemia
Renal Ultrasound:
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Size of the Kidneys:
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Normal sized kidneys are expected in AKI
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Kidneys may be nomal size in CKD due to diabetic nephropathy, HIV-associated nephropathy, or infiltrative diseases.
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Small, shrunken kidneys are suggestive of CKD
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Enlarged kidneys in a patient with AKI suggests the possibility of acute interstitial nephritis
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May show obstruction and dilation of the collecting system and hydroureteronephrosis
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Dopplers may be useful in ruling out renal vein thrombi
Kidney Biopsy
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A biopsy can give diagnostic information when prerenal, postrenal,
ischemia and nephrotoxic etiologies are unlikely.
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Useful in diagnosing glomerulonephritis, vasculitis, interstitial nephritis,
myeloma kidney, HUS and TTP, and allograft dysfunction.
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This procedure carries a risk of serious bleeding, especially when patients
are coagulopathic.
Complications of AKI
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Hypervolemia
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Uremia
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Uremia poses little direct toxicity at levels below 100 mg/dL.
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At higher concentrations can cause mental status changes and bleeding
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Electrolyte abnormalities including hyperkalemia, hyponatremia,
hyperuricemia, hyperphosphatemia, hypocalcemia, and
hypomagnesemia
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Metabolic acidosis
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Cardiac complications can include arrhythmias, pericarditis, and
pericardial effusion
Indications for Emergent Dialysis
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AEIOU mnemonic:
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Acidemia: Persistent academia that is either non-responsive to bicarb or when
giving bicarb would result in volume overload
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Electrolyte abnormalities such as hyperkalemia in setting of EKG changes
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Intoxications: Salicyclic acid, lithium, isopropanol, magnesium and ethylene
glycol
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Overload
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Uremia causing complications such as pericarditis, encephalopathy, bleeding
Treatment of AKI
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Treatment depends on the etiology and focuses on treating underlying
insult
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For instance, in setting of post-renal obstruction, relieving the obstruction or in
prerenal etiologies such as hypovolemia, correcting the hypovolemia.
Patients may need medications renally dose in the setting of AKI.
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Avoid NSAIDs and consider holding ACEi/ARBs in the setting of acute AKI