ACUTE KIDNEY INJURY

Nephrology: Dr.Ngo
Acute Kidney Injury
72 yo male with DM , developed CHF, decreasing UO and
azotemia. Anti-CHF regimen was instituted. Patient
started to have increasing urine UO and his azotemia
resolved
59 yo HTN male underwent coronary angiogram. The
next day he developed oliguria and was noted to be
azotemic. U/A showed pyuria and slight proteinuria.
After a week azotemia resolved and the u/a was normal
81 yo male underwent coronary bypass. The operation
lasted for 16 hours and during the operation there were
3x had BP of 70 to 80 mmhg systolic. After the
operation the pt. Had anuria despite normalization of his
BP to 130-150mmhg systole
42 yo female with community acquired pneumonia was
confined 7 days after the onset of her symptoms. Dx on
admission was septicemia. She was oliguric and with
azotemia. Parenteral antibiotics were instituted and the
patient recovered. Urine output increased day by day
and her azotemia resolved.

ACUTE KIDNEY INJURY

o functional or structural abnormality
o manifested within 48 hours
o determined by blood, urine, tissue tests or
imaging studies
o increased creatinine of 0.3 mg/dl or 26umol/l or
50% increase in serum creatinine
o decreased urine output less than 0.5
ml/kg/hour for longer than 6hours
Know first the hydration of the pt. and
see if the urine output is cured
give fluid challenge 200ml PNSS
auscultate lungs if with crackles
possible pulmonary edema upon fluid
challenge
COPDcrackles will not disappear
even with diuretics(furosemide) given
CAUSES OF ACUTE KIDNEY INJURY
o PRE RENAL-60-70% d/t renal hypoperfusion
secondary to hypovolemia, low cardiac output,
systemic vasodilation or selective
vasoconstriction
sepsis
trauma
blood loss
concealed (PUD, fracture of
the pelvic bone)
obvious/apparent
surgery (major)
o INTRINSIC RENAL DISEASE -25-40%
lupus( sudden flare up)
element of reversibility(AKI) or maylead
to CKD
glomerulonephritis
o POST RENAL 5-10% d/t acute obstruction of
urine flow

can be in the ureter, ureterovesical

/pelvic junction, bladder or in the
urethra
ovarian mass that impinges the ureter
malignancy in the pelvic organ (cervix)
(BPH) feeling of retention
small stream of urine
treatment: finasteride

In acute kidney injury, neurohormonal cascade results to

afferent arteriolar dilatation and efferent arteriolar
constriction to maintain normal GFR
o Afferent arteriole will dilate function is
impaired if given NSAIDS and ..
o Efferent arteriole will constrict to maintain the
perfusion pressure constriction of the efferent
is mediated by the release of the RAS
formation of AT2 constriction of the efferent
arteriole
ACEi & ARB given, prevention of the
compensatory mechanism if
impaired Ischemia
When compensatory mechanism fails, progression to
ischemic renal injury occurs
Progression occurs depending on the severity and
duration of the insult

ISCHEMIC NEPHROPATHY
o occurs in more severe or prolonged
hypoperfusion
o injury to the terminal medullary portion of the
proximal tubule and the medullary portion of
the thick ascending limb of Loop of Henle
o recovery takes 1-2 weeks
tubular cells may shed to the tubular
lumen leading to tubular
obstructiontubular edema

CONDITIONS THAT LEAD TO ISCHEMIC NEPHROPATHY

o Intravascular volume depletion and hypotension
Hemorrhage, GI , real and dermal
losses
o Decreased effective intravascular volume

CHF
Liver cirrhosis
Hepatorenal syndrome
Peritonitis
Water is not in the blood vessels but in
the interstitial fluid compartment
third spacing
o Systemic vasodilation/ renal vasoconstriction
Sepsis
Hepatorenal syndrome
o Large renal vascular disease
Renal artery thrombosis/ embolism
Intraoperative arterial cross clamping
Renal artery stenosis
Cholesterol embolism
o Small vessel renal vascular disease
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ACUTE KIDNEY INJURY

Nephrology: Dr.Ngo

Sepsis
Vasculitis
Hus
Malignant hypertension
Scleroderma
Preeclampsia
Sickle cell anemia
Transplant rejection
o Impaired renal blood flow
Cyclosporine
Tacrolimus
Acei
Arb
Nsaid
Radiocontrast agents
INTRINSIC RENAL DISEASE
o Tubular injury d/t ischemia, inflammation or
d/t toxins
Renal tubular toxins
Aminoglycosides
Radiocontrast agents
Antiviral acyclovir
Anticancer ( methotrexate ,
cisplatin)
Immunosuppressive drugs
cyclosporine , tacrolimus
o Acute Interstitial Nephritis
meds a/w acute interstitial nephritis
penicillin , cephalosporin,
ampcillin, sulfonamide,
vancomycin, rifampicin,
acyclovir, nafcillin
furosemide,
hydrochlorothiazide
Ibuprofen, naproxen m
indomethacine

infections (thyphoid,
leptospirosis and dengue)
hematuria, pus cells,
protienuria (+2/3)
normal BP

Acute Glomerulonephritis
U/A hematuria , marked proteinuria .
RBC casts , granular casts
Rapidly progressive glomerulonephritis
Glomerulinephritis triggered by
ischemia , preganancy and
nephrotoxins

POST RENAL ACUTE INJURY

o Outflow Obstruction
Prostatic enlargement
Prostate or cervical cancer
Retroperitoneal d/o
o Functional Obstruction
Neurogenic bladder
o Intraluminal Obstruction
Retroperitoneal fibrosis
Colonic ca
Lymphoma
Crystalization of compounds such as
uric acid, ca oxalate, acyclovir,
sulfonamide , methotrexate , myeloma
light chain
URINALYSIS
o PRE RENAL INJURY
normal u/a or with hyaline casts
o INTRINSIC RENAL PARENCHYMAL INJURY
Tubular cell injury mudd brown
granular epithelial casts
Interstitial nephritis pyuria,
hematuria, granular and epithelial
casts, eosinophilia
Glomerulonephritis hematuria , rbc
casts, marked proteinuria
Vascular d/o normal or with
hematuria , mild proteinuria
o POST RENAL INJURY
Normal or with hematuria(3-5/5-10
rbc), granular casts or pyuria
URINARY INDICES
o FeNA = urine Na X plasma creatinine X 100
plasma Na X urine creatinine
o pre renal <1 %
o Intrinsic renal injury disease
Tubular injury >1%
Interstitial nephritis >1%
Early Glomerulonephritis <1%
Early Vascular d/o <1%
o Post renal injury >1%
BUN / Creatinine Ratio
o PRERENAL >20 / 1
o INTRINSIC RENAL DISEASE
o POST RENAL > 20 / 1

< 10-15 / 1

proteinura +3/4
full blown glomerulonephritis when
pregnant
high BP
tendency of hypovolemia
edema
strep. infection AKI

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