1. Acute kidney injury (AKI) can be diagnosed by assessing urine and serum markers such as a urine sodium level greater than 20 or a serum urea/creatinine ratio greater than 40, which indicates pre-renal AKI. 2. Laboratory tests that can help determine the underlying cause of AKI include checking for hypercalcemia, which can indicate multiple myeloma or lymphoma, and measuring CPK to check for rhabdomyolysis. 3. An elevated osmolar gap on lab tests, particularly one over 25, along with an otherwise unexplained high anion gap metabolic acidosis, suggests ethylene glycol or methanol intoxication in a patient suspected of poisoning.

1. LABORATORY TOOLS IN AKI
myeloma kidney
HOW DX AKI?
- low renal blood flow- o kidney reabsorb whatever it can
- urea/cr >2 = prerenal-- must give fluid to ressucitate
- kidney reabsorb na
- in prerenal syndrome- absorb everything it can
(see below)
- prerenal- kidney works ok
- if it was renal: then it would be dilute due to inability to reabsorb water (not osmotic urine)
URINE URINE Serum uera/
OSMOLARITY SODIUM creatinine
300 ≥ ≥20 40 ≥ ARF
300 ≤ 20 ≥ 40 ≤ PRERENAL
The fractional excretion of sodium (FENa
<1=Prerenal
>1=RENAL
UNa x PCr
FENa, percent = ————————— x 100
PNa x UCr
- How much Na is filtrated in kidney in a day:
- GFR (100) * concentration of Na (145)*1440
(min in 24h)= 175 000 miliequiv
- only 1% from this goes into the urine
DD :ANURIA
anuria: no urine
1.Obstruction (vast majority of patients with anuria) BPH
2.Bilateral renal cortical necrosis- very severe- usually caused by DIC or
disease: hemolytic syndrome (usually post partum or post abortion- today is very rare)=
caused renal shut-down
3.Fulminant glomerulonephritis (usually some type of rapidly
progressive glomerulonephritis)- also severe
4.Acute bilateral renal artery or vein occlusion (rare)

2. 5. severe aortic dissection (another thing that shutdown
kidney)
LABORATORY TEST IN AKI
UREA/CR>40; PRE RENAL
HYPERCALCEMIA : MM, LYMPHOMA
TUMUR LYSIS SYNDROME:, HYPERURICEMIA
CPK: RHABDOMYOLISIS
- EOSINOPHILIA ALLERGIC INTERSTITIAL NEPHRITIS
– OSMOLAR GOP : TOXINS: ETHYLENE GLYCOL ,ETHANOL
C3,C4,ANA,DS DNA,CRYOGLOBULIN,ANTI-GBM:ACUTE
GLOMERULONEPHRITIS
Osmolar Gap
pt of osmolar gap: to narrow down dx even further
Plasma osmolarity = 2(Na) + glucose/18 + BUN/2.8.
(BUN= urea/2)
Osmolar Gap = Measured Posm – Calculated Posm
The normal osmolar gap is 10-15 mmol/L H20 .The osmolar gap is increased
in the presence of low molecular weight substances that are not included in
the formula for calculating plasma osmolarity. Common substances that
increase the osmolar gap are ethanol, ethylene glycol, methanol, acetone,
isopropyl ethanol and propylene glycol.
In a patient suspected of poisoning, a high osmolar gap (particularly
if ≥ 25) with an otherwise unexplained high anion gap metabolic
acidosis is suggestive of either methanol or ethylene glycol
intoxication.
BIOMARKERS IN AKI
Neutrophil gelatinase-associated lipocalin
(NGAL) is a relatively new biomarker for
acute renal injury
The lipocalins are a family of proteins which transport small hydrophobic
molecules such as steroids, retinoids, and lipids. Lipocalin proteins are
involved in inflammation processes caused by immune system activation in
mammals.

3. Other emerging bio-markers for diagnosis of AKI
KIM-1
IL-18
Indications of dialysis in acute renal failure (ARF)
• ABSULUTE INDICATIONS
• Severe fluid overload (pulmonary edema)
• Refractory hypertension
• Uncontrollable hyperkalemia (ABOVE 6.5 OR 7)
o but more imp than absolute level: arrhythima (complication)- so start dialysis
in abnormal EKG: T wave elevation and QRS elongation
• Severe metabolic acidosis

4. • RELATIVE INDICATIONS
• Lethargy, malaise, somnolence, stupor, coma, delirium, ,
seizures,
• Pericarditis (risk of hemorrhage or tamponade)
• bleeding diathesis (epistaxis, gastrointestinal (GI)
bleeding and etc.)
TREAT THE PTS CUASE
S/T NEED TO START DIALYSIS: TO KEEP PT ALIVE