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DEFINITION
form of acute renal failure characterized
by insufficient renal perfusion for the
maintenance of adequate glomerular
filtration rate.
PRERENAL ACUTE RENAL FAILURE
MECHANISMS:
• hypovolemia
– hemorrhagic losses
– digestive losses
– renal losses
– cutaneous losses
• reductions of effective circulanting blood volume
- redistribution
– peripheral vasodilatation
– peripheral edema
– third space losses
• reduction of cardiac output
• dysfunction of renal autoregulation
PRERENAL ACUTE RENAL FAILURE
CLINICAL FEATURES
• Clinical signs and symptoms of causative disorder are
prevalent (trauma, burns, acute surgical abdomen, acute
myocardial infarction, anaphylactic shock, etc.)
• Patient history, clinical signs and hemodynamic
parameters will identify the characteristic hemodynamic
status for each mechanism (hypovolemia, reduction of
effective circulanting blood volume through redistribution,
reduction of cardiac output).
• urinary volume is variable, but most frequently is
decreased (oliguria– urinary output <0,5ml/kg/hour).
PRERENAL ACUTE RENAL FAILURE
• Diagnosis:
– Identification of the causes;
– variable dysfunction of urinary output;
• usual, oliguria ( urinary output <0,5ml/kg/hour);
• Urinary output can be normal or elevated in the case of
diuretics and osmotic drugs administration;
– Elevations of blood ureea nitrogen (BUN) and serum
creatinine ;
• The elevation of blood ureea nitrogen is more pronunced
than serum creatinine elevation
• Plasma BUN/serum creatinine is elevated (normal 10/1; în
IRA prerenal 20/1);
• It is very important to make differential diagnosis with
diseases accompanied by BUN/serum creatinine elevations
without glomerular filtration rate reduction (table 3);
– Characteristic urinary analysis
– Imagistic explorations for the exclusion of postrenal
causes (Rx T, abdominal ecography).
PRERENAL ACUTE RENAL FAILURE
Causes of BUN/serum creatinine elevations without
glomerular filtration rate reduction:
• Elevation of BUN synthesis
– Gastro-intestinal bleeding
– drugs: steroids, tetraciclyne
– Elevated protein intake
– Elevated intake of aminoacids
– Hypercatabolism and fever
• Elevation of creatinine synthesis
• Elevation of creatinine release from the muscles
(rhabdomyolysis)
• Drugs which interfere with tubular secretion of creatinine
• Cimetidine, trimetoprim
PRERENAL ACUTE RENAL FAILURE
• PRINCIPLES OF TREATMENT
– early and agressive treatment of the
causative disorder for normalisation of renal
perfusion before occurance of ischemic
damage
– Hemodynamic optimization: normalisation of
intravascular volume, cardiac output and
systemic vascular resistance - by volemic
repletion, inotropic and vasoactive drugs
– Promotion of urinary output with diuretics
(manitol, furosemid)
ACUTE RENAL FAILURE
PROPHYLAXIS
• Identification of the patients with high risk
• Early correction of hemodynamic
disorders which can induce or aggravate
renal dysfunction
• Promoting of urinary output - diuretics
• Use catecholamines for renal protection
• Other drugs used in renal protection
POSTRENAL ACUTE RENAL FAILURE
DEFINITION
CLINICAL FEATURES
• Clinical signs of the causative disorder
– Frequently – slow progression, late and discreet signs
of acute renal failure.
• Urinary output is variable.
– Sometimes suddenly instalation of a complete anuria
dominate clinical picture and in this case a complete
obstruction must be suspected.
– Other times the obstruction is incomplete and urinary
output is present and even polyuria is possible
POSTRENAL ACUTE RENAL FAILURE
DIAGNOSIS
– Identification of the obstructive causes ;
• Ultrasonography is the screening and often diagnostically
examination (shows level of obstruction and retrograde
dilatation and often also the cause : lithiasis, tumors, etc.);
• for complete diagnosis of the causative disorder all
necessary investigations should be made ;
– Variable urinary output;
• Sometimes compete anuria, suddenly instalated ; other times
polyuria (loss of urinary concentrating capacity);
– Plasma BUN and creatinine are elevated; plasma
BUN/ plasma creatinine ratio is elevated
– Hyperkalemia;
– Variable and uncharacteristic urinary analysis:
• loss of urinary concentrating and dilution ability
• reduction of the urinary acidification capacity
• variable Na excretion (FENa<1% in early phases , FENa>3%
in late phases).
POSTRENAL ACUTE RENAL FAILURE
• PRINCIPlES OF TREATMENT
• Treatment of causative disorder
• Early removal of the obstruction
– Emergency urine drainage through urinary catheter,
cistostomy, ureteral stents or percutaneous
nephrostomy
• Hemodynamic and renal perfusion optimization
for functional renal recovery
• Treatment of urinary infection which is frequent
associated with obstruction.
INTRINSIC ACUTE RENAL FAILURE
Intrinsic acute renal failure causes:
• Renal ischemia
• Nephrotoxic substances:
– Drugs : antibiotics, NSAID, cyclosporine, etc.
– Radiocontrast agents
– Toxins: tetraclorura de carbon, ethylene glycol, heavy metals,
pesticides, fungicides, etc.
• Glomerulonephritis and vasculitis:
– poststreptococcal glomerulonephritis, bacterial endocarditis, systemic
erythematosus lupus, malignant hypertension, thrombotic
microanghiopathy, Henoch-Schönlein purpura, polyarteritis nodosa,
rapidly progressive glomerulonephritis, Goodpasture syndrome,
Wegener granulomatosis, etc.
– bilateral thrombosis of renal veins, dissecting aneurysm of renal artery,
renal artery embolism, etc.
• Interstitial nephritis:
– antibiotics, furosemide, alopurinol, fenitoine,etc.
INTRINSIC ACUTE RENAL FAILURE
PATHOGENESIS:
– afferent arterioles vasoconstriction
• catecholamines, angiotensin II, impaired prostaglandin
regulation
– decreased permeability of glomerulo-capillary
membrane
• inflammatory/immunological processes
– tubular basement membrane disrupption
• primary urine back leak to interstitium
– intratubular obstruction
• cell debris
INTRINSIC ACUTE RENAL FAILURE
DIAGNOSIS:
– history
• consistent with causative condition
– clinical examination
• data according to causative disorder
• urine output according to form (anuria, oliguria, preserved urinary
flow/polyuria)
• clinical signs of renal failure and complication
– laboratory
• urinary specific gravity ~1010 (isosthenuria)
• urinary urea/blood urea nitrogen < 3
• urinaru creatinine/blood creatinine < 20
• urinary Na > 40mEq/l
• fractional sodium excretion > 3%
– other diagnostic tests – to exclude postrenal causes
INTRINSIC ACUTE RENAL FAILURE
PHASES:
– phase I:
• dominated by causative condition
– phase II:
• dominated by anuria and clinical signs of nitrogen waste
products retention
• attenuated by the use of renal replacement therapies
– phase III:
• reappearance of urinary output, followed by polyuria
ACUTE RENAL FAILURE
PROPHYLAXIS
• Identification of the patients with high risk
• Early correction of hemodynamic
disorders which can induce or aggravate
renal dysfunction
• Promoting of urinary output - diuretics
• Use catecholamines for renal protection
• Other drugs used in renal protection
INTRINSIC ACUTE RENAL FAILURE
PRINCIPLES OF TREATMENT:
• Causative treatment
• Hemodynamic optimization
• Urinary output promotion
• Fluid-electrolyte treatment
• Prophylaxis and treatment of complications
• Nutritional support
• Renal replacement therapies
RENAL REPLACEMENT
TECHNIQUES