May 3, 2016 - Acute Tubular Necrosis Flashcards
Insults Leading to ATN
- Ischemia
- Toxins
Ischemia and ATN
Ischemia is a big cause of ATN.
Can be caused by hypotension, sepsis, peri/post operative (low blood supply after surgery), heart failure, and drugs.
Toxins and ATN
Toxins can be exogenous such as drugs. May be radio contrast dyes, aminoglycosides, cisplatin, and amphotericin B.
Endogenous toxins are usually pigments such as hemoglobin and myoglobin.
Phases of ATN
- Injury phase (changes in hemodynamics and cell injury)
- Maintenance phase (impaired renal function)
- Recovery phase (proliferation and repopulation)
Clinical Presentation of ATN
Usually occurs in patients already in the hospital.
First recognized by decreased urine output, followed by a rise in serum creatinine.
Tubular Casts
When cells plug up the nephron and form a cast around the tubule. These can later be passed in the urine.
Tubuloglomerular Feedback
Abnormal ultrafiltrate is detected by the macula densa which signals the afferent arteriole to vasoconstrict, essentially shutting down a faulty nephron.
In ATN, much of the kidney completely shuts down and GFR drops significantly or completely to 0.
Diagnosis of ATN
Blood
Protein (<1g / day)
Casts
Urine Na usually > 40
FE Na > 2% as the tubules are unable to conserve Na
Pre-Renal Failure vs ATN
Pre-renal failure the kidney is intrinsically normal and is quickly reversible, the urine is bland, urine osmolality is high, FENa < 1%, urine Na usually <10
ATN the kidney is intrinsically abnormal and is slowly reversible, urine is not bland, urine osmolality same as the plasma, FENa > 1% (usually >2%), urine Na is usually >40
ATN Management
Supportive care
Prevention is critical
Indications for Hemodialysis
A - acidosis
E - electrolyte abnormalities
I - intotoxins
O - volume overload
U - uremia
