Flashcards in 16 ) Acute kidney injury Deck (10)
prerenal acute kidney injury etiology ?
any condition leading to decreased renal perfusion
Volume depletion: e.g., hemorrhage, vomiting, diarrhea,
Decreased circulating volume: e.g., hepatorenal syndrome, cirrhosis, liver failure, nephrotic syndrome,
Hypotension: e.g., sepsis, dehydration, cardiogenic shock (decreased cardiac output)
Renal artery stenosis
Drugs affecting glomerular perfusion: e.g., cyclosporine,
intrinsic acute kidney injury etiology ?
any disease that leads to severe direct kidney damage.
Acute tubular necrosis (causes ∼ 85% of intrinsic AKIs): most commonly caused by sepsis, infection, ischemia
Glomerulonephritis (e.g., rapidly progressive glomerulonephritis
Hemolytic uremic syndrome (HUS)
Thrombotic thrombocytopenic purpura
acute tubulointerstitial nephritis
what is the etiology of post renal acute kidney injury ?
any condition that results in bilateral obstruction of urinary flow
Congenital malformations posterior urethral valves
Benign prostatic hyperplasia (BPH)
neurogenic badder - MS
what are the 4 phases of AKI ? !
Initiating event (kidney injury)
= hours to days
Oliguric or anuric phase (1-3wks)
oliguria = < 400 mL per 24 hours
anurea = < 50 ml/24 hrs = anuria
complication = pulmonary edema , hyperkalemia , metabolic acidosis , asterisks
- 2 wks
Generally, the glomeruli recover faster than the tubular system,
Glomerular filtration returns to normal, which increases urine production (polyuria), while tubular reabsorption remains disturbed.
recovery phase = months to years
Kidney function and urine production normalize
clinical features of AKI ?
Oliguria or anuria
Signs of volume depletion
(in prerenal AKI caused by volume loss)
Orthostatic or frank hypotension and tachycardia
Reduced skin turgor
Signs of fluid overload
Shortness of breath
Signs of uremia
decreased alertness and confusion
Signs of renal obstruction (in postrenal AKI)
Pain over the bladder or flanks
In severe cases: seizures or coma
acute tubular necrosis usually take place where ?
straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb)
= most susceptible to ischemic changes
etiology of acute tubular necrosis ?
Ischemic: Injury occurs secondary to decreased renal blood flow:
Injury occurs directly due to nephrotoxic substances.
Medication: aminoglycosides, cisplatin, amphotericin,
Myoglobinuria due to rhabdomyolysis (crush syndrome)
diagnosis of tubular necrosis ?
Blood findings: azotemia, hyperkalemia, and metabolic acidosis
↑ Fractional excretion of sodium (FENa)
Muddy brown granular casts
Epithelial cell casts
Free renal tubular epithelial cells (due to denudation of the tubular basement membrane)
diagnosis of AKI
serum creatinine increase by 0.3mg/dl within 48hr
urine output less than 0.5 ml/kg/h for 6-12hr
serum creatinine 2-2.9 times higher than baseline
urine output less that 0.5ml/kg/hr for more than 12 hrs
more than or equal 3 times higher
urine output less than 0.3ml/kg/hr for or at 24hrs
Elevated serum creatinine concentration
Serum BUN:creatinine ratio > 20:1
Low urine sodium concentration (< 20 mEq/L)
Low fractional excretion of sodium (FeNa < 1%)
High urine osmolality (> 500 mosm/kg) and specific gravity (> 1.010)
Elevated serum creatinine concentration and rapidly rising serum creatinine level
BUN:creatinine ratio < 15:1
metabolic acidosis, hyperphosphatemia, hypocalcemia,
hyperuricemia, and/or dyslipidemia
anemia - due to decreased EPO
Renal tubular epithelial cells or granular, muddy brown, or pigmented casts
Urine dipstick is positive for blood but negative for RBCs in rhabdomyolysis
Elevated serum creatinine concentration in bilateral obstruction
how you test fo rtsones and blocks