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					Acut renal failure and
treatment


   Székely Andrea
Objectives
 To define acute renal failure
 To discuss causes of acute renal
  failure
 Diagnosis and Treatment of ARF
 Introduce Chronic renal failure

 Methods using case presentations
Case 1
 24 year old student collapsed after running
  the Dublin Marathon
 Had complained of muscle cramps during
  race and these continued
 Admitted to A/E after passing a small
  amount of red urine
 O/E normal BP and Pulse
 Urinalysis 2+ Protein, 4+ Blood
 Light microscopy renal tubular casts
Case History continued

     Urea 20 mmol/L
     Creatinine 350 micromol/L
     Sodium 140
     Potassium 6.1
     Calcium 2.01 mmol/l
     Phosphate 2.4 mmol/l
     Urate 500 micromol/l
     Bicarbonate 17 mmol/l
     Creatinine Kinase markedly elevated
Diagnosis
   Raised muscle enzymes
   Assume urinary myoglobin
   Kidneys normal size and shape on U S
   Acute renal failure

 Acute tubular necrosis due to
  Rhabdomyolysis
Acute Renal Failure
Treatment
   Establish the cause of acute renal failure
    exclude other causes
   Intrinsic renal disease sepsis obstruction
    Background chronic renal disease
   ATN due to Rhabdomyolysis requires
    aggressive volume expansion (With What ?)
    with correction of acidosis with close
    monitoring of urine output blood pressure,
    pulse, breathing and blood gases and
    electrolyte and renal function
   Even if late presentation and established
    ATN will recover function to normal
What does the kidney do?
   Extracellular Environment maintenance

   Excretes by-products of metabolism like urea,
    creatinine, uric acid
   Individual regulation of salt, water and H+ by
    changes in tubular reabsorbtion and secretion
   Hormonal function Ca PO4 via 1,25 cholecalciferol
   Systemic and Renal haemodynamics Renin
    angiotensin 2, prostaglandins, bradykinin
   Red cell production via erythropoiten
   Potential dysfunction depends on type and extent of
    renal disease
Assessment of Renal Function
   Blood Urea
   Serum Creatinine
   GFR: Used clinically to assess the level of renal
      function no information on cause
   GFR is the sum of filtration rates of all nephrons
  Is the GFR changing or Stable Creatinine is used if
      monitoring change
  Creatinine clearance UCr* V(mls) / PCr gives ml/day
   Chromium EDTA in children
   MAG 3 isotope scanning
Urea and Creatinine as
measures of function
 Urea can be higher in prerenal failure due to
  volume changes Avid tubular reabsorbtion
 Blood loss into GI tract
 Excessive breakdown of Protein Catabolism
 Creatinine lower in small frame, poor muscle
  mass
 Creatinine higher if muscle breakdown
 Creatinine is freely filtered by the kidney and
  is not reabsorbed or metabolised 15% is
  secreted into proximal tubule How does this
  affect functional assessment???
3 Categories of Renal Failure
 Pre-Renal
   Condition that causes a decrease in blood flow to
    the kidneys
   Reduced HP at glomeruli results in poor filtration
 Post-Renal
   An obstruction in the outflow of urine
   Increase HP in Bowman’s capsule results in poor
    filtration
 Intra-Renal
   Direct damage to kidneys, esp. glomeruli
   Less effective surface area results in poor filtration
   Post-Renal: Ureteral Stone
 The material that
  makes up the stones
  often consists of
  calcium deposits,
  among other things
 These can cause
  blockage of urine
  flow
 Urine backs up into
  the kidneys causing
  nephrons to shut
  down due to an
  increase in pressure
Analogy
 In this analogy the
  ureter acts as a
  stream
 Beavers come and
  build a dam (ureter
  stones) that block the
  passage of water down
  the stream
 The dam causes a
  backflow of water that
  damages the
  surrounding habitat
  (kidneys)
Pre-Renal: Myocardial Infarction
                The heart weakens
                 and cannot pump
                 sufficient amounts of
                 blood to the kidneys
                Glomerular filtration
                 rate decreases (kidney
                 failure ensues)
                The kidneys may
                 compensate by
                 retaining more salt
                 and water to increase
                 blood volume
Analogy
 In this analogy blood
  is represented by
  water
 A drought occurs
  (myocardial infarction)
 Kidneys act as a dam
  conserving water
  (blood), which supplies
  the people with
  enough water to
  survive (i.e. blood
  supplying tissues)
Intra-Renal: Glomerulonephritis
 A Streptococcus
  bacterial infection of the
  throat or skin can lead
  to acute post-
  streptococcal
  glomerulonephritis
 Strep antigens and
  antibodies form
  complexes that attach to
  the glomerulus
 The inflammation
  impairs the kidney‟s
  ability to filter and
  eliminate waste causing
  low output of urine
Analogy
 In this analogy a river
  represents the kidneys
 An oil spill represents
  Acute post-strep
  glomerulonephritis
 The river cannot filter
  out or diffuse all the
  sticky oil
 Therefore the oil ends
  up disturbing natural
  habitat around the
  river and it cannot
  function properly
What can go wrong (Cause)
Acute = Hours Days weeks
 Blood from renal artery is delivered to
  glomeruli Perfusion
 Glomeruli form Ultrafiltrate which flows into
  tubules Glomerular Diseases
 Tubules reabsorb and secrete water
  electrolytes from the ultrafiltrate ATN
 Urine leaves the kidney and drains into the
  renal pelvis ureters bladder and urethra
  Obstruction
Prerenal Disease
   Prerenal
   Anything which affects the renal perfusion
      through volume loss hypotension or
      effective volume depletion
  What is the hydration status of the patient
  History and Physical Examination
  Background History
  Risk Factors for Acute renal failure
  If impaired perfusion is prolonged severe and
      untreated, prerenal failure manifests as
      Acute Tubular Necrosis
Post Renal Failure
 Causes of renal impairment due to
  Obstruction of the renal tract
 Tumours
 Fibrosis
 Blood clots
 Stones
 Papillae
Case 2
 76 year old man admitted with urinary symptoms and
  incontinence found by GP to have abnormal renal
  function
 Main complaints were urinary frequency nocturia
  double micturition and poor stream
 Past history of MI and TIA
 O/E Hypertension 180/95 with evidence of volume
  expansion Raised JVP and cardiomegaly sacral and leg
  oedema
 Abdominal examination revealed a large mass arising
  from the pelvis which was dull to percussion
 PR no rectal masses but prostate enlarged with
  smooth nodularity
Investigations
   Urea 20
   Creatinine 600
   Sodium 136
   Potassium 6.0mmol/l
   Bicarbonate 18 mmol/l
   Renal Ultrasound Severe bilateral
    hydronephrosis with dome like bladder
    expansion
   Chest Xray Cardiomegaly with upper lobe
    diversion
   ECG Twave tenting
Treatment
 Renal Failure
 Time frame to presentation not clear unwell
  for weeks ++
 Clinical examination suggests obstruction
  as cause probably due to prostatic
  hypertrophy
 Catheter inserted and achieved massive
  diuresis
 As bladder reduced in size developed
  haematuria
 Urologistsarranged TURP for 4 weeks after
  presentation
Intrinsic renal disease
 Systemic Disease
SLE, Amyloidosis, Wegeners
  Granulomatosis, Diabetes mellitus

 Primary renal disease
Glomerulonephritis, Acute interstitial
  nephritis, Acute tubular nephritis
Urinalysis and Urinary
microscopy
1. Haematuria heavy         1.   Glomerular disease or
   proteinuria                   vasculitis
   dysmorphic red cells     2.   Tubular or interstitial
                                 disease or Obstruction
2. Pyuria with white cell   3.   Renal tract infection or
   casts no proteinuria          TB
3. Pyuria alone             4.   Prerenal disease renal
                                 ischaemia some cases
4. Few cells low grade           of ATN, tubular
   proteinuria –Bland            interstitial disease
   urinary sediment         5.   IgA or Thin BM will
5. Haematuria Alone              have some proteinuria,
                                 Renal tract tumours
                                 Renal calculi, sloughed
                                 papillae
Case 3
 A 59 year old man presents with weight loss and night
  sweats. He had recurrent sinusitis aching joints and a
  painful left ear. He had shortness of breath for 4 days
  before and had a small amount of haemoptysis
 On examinatio . Tender over maxillary sinus and left
  ear drum was inflamed. He appeared pale he was
  hypertensive 190/100 he had bilateral fine
  crepitations in his lungs and his JVP was mildly raised.
  He had moderate leg oedema and all peripheral
  pulses were present with no femoral or aortic bruits.
  He had a purpuric rash on his lower limbs with some
  bullae
Investigations
 Urinalysis showed 3+ Proteinuria and 3+ Blood,
  microscopy saw some dysmorphic red cells
 Spot urinary protein 8g/24 hours
 Hb was low 8.8g/dl
 Urea 35 mmol/l, Creatinine 480 micromol/l
 Chest Xray showed interstitial infiltrates
 Auto antibodies were sent
 ANCA ANA dsDNA complement Anti GBM antibodies
 A definitive Test was preformed
ANCA related disease
 Antibodies to neutrophil cytoplasmic
  antigen are found in 90% of vasculitides
 C-ANCA diffuse cytoplasmic stippling PAN,
  now known as anti myeloperoxidase
  antibody
 P-ANCA perinuclear staining Wegeners now
  known as anti proteinase 3
 Initially by indirect immunoflourescence
  now by ELIZA gives more accurate
  quantification
Multisystem disease
Wegeners Granulomatosis
 Active urinary sediment with haematuria
  and proteinuria glomerular
 Biopsy Rapidly progressive GN with focal
  segmental necrotizing GN with crescent
  formation. Immunofluorescence negative
  findings or traces only of IgG and C3
  Pauciimmune on renal biopsy
 Systemic disease due to small vessel
  vasculitis with granuloma causes areas of
  focal necrosis
Treatment
   Assess organ involvement
   Exclude other causes
   Treat Disease process
   Immunosupression with pulse
    methylprednisolone and
    cyclophosphamide has revolutionised
    outcome from Wegeners
RIFLE Global description of ARF
 R-risk of renal impairment Creatinine
  >1.5 x Normal UO <0.5 mls/kg/hour for 6
  hours
 I-Injury renal injury Creatinine>2 x
  Normal UO <0.5 mls/kg/hour for 12 hours
 F – Failure Creatinine > 3 x Normal or
  >350 Anuria for 12 hours
 L –Loss complete loss of renal function for
  more than 4 weeks (Needing renal
  replacement)
 E ESRF complete loss of function needing
  renal replacement for> 12 weeks
Summary
 Renal Impairment can be acute or chronic
 Rate of change of function and baseline
  function is important
 Prerenal failure is a term to describe
  reduced renal perfusion
 Intrinsic renal disease is important as it
  may be treatable or may be systemic
 Obstruction is an important cause of renal
  failure especially in the elderly
 RIFLE criterion is a new method of
  describing acute renal failure
Questions

1.   Does the patient have
     ARF?
2.   Why does the patient
     have ARF?
3.   What is the immediate
     management?
4.   What is the intermediate
     management?
5.   Does the patient need to
     be transferred?
6.   Does the patient need
     RRT?
What is ARF?

 Acute, usually reversible, decline in
  GFR

  ........over days, occasionally weeks
  ........not necessarily from normal
  baseline
  ........usually with a rising plasma urea
  ........usually with a rising plasma creatinine
  ........often, but not always with
  oliguria
What is not ARF?

 Oliguria due to fluid retention
  .......post-operatively
  .......as initial response to ECF depletion
  .......in cardiac failure and other diseases

 Urinary retention

 ESRF presenting as uraemic emergency
Consequences of ARF

   Acute metabolic complications
   Acute cardiovascular complications
   Prolonged hospitalisation
   Resource consumption

 Patient Death       Common
 Renal Death         Uncommon
ARF in Hospital                                                 (Boston Study)

                            60

                                                                                    50
                            50
% of cases developing ARF




                            40


                            30
                                                                                         25
                                            20                       20
                            20

                                 10                   10
                            10
                                                 5          5             5
                                      2
                             0
                                 Hospital   Trauma   Elective AAA   Open Heart   Emergency AAA
Incidence of ARF                                          (RA Study)



                        2500

                                    2058
 Annual Incidence pmp




                        2000


                        1500


                        1000                        872


                         500
                                                                       137
                           0

                               Creatinine >150   Transiently      Severe ARF
Causes of Severe ARF                                        (RA Study)


             40      36


             30
% of cases




             20
                                  14            13
                                                             10           9
             10


             0
                  Obstruction   Surgical   Cardiovascular   Sepsis   ECF Depletion
Survival to hospital discharge with ARF   (RA/ICS)


                                100
 ARF alone       90%

 SCARRF         40-50%          75
Severe Combined Acute Renal
   and Respiratory Failure
                                 50
 SCARRF +1 5-10%

                                 25
  All cases of MODS with ARF
         should have RRT
   if other therapy continues     0


                                      ARF    SCARRF   MODS
Causes of ARF

 Pre-Renal Azotemia             ischaemic
 Acute Tubular Necrosis
        ischaemic
        toxic
 Acute Interstitial Nephritis
     immunological
     toxic

 Acute Glomerulonephritis       immunological


 Obstruction / Thrombo-embolic
Why does ARF occur?

 Insult                 Risk Factors

Usually identifiable    Usually identifiable

Often predictable

Sometimes preventable   Sometimes correctable
W.R.I.S.T.

 W..        kers!

   R   isk Factors
   I   nsults
   S   tatus
   T   reatment
Risk Factors

 Age
 Pre-existing renal disease
 Co-existing cardiac and hepatic disease
 Generalised vascular disease
 Conditions interfering with fluid balance
    (includes dementia & broken legs)
 ‘Usual medications’
Insults

   Disturbance of ECF volume status
   Disturbance of cardiovascular functioning
   Disturbance of renal haemodynamics
   Sepsis
   Operative procedures/anaesthesia
   Obstruction
   Prescription of nephrotoxic agents
Status
 Compromised?

  ECF status
    Hyperkalaemia
         Acidosis
         „Uraemia‟

 Likely to improve?
ECF Volume Status

 Is established on clinical examination

 Corrected and repeatedly re-assessed
  with rational/detailed/appropriate fluid
  therapy

 Facilitated when appropriate by.....
                        CVP Monitoring
                    PCWP Monitoring
Treatment

 Resuscitate/review

 Correct other contributors

 Predict outcome

 RRT or other investigations as needed

 Wait………………..
Hyperkalaemia
 Calcium carbonate/chloride

 Insulin/Dextrose (1unit:5g)
 Nebulised Salbutamol

 30mins       90mins           6hrs

 Bicarbonate/Calcium resonium
Magic bullets…………….

 Loop diuretics




                       11 3
 Mannitol

 Atrial natriuretic
  peptide

 Dopamine
Kellum JA, M Decker J.
Use of dopamine in acute renal failure: a meta-analysis.
Crit Care Med 2001; 29:1526-31.




 1966-2000                       Mortality 0.44-1.83
 Prevention/Treatment
                                  ARF          0.55-1.19

 58 (n=2149) studies
                                  RRT          0.55-1.24
 24 (n=1019) outcome
 17 (n=854) RCT
                                   Power for >50% effect on
                                             ARF/RRT
Is it bad for you……?

 Skin necrosis

 Tachydysrythmia

 Ventilatory dysfunction

 Gut hypoperfusion

 Ineffective pressor
Until proven otherwise....
 The patient has not had.....

          Risk Factors   identified
          Insults        identified

          ECF volume depletion
          Cardiovascular dysfunction
          Drug toxicity
          Obstruction
Indication of RRT (renal
replacement therapy)

 Rescuscitated

 Precipitating event
  corrected

 Unlikely to recover
  quickly

 MODS
Emergent Indications For Initiation
of RRT
 K > 6.5
 Volume overload: Refractory to
  diuretics.
 Severe Acidosis
 Uremic complications :Pericarditis
 Drug Overdose
Principles of CRRT
Solute removal
 Diffusion
 Convection
Diffusion




    Diffusion: The movement of solutes from a
    higher to a lower solute concentration area.
Hemodialysis
     to waste

       Dialysate Out     Blood In
                             (from patient)




       Dialysate In      Blood Out

                              (to patient)

          LOW CONC     HIGH CONC
Convection




Convection: The movement of solutes with a water-flow,
“solvent drag”, e.g., the movement of membrane-permeable
solutes with ultra filtered water.
Hemofiltration


    to waste      Blood In
                      (from patient)
                                       Replacement.
                                         Solution




                  Blood Out

                       (to patient)

    LOW PRESS    HIGH PRESS
Hemodiafiltration
 Diffusive clearance (hemodialysis) +

  Convective clearance
  (hemofiltration)

 Use of dialysate on fluid side of filter
  and replacement solution on the
  blood side of the filter.
Hemodiafiltration
       to waste
                                    Blood In
                               (from patient)
Dialysate
Solution                                          Replacement
                                                    Solution



                               Blood Out

                                   (to patient)


             LOW PRESS       HIGH PRESS

                  LOW CONC   HIGH CONC
Dialysis Access
 Arterial Venous (AV)
 Needs 2 catheters one in artery and
  other in vein
 No blood pump required: Depends on
  systemic BP
 Complications: embolization,
  bleeding, pseudoaneurysm
 Not used anymore
Dialysis Access
 Veno-venous (VV)
 One dialysis catheter in vein
 Less complications
 Blood flow more reliable since
  external blood pump +
 Technically more complicated.
 Widely used
The
      M EDUWAY
        To Care For Patients




       Types of CRRT
       SCUF - Slow Continuous Ultra Filtration

       CVVH - Continuous Veno-Venous
          Hemofiltration

       CVVHD - Continuous Veno-Venous
          HemoDialysis

       CVVHDF -     Continuous Veno-Venous
          HemoDiaFiltration
 Types of CRRT

CAVH   -       Continuous Arterio-Venous   Hemofiltration



CAVHD      -     Continuous Arterio-Venous HemoDialysis



CAVHDF     –  Continuous Arterio-Venous
 HemoDiaFiltration
SCUF
 Primary therapeutic goal:
• Safe management of fluid removal
 UF rate ranges up to 2 L/Hr
 No dialysate
 No replacement fluids
 Large fluid removal via ultrafiltration
 Blood Flow rates = 10-180 ml/min
CVVH
 Primary therapeutic goal
• Convective solute removal
• Safe fluid management
 UF rate ranges 12-20 L/24 hours (>500
  ml/hr)
 Requires replacement solution to drive
  convection
 No dialysate
CVVHD
 Primary therapeutic goal
• Solute removal by diffusion
• Safe fluid volume management
 Requires dialysate solution
 UF rate ranges 2-7 L/24 hours (~300 ml/hr)
 Dialysate Flow rate = 15-45 ml/min (~1-3
  L/hr)
 Blood Flow rate = 10-180 ml/min
 No replacement solution
 Solute removal determined by Dialysate Flow
CVVHDF
 Primary therapeutic goal:
• Solute removal by diffusion and convection
• Safe fluid management
 Combines CVVH and CVVHD therapies
 UF rate ranges 12-20L/24hr
 Uses dialysate solution
 Uses replacement solution
 Blood Flow rate = 10-180ml/min
   Dialysate Flow rate = 15-45 ml/min
 Summary

                                                  Dialysate                     Dialysate
            Access                Access                              Access                            Access

             Return                Return                              Return                            Return

                                   Replacement                                                               Replacement
                                   (pre or post                                               I              (pre or
                                   dilution)                                                                 post dilution)




 Effluent              Effluent                                 Effluent                          Effluent




SCUF                  CVVH                                    CVVHD                         CVVHDF
Complication: Vascular access
 Monitor for complications
   Subclavian or jugular vein
         Respiratory distress
         Hematoma/bleeding at site
         Infection
         Cardiac arrhythmia during placement
         Tubing disconnection
           Hemorrhage/air embolism
Potential patient problem
 Air embolism

 Hypothermia

 Blood leak

 Ekg interference
 Peritoneal Dialysis (PD)

 Use of the peritoneal membrane for
   ultrafiltration and diffusion
 Acute PD -temporary catheter -2 days
 Chronic PD- permanent catheter
Continuous ambulatory peritoneal dialysis-
   CAPD
4 exchanges/day
Ultrafiltration- osmotic pressure 1.5-4.25 %
   glucose
Peritoneal dialysis - advantages
   Dependency on medical staff
   Restriction of fluid and food intake
   Continued dialysis-stable
    hemodynamic and metabolic
    conditions
eritoneal dialysis- disadvantages
  Hypoalbuminemia and malnutrition
  Exacerbation of DM
  Exacerbation of respiratory disturbances
  Efficiency -“BIG”patients,low residual
   function
  Less efficient for emergent fluid and K
   removal
  Peritonitis, sclerosing peritonitis
  Burnout
COMPLICATIONS OF PERMANENT
DIALYSIS
 CARDIOVASCULAR                BONE and JOINTS
     Accelerated                disease
      Atherosclerosis           secunder
     Coronary calcification     hyperparathyroidism
     Ischemic heart disease
                                b 2 microglobuline
     Peripheral vascular
      disease
                                 amyloidosis
     Left ventricular
      hypertrophy- HTN,
      Anemia
     Valvular calcification
     Heart failure
Renal Transplantation
 Cadaveric renal transplantation (CRT)
 Living related renal transplantation
  (LRD)
 Living unrelated renal transplantation
 Kidney and pancreas transplantation
IMMUNOSUPPRESSION
 Steroids
 Calcineurin Inhibitors- cyclosporine,
  FK506
 Azothioprine, Mycophenolate mofetil
 ATG, OKT3
 Rapamycin
 Anti IL2 antibodies
Renal Transplantation -
Common Complications
     Ischemia-ATN
     Rejection
     Infections- Bacterial
     CMV
     Opportunistic infections
 Renal Transplantation -
Late Complications
    Rejection
    Cyclosporine toxicity
    Recurrence of primary disease- FGS
    Renal artery stenosis
    Chronic allograft dysfunction
    Atherosclerosis, osteoporosis
 Advantages of transplantation

 Freedom from dialysis
 Improvement in nutritional state
 Improvement in Fertility and sexual
  function
 Less restriction of food and fluid intake
 Improved QOL and survival
 Limitations of transplantation
                 Early
Medication - need for compliance
Immunosupression and infections
Exacerbation of diabetes
Hyperkalemia and volume overload-
possible
Procedures during follow up- biopsies
etc
 Limitations of transplantation
                  Late
 Chronic allograft dysfunction-T1/2=7
  years
 Atherosclerosis, osteoporosis

 Exacerbation of hepatitis B and C

 Malignancy-frequency and severity

				
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