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 Rapid loss of renal function leading to
  abnormal water, electrolyte and solute
  balance.
 Occurs over a period of hours to days.
 Usually associated with oliguria. Some
  patients develop non oliguric ARF eg. After
  radiocontrast media.
 It can be reversed with treatment of the
  cause.
 Acute-on top of chronic renal failure may
  occur.                                     2
RIFLE classification of acute kidney injury


 Grade                GFR criteria                    UO criteria
                          SCr × 1.5                UO < 0.5 mL/kg/hour
 Risk                                                   × 6 hours
                           SCr × 2                 UO < 0.5 mL/kg/hour
 Injury                                                × 12 hours
                    SCr × 3 or SCr > 350           UO < 0.3 mL/kg/hour
 Failure          mol/L with an acute rise             × 24 hours
                         > 40 mol/L
                  Persistent AKI > 4 weeks
 Loss
                  Persistent renal failure >
 ESKD                    3 months

AKI, acute kidney injury; ESKD, end-stage kidney disease, GFR,
glomerular filtration rate; SCr, serum creatinine; UO, urine output.
                                                                         3
Acute Renal Failure

Pre-renal        Intrinsic renal             Post-renal
 causes              causes                   causes

Glomerular   Tubular         Interstitial   Vascular
disease      injury          nephritis      disease
                 Ischaemic

                 Toxic
                                                          4
Causes of Acute Renal Failure
Prerenal (Reduced renal perfusion)
1) Volume depletion:
    Renal loss – diuretics, osmotic diuresis (DKA).
     Addisonian crisis.
    Extrarenal loss – vomiting, diarrhea, skin
     losses (burns, excessive sweating).
    Hemorrhage.
    Pancreatitis.
2) Hypotension (regardless of cause):
3) Cardiovascular:
    Congestive heart failure, reduced myocardial
     function, arrhythmias.
    Severe valvular heart disease.
                                                   5
4) Hemodynamic (intense intrarenal
   vasoconstriction):
      Radiographic contrast.
      Prostaglandin inhibition (NSAIDs).
      Cyclosporine and tacrolimus.
      ACE inhibitors.
      Amphotericin.
      Hypercalcemia.

5) Hepatorenal syndrome (bland urinary
   sediment, oliguria, low urine sodium, not
   reversed with volume repletion, reversible with
   successful liver transplant).
                                                     6
Intrinsic or intrarenal
1) Vascular:
  Renal infarction, renal artery stenosis, renal vein
   thrombosis.
  Malignant hypertension, scleroderma renal crisis,
   atheroemboli.

2) Tubular:
  Ischemic-prolonged prerenal state, sepsis syndrome,
   systemic hypotension.
  Nephrotoxic-aminoglycosides, methotrexate, cisplatin,
   myoglobin (rhabdomyolysis), hemoglobin
   (intravascular hemolysis).
                                                       7
3) Glomerular:
    Acute glomerulonephritis.
    Good pasture syndrome.
    Vasculitis (Wegener’s granulomatosis, polyarteritis).
    Thrombotic microangiopathy (hemolytic uremic
     syndrome, TTP).

4) Interstitium:
  Medications–penicillins, cephalosporins, ciprofloxacin,
   NSAIDs, phenytoin.
  Tumor infiltration (lymphoma, leukemia).
  Sarcoidosis, sjogren syndrome.
                                                         8
Postrenal (obstruction)
 Prostate hypertrophy, neurogenic bladder
 Intraureteral obstruction-crystals stones, clots,
  tumor.
 Extraureteral obstruction-tumor (cervical,
  prostate), retroperitoneal fibrosis.
 Ureteric ligation during pelvic surgery.




                                                      9
* Pre-renal failure :
  - There is hypotension with signs of poor preripheral
    perfusion.
  - Postural hypotension.
  - Signs of hypovolemia.
  - Manifestations of the cause.
  - Metabolic acidosis and ↑ K may be present.

* Established renal ARF :
  - Oliguria (urine volume < 400ml/d) or anuria
    (< 100ml/d).
  - Disturbances of water, electrolyte and acid base
    balance (↑ K, ↓ pH, Dilutional ↓ Na).
  - Uremic features include anorexia, nausea, vomiting,
    hiccough, acidotic breathing ….                   10
* Post-renal (ARF) :
 - Loin pain (which may be constant or intermittent)
 - Complete    anuria   with   bilateral   obstruction   or
   complete obstruction of single kidney.
 - Infection may → fever, septicaemia.
 - Bladder outflow obstruction → Hesitancy, weak
   urine stream, terminal drippling, re-tension with
   overflow may occur
 - Screening of urinary tract by sonar is essential.

                                                         11
Probable Causes of Acute Renal Failure
            Based on the Findings of The History

History                                  Probable causes of acute
                                         renal failure
Review of systems
Pulmonary system
   Sinus, upper respiratory or pulmonary Pulmonary-renal syndrome or vasculitis
   symptoms
Cardiac system
   Symptoms of heart failure          Decreased renal perfusion
   Intravenous drug abuse, prosthetic Endocarditis
   valve or valvular disease
Gastrointestinal System
   Diarrhea, vomiting or poor intake.    Hypovolemia
   Colicky abdominal pain radiating from Urolithiasis
   flank to groin
Genitourinary System
   Symptoms      of    benign prostatic Obstruction
   hypertrophy.
   Bone pain in the elderly             Multiple myeloma or prostate cancer
   Trauma or prolonged immobolization   Rhabdomyolysis (pigment nepbropathy)12
(Cont.)
History                                      Probable causes of acute
                                             renal failure
Skin
   Rash                                      Allergic interstitial nephritis, vasculitis,
                                             systemic lupus erythematosus,
                                             atheroemboli or thrombotic
                                             thrombocytopenic purpura.
Constitutional symptoms
   Fever, weight loss, fatigue or anorexia   Malignancy or vasculitis
Past medical history
Multiple sclerosis, diabetes mellitus Neurogenic bladder
or stroke
Past surgical history
Recent surgery or procedure                  Ischemia, atheroemboli, endocarditis
                                             or exposure to contrast agent
Medication history
Angiotensin-converting       enzyme Decreased renal perfusion, acute
inhobitors,     nonsteroidal    anti- tubular necrosis or allergic interstitial
inflammatory drugs, antibiotics or nephritis
acyclovir (Zovirax)                                                         13
Probable Causes of Acute Renal Failure
             Based on the Physical Findings

Physical    Probable causes of acute renal failure
Examination
Vital signs
  Temperature    Possible infection.
  Blood          Hypertension: G.N or malignant hypertension.
  pressure       Hypotension: volume depletion or sepsis.
Weight loss or   Hypovolemia or hypervolemia.
gain
Mouth            Dehydration
Jugular veins    Hypovolemia or hypervolemia
and axillae
(perspiration)
Pulmonary        Signs of pneumonia, cavitations, pleurisy.
system
Heart            New murmur of endocarditis or signs of
                 congestive heart failure

                                                                14
(Cont.)

Physical    Probable causes of acute renal failure
Examination
Abdomen      Bladder distention suggesting uretheral
             obstruction
Pelvis       Pelvic mass
Rectum       Prostate enlargement
Skin         Rash of interstitial nephritis, purpura of
             microvascular disease, livedo reticularis
             suggestive of atheroembolic disease, or splinter
             hemorrhages or Osler’s nodes of endocarditis.




                                                            15
* Blood urea nitrogen and serum creatinine are
  elevated.
* ABG, electrolytes, CBC, and serology.
* U/S kidneys (The size of the kidneys is usually
  normal.
* Serology: ANA, ANCA, Anti DNA, HBV, HCV, Anti
 GBM. Cryoglobulin, CK, urinary myoglobin.




                                               16
* Urine analysis :
 - Unremarkable in pre and post renal causes.
 - Differentiates ATN vs. AIN. vs. AGN
    Granular casts in ATN.
    WBC casts in AIN.
    RBC casts in AGN.

 - Urine electrolytes (Na) and osmolality.

* Hansel stain for Eosinophiluria.

                                                17
LAB Findings of Specific Types of
                      Acute Renal Failure

 Findings on blood tests                   Diagnosis to consider
Very high uric acid level            Suggestive of malignancy or tumor lysis
                                     syndrome leading to uric acid crystals;
                                     also seen in prerenal acute renal failure.
Elevated creatinine kinase or        Rhabdomyolysis.
myoglobin levels
Elevated prostate-specific antigen   Prostate cancer.
Abnormal serum protein               Multiple myeloma.
electrophoresis
Low complement levels                Systemic lupus erythematosus,
                                     postinfectious glomerulophritis,
                                     subacute bacterial endocarditis
Positive antineurtrophic             Small-vessel vasculitis (Wegener’s
cytoplasmic antibody (ANCA)          granulomatosis or polyartheritis nodosa)

                                                                            18
LAB Findings of Specific Types of
                 Acute Renal Failure (Cont.)

 Findings on blood tests                 Diagnosis to consider
Positive antinuclear antibody to Systemic lupus erythematosus
double-stranded DNA

Positive antibody to glomerular Goodpasture’s syndrome
basement membrane

Positive antibodies to streptolysin Poststreptocaccal glomerulonephritis.
O, streptokinase or hyaluronidase

Schistocytes on peripheral smear, Hemolytic uremic syndrome or
decreased hepatoglobin level, thrombotic thrombocytopenic purpura
elevated lactate dehydrogenase
level or elevated serum bilirubin
level

Low albumin levels                 Liver disease or nephrotic syndrome

                                                                         19
Laboratory Findings in Acute Renal Failure To
         Differentiate Pre-Renal from Renal Failure

      Index            Prerenal Azotemia Oliguric Acute Renal
                                             Failure (ATN)
  BUN/PCR Ratio             > 20 : 1                10-15 : 1
Urine sodium (UNa)            < 20                    > 40
      meg/L
 Urine osmolality,           > 500                   < 350
  mosmol/L H2O
Fractional excretion         <1%                     >2%
     of sodium
   Response to            Improvement          No improvement
     volume
 Urinary Sediment            Bland       ATN: muddy brown granular
                                         casts, cellular debris, tubular
                                                 epithelial cells

                                                                    20
   ARF is common in the ICU.
   ARF is an independent factor for prognosis
    in the ICU.
   The incidence of ARF in the ICU 40-60%
    compared to 1-3% in the ward.
   ARF still has a mortality of 50% since it
    occurs in very sick patients with multiorgan
    failure.
                                              21
   Predisposing factors to ARF include old age
    sepsis pre existing renal disease heart
    disease and chronic liver disease.


   Mechanical ventilation has an adverse effect
    on renal blood flow and GFR and subsequent
    renal function.
                                              22
• Patients with ICU acquired ARF were classified
  into the following :
  A) According to the urine output:
    - Oliguric (urine volume of < 400 ml/day).
    - Nonoliguric (urine volume of > 400 ml/day).
    - Anuric (urine volume of < 100 ml/day).
 B) According to the cause:
    1)   Prerenal ARF.
    2)   Ischemic acute Tubular necrosis.
    3)   Nephrotoxic ARF (ATN or AIN).
    4)   Sepsis induced ARF.
    5)   Hepato-renal syndrome.
    6)   Other causes (e.g. obstructive uropathy,
         pigment nephropathy, microangiopathies).
                                                    23
1) Prerenal ARF was defined as ARF to renal
  hypoperfusion with recovery after correction of
  hemodynamic disturbances.

2) Ischemic Acute tubular necrosis (IATN) was
  diagnosed when renal function did not improve after
  correction of possible prerenal causes, and when
  hepatorenal    syndrome,    vascular,   interstitial,
  glomerular and obstructive aetiologies were
  excluded.

                                                     24
• Decreased renal perfusion was identified by
  the following observations :

   Any documented decline in blood pressure to less
    than 90/60 mmHg.
   Overt volume contraction on physical examination
    (postural hypotension, decreased skin turgor, …),
    and central venous pressure (CVP) less than 5 cm
    H2O.
   Clinically evident congestive heart failure with
    improvement      in  renal    function  following
    appropriate treatment of heart failure.
                                                   25
3) Nephrotoxic ARF (either AIN or ATN)

    Nephrotoxic Acute Interstitial Nephritis
     (AIN): history of drug ingestion, fever, rash, or
      arthralgias. Urinary increase in WBCs (frequently
      eosirophiluria),   WBC      casts  RBCs,     and
      proteinuria, with systemic eosinophilia, if
      histologically demonstrated by renal biopsy or
      when there was a high grade of clinical
      suspicion.
                                                     26
 Nephrotoxic Acute Tubular Necrosis
  (ATN): was defined as ARF occurring after
  administration of drugs known to cause ATN (e.g.
  aminoglycosides, amphotericin, contrast media
  etc …).

Concurrent administration of vancomycin &
aminoglycosides to critically ill septic
patients with normal renal function of
baseline induces mainly slight and transient
toxic tubular effects.
                                                27
   Radiographic contrast media, were determined to
    be the cause of renal insufficiency when the
    serum creatinine concentration increased – as
    defined – within 72 hours following a radiologic
    procedure    employing   these    agents    (e.g.
    intravenous pyelogram – angiography – computed
    tomography scan).




                                                   28
4) Sepsis induced ARF was diagnosed if ARF is
  associated with at least one of the following three
  conditions:
    Documented bacteremia.
    A known focus of infection
    Immunosuppression with neutropenia,

   and at least two additional findings: rigors –
   unexplained hyperventilation unexplained sudden
   fall in blood pressure – abrupt rise in temperature to
   more than 38C not due to transfusion reaction –
   unexplained leukocytosis of more than 15.000 mm3.
                                                       29
5) Hepatorenal syndrome was assigned as the
  cause of renal failure if the patient had severe liver
  failure   (e.g.   ascites    –    jaundice,    hepatic
  encephalopathy) – and a urine sodium concentration
  less than 10 mEq/Liter, and the renal function did not
  respond to a volume expansion.




                                                      30
6) Other causes:

      Obstruction was determined to be the cause of
       renal failure if obstruction was present by
       physical examination (as enlarged bladder) or by
       radiological evaluation and if improvement in
       renal function followed relief of obstruction.



                                                        31
   Pigment      induced-ARF,   history   suggestive   of
    rhabdomyolysis, urine dispstick positive for blood
    (heme)       without   microscopic    haematuria
    hyperkalemia, hyperphosphatemia, hypocalcemia,
    increased creatine kinase-MM fraction and serum
    uric acid.




                                                       32
 Atheroembolic ARF:
      Associated with emboli of fragments of
atherosclerotic plaque from aorta and other large
arteries.
      Diagnose by history, physical findings
(evidence of other embolic phenomena, ischemic
digits, “blue toe” syndrome, etc), low serum C3
and C4, peripheral eosinophiluria, rarely WBC
casts.
      Commonly      occur   after   intravasculer
procedures or cannulation (cardiac catheter,
CABG).
                                               33
Number of patients admitted in different
              ICUs with acquired ARF in each ICU
      ICU            No. of admitted   No. & % of patients
                        patients       with ICU acquired
                                        ARF in each ICU
   Medical ICU            1123              402 (35.7 %)
 Gynecology ICU            431              98 (22.7 %)
   Surgical ICU            336              53 (15.7 %)
  Neurology ICU            116              17 (14.6 %)
    Chest ICU              409              57 (13.9 %)
Coronary Care Unit         722              78 (10.1 %)
Cardiosurgery ICU          425              43 (10.1 %)
      Total               3562              748 (21 %)

                                                           34
Causes of ICU acquired-ARF in 748 patients

              Causes             No. & % of patients
                 iATN                    283 (37.8 %)
               Prerenal                  198 (26.5 %)
              Toxic ARF                  80 (10.6 %)
         Sepsis induced ARF              89 (11.9 %)
                 HRS                      73 (9.8 %)
                Others                    25 (3.4 %)



iATN = ischemic acute tubuler necrosis. Toxic ARF = toxic acute renal
failure. HRS – hepatorenal syndrome.

                                                                        35
Number & Percentage of patient mortality
                             in each ICU

      ICU             No. of patients    Mortality No. & %
                     with ICU acquired     in each ICU
                            ARF
   Medical ICU              402              261 (64.9 %)
Coronary Care Unit          78               20 (25.6 %)
    Chest ICU               57               28 (49.1 %)
  Neurology ICU             17                9 (52.9 %)
   Surgical ICU             53               10 (18.8 %)
Cardiosurgery ICU           43               19 (44.1 %)
Gyne & obst. ICU            98               42 (42.8 %)
      Total                 748                  389

                                                             36
* The initiation of RRT in patients with AKI prevents
  uremia and immediate death from the adverse
  complications of renal failure.
* It is possible that variations in the timing of
  initiation, modalities, and/or dosing may affect
  clinical outcomes.
* Multiple modalities of RRT are currently available.
  These include intermittent hemodialysis (IHD),
  continuous renal replacement therapies (CRRTs),
  and hybrid therapies, such as sustained low-
  efficiency dialysis (SLED). Despite these varied
  techniques mortality in patients with ARF remains
  high greater than 50% in severely ill patients.  37
1.   Indications for dialysis.
2.   Timing of initiation of dialysis.
3.   Optimal modality.
4.   Optimal Dosing.
5.   Discontinuation of therapy.



                                         38
1) Refractory fluid overload.
 2) Hyperkalemia (plasma potassium concentration >
    6.5 meq/L) or rapidly rising potassium levels.
 3) Metabolic acidosis (pH less than 7.1).
 4) Signs of uremia e.g. pericarditis and decline in
    mental state.
 5) Certain alcohol and drug intoxications.


* The likelihood of requiring RRT is increased in
  patients with underlying CKD (Acute on top of
  chronic).
                                                  39
   Studies published during the 1960s and 1970s
    suggested that improved outcomes were associated
    with the initiation of hemodialysis when BUN reached
    exceeded 150 to 200 mg/dL.




                                                     40
   More recent studies have evaluated the relationship
    between the timing of RRT initiation and clinical
    outcomes. Several non-randomized studies have
    reported that improved outcomes, including survival,
    are associated with early versus late initiation of RRT.
   It has been suggested that initiation of RRT dialysis
    prior to the development of overt symptoms and signs
    of renal failure due to AKI improves the outcome.


                                                          41
Can dialysis delay recovery
            of renal function ?
   There is at least theoretical concern that dialysis
    might have detrimental effects on renal function.
   Three factors may be important in this regard:
    1) A reduction in urine output; Both removal of
       excess volume and of urea contribute to a
       reduction in or even cessation of the urine output.
       The fall in urine output should not delay the
       regeneration of tubules.

    2) Induction of hypotension; Autoregulation is
       impaired in ATN, because vascular endothelial
       injury reduces the release of vasodilating
       substances so recurrent ischemic tubular injury is
       more likely to occur, thereby delaying the
       restoration of function.
                                                       42
3) Complement activation resulting from a blood-
   dialysis membrane interaction, can lead to
   neutrophilic infiltration into the kidney (and other
   tissues) and prolonged acute kidney injury.

4) High flux membranes can enhance removal of
   putative toxins and improve outcome, but may
   also allow the back transport (from dialysate to
   blood).




                                                    43
1) Intermittent hemodialysis (IHD).
2) Continuous renal replacement therapy (CRRT).
3) Peritoneal dialysis.




                                                  44
Principles of dialysis

 Dialysis     =  diffusion =
   passive    movement      of
   solutes across a semi-
   permeable membrane down
   concentration gradient.
   * Good for small molecules.
 (Ultra)      filtration     =
  convection = solute + fluid
  removal      across     semi
  permeable membrane down
  a pressure gradient (solvent
  drag).
  * Better for removal of fluid   Figure (1): Principles of dialysis
     and medium-size molecules.      (top panel) and filtration
                                           (lower panel).        45
Principles of dialysis

 Hemodialysis = solute passively diffuses down
   concentration gradient.
    Dialysate flows countercurrent to blood flow.
    Urea, creatinine, K move from blood to dialysate.
    Ca and bicarb move from dialysate to blood.

 Ultrafiltration = This is the convective flow of water
   and dissolved solutes down a pressure gradient
   caused by hydrostatic or osmotic forces.
 Hemodiafiltration = combination of dialysis and
   ultrafiltration

                                                         46
Intermittent hemodialysis (IHD)

 Oldest and most common technique.
 Primarily diffusive treatment: blood                  and
   dialysate are circulated in countercurrent manner.
    Also some fluid removal by ultrafiltration due to
     pressure driving through circuit.

 Best for removal of small molecules.
 Typically performed 4 hours 3x / wk or daily.




                                                         47
Continuous Renal Replacement
              Therapy (CRRT)
 CRRT strategies are particularly useful in haemo-
  dynamically compromised patients with ARF.
 They allow slow and gentle removal of solutes and
  fluid, avoiding major intravascular fluid shifts and
  minimizing electrolyte disturbances, hypotension and
  arrhythmias.
 Inflammatory mediators may also be continuously
  removed by CRRT, so it may be useful in sepsis
  syndrome.


                                                    48
Types of Continuous Renal
       Replacement Therapies (CRRT)
Blood access
Continuous arteriovenous hemofiltration (CAVH).
Continuous arteriovenous hemodialysis (CAVHD).
Continuous arteriovenous hemodiafiltration (CAVHDF).
Continuous venovenous hemofiltration (CVVH).
Continuous venovenous hemodialysis (CVVHD).
Continuous venovenous hemodiafiltration (CVVHDF).
Slow low efficiency dialysis (SLED).
Slow continuous ultrafiltration (SCUF).
Extended daily dialysis (EDD).

Peritoneal access
Continuous equilibrium peritoneal dialysis.Blood acce

                                                       49
Haemofiltration

 Provides solute clearance by convection as
  solutes are dragged down pressure gradient
  with water.
 It provides better removal of large MW solutes
  e.g. B2-microglobulin, improved clearance of
  low MW uraemic toxins and better
  cardiovascular stability and Bp control than
  HD.
 Inflammatory markers are improved.

                                              50
Sustained low-efficiency daily dialysis
    (SLED):
 Uses conventional dialysis machines but blood flow
  of 100-200 ml/M and dialysate flow of only 100 ml/M
  for 8-24 hr/D.
 Major advantages: Flexibility     of   duration   and
  intensity, reduced costs.
 Excellent tolerability, cardiovascular stability and
  solute removal.




                                                     51
Slow continuous ultrafiltration ((SCUF):
 Used for fluid removal in overloaded CHF patients
  with refractory edema without severe renal failure.
 Blood is driven through a highly permeable filter in a
  venovenous mode to primarily remove water, not
  solute.
 The ultrafiltrate produced during membrane transit is
  not replaced.

Haemodiafiltration (HDF):
 Simultaneous use of HD and UF.
 It is good with CVS instability.
 It can remove the inflammatory mediators.

                                                      52
* Current data suggest that survival and recovery
  of renal function are similar with both CRRT
  and IHD.
* Advocates for CRRT have claimed that CRRT is
  associated with the following advantages
  compared with IHD:
 1) Enhanced hemodynamic stability, in hemodynamically
    unstable patients.
 2) Increased net salt and water removal, thereby
    permitting superior management of volume overload
    and nutritional requirements.
                                                    53
3)    Enhanced clearance of inflammatory mediators, which
     may provide benefit in septic patients, particularly
     using convective modes of continuous therapy.

4) Among patients with acute brain injury or fulminant
   hepatic failure, continuous therapy may be associated
   with better preservation of cerebral perfusion.




                                                       54
Peritoneal dialysis:

 Least useful form of CRRT in the ICU.
 Diffusive treatment: Blood in capillaries of peritoneal
  membrane exposed to dialysate in abdomen.
 Continuous or intermittent.
 Inefficient solute/ volume clearance if unstable or
  poor intestinal blood flow.
 Can’t use if intra-abdominal pathology – risk of
  peritonitis.
 Respiratory burden.

                                                       55
* Intermittent hemodialysis – Dosing in IHD is
  based upon the dose delivered per session
  plus the frequency of sessions.
* Improved survival was observed with a higher
  Kt/V (greater than 1), which was particlarly
  evident among patients with intermediate
  levels of illness severity.
* Compared with every other day dialysis, daily
  therapy was associated with a significant
  reduction in mortality, fewer hypotensive
  episodes during hemodialysis, and more rapid
  resolution of acute renal failure.
                                             56
* In contrast, the Acute Renal Failure Trial
  Network (ATN) Study did NOT find a difference
  in mortality associated with a more intensive
  dosing strategy for renal replacement therapy.
* The Hanover Dialysis Outcome study compared
  extended duration dialysis, provided for
  approximately 8 hours per day, to a more
  intensive regimen where additional 8-hour
  treatment sessions were provided to maintain
  the BUN < 42 mg/dL. No difference in survival
  or recovery of kidney function was observed
  with more intensive treatment.
                                              57
• The Randomized Evaluation of Normal versus
  Augmented Legal of RRT study and two meta-
  analyses were performed. All studies found
  that, compared with standard intensity dialysis,
  higher intensity dialysis did not result in
  improved survival or clinical benefits.
• It is recommended that IHD be provided 3
  times/week with monitoring of the delivered
  dose of therapy to ensure a minimum delivered
  Kt/V of 1.2 per treatment.

                                                58
RRT is usually continued until the patient
manifests evidence of recovery of kidney
function.
1. Increase in urine output.
2. A progressive decline in serum creatinine
   concentration after initial attainment of stable values
   (assessed daily during CRRT or predialysis in
   patients managed with IHD) despite a constant dose
   of renal support.
3. Measurement of creatinine clearance e.g. on six-
   hour timed urine collections obtained when the urine
   output exceeded 30 mL/hour based on an average
   serum creatinine at the beginning and end of the
   timed collection.
                                                        59
A precise level of kidney function needed to
allow discontinuation of renal support has not
been established; however,
Creatinine clearance < 12 mL/min → no discontinuation.
Creatinine clearance > 20 mL/min → discontinue.
Creatinine clearance 12 to 20 mL/min → optional.




                                                         60
1) No drugs are currently available to enhance
   or hasten renal recovery once ARF occurs.
2) There is now clear evidence that ARF is
   associated with excess mortality, irrespective
   of whether the patient requires renal
   replacement therapy.

3) Hense prevention is the only powerful
   tool to improve outcome of AKI.

                                               61
Identification of patients at high risk to develop
AKI-Elderly, DM, HT. Sepsis etc ....
    Non Pharmacological         Pharmacological
   Ensuring adequate         Loop diuretics,
    hydration (reversing      Mannitol,
    dehydration,              Dopamine &
   Maintenance of             Fenoldopam.
    adequate mean             Natriuretic Peptides.
    arterial pressure,
   Minimizing exposure
    to nephrotoxins.
                                                   62
 NS, albumin, plasma ….
 CVP = 8-12 cm H2O, MAP > 65 mmHg.
 Optimal rate of infusion remain unclear and
  should be individualized.



 Target MAP ≥ 65 mmHg.
 Which vasopressors to be used.
 Role of low dose dopamine..
                                           63
 Noradrenaline is the drug of choice in AKI in
  sepsis.
 Norepinephrine has been demonstrated to
  preserve splanchnic blood flow better than
  dopamine.
 Optimise fluid before starting vasopressors.
 Low dose dopamine should not be used for
  renal protection in severe sepsis.
                                             64
Meta-analysis: Low-Dose Dopamine Increases
Urine Output but Does Not Prevent Renal
Dysfunction or Death

Low-dose dopamine offers transient
improvements in renal physiology, but no
good evidence shows that it offers
important clinical benefits to patients with
or at risk for acute renal failure.


                                          65
   In animal studies the use of mannitol and loop
    diuretic minimize the degree of renal injury if
    given at the time of ischemic injury.
   Loop   diuretics   decrease    the   active    Na
    transport   in   the   thick   ascending      loop
    decreasing the energy requirement.

                                                    66
   Increasing the urine output by loop diuretic
    make the management easier but does not
    affect cell injury or the severity of the renal
    damage.
   Loop diuretic increase the urine output in the
    remaining   nephrons    and   therefore   huge
    doses are required that may cause deafness.
                                                 67
   ANP had been tried in experimental models
    without any benefit despite their ability to
    increase renal blood flow and Na excretion.
   Calcium channel blockers decrease Ca influx
    to the cells that lead to cell injury.
   Most human studies were done on
    established ATN.
                                              68
   Uncontrolled   studies     showed      that   those
    patients who respond to diuretics or mannitol
    may have better outcome but these patients
    has less severe disease.
   Controlled   studies     failed   to   show    any
    evidence that low dose dopamine have any
    protection of cell injury in ischemic renal
    damage.                                          69
70

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Acute renal failure in icu .....

  • 1.  Rapid loss of renal function leading to abnormal water, electrolyte and solute balance.  Occurs over a period of hours to days.  Usually associated with oliguria. Some patients develop non oliguric ARF eg. After radiocontrast media.  It can be reversed with treatment of the cause.  Acute-on top of chronic renal failure may occur. 2
  • 2. RIFLE classification of acute kidney injury Grade GFR criteria UO criteria SCr × 1.5 UO < 0.5 mL/kg/hour Risk × 6 hours SCr × 2 UO < 0.5 mL/kg/hour Injury × 12 hours SCr × 3 or SCr > 350 UO < 0.3 mL/kg/hour Failure mol/L with an acute rise × 24 hours > 40 mol/L Persistent AKI > 4 weeks Loss Persistent renal failure > ESKD 3 months AKI, acute kidney injury; ESKD, end-stage kidney disease, GFR, glomerular filtration rate; SCr, serum creatinine; UO, urine output. 3
  • 3. Acute Renal Failure Pre-renal Intrinsic renal Post-renal causes causes causes Glomerular Tubular Interstitial Vascular disease injury nephritis disease Ischaemic Toxic 4
  • 4. Causes of Acute Renal Failure Prerenal (Reduced renal perfusion) 1) Volume depletion:  Renal loss – diuretics, osmotic diuresis (DKA). Addisonian crisis.  Extrarenal loss – vomiting, diarrhea, skin losses (burns, excessive sweating).  Hemorrhage.  Pancreatitis. 2) Hypotension (regardless of cause): 3) Cardiovascular:  Congestive heart failure, reduced myocardial function, arrhythmias.  Severe valvular heart disease. 5
  • 5. 4) Hemodynamic (intense intrarenal vasoconstriction):  Radiographic contrast.  Prostaglandin inhibition (NSAIDs).  Cyclosporine and tacrolimus.  ACE inhibitors.  Amphotericin.  Hypercalcemia. 5) Hepatorenal syndrome (bland urinary sediment, oliguria, low urine sodium, not reversed with volume repletion, reversible with successful liver transplant). 6
  • 6. Intrinsic or intrarenal 1) Vascular:  Renal infarction, renal artery stenosis, renal vein thrombosis.  Malignant hypertension, scleroderma renal crisis, atheroemboli. 2) Tubular:  Ischemic-prolonged prerenal state, sepsis syndrome, systemic hypotension.  Nephrotoxic-aminoglycosides, methotrexate, cisplatin, myoglobin (rhabdomyolysis), hemoglobin (intravascular hemolysis). 7
  • 7. 3) Glomerular:  Acute glomerulonephritis.  Good pasture syndrome.  Vasculitis (Wegener’s granulomatosis, polyarteritis).  Thrombotic microangiopathy (hemolytic uremic syndrome, TTP). 4) Interstitium:  Medications–penicillins, cephalosporins, ciprofloxacin, NSAIDs, phenytoin.  Tumor infiltration (lymphoma, leukemia).  Sarcoidosis, sjogren syndrome. 8
  • 8. Postrenal (obstruction)  Prostate hypertrophy, neurogenic bladder  Intraureteral obstruction-crystals stones, clots, tumor.  Extraureteral obstruction-tumor (cervical, prostate), retroperitoneal fibrosis.  Ureteric ligation during pelvic surgery. 9
  • 9. * Pre-renal failure : - There is hypotension with signs of poor preripheral perfusion. - Postural hypotension. - Signs of hypovolemia. - Manifestations of the cause. - Metabolic acidosis and ↑ K may be present. * Established renal ARF : - Oliguria (urine volume < 400ml/d) or anuria (< 100ml/d). - Disturbances of water, electrolyte and acid base balance (↑ K, ↓ pH, Dilutional ↓ Na). - Uremic features include anorexia, nausea, vomiting, hiccough, acidotic breathing …. 10
  • 10. * Post-renal (ARF) : - Loin pain (which may be constant or intermittent) - Complete anuria with bilateral obstruction or complete obstruction of single kidney. - Infection may → fever, septicaemia. - Bladder outflow obstruction → Hesitancy, weak urine stream, terminal drippling, re-tension with overflow may occur - Screening of urinary tract by sonar is essential. 11
  • 11. Probable Causes of Acute Renal Failure Based on the Findings of The History History Probable causes of acute renal failure Review of systems Pulmonary system Sinus, upper respiratory or pulmonary Pulmonary-renal syndrome or vasculitis symptoms Cardiac system Symptoms of heart failure Decreased renal perfusion Intravenous drug abuse, prosthetic Endocarditis valve or valvular disease Gastrointestinal System Diarrhea, vomiting or poor intake. Hypovolemia Colicky abdominal pain radiating from Urolithiasis flank to groin Genitourinary System Symptoms of benign prostatic Obstruction hypertrophy. Bone pain in the elderly Multiple myeloma or prostate cancer Trauma or prolonged immobolization Rhabdomyolysis (pigment nepbropathy)12
  • 12. (Cont.) History Probable causes of acute renal failure Skin Rash Allergic interstitial nephritis, vasculitis, systemic lupus erythematosus, atheroemboli or thrombotic thrombocytopenic purpura. Constitutional symptoms Fever, weight loss, fatigue or anorexia Malignancy or vasculitis Past medical history Multiple sclerosis, diabetes mellitus Neurogenic bladder or stroke Past surgical history Recent surgery or procedure Ischemia, atheroemboli, endocarditis or exposure to contrast agent Medication history Angiotensin-converting enzyme Decreased renal perfusion, acute inhobitors, nonsteroidal anti- tubular necrosis or allergic interstitial inflammatory drugs, antibiotics or nephritis acyclovir (Zovirax) 13
  • 13. Probable Causes of Acute Renal Failure Based on the Physical Findings Physical Probable causes of acute renal failure Examination Vital signs Temperature Possible infection. Blood Hypertension: G.N or malignant hypertension. pressure Hypotension: volume depletion or sepsis. Weight loss or Hypovolemia or hypervolemia. gain Mouth Dehydration Jugular veins Hypovolemia or hypervolemia and axillae (perspiration) Pulmonary Signs of pneumonia, cavitations, pleurisy. system Heart New murmur of endocarditis or signs of congestive heart failure 14
  • 14. (Cont.) Physical Probable causes of acute renal failure Examination Abdomen Bladder distention suggesting uretheral obstruction Pelvis Pelvic mass Rectum Prostate enlargement Skin Rash of interstitial nephritis, purpura of microvascular disease, livedo reticularis suggestive of atheroembolic disease, or splinter hemorrhages or Osler’s nodes of endocarditis. 15
  • 15. * Blood urea nitrogen and serum creatinine are elevated. * ABG, electrolytes, CBC, and serology. * U/S kidneys (The size of the kidneys is usually normal. * Serology: ANA, ANCA, Anti DNA, HBV, HCV, Anti GBM. Cryoglobulin, CK, urinary myoglobin. 16
  • 16. * Urine analysis : - Unremarkable in pre and post renal causes. - Differentiates ATN vs. AIN. vs. AGN  Granular casts in ATN.  WBC casts in AIN.  RBC casts in AGN. - Urine electrolytes (Na) and osmolality. * Hansel stain for Eosinophiluria. 17
  • 17. LAB Findings of Specific Types of Acute Renal Failure Findings on blood tests Diagnosis to consider Very high uric acid level Suggestive of malignancy or tumor lysis syndrome leading to uric acid crystals; also seen in prerenal acute renal failure. Elevated creatinine kinase or Rhabdomyolysis. myoglobin levels Elevated prostate-specific antigen Prostate cancer. Abnormal serum protein Multiple myeloma. electrophoresis Low complement levels Systemic lupus erythematosus, postinfectious glomerulophritis, subacute bacterial endocarditis Positive antineurtrophic Small-vessel vasculitis (Wegener’s cytoplasmic antibody (ANCA) granulomatosis or polyartheritis nodosa) 18
  • 18. LAB Findings of Specific Types of Acute Renal Failure (Cont.) Findings on blood tests Diagnosis to consider Positive antinuclear antibody to Systemic lupus erythematosus double-stranded DNA Positive antibody to glomerular Goodpasture’s syndrome basement membrane Positive antibodies to streptolysin Poststreptocaccal glomerulonephritis. O, streptokinase or hyaluronidase Schistocytes on peripheral smear, Hemolytic uremic syndrome or decreased hepatoglobin level, thrombotic thrombocytopenic purpura elevated lactate dehydrogenase level or elevated serum bilirubin level Low albumin levels Liver disease or nephrotic syndrome 19
  • 19. Laboratory Findings in Acute Renal Failure To Differentiate Pre-Renal from Renal Failure Index Prerenal Azotemia Oliguric Acute Renal Failure (ATN) BUN/PCR Ratio > 20 : 1 10-15 : 1 Urine sodium (UNa) < 20 > 40 meg/L Urine osmolality, > 500 < 350 mosmol/L H2O Fractional excretion <1% >2% of sodium Response to Improvement No improvement volume Urinary Sediment Bland ATN: muddy brown granular casts, cellular debris, tubular epithelial cells 20
  • 20. ARF is common in the ICU.  ARF is an independent factor for prognosis in the ICU.  The incidence of ARF in the ICU 40-60% compared to 1-3% in the ward.  ARF still has a mortality of 50% since it occurs in very sick patients with multiorgan failure. 21
  • 21. Predisposing factors to ARF include old age sepsis pre existing renal disease heart disease and chronic liver disease.  Mechanical ventilation has an adverse effect on renal blood flow and GFR and subsequent renal function. 22
  • 22. • Patients with ICU acquired ARF were classified into the following : A) According to the urine output: - Oliguric (urine volume of < 400 ml/day). - Nonoliguric (urine volume of > 400 ml/day). - Anuric (urine volume of < 100 ml/day). B) According to the cause: 1) Prerenal ARF. 2) Ischemic acute Tubular necrosis. 3) Nephrotoxic ARF (ATN or AIN). 4) Sepsis induced ARF. 5) Hepato-renal syndrome. 6) Other causes (e.g. obstructive uropathy, pigment nephropathy, microangiopathies). 23
  • 23. 1) Prerenal ARF was defined as ARF to renal hypoperfusion with recovery after correction of hemodynamic disturbances. 2) Ischemic Acute tubular necrosis (IATN) was diagnosed when renal function did not improve after correction of possible prerenal causes, and when hepatorenal syndrome, vascular, interstitial, glomerular and obstructive aetiologies were excluded. 24
  • 24. • Decreased renal perfusion was identified by the following observations :  Any documented decline in blood pressure to less than 90/60 mmHg.  Overt volume contraction on physical examination (postural hypotension, decreased skin turgor, …), and central venous pressure (CVP) less than 5 cm H2O.  Clinically evident congestive heart failure with improvement in renal function following appropriate treatment of heart failure. 25
  • 25. 3) Nephrotoxic ARF (either AIN or ATN)  Nephrotoxic Acute Interstitial Nephritis (AIN): history of drug ingestion, fever, rash, or arthralgias. Urinary increase in WBCs (frequently eosirophiluria), WBC casts RBCs, and proteinuria, with systemic eosinophilia, if histologically demonstrated by renal biopsy or when there was a high grade of clinical suspicion. 26
  • 26.  Nephrotoxic Acute Tubular Necrosis (ATN): was defined as ARF occurring after administration of drugs known to cause ATN (e.g. aminoglycosides, amphotericin, contrast media etc …). Concurrent administration of vancomycin & aminoglycosides to critically ill septic patients with normal renal function of baseline induces mainly slight and transient toxic tubular effects. 27
  • 27. Radiographic contrast media, were determined to be the cause of renal insufficiency when the serum creatinine concentration increased – as defined – within 72 hours following a radiologic procedure employing these agents (e.g. intravenous pyelogram – angiography – computed tomography scan). 28
  • 28. 4) Sepsis induced ARF was diagnosed if ARF is associated with at least one of the following three conditions:  Documented bacteremia.  A known focus of infection  Immunosuppression with neutropenia, and at least two additional findings: rigors – unexplained hyperventilation unexplained sudden fall in blood pressure – abrupt rise in temperature to more than 38C not due to transfusion reaction – unexplained leukocytosis of more than 15.000 mm3. 29
  • 29. 5) Hepatorenal syndrome was assigned as the cause of renal failure if the patient had severe liver failure (e.g. ascites – jaundice, hepatic encephalopathy) – and a urine sodium concentration less than 10 mEq/Liter, and the renal function did not respond to a volume expansion. 30
  • 30. 6) Other causes:  Obstruction was determined to be the cause of renal failure if obstruction was present by physical examination (as enlarged bladder) or by radiological evaluation and if improvement in renal function followed relief of obstruction. 31
  • 31. Pigment induced-ARF, history suggestive of rhabdomyolysis, urine dispstick positive for blood (heme) without microscopic haematuria hyperkalemia, hyperphosphatemia, hypocalcemia, increased creatine kinase-MM fraction and serum uric acid. 32
  • 32.  Atheroembolic ARF: Associated with emboli of fragments of atherosclerotic plaque from aorta and other large arteries. Diagnose by history, physical findings (evidence of other embolic phenomena, ischemic digits, “blue toe” syndrome, etc), low serum C3 and C4, peripheral eosinophiluria, rarely WBC casts. Commonly occur after intravasculer procedures or cannulation (cardiac catheter, CABG). 33
  • 33. Number of patients admitted in different ICUs with acquired ARF in each ICU ICU No. of admitted No. & % of patients patients with ICU acquired ARF in each ICU Medical ICU 1123 402 (35.7 %) Gynecology ICU 431 98 (22.7 %) Surgical ICU 336 53 (15.7 %) Neurology ICU 116 17 (14.6 %) Chest ICU 409 57 (13.9 %) Coronary Care Unit 722 78 (10.1 %) Cardiosurgery ICU 425 43 (10.1 %) Total 3562 748 (21 %) 34
  • 34. Causes of ICU acquired-ARF in 748 patients Causes No. & % of patients iATN 283 (37.8 %) Prerenal 198 (26.5 %) Toxic ARF 80 (10.6 %) Sepsis induced ARF 89 (11.9 %) HRS 73 (9.8 %) Others 25 (3.4 %) iATN = ischemic acute tubuler necrosis. Toxic ARF = toxic acute renal failure. HRS – hepatorenal syndrome. 35
  • 35. Number & Percentage of patient mortality in each ICU ICU No. of patients Mortality No. & % with ICU acquired in each ICU ARF Medical ICU 402 261 (64.9 %) Coronary Care Unit 78 20 (25.6 %) Chest ICU 57 28 (49.1 %) Neurology ICU 17 9 (52.9 %) Surgical ICU 53 10 (18.8 %) Cardiosurgery ICU 43 19 (44.1 %) Gyne & obst. ICU 98 42 (42.8 %) Total 748 389 36
  • 36. * The initiation of RRT in patients with AKI prevents uremia and immediate death from the adverse complications of renal failure. * It is possible that variations in the timing of initiation, modalities, and/or dosing may affect clinical outcomes. * Multiple modalities of RRT are currently available. These include intermittent hemodialysis (IHD), continuous renal replacement therapies (CRRTs), and hybrid therapies, such as sustained low- efficiency dialysis (SLED). Despite these varied techniques mortality in patients with ARF remains high greater than 50% in severely ill patients. 37
  • 37. 1. Indications for dialysis. 2. Timing of initiation of dialysis. 3. Optimal modality. 4. Optimal Dosing. 5. Discontinuation of therapy. 38
  • 38. 1) Refractory fluid overload. 2) Hyperkalemia (plasma potassium concentration > 6.5 meq/L) or rapidly rising potassium levels. 3) Metabolic acidosis (pH less than 7.1). 4) Signs of uremia e.g. pericarditis and decline in mental state. 5) Certain alcohol and drug intoxications. * The likelihood of requiring RRT is increased in patients with underlying CKD (Acute on top of chronic). 39
  • 39. Studies published during the 1960s and 1970s suggested that improved outcomes were associated with the initiation of hemodialysis when BUN reached exceeded 150 to 200 mg/dL. 40
  • 40. More recent studies have evaluated the relationship between the timing of RRT initiation and clinical outcomes. Several non-randomized studies have reported that improved outcomes, including survival, are associated with early versus late initiation of RRT.  It has been suggested that initiation of RRT dialysis prior to the development of overt symptoms and signs of renal failure due to AKI improves the outcome. 41
  • 41. Can dialysis delay recovery of renal function ?  There is at least theoretical concern that dialysis might have detrimental effects on renal function.  Three factors may be important in this regard: 1) A reduction in urine output; Both removal of excess volume and of urea contribute to a reduction in or even cessation of the urine output. The fall in urine output should not delay the regeneration of tubules. 2) Induction of hypotension; Autoregulation is impaired in ATN, because vascular endothelial injury reduces the release of vasodilating substances so recurrent ischemic tubular injury is more likely to occur, thereby delaying the restoration of function. 42
  • 42. 3) Complement activation resulting from a blood- dialysis membrane interaction, can lead to neutrophilic infiltration into the kidney (and other tissues) and prolonged acute kidney injury. 4) High flux membranes can enhance removal of putative toxins and improve outcome, but may also allow the back transport (from dialysate to blood). 43
  • 43. 1) Intermittent hemodialysis (IHD). 2) Continuous renal replacement therapy (CRRT). 3) Peritoneal dialysis. 44
  • 44. Principles of dialysis  Dialysis = diffusion = passive movement of solutes across a semi- permeable membrane down concentration gradient. * Good for small molecules.  (Ultra) filtration = convection = solute + fluid removal across semi permeable membrane down a pressure gradient (solvent drag). * Better for removal of fluid Figure (1): Principles of dialysis and medium-size molecules. (top panel) and filtration (lower panel). 45
  • 45. Principles of dialysis  Hemodialysis = solute passively diffuses down concentration gradient.  Dialysate flows countercurrent to blood flow.  Urea, creatinine, K move from blood to dialysate.  Ca and bicarb move from dialysate to blood.  Ultrafiltration = This is the convective flow of water and dissolved solutes down a pressure gradient caused by hydrostatic or osmotic forces.  Hemodiafiltration = combination of dialysis and ultrafiltration 46
  • 46. Intermittent hemodialysis (IHD)  Oldest and most common technique.  Primarily diffusive treatment: blood and dialysate are circulated in countercurrent manner.  Also some fluid removal by ultrafiltration due to pressure driving through circuit.  Best for removal of small molecules.  Typically performed 4 hours 3x / wk or daily. 47
  • 47. Continuous Renal Replacement Therapy (CRRT)  CRRT strategies are particularly useful in haemo- dynamically compromised patients with ARF.  They allow slow and gentle removal of solutes and fluid, avoiding major intravascular fluid shifts and minimizing electrolyte disturbances, hypotension and arrhythmias.  Inflammatory mediators may also be continuously removed by CRRT, so it may be useful in sepsis syndrome. 48
  • 48. Types of Continuous Renal Replacement Therapies (CRRT) Blood access Continuous arteriovenous hemofiltration (CAVH). Continuous arteriovenous hemodialysis (CAVHD). Continuous arteriovenous hemodiafiltration (CAVHDF). Continuous venovenous hemofiltration (CVVH). Continuous venovenous hemodialysis (CVVHD). Continuous venovenous hemodiafiltration (CVVHDF). Slow low efficiency dialysis (SLED). Slow continuous ultrafiltration (SCUF). Extended daily dialysis (EDD). Peritoneal access Continuous equilibrium peritoneal dialysis.Blood acce 49
  • 49. Haemofiltration  Provides solute clearance by convection as solutes are dragged down pressure gradient with water.  It provides better removal of large MW solutes e.g. B2-microglobulin, improved clearance of low MW uraemic toxins and better cardiovascular stability and Bp control than HD.  Inflammatory markers are improved. 50
  • 50. Sustained low-efficiency daily dialysis (SLED):  Uses conventional dialysis machines but blood flow of 100-200 ml/M and dialysate flow of only 100 ml/M for 8-24 hr/D.  Major advantages: Flexibility of duration and intensity, reduced costs.  Excellent tolerability, cardiovascular stability and solute removal. 51
  • 51. Slow continuous ultrafiltration ((SCUF):  Used for fluid removal in overloaded CHF patients with refractory edema without severe renal failure.  Blood is driven through a highly permeable filter in a venovenous mode to primarily remove water, not solute.  The ultrafiltrate produced during membrane transit is not replaced. Haemodiafiltration (HDF):  Simultaneous use of HD and UF.  It is good with CVS instability.  It can remove the inflammatory mediators. 52
  • 52. * Current data suggest that survival and recovery of renal function are similar with both CRRT and IHD. * Advocates for CRRT have claimed that CRRT is associated with the following advantages compared with IHD: 1) Enhanced hemodynamic stability, in hemodynamically unstable patients. 2) Increased net salt and water removal, thereby permitting superior management of volume overload and nutritional requirements. 53
  • 53. 3) Enhanced clearance of inflammatory mediators, which may provide benefit in septic patients, particularly using convective modes of continuous therapy. 4) Among patients with acute brain injury or fulminant hepatic failure, continuous therapy may be associated with better preservation of cerebral perfusion. 54
  • 54. Peritoneal dialysis:  Least useful form of CRRT in the ICU.  Diffusive treatment: Blood in capillaries of peritoneal membrane exposed to dialysate in abdomen.  Continuous or intermittent.  Inefficient solute/ volume clearance if unstable or poor intestinal blood flow.  Can’t use if intra-abdominal pathology – risk of peritonitis.  Respiratory burden. 55
  • 55. * Intermittent hemodialysis – Dosing in IHD is based upon the dose delivered per session plus the frequency of sessions. * Improved survival was observed with a higher Kt/V (greater than 1), which was particlarly evident among patients with intermediate levels of illness severity. * Compared with every other day dialysis, daily therapy was associated with a significant reduction in mortality, fewer hypotensive episodes during hemodialysis, and more rapid resolution of acute renal failure. 56
  • 56. * In contrast, the Acute Renal Failure Trial Network (ATN) Study did NOT find a difference in mortality associated with a more intensive dosing strategy for renal replacement therapy. * The Hanover Dialysis Outcome study compared extended duration dialysis, provided for approximately 8 hours per day, to a more intensive regimen where additional 8-hour treatment sessions were provided to maintain the BUN < 42 mg/dL. No difference in survival or recovery of kidney function was observed with more intensive treatment. 57
  • 57. • The Randomized Evaluation of Normal versus Augmented Legal of RRT study and two meta- analyses were performed. All studies found that, compared with standard intensity dialysis, higher intensity dialysis did not result in improved survival or clinical benefits. • It is recommended that IHD be provided 3 times/week with monitoring of the delivered dose of therapy to ensure a minimum delivered Kt/V of 1.2 per treatment. 58
  • 58. RRT is usually continued until the patient manifests evidence of recovery of kidney function. 1. Increase in urine output. 2. A progressive decline in serum creatinine concentration after initial attainment of stable values (assessed daily during CRRT or predialysis in patients managed with IHD) despite a constant dose of renal support. 3. Measurement of creatinine clearance e.g. on six- hour timed urine collections obtained when the urine output exceeded 30 mL/hour based on an average serum creatinine at the beginning and end of the timed collection. 59
  • 59. A precise level of kidney function needed to allow discontinuation of renal support has not been established; however, Creatinine clearance < 12 mL/min → no discontinuation. Creatinine clearance > 20 mL/min → discontinue. Creatinine clearance 12 to 20 mL/min → optional. 60
  • 60. 1) No drugs are currently available to enhance or hasten renal recovery once ARF occurs. 2) There is now clear evidence that ARF is associated with excess mortality, irrespective of whether the patient requires renal replacement therapy. 3) Hense prevention is the only powerful tool to improve outcome of AKI. 61
  • 61. Identification of patients at high risk to develop AKI-Elderly, DM, HT. Sepsis etc .... Non Pharmacological Pharmacological  Ensuring adequate  Loop diuretics, hydration (reversing  Mannitol, dehydration,  Dopamine &  Maintenance of Fenoldopam. adequate mean  Natriuretic Peptides. arterial pressure,  Minimizing exposure to nephrotoxins. 62
  • 62.  NS, albumin, plasma ….  CVP = 8-12 cm H2O, MAP > 65 mmHg.  Optimal rate of infusion remain unclear and should be individualized.  Target MAP ≥ 65 mmHg.  Which vasopressors to be used.  Role of low dose dopamine.. 63
  • 63.  Noradrenaline is the drug of choice in AKI in sepsis.  Norepinephrine has been demonstrated to preserve splanchnic blood flow better than dopamine.  Optimise fluid before starting vasopressors.  Low dose dopamine should not be used for renal protection in severe sepsis. 64
  • 64. Meta-analysis: Low-Dose Dopamine Increases Urine Output but Does Not Prevent Renal Dysfunction or Death Low-dose dopamine offers transient improvements in renal physiology, but no good evidence shows that it offers important clinical benefits to patients with or at risk for acute renal failure. 65
  • 65. In animal studies the use of mannitol and loop diuretic minimize the degree of renal injury if given at the time of ischemic injury.  Loop diuretics decrease the active Na transport in the thick ascending loop decreasing the energy requirement. 66
  • 66. Increasing the urine output by loop diuretic make the management easier but does not affect cell injury or the severity of the renal damage.  Loop diuretic increase the urine output in the remaining nephrons and therefore huge doses are required that may cause deafness. 67
  • 67. ANP had been tried in experimental models without any benefit despite their ability to increase renal blood flow and Na excretion.  Calcium channel blockers decrease Ca influx to the cells that lead to cell injury.  Most human studies were done on established ATN. 68
  • 68. Uncontrolled studies showed that those patients who respond to diuretics or mannitol may have better outcome but these patients has less severe disease.  Controlled studies failed to show any evidence that low dose dopamine have any protection of cell injury in ischemic renal damage. 69
  • 69. 70