Acute Renal Failure Flashcards
What is acute kidney injury?
an abrupt (within 48 hrs) reduction in kidney function currently defined as an absolute increase in serum creatinine of either 0.3 mg/dl or 50% increase, or reduction in urine output (documented oliguria of 0.5 ml/kg per hour for 6 hours).
What is the impact of the magnitude of increase in serum creatinine on mortality?
as serum creatinine doubles, triples, or quadruples, mortality increases exponentially!
*** What is important to remember about rises in serum creatinine?
It will not begin to rise until you have a significant loss in your GFR!!!
What are some important conditions that will cause an increase in levels of urea or creatinine in the blood without decreasing GFR?
- bactrim (sulfamethoxazole-trimethoprim), which decreases tubular secretion of creatinine (remember this is why creatinine isn’t as good as inulin bc it can also be secreted).
- cephalosporins
- ketones (DKA)
- rhabdomyolysis
- Excessive protein intake, amino acid infusion, tetracyclines, or corticosteroids will increase BUN. Not as important as creatinine bc too many factors will increase BUN without affecting GFR.
*** What are the 5 etiologies of acute kidney injury (AKI)?
- pre-renal azotemia (decreased blood flow to kidneys; decreased effective circulating volume).
- acute tubular necrosis
- obstructive uropathy
- acute glomerulonephritis
- vasomotor nephropathy
** What are some causes of renal hypoperfusion (prerenal azotemia) associated with ARF?
- intravascular volume depletion (trauma, hemorrhage, hypoalbuminemia…).
- decreased cardiac output (CHF, pts on ventilators leading to pulmonary hypertension).
- increased renal/systemic vascular resistance ratio (NSAIDs, norepinephrine…).
Will acute tubular necrosis often be non-oliguric (aka normal urine production)?
YES so be wary
In postrenal azotemia (obstructive uropathy), what do the size of the casts indicate?
- thin casts= early and more acute
- broad casts= late and chronic
Will unilateral hydronephrosis have an impact on renal function?
NO and will NOT cause a rise in serum creatinine.
*If a pt does have this and their creatinine does rise, then they definitely have CKD.
** What is vasomotor nephropathy?
- aberration in afferent or efferent arteriole (hemodynamic compromise).
- NSAIDs (decrease vasodilating prostaglandins= decreased renal blood flow), ACE inhibitors or ARBs (decreased intrarenal angiotensin II= decreased intraglomerular pressure).
** What must you always get before you prescribe a diuretic?
urine electrolytes!
Is urine creatinine influenced by diuretics?
NO
** Is a DECREASED urine Na+ and INCREASED urine:plasma creatinine ratio (>40) consistent with a decreased effective circulating volume (PRERENAL AZOTEMIA)?
YES.
*So BUN is reabsorbed (hence high BUN:Cr ratio) but creatinine is not (hence high urine:plasma creatinine ratio).
Will a pt’s urine have an odor if they have acute loss in GFR?
NO because they have little solute due to decreased filtration.
When should be treat hypocalcemia?
only if pt is symptomatic
