Shokoufeh Savaj MD Associate Professor of Medicine Firouzgar
hospital Iran University of Medical Sciences Acute Kidney Injury
(Acute Renal Failure )
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Definition Rapid decline in glomerular filtration rate (GFR)
over hours to days
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Diagnostic criteria for ARF Abrupt (within 48 hours) absolute
increase in the serum creatinine concentration of 0.3 mg/dL from
baseline A percentage increase in the serum creatinine
concentration of 50 percent Oliguria of less than 0.5 mL/kg per
hour for more than six hours
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Classifications for Acute Renal Failure
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Classification Prerenal (55%) Renal(40%) Post renal (5%)
Prerenal (55%) Renal(40%) Post renal (5%)
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Pathogenesis of prerenal Azotemia Fall in mean systemic
arterial pressure, Reduced stretch by arterial (e.g., carotid
sinus) and cardiac baroreceptors Neurohormonal responses t(
activation sympathetic nervous system,RAS system and vasopressin
release. Vasoconstrictrion in musculocutaneous and splanchnic
circulations Preserved cardiac and cerebral perfusion pressure
Decrease salt loss and stimulation of thirst and salt appetite
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Local myogenic reflex (autoregulation). Angiotensin II
increases biosynthesis of vasodilator prostaglandins (e.g.,
prostaglandin E 2 and prostacyclin Afferent arteriolar vasodilation
Constriction of efferent arterioles. Increased filtration fraction
Maintenance of intraglomerular pressure and GFR Severe
hypoperfusion, GFR falls, leading to prerenal ARF.
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Prerenal ARF Hypovolemia A. Increased extracellular fluid
losses B. Gastrointestinal fluid loss C. Renal fluid loss D.
Extravascular sequestration E. Decreased intake Altered renal
hemodynamics resulting in hypoperfusion A. Low cardiac output state
B. Systemic vasodilation C. Renal vasoconstriction D. Impairment of
renal autoregulatory responses E. Hepatorenal syndrome
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Glomerular and microcirculation Interstitial nephritis Acute
tubular necrosis Diseases of larger renal vessels Intrinsic
ARF
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Renovascular obstruction A. Renal artery obstruction B. Renal
vein obstruction Diseases of the glomeruli or vasculature A.
Glomerulonephritis or vasculitis B. thrombotic microangiopathy,
malignant hypertension, collagen vascular diseases (systemic lupus
erythematosus, scleroderma), disseminated intravascular
coagulation, preeclampsia
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Renal Vein thrombosis
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Renal artery stenosis
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Post Streptococcal Glomerulonephritis
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Acute tubular necrosis A. Ischemia B. Infection, with or
without sepsis syndrome C. Toxins: 1. Exogenous: 2. Endogenous:
rhabdomyolysis, hemolysis
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Decrease blood flow and oxygen delivery Increase oxygen
consumption and direct cellular toxicity Renal medullary
hypoxia
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Interstitial nephritis A. Allergic B. Infection C.
Infiltrations D. Inflammatory, nonvascular: Sjgren's syndrome,
tubulointerstitial nephritis with uveitis Intrinsic ARF
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Intratubular obstruction A. Endogenous B. Exogenous Intrinsic
ARF
Fractional Excretion of Sodium U Na x P Cr FE Na % = x 100 P Na
x U Cr U Na x P Cr FE Na % = x 100 P Na x U Cr
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Diagnosis of ARF EtiologyEpidemiologyClinical features Serum
studiesUrine studies Prerenal ARFMost common History of poor fluid
intake,Worsening heart failure Treatment with ACE/ARB/NSAI D
Clincal signs of volume depletion High BUN /Cr > 20 is
suggestive Hyaline casts FENa < 1% Urine Na < 10 mmol/L Urine
SG > 1018
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Diagnosis of ARF EtiologyEpidemiologyClinical features Serum
studies Urine studies IschemiaSevere hemorrhage or hypotension
Muddy browun tubular or epithelial cast casts FENa > 1% Urine Na
>20 mmol/L Urine SG
EtiologyEpidemiologyClinical featuresSerum studies Urine
studies Exposure to endogenus toxins RhabdomyolysisPost
ictal,prolonged ischemia or immobilization Increased myoglobin and
Creatine kinase U/A positive for heme With no RBC Hemolysis :recent
blood transfusion Fever, transfusion reaction Pink plasma,
increased LDH same as above Tumor lysis :recent chemotherapy
Hyperuricemi a,increased LDH Urate crystals Multiple
myelomaIndividuals >60yrs age, contitutional symptoms
Anemia,mono clonal spike Proteinuria spike on urine electrophoresis
Ethylene glycolHistory of alcohol abuse,altered mental state High
anion gap acidosis,with osmolal gap,positive toxicity Oxalate
crystals
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EtiologyEpidemiologyClinical features Serum studies Urine
studies Allergic interstitial nephritis Recent medication exposure
Fever,rash, arthralgia EosinophiliaWhite cell casts,eosinophiluria
Acute bilateral pyelonephritis Fever, flank pain and tenderness
Positive blood cultures leukocytes, proteinuria,positive urine
culture Postrenal ARFHistory of renal stones or prostatic disease
Palpable bladder, flank or abdominal pain Usually normal.hematuria
if due to stones
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Novel biomarkers of acute kidney injury *Low molecular weight
proteins: ( Alpha1-Microglobulin (alpha1-M), beta2-Microglobulin
(beta2-M), retinol binding protein (RBP), adenosine deaminase
binding protein (ABP), and urinary cystatin C *Tubular enzymes
:Urinary tubular enzymes consist of proximal renal tubular
epithelial antigen (HRTE-1), alpha-Glutathione S- transferase
(alpha-GST), pi-Glutathione S-transferase (pi-GST),
gamma-Glutamyltranspeptidase (gamma-GT), Alanine aminopeptidase
(AAP), Lactate dehydrogenase (LDH), N-acetyl-beta- glucosaminidase
(NAG), and Alkaline phosphatase (ALP).
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Kidney injury molecule 1 (KIM1) Transmembrane protein in
proximal tubular cells Phagocytic properties of tubular cell DD
prerenal from ATN Neutrophil gelatinase associated lipocalin (NGAL)
Protein in granules with tissue Protective effect of in proximal
Increases 2 hours after ischemic injury Novel biomarkers of acute
kidney injury
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Classification/staging system for acute kidney injury*