ACUTE RENAL FAILURE

ACUTE RENAL FAILURE

DEFINITION
clinical syndrome induced by various causes
and characterized by the incapacity of the
kidney to maintain organism homeostasis
manifested as retention of nitrogenous waste
products and variable volume of diuresis.
 ACUTE RENAL FAILURE
CLASSIFICATION:
– Prerenal acute renal failure
Reduction of renal blood flow
– Intrinsic acute renal failure
Agression of renal parenchyma (toxic,
ischemic, imunological, etc)
– Postrenal acute renal failure
Urinary tract obstruction
 PRERENAL ACUTE RENAL FAILURE
( functional renal failure, prerenal azotemia)
CAUSES:
– Reduction of effective circulant blood volume
• Hypovolemia caused by hemorrhage
• Hipovolemia caused by non-hemorrhagic losses
(see hypovolemic shock)
– Low cardiac output
• Cardiogenic shock or extracardiac obstructive shock
• Chronic heart failure
• Ischemic, toxic, dilated cardiomyopathy
• Cardiac disrhytmias, etc.
– Blood flow maldistribution
• Excessive vasodilatation ( septic shock, excess of
antihypertensive drugs)
• Cirrhosis
 PRERENAL ACUTE RENAL FAILURE
( functional renal failure,prerenal azotemia)
• Functional renal dysfunction induced by alterations of
renal perfusion.
• General features:
– Functional deterioration without structural damage;
– Prompt correction of the renal perfusion reestablishes renal
function;
– Healing - complete recovery of renal function;
– Good prognosis;
– Dyalisis is not necessary;
– Is the form of acute renal failure in which prophylaxis and early
treatment have maximum efficiency and the most chances of
success;
– Without early correction of renal hypoperfusion, intrinsic renal
failure develops through ischemic mechanism (acute tubular
necrosis).
 INTRINSIC ACUTE RENAL FAILURE
CAUSES:
– Renal parenchyma ischemia
• Prerenal acute renal failure (late treatment)
• All the shock states (late treatment)
– Nephrotoxic agents
• Radiocontrast agents
• Antibiotics (aminoglycosides, vancomycin, cyclosporine)
• Toxins ( heavy metals: Pb, Cd, Hg, ethylene glycol,
poisonous mushrooms)
– Disorders of glomeruli and blood vessels
• Glomerulonephritis
• Vasculitis
• Diabetic nephropathy
– Interstitial disorders
• Interstitial nephritis
• Antibiotics (cephalosporins)
 Renal acute failure
(intrinsic renal failure)
• Agression of renal parenchyma triggered by different
mechanisms: ischemic, nephrotoxic, imunological, etc.
• General features:
– Morphological alterations of the kidney are present;
– Long time of evolution;
– Requires often dialysis;
– Poor prognosis (variable mortality depending by the
cause);
– Recovery can be complete or with residual
functional deficit.
 POSTRENAL ACUTE RENAL FAILURE
(obstructive renal failure)
CAUSES:
– Nephrolithiasis
– Prostate adenoma
– Pelvic tumors
– Retroperitoneal pathological process
(retroperitoneal fibrosis, tumors, abcess,
hematoma)
– Accidental ureteral ligation,etc.
POSTRENAL ACUTE RENAL FAILURE
(obstructive renal failure)
• result of bilateral ureteral obstruction or unilateral
obstruction in patients with solitary kidney.
• General features:
– Obstruction results in renal parenchyma
damage;
– Prognosis depends on the precociousness of
urinary output resumption and the presence of
urinary infection
– Early urinary output resumption results in
complete recovery of renal function
 ACUTE RENAL FAILURE
FORMS:
– Anuric renal failure
urinary output < 100ml/24 ore
– Oliguric renal failure
urinary output < 500ml/24 ore
– Renal failure with preserved diuresis
urinary output >1000ml/24 ore
 MONITORING OF THE PATIENT WITH
RENAL FAILURE
• Respiratory monitoring
• Number of respirations per minute
• Type of respirations
• Pulse oximetry
• Blood gas analysis
• Cardio-vascular monitoring
• BP , HR
• ECG
• Pulse oximetry
• Skin colour and temperature
• CVP
• Neurological monitoring
• State of consciousness
• Temperature monitoring
• Measurement of central/peripheral temperature
• Diuresis monitoring
• Hourly monitoring of diuresis – urinary catheter
• Acido-basic monitoring
• Blood gas analyses
 ACUTE RENAL FAILURE
PRINCIPILES OF TREATMENT
• Treatment of the causative disease
• Circulanting blood volume restoration
– Volemic solutions (see hypovolemic shock)
• Correction of cardiac output and renal perfusion
– inotropic drugs (dobutamine, dopamine)
• Removal of the nephrotoxic drugs
• Fluid-electrolyte and nutritional support
• Infection prophylaxis
• Dialysis (when necessary)
• Obstacle removal (when necessary)
PRERENAL ACUTE RENAL FAILURE
 PRERENAL ACUTE RENAL FAILURE

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

REDUCTION OF EFFECTIVE CIRCULANTING BLOOD

VOLUME - HYPOVOLEMIA
•hemorrhagic losses
trauma
upper/lower GI bleeding
epistaxis
hemoptysis,etc.
•digestive losses
vomiting
diarrhea
surgical drainage, etc.
•renal losses
diuretics
osmotic drugs
renal diseases with salt losses
adrenal insufficiency, etc.
•cutaneous losses
burns
excessive sweating, etc.
 PRERENAL ACUTE RENAL FAILURE

REDUCTIONS OF EFFECTIVE CIRCULANTING BLOOD

VOLUME - REDISTRIBUTION
• peripheral vasodilatation
vasodilators, anaphylaxis, sepsis, anesthetics
peripherical edema
hipoalbuminemia, nephrotic syndrome, cirrhosis
• third space losses
peritonites, pancreatits, intestinal oclussion,etc.
Reduction of cardiac output
cardiac tamponade, acute myocardial infarction, valvular heart
disease, cardiomyopathys, arrhytmias, etc.
Dysfunction of renal autoregulation
treatment with cu NSAID or ACE inhibitors
 PRERENAL ACUTE RENAL FAILURE -
PATHOGENESIS

Reduction of effective circulanting blood volume

Reduction of cardiac output

– Systemic arterial hypotension which reduces renal

perfusion pressure;
– Compensatory mechanisms : sympatic stimulation,
stimulation of SRAA and ADH.

Reduction of renal perfusion

 PRERENAL ACUTE RENAL FAILURE -
PATHOGENESIS
Reduction of renal perfusion
• afferent arteriolar vasoconstriction

glomerular hidrostatic pressure

glomerular filtration rate
predominantly in renal cortex
• Stimulation of SRAA şi ADH
renal vasoconstriction
reabsorbtion of sodium, water and
bicarbonate.
 PRERENAL ACUTE RENAL FAILURE -
PATHOGENESIS

• In prerenal acute renal failure the kidney

tends to conserve water and sodium
producing a concetrated urine, with small
volume and reduced Na excretion.
 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

– characteristic urinary analysis:

• Urine specific gravity >1020 or urine
osmolarity>500mOsm/l
• plasma BUN/ plasma creatinine ratio>20/1
• Urine urea nitrogen /plasma urea nitrogen ratio >10
• urinary sodium <10-20 mEq/l
• Fractional Na excretion <1%; the ratio between
sodium and creatinine excretion;
FENa = UNa : PNa / Ucr : Pcr
FENa = UNa x Pcr / Ucr x PNa
 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

postrenal acute renal failure is the form of

renal failure caused by urinary output
obstruction
 POSTRENAL ACUTE RENAL FAILURE
• Postrenal acute renal failure causes:
• Tumors: renal adenocarcinoma, limfomas, bladder cancer ,
gynecological tumors, prostate carcinoma, others pelvic
tumors, etc.;
• inflamatory process: tuberculosis,retroperitoneal abcess,
retroperitoneal fibrosis, inflamatory disease of the large
bowel, etc.;
• Vascular diseases: aneurysm of renal artery, aortic
aneurysm;
• Papilar necrosis: diabetes mellitus, hemoglobinopathy C,
analgetic abuse , inhibition of prostaglandins, cirrhosis
• Intratubular obstruction: uric acid ,calcium phosphate
fosfate, Bene-Jones proteins , metotrexat, acyclovir,
sulfonamide;
• Diverse: nephrolithiasis, ureteral ligature, ureteral
pielography, pielography with ureteral edema, neurological
bladder,etc.
 POSTRENAL ACUTE RENAL FAILURE
• PATHOGENESIS
• Reduction of urinary output is realized
through multiple mechanisms:
– obstruction generates retrograde hiperpressure
which reduces or stops glomerular filtration;
– ureteral obstruction produces renal
vasoconstriction, response mediated by
thromboxan;
– Depending on the duration of obstruction –
structural renal damage.
 POSTRENAL ACUTE RENAL FAILURE

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

CLINICAL SINGS AND COMPLICATIONS OF ARF:

– water and electrolytes balance
• water and salt overload (anuria);
– treatment: water restriction
• volume depletion (rare; vomiting, diarrhea, etc.)
– treatment: volume repletion
• dillutional hyponatremia
– treatment: fluid restriction
• hypernatremia
– treatment: hemodialysis
• hyperkaliemia
– treatment: correction of metabolic acidosis
infusion of glucose + insulin, bicarbonate
hemodialysis
 INTRINSIC ACUTE RENAL FAILURE
CLINICAL SINGS AND COMPLICATIONS OF ARF:
– acid-base balance
• metabolic acidosis
– treatment: sodium bicarbonate, hemodialysis
– complications
• of nitrogen waste products retention
– encephalopathy, pulmonary edema, pericarditis, HTA, etc.
– absent in case of hemodialysis
• infections
– sites: urinary, intravascular catheters, intraabdominal
– no antibiotic prophylaxis
– search for the source
• gastro-intestinal bleeding (stress ulcerations)
– prophylaxis: aniacids, histamine H2 blockers, etc.
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

PATIENTS AT RISK FOR RENAL FAILURE:

• chronic renal failure
• volume depletion
• diabetes mellitus
• elderly patients
• surgery
• chronic heart failure
• urinary tract infection
• prior history of acute renal failure
 INTRINSIC ACUTE RENAL FAILURE
USE OF DIURETICS IN PREVENTION / TREATMENT
OF ACUTE RENAL FAILURE
– MANITOL
• expans blood volume (colloid solution)
• may induce vasodilation (if vasoconstriction is present)
• promotes osmotic diuresis
• solutions: 10%, 20%;
• effective in high risk conditions, before occurrence of renal insult
• should not be use in anuric intrinsic renal failure
– FUROSEMIDE
• may induce vasodilation (if vasoconstriction is present)
• may diminish renal oxygen demand (protects nephron during
ischemia); redistribution of renal blood flow
• may convert oliguric ARF to ARF with preserved urinary flow
 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

Indications of hemodialysis în ARF:

• volume overloaded (HTA, pulmonary oedema)
• Electrolyte abnormalities: K> 7mEq/l, Na< 120mEq/l, Na>155mEq/l
• acido-basic abnormalities (pH <7,20 sau pH >7,54)
• Retention of nitrogenous waste products (BUN>200mg%, creatinine
>8-10mg%)
Mnemotehnique formula for hemodialysis indications:
A – metabolic acidosis
E - electrolyte: hyperkalemia
I - intoxications
O - fluid overload
U - uremia
 RENAL REPLACEMENT
TECHNIQUES
• PERITONEAL DIALYSIS
• TECHNIQUES WITH PARENTERAL ACCESS
 Renal replacement duration
• Intermittent (for 4-8 hours/day)
• Continous (24 hours/day)
 Type of vascular access
• arterial access and venous access
• venous access
 Type of renal replacement technique
• Hemodialysis
• Hemofiltration
• Hemodiafiltration