Acute Kidney Failure Flashcards
AKF: define:
- Kidney can’t maintain homeostasis, leading to nitrogenous waste buildup
NOT SAME AS renal insufficiency where kidney function is deranged, but can still support LIFE!!
AKI defined as; define anuria, oliguria, polyuria
occurring over hrs/days; lab definition is increase in baseline creatinine by 50% or decrease in clearance by 50%; often a deterioration of renal function which requires dialysis;
anuria: less than 100 mls/24 hr OR no urine output
oliguria: 2.5 L/24hr
Causes of AKI:
- pre-renal (inadequate perfusion with absolute and relative hypovolemia, reduced CO, renovascular occlusion: check volume status)
- Renal (AKI despite perfusion and excretion with ATN, AIN, atheroemboli: check UA, full blood count, autoimmune screen)
- Post-renal (blocked outflow with pelvi-calyceal, ureteric, vesicoureteric junction, bladder neck: check bladder, catheter, US)
For ATN, causes?
- ischemic
- nephrotoxic: endogenous toxins (heme pigments like myoglobin and hemoglobin; myeloma light chains) vs exogenous (aminoglycosides, amphotericin B, radiocontrast agents, heavy metals with cis-platinum, mercury, poisons like ethylene glycol) HARP
For AIN, causes? Clinically?
- allergic IN (drugs)
- infections (bacterial, viral)
- sarcoidosis; SIA!!!
fever, rash, arthralgias, eosinophilia, UA (microscopic hematuria, sterile pyuria, eosinophiluria) FU RAE
Contrast-induced AKI: prev? risk factors?
Less than 1% in patients with normal renal function;
- renal insufficiency
- DM
- multiple myeloma
- high osmolar contrast media (try low-osmolar)
- contrast medium volume (try and minimize)
The RM DOVe
clinical characteristics of contrast-induced AKI and pre-procedure prophylaxis?
24-48 hrs after exposure, lasts 5-7 days, non-oliguric (majority), dialysis rarely needed, urinary sediment (variable), low fractional excretion of Na;
IV fluid, mucomyst (N-acetylcysteine), bicarb, maybe fenoldopam but the go-to is IV fluid!!
Glomerulonephritis is characterized by
inflamm and damage of the glomeruli; allows leak of protein w/w/o blood in urine
Proliferative vs. non-prolif glomerulonephritis examples:
- Membranoproliferative, post-infectious, IgA nephropathy, rapidly progressive glomerulonephritis (Goodpasture vs. vasculitic disorders like Wegeners and microscopic polyangiitis)
- Membranous, minimal change, FSGS
AKI post-renal causes:
- Intra-renal obstruction: acute uric acid nephropathy, drugs (acyclovir)
- extra-renal obstruction (renal pelvis or ureter like stones, clots, papillary necrosis, tumors), bladder (BPH), urethra (stricture)
Bland urinary sediment seen in
pre-renal azotemia and urinary outlet obstruction
RBC casts or dysmorphic RBCs seen in
acute glomerulonephritis and small vessel vasculitis
WBC’s and WBC casts seen in
AIN, acute pyelonephritis
ATN would show _____ in urinary sediment:
- renal tubular epithelial cells,
- RTE cell casts
- pigmented granular (muddy brown) casts
FeNa < 1% in; 1-2% in; >2% in
- prerenal
- ATN (unusual)
- glomerular or vascular injury;
- prerenal
- ATN sometimes
- AIN: higher FeNa b/c of tubular damage;
- ATN