Acute kidney injury (AKI) Flashcards
Define AKI
- abrupt decline in renal function leading to increased nitrogenous waste products normally excreted by the kidney
- formerly known as Acute Renal Failure (ARF)
Px of AKI
- azotemia (increased BUN, Cr)
* abnormal urine volume (anuria, oliguria, polyuria)
Ix of AKI
- blood: CBC, electrolytes, Cr, urea, Ca2+, PO4 3-
- urine volume, C&S, R&M: sediment, casts, crystals
- urinary indices: electrolytes, osmolality
- Foley catheterization (rule out bladder outlet obstruction)
- fluid challenge (i.e. fluid bolus to rule out most pre-renal causes)
- imaging: abdo U/S (assess kidney size, hydronephrosis, post-renal obstruction)
- kidney biopsy if indicated (Dx not certain, unlikely prerenal azotemia/ATN & >4wk oliguria)
When should you think of pre-renal cause as the cause of AKI?
if increase in urea is relatively greater than increase in Cr
Pre-renal causes of AKI
- Shock, sepsis, haemolysis, rhabdomyolysis (breakdown of skeletal muscle), nephrotoxic drugs (which actually cause tubulo-interstitial nephritis, a renal cause)
- Haemolysis & rhabdomyolysis toxins: Hb & myoglobin à tubular necrosis à block GFR intrarenally
- Shock & haemorrhage
ATN is a result of shock/pre-renal cause
How does shock & haemorrhage lead to AKI?
- Shock & haemorrhage -> low BP -> low GFR -> stasis in proximal tubule etc -> anoxia of tubular cells -> casts formation & death of tubular cells -> acute tubular necrosis due to decreased RBF
Renal causes of AKI
o Glomerular disease
o Interstitial nephritis (tubulo-interstitial): inflammatory reaction (IgA), often drug-related
- Streptococcal infections Grp A: penicillin for a long period of time so that the patient does not mount their own immune response against Strep. Otherwise, it leads to deposition in immune complexes to glomerulus -> glomerulonephritis
o Tubular damage
- Ischaemia – ATN, vascular obstruction
- Toxins – antibiotics (aminoglycoside), X-ray contrast media (invariably toxic), myoglobin/Hb
Post renal causes of AKI
o Outlet obstruction
- Ureteric, cystic or urethral (e.g. Enlarged prostate in BPH)
- Stones, clots, fibrosis, tumours
What are the 2 things to worry about in renal failure?
rise early on: K+ & H+ (very critical)
o Acidosis o Hyperkalaemia (low aldosterone -> low reabsorption of sodium in exchange of excretion of potassium)
Rx of pre-renal AKI
correct prerenal factors:
- optimize VOLUME status and cardiac performance using fluids that will stay in the plasma subcompartment (NS, albumin, blood/plasma)
- hold ACEI/ARB (gently rehydrate when needed, i.e. CHF)
Rx of renal AKI
address reversible renal causes:
- d/c nephrotoxic drugs
- treat infection
- optimize electrolytes
Rx of post-renal AKI
- consider obstruction: structural (stones, strictures) vs. functional (neuropathy)
- treat with Foley catheter, indwelling bladder catheter, nephrostomy, stenting
How do casts help you identify renal etiology in AKI?
- Pigmented granular: acute tubular necrosis
- WBC: acute interstitial nephritis
- RBC: glomerulonephritis
Clinical clues to post renal etiology
- known solitary kidney
- older man
- recent retroperitoneal surgery
- anuria
- palpable bladder
- US shows hydronephrosis
4 types of drugs implicated in pre-renal azotemia
- Anti-hypertensives
- Diuretics
- NSAIDs
- ACEI/ARBs
