Acute Kidney Injury

Thanks to Dr. Jessica Weiss for the noon conference on AKI!

AKI definition - an abrupt decrease in glomerular and tubular function.

• KDIGO
  - increase in Cr > 0.3 within 48hrs
  - Increase in Cr > 1.5 times baseline
  - Urine volume <0.5ml for 6 hours

• ** need to identify baseline!!
  ** CANNOT estimate GFR in AKI, only in steady state

• AKI stages matter!
  - Kaplan-Meier plot of cumulative rates of in-hospital death by AKI stage

• Lower baseline Cr seen in older age, less muscle mass, amputation, malnutrition, cancer, liver disease, chronic inflammation, vegetarian diet
  Higher baseline Cr seen in patients with higher muscle mass (athletes), diets high in protein.

• Risk factors for AKI – basically, less renal reserve
  -older age
  -diabetes
  -male gender
  -CKD
  -recurrent AKIs
  -socioeconomic status
  -field work

• AKI is associated with increased risk of death (especially in ICU), increased risk of CKD, and increased costs.

Evaluation of AKI

Pre-renal

Key questions
-food/fluid intake + outs/changes in urine output
-what is BP at home typically
- mucus membranes, lung sounds, edema
-almost always check a CK
-if urine sodium is low, it is meaningful
-diarrhea? -  anyone else sick around them?
-give small bolus 250mg and see if BP goes up to check if fluid responsive

3 flavors of pre-renal
-hypovolemia – (dehydration, blood loss, GI loss, excessive diuresis)
-change in vascular resistance- (sepsis, cirrhosis, burns, anaphylaxis, vasodilators)
-decreased flow to kidney – (heart failure, arrhythmia, pulmonary embolism, tamponade, cardiac valvular disease, changes in renal vasculature)

Intra-renal (ischemic injury resulting in destruction of tubular cells)

• -ischemia (hypovolemia vs vascular blockage), toxins, septic shock
  -NSAIDs use
  -muddy brown casts = tubular injury

• **might not be only one type of AKI going on.
  **pre-renal and ATN are most common types of AKI.

• urine spot sodium: to look at Na+, if not as much forward flow in glomerulus, will kick up mechanisms to reabsorb Na+
  if pre-renal, should be letting very little sodium go out to the urine
  If ATN, tubules not working (this is the idea behind FeNa)
  BUT can see low FeNa in cardiorenal syndrome, liver cirrhosis, rhabdo, and contrast nephropathy (maybe due to vaso-constriction from dye…?)! (know these limitations)

• BUN/Cr ratio: Pre-renal 20:1, ATN 10:1 – not the be all end all, but can look to give more evidence to your hypothesis

• *** don’t forget about insensible loses, post ATN diuresis can lead to pre-renal if can’t drink to keep up (robust output is more than 3L a day, need to check electrolytes at least twice a day)

Post-renal (obstructive)

• check retention

Limitations of common renal labs

• ***Urine spot protein/creatinine ratios are not generally accurate in the setting of AKI, should only due when creatinine in steady state

Address AKI associated hyperkalemia
-          Is it real (hemolysis??)
-          EKG – worry about prolonged QRS or bradycardia (is this where they always are??), consider ongoing tele if severe enough
-          Shift K
-          Remove K – patiromer (Veltassa) effective 7 hours | zirconium cyclosilicate (Lokelma) effective within 1 hour, thus thought to be best
-          Shift K again if needed (insulin + D50 (2 hour shift) and beta agonist therapy (albuterol – 1 hour shift)) (shifts for 1-2 hours then gone so need to consider doing again after 3-4 hours)
-          Stabilize with Ca gluconate, and can give bicarb if acidotic
-          Address underlying causes
-          Remove K and shift again