#12 Press - Acute Kidney Injury Flashcards
What constitutes acute kidney injury?
- Increase in serum creatinine of = or > 0.5 mg per deciliter over the baseline value
- hours to days
Patient comes in with orthostatic hypertension with presence of edema. Upon examination you hear a pericardial rub. What type of offending agents might have induced the acute kidney injury?
- IV contrast
- antibiotics
What labs would you order to investigate AKI?
BUN/creatinine ratio (>20:1 is consitent with pre-renal azotemia)
Chem7 - electrolytes and acid/base status
UA - look for WBC/RBC/granular casts
US - exclude obstruction
Is all elevated creatinine AKI?
NO Factitious ARF also has elevated creatinine.
Bactrim can interfere with creatinine levels, showing increased creatinine.
Opposite is also true. Elderly, malnutrition and liver disease patients may have AKI without elevated creatinine.
You look at the patient’s file at the hospital and their creatinine is at 6. Is this acute or chronic kidney disease?
You would need their history to determine. If their baseline has been 6 for years then chronic. If their baseline was 1 a year ago –> acute.
Is all elevated BUN AKI?
No.
Steroids
Increased catabolic rate (febriile, bed-bound, septic ICU)
Tetracycline
Parenteral nutrition
GI bleed
Patient’s labs show a FeNa less than 1%. What type of AKI is most likely?
Pre-renal azotemia
[FeNa >2% is likely ATN]
What are the ddx for a FeNa less than 1%?
Renal Artery Stenosis
Acute GN
Non-oliguric ATN
ATN when pigment or contrast nephropathy
Early urinary tract obstruction
FeNa is over 1%. What pre-renal ddx might it be?
Elderly
CKD
Diuretic use
Poor nutritional intake
What are the most common causes of pre-renal azotemia?
Decreased intravascular volume
- hemorrhage
- renal losses (osmotic diuresis, DI, salt wasting nephritis)
- GI losses (V/D)
- Insensible losses (fever, mechanical respiration)
- 3rd spacing (burns, pancreatitis, peritonitis, Ileus)
How will low BP affect kidneys?
Low perfusion
No BP, no pee pee
Decrease cardiac output can lead to pre-renal azotemia
In what scenarios might you find decreased cardiac output leading to pre-renal azotemia?
Acute MI
CHF
Pulmonary embolus
Cardiac tamponade
Patient in the hospital with peripheral vasodilation could be due to?
BP meds
Gram-negative shock
Anaphylactic reaction
Hepato-renal syndrome
Which drugs are the biggest offenders of increased vascular resistance causing pre-renal azotemia?
NSAIDS
Calcineurin inhibitors (cyclosporine)
Radiocontrast dye
ACE/AT II inhibitors
Patient has a fast rise in creatinine and granular casts are seen in urinalyssis. FeNa is above 2%. What type of AKI is the patient likely to have?
ATN
Most severe in the early proximal tubule
What are the two major histological changes in ATN?
Loss of intact or necrotic tubular changes
Occlusion of the tubular lumen by cellular debris
Identify
ATN
Muddy brown casts
Cola casts
Identify
ATN
Loss of nuclei
Labs return and the patient’s BUN:Cr is 12:1 and FeNa is > than 2%. Specific gravity is isosthenuric 1.010. What do you suspect?
ATN
Tx: Dopamine may be HARMFUL
Minimize hypotension
Remove offending agents
Diuretics to convert oliguric ATN to non-oliguric ATN*
*DOES NOT Decrease mortality
What are indications for dialysis?
AEIOU (**Digoxin is not dialyzable)
Acidosis
Electrolytes
Intoxicants (LISA MET BARB)
[LIthium, SAlicylates, Methanol, Ethylene glycol, Theophylline, BARBituates]
Overload
Uremia
65 year old man with diabetes and a creatinine of 4 mg/dL comes in complaining of chest pain but is worried about having to go on dialysis from contrast nephropathy. What imaging would you use that would not need radiocontrast agents?
US
MRI
CT w/o contrast
Withhold certain offending medication (NSAIDS, DM-metformin)
Avoid volume depletion
What pre-procedure prophylaxis would be used IV?
Isotonic IVF
0.9 NS
1 ml/kg/hour x 12 hours prior and 6-12 hours after procedure
You have an elderly patient who was given gentamyacin by a local urgent clinic. What toxicity may result?
Aminoglycoside nephrotoxicity
Susceptible groups:
Volume depletion
Sepsis
Preexisting renal disease
Hypokalemia
Elderly
A patient comes in with suspected ethylene glycol ingestion. What examination of the urine would you order and how would you treat it?
Wood’s light (ultraviolet)
Calcium oxalate crystals
Tx: alcohol or fomepizole +dialysis
Fomepizole - prevents metabolism of ethylene glycol
If suicide attempt, refer after treatment
Patient comes in with livedo retularis from a cardiovascular cath procedure. Dx?
Atheroembolic Renal disease (rare but looks like contrast induced nephropathy [CIN])
-small artery occlusion leading to organ ischemia
*blood thinners may also be causative
Patient comes in after labs indicated decrease in GFR and on renal biopsy crescent formations were found. Dx?
Rapidsly Progressive GN (RPGN)
RPGN has three main classes. Type I, II, III. Classification is based on immunofluorescent. What pattern is seen in each?
Type I (Goodpastures)- IF –>linear deposition
Type II (PSGN, Lupus, IgA, HS, MPGN)- IF–> granular deposition
Type III (Wegener’s, MicroPolyangitis, Idiopathic crescenteric) - IF –> Pauci immune deposition, ANCA
A patient comes in with a rash, fever and eosinophilia. You go through the history and find he is currently on ibuprofen. After asking more questions you find he had an injury 13 months ago after cycling. You immediately think?
Allergic Interstitial Nephritis
(May take weeks after initial exposure. NSAIDS can take up to 18 months!)
You send your cyclist patient in for labs upon suspicion of allergic interstitial nephritis. If he has AIN, what will be on the report?
Bland sediment or WBCs, RBCs, non-nephrotic proteinuria
WBC casts
Normal or mildley increased protein excretion
Urine eosinophils on Wright’s or Hansel’s stain
Your cyclist patient comes back with WBC casts and eos. Based on labs and clinical findings, how would you treat his allergic interstitial nephritis?
Remove the offending agent.
If severe, he should undergo a renal biopsy to confirm.
If poor candidate for renal biopsy, then prednisone.
2-3 month therapy
