ACUTE RENAL FAILURE

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ACUTE RENAL FAILURE
University of Medicine and Pharmacy, Iasi School
of Medicine ANESTHESIA and INTENSIVE CARE Conf.
Dr. Ioana Grigoras
MEDICINE 4th year English Program Suport de curs
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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.

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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

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PRERENAL ACUTE RENAL FAILURE( functional renal
failure, prerenal azotemia)

• CAUSES
• Reduction of effective circulanting blood volume
• Hypovolemia due to hemorrhage
• Hipovolemia due to non-hemorrhagic losses
• (see hypovolemic shock)
• Low cardiac output
• Cardiogenic shock or extracardiac obstructive
  shock
• Chronic heart failure
• Ischemic, toxic, dilated cardiomyopathy
• Cardiac disrhythmias, etc.
• Blood flow maldistribution
• Excessive vasodilatation ( septic shock, excess
  of antihypertensive drugs)
• Cirrhosis

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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
  normalizes renal function
• Healing - complete recovery of renal function
• Good prognosis
• Dialysis is not necessary
• 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).

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INTRINSIC ACUTE RENAL FAILURE

• CAUSES
• Renal parenchymal ischemia
• Prerenal acute renal failure (late treatment)
• All 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)

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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
• Dialysis often required
• Poor prognosis (variable mortality depending on
  cause)
• Recovery can be complete or with residual
  functional deficit.

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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.

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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 parenchymal 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

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ACUTE RENAL FAILURE

• FORMS
• Anuric renal failure
• urinary output lt 100ml/24 ore
• Oliguric renal failure
• urinary output lt 500ml/24 ore
• Renal failure with preserved diuresis
• urinary output gt1000ml/24 ore

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MONITORING OF THE PATIENT WITH RENAL FAILURE

• Respiratory monitoring
• Respiratorz rate
• Pattern of respiration
• Pulsoximetry
• Blood gas analysis
• Cardio-vascular monitoring
• BP , HR
• ECG
• Pulsoximetry
• 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

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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
• Water, electrolytes and nutritional support
• Infection prophylaxis
• Dialysis (when necessary)
• Obstacle removal (when necessary)

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• PRERENAL ACUTE RENAL FAILURE

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PRERENAL ACUTE RENAL FAILURE

• DEFINITION
• form of acute renal failure characterized by
  insufficient renal perfusion for the maintenance
  of adequate glomerular filtration rate.

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PRERENAL ACUTE RENAL FAILURE

• MECHANISMS
• hypovolemia
• reductions of effective circulanting blood volume
  
• reduction of cardiac output
• dysfunction of renal autoregulation

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PRERENAL ACUTE RENAL FAILURE
REDUCTION OF EFFECTIVE CIRCULANTING BLOOD VOLUME
- HYPOVOLEMIA
renal losses diuretics osmotic drugs renal
diseases with salt losses adrenal insufficiency,
etc. skin losses burns excessive sweating, etc.
hemorrhagic losses trauma upper/lower GI
bleeding epistaxis hemoptysis,etc. digestive
losses vomiting diarrhea
surgical drainages, etc.
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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

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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 sympathetic
  stimulation, stimulation of SRAA and ADH.
• Reduction of renal perfusion

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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 and ADH
• renal vasoconstriction
• reabsorbtion of sodium, water and
  bicarbonate.

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PRERENAL ACUTE RENAL FAILURE - PATHOGENESIS

• In prerenal acute renal failure the kidney tend
  to conserve water and sodium producing a small
  volume high concetration urine and decreased Na
  excretion.

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PRERENAL ACUTE RENAL FAILURE

• CLINICAL FEATURES
• Clinical signs and symptoms of the 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
  lt0,5ml/kg/hour).

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PRERENAL ACUTE RENAL FAILURE

• Diagnosis
• Identification of etiology
• variable amount of urine
• usual, oliguria ( urinary output lt0,5ml/kg/hour)
• urinary output may be normal or elevated in the
  case of diuretics and osmotic drugs
• Elevation 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 in prerenal ARF 20/1)
• 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 (chest Rx, abdominal ultrasound).

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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

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PRERENAL ACUTE RENAL FAILURE

• characteristic urinary analysis
• urine specific gravity gt1020
• urine osmolaritygt500mOsm/l
• plasma BUN/ plasma creatinine ratio gt20/1
• urine urea nitrogen /plasma urea nitrogen ratio
  gt10
• urinary sodium lt10-20 mEq/l
• fractional Na excretion lt1
• the ratio between sodium and creatinine
  excretion
• FENa UNa PNa / Ucr Pcr
• FENa UNa x Pcr / Ucr x PNa

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PRERENAL ACUTE RENAL FAILURE

• PRINCIPLES OF TREATMENT
• early and agressive treatment of the causative
  disorder for normalization 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)

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ACUTE RENAL FAILURE PROPHYLAXIS

• Identification of high risk patients
• Early correction of hemodynamic disorders which
  can induce or aggravate renal dysfunction
• Promotion of urinary output - diuretics
• Use catecholamines for renal protection
• Other drugs used in renal protection

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POSTRENAL ACUTE RENAL FAILURE
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POSTRENAL ACUTE RENAL FAILURE

• DEFINITION
• postrenal acute renal failure is the form of
  renal failure caused by urinary output obstruction

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POSTRENAL ACUTE RENAL FAILURE

• Causes
• Tumors
• renal adenocarcinoma, limfomas, bladder cancer,
  gynecological tumors, prostate carcinoma, others
  pelvic tumors, so
• inflamatory process
• tuberculosis, retroperitoneal abcess,
  retroperitoneal fibrosis, bowel inflammatory
  disease, so
• Vascular diseases
• Renal artery aneurysm, aortic aneurysm
• Papilar necrosis
• diabetes mellitus, hemoglobinopathy C, analgetic
  abuse, inhibition of prostaglandins, cirrhosis
• Intratubular obstruction
• uric acid, calcium phosphate, Benes-Jones
  proteins, metotrexat, acyclovir, sulfonamide
• Others
• nephrolithiasis, ureteral ligature, ureteral
  pielography, pielography with ureteral edema,
  neurological bladder,etc

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POSTRENAL ACUTE RENAL FAILURE

• PATHOGENESIS
• Mechanisms of urinary output reduction
• Urinary obstruction retrograde
  overpressure
• reduced or suspended glomerular
  filtration
• Ureteral obstruction thromboxan
  mediated renal vasoconstriction
• Long lasting obstruction structural renal
  damage.

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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

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POSTRENAL ACUTE RENAL FAILURE

• DIAGNOSIS
• Identification of the obstructive cause
• Ultrasonography is the screening test and often a
  diagnostic examination
• level of obstruction
• retrograde dilatation
• the cause lithiasis, tumors, so
• Investigations for complete diagnosis of the
  causative disorder
• 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 (FENalt1 in early phases,
  FENagt3 in late phases)

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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.

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INTRINSIC ACUTE RENAL FAILURE
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INTRINSIC ACUTE RENAL FAILURE

• Causes
• Renal ischemia
• Nephrotoxic substances
• Drugs antibiotics, NSAID, cyclosporine, etc.
• Radiocontrast agents
• Toxins 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.

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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

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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 lt 3
• urinaru creatinine/blood creatinine lt 20
• urinary Na gt 40mEq/l
• fractional sodium excretion gt 3
• other diagnostic tests to exclude postrenal
  causes

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INTRINSIC ACUTE RENAL FAILURE

• CLINICAL SINGS AND COMPLICATIONS
• 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

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INTRINSIC ACUTE RENAL FAILURE

• CLINICAL SINGS AND COMPLICATIONS
• 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.

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INTRINSIC ACUTE RENAL FAILURE

• PHASES
• phase I
• dominated by the 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

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ACUTE RENAL FAILURE PROPHYLAXIS

• Identification of high risk patients
• Early correction of hemodynamic disorders which
  can induce or aggravate renal dysfunction
• Promotion of urinary output - diuretics
• Use catecholamines for renal protection
• Other drugs used in renal protection

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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

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INTRINSIC ACUTE RENAL FAILURE

• USE OF DIURETICS IN PREVENTION / TREATMENT OF
  ACUTE RENAL FAILURE
• MANITOL
• expands 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

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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

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RENAL REPLACEMENT TECHNIQUES

• Indications of hemodialysis în ARF
• volume overloaded HTA, pulmonary edema
• electrolyte abnormalities Kgt 7mEq/l, Nalt
  120mEq/l, Nagt155mEq/l
• acido-base abnormalities pH lt7,20 sau pH gt7,54
• retention of nitrogenous waste products
  BUNgt200mg, creatinine
• gt8-10mg
• Mnemotehnique formula for hemodialysis
  indications
• A metabolic acidosisE - electrolyte
  hyperkalemiaI - intoxicationsO - fluid
  overload U - uremia

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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