Download Acute Kidney Injury

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Prenatal testing wikipedia , lookup

Forensic epidemiology wikipedia , lookup

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