Acute Kidney Injury - Regner Flashcards
What criteria are used to diagnose acute kidney injury?
Increase in serum creatinine (+0.3 mg/dL or a 50% increase)
Reduction in urine output to <500mL/day
*These must occur abruptly (within 48hrs)
Distinguish between azotemia and uremia.
Azotemia is an elevation of nitrogenous products normally filtered by the kidney.
Uremia is the clinical syndrome caused by this accumulation.
How is GFR related to serum creatinine? To creatinine clearance?
Why is creatinine clearance used to estimate GFR?
Inversely related to serum creatinine, directly related to creatinine clearance.
Creatinine is produced at a constant rate over time. It is freely filtered and not reabsorbed (but it is secreted slightly; therefore Inulin is more accurate)
Why is BUN less precise than creatinine in predicting GFR?
Nitrogen levels can be influenced by many factors, including protein intake, protein catabolism, tubular reabsorption, and presumably many other factors.
What factors influence the autoregulation of GFR & RBF?
How does this autoregulation actually occur?
Responses such as the myogenic reflex as well as tubuloglomerular feedback.
Autoregulation occurs through selective constriction or dilation of the efferent and afferent arterioles (via PGs or AngII, for example) to influence GFR.
In each of the following glomerular conditions, state whether GFR and RBF increase, decrease, or remain the same.
Dilation of afferent arteriole / Dilation of efferent arteriole
Constriction of afferent arteriole / Constriction of efferent arteriole;
Dilation of afferent arteriole / Constriction of efferent arteriole
Construction of afferent arteriole / Dilation of efferent arteriole
RBF++, GFR++.
RBF–, GFR–.
RBF–, GFR++
RBF–, GFR–
Under what conditions is GFR autoregulation impaired?
In hypertension, with age, chronic kidney disease, and use of NSAIDs and/or RAS blockers.
Are uremic signs generally present in AKI?
What are the most common forms of AKI?
How is the prognosis?
No, uremia is usually absent.
Most common forms are intrarenal (usually ATN which has ischemic or toxic etiologies), then pre-renal.
AKI is usually reversible, but correlates with high mortality.
What is the etiology of a pre-renal AKI?
What are the lab findings in a pre-renal AKI?
Decreased renal perfusion (eg heart failure, volum depletion).
Elevation of BUN (BUN:Cr > 20), FENa < 1%. This indicates that there is no tubular defect; the nephron is still largely working.
What are some possible causes of intrarenal AKI?
ATN, inflammation, thromboembolism, neoplasms…
ATN most common by far.
How does endothelial dysfunction contribute to ATN?
Why would intratubular pressure increase in ATN?
Endothelial dysfunction can lead to impaired autoregulation (failure of production of vasodilatory factors)
Necrosed tubular cells fall into the tubular lumen and cause obstruction.
Describe the morphological features of a nephron under ATN.
Dilation of the tubules, loss of epithelium & brush border, granular casts, and mitotic figures.
Why is it expected that Oliguria would persist for 2-3 weeks following a bout of ATN?
Regeneration of the tubule cells takes time, as they must undergo dedifferentiation, proliferation and migration to repair the kidney.
What are the lab findings regarding ATN?
FENa > 2% (failure of sodium reabsorption), BUN:Cr < 15.
Urinalysis reveals presence of muddy brown granular casts.
What pathology should be considered in any patient with oliguria?
What changes can this condition cause to the kidneys?
Oliguric patients should be considered for post-renal AKI.
May result in hydronephrosis (dilation of the renal calyces).
What type of kidney injury is shown here?
This is Acute Tubular Necrosis; observe the loss of epithelial border & cells, as well as the obstruction of tubules by anucleate tubular cell debris.
