Acute Kidney Injury Flashcards
ATN is used to describe
a clinical situation in which there is adequate renal perfusion to largely maintain tubular integrity, but not to sustain glomerular filtration.
AKI is divided into 3 mainly
Prerenal — as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons
Intrinsic — in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage
Postrenal — from obstruction to the passage of urine.
Oliguria is
defined as a daily urine volume of less than 400 mL/d
Anuria is defined as
a urine output of less than 100 mL/d
Examples of causes of prerenal AKI
Volume loss from GI, renal,
cutaneous losses (eg, burns, Stevens-Johnson syndrome)
internal or external hemorrhage
decreased renal perfusion in patients
with heart failure or shock (eg, sepsis, anaphylaxis).
Hepatorenal syndrome
Renal losses (diuretics, polyuria) GI losses (vomiting, diarrhea)
Pancreatitis
Decreased cardiac output Heart failure Pulmonary embolus Acute myocardial infarction Severe valvular disease Abdominal compartment syndrome (tense ascites) Systemic vasodilation Sepsis Anaphylaxis Anesthetics Drug overdose Afferent arteriolar vasoconstriction Hypercalcemia Drugs (NSAIDs, amphotericin B, calcineurin inhibitors, norepinephrine, radiocontrast agents) syndrome
Efferent arteriolar vasodilation – ACEIs or ARBs
Examples of renL causes of AKI
ATN ( isosthenuria)
Rapidly progressing glomerulonephritis ( glomerulo crescents found on ultrasound )
Vascular (large and small vessel)
Renal artery obstruction (thrombosis, emboli, dissection, vasculitis)
Renal vein obstruction (thrombosis)
Microangiopathy (TTP, hemolytic uremic syndrome [HUS], DIC,
preeclampsia)
Malignant hypertension
Scleroderma
renal crisis Transplant rejection
Atheroembolic disease
Glomerular
(Goodpasture syndrome, ANCA associated GN , immune complex GN e.g lupus , postinfection)
Acute interstitial nephritis (
Drugs (penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, indinavir, mesalamine, sulfonamides)
Infection (pyelonephritis, viral nephritides)
Systemic disease (Sj ö gren syndrome, sarcoid, lupus, lymphoma, leukemia, tubulonephritis, uveitis)))
What is isosthenuria ?
A physiologic hallmark of ATN is a failure to maximally dilute or concentrate urine
diagnostic clue in distinguishing prerenal from intrinsic renal disease?
in prerenal azotemia, urine osmolality is typically more than 500 mOsm/kg, whereas in intrinsic renal disease, urine osmolality is less than 300 mOsm/kg.
Causes of post renal AKI
Stones stricture; and intraluminal, extraluminal, or intramural tumors Prostrate enlargement( BPH) Cancer of prostrate Neurogenic bladder
Abrupt
anuria suggests
acute urinary obstruction, acute and severe glomerulonephritis, or
embolic renal artery occlusion
People with the following comorbid conditions are at a higher risk for
developing AKI:
Hypertension Diabetes Congestive cardiac failure Multiple myeloma Chronic infection Myeloproliferative syndrome
Medications associated with ATN
NSAIDS Aminoglycosides ACEIs ARB Amphotericin B Cisplastin Iodinated contrast Pentamidine
AKI is
diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria.
AKI based on AKIN criteria
Rapid time course (less than 48 hours)
Reduction of kidney function
Rise in serum creatinine
Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μmol/l) Percentage
increase in serum creatinine of ≥50%
Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours
Treatment of AKI
Fluid rescuacitation
Loop diuretics
Nutritional support
