Transcript from patient

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
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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
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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 poststreptococcal
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
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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
proteinuria
dysmorphic red cells
2. Pyuria with white cell
casts no proteinuria
3. Pyuria alone
4. Few cells low grade
proteinuria –Bland
urinary sediment
5. Haematuria Alone
1.
2.
3.
4.
5.
Glomerular disease or
vasculitis
Tubular or interstitial
disease or Obstruction
Renal tract infection or
TB
Prerenal disease renal
ischaemia some cases
of ATN, tubular
interstitial disease
IgA or Thin BM will
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
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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.
2.
3.
4.
5.
6.
Does the patient have
ARF?
Why does the patient
have ARF?
What is the immediate
management?
What is the intermediate
management?
Does the patient need to
be transferred?
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
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Acute metabolic complications
Acute cardiovascular complications
Prolonged hospitalisation
Resource consumption
 Patient Death
 Renal Death
Common
Uncommon
ARF in Hospital
(Boston Study)
60
50
% of cases developing ARF
50
40
30
25
20
20
20
10
10
10
2
5
5
5
0
Hospital
Trauma
Elective AAA
Open Heart
Emergency AAA
Incidence of ARF
(RA Study)
Annual Incidence pmp
2500
2058
2000
1500
872
1000
500
137
0
Creatinine >150
Transiently
Severe ARF
Causes of Severe ARF
40
(RA Study)
36
% of cases
30
20
14
13
10
10
9
0
Obstruction
Surgical
Cardiovascular
Sepsis
ECF Depletion
Survival to hospital discharge with ARF
 ARF alone
90%
 SCARRF
40-50%
(RA/ICS)
100
75
Severe Combined Acute Renal
and Respiratory Failure
 SCARRF +1 5-10%
50
25
All cases of MODS with ARF
should have RRT
if other therapy continues
0
ARF
SCARRF
MODS
Causes of ARF
 Pre-Renal Azotemia
 Acute Tubular Necrosis
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
ischaemic
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..
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R
I
S
T
kers!
isk Factors
nsults
tatus
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’
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Insults
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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
 Mannitol
 Atrial natriuretic
peptide
 Dopamine
11 3
Kellum JA, M Decker J.
Use of dopamine in acute renal failure: a meta-analysis.
Crit Care Med 2001; 29:1526-31.
 1966-2000
 Prevention/Treatment
 58 (n=2149) studies
 24 (n=1019) outcome
 17 (n=854) RCT
 Mortality 0.44-1.83
 ARF
0.55-1.19
 RRT
0.55-1.24
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
Insults
identified
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
LOW CONC
HIGH PRESS
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
-
CAVHD
Continuous Arterio-Venous
-
CAVHDF
Hemofiltration
Continuous Arterio-Venous HemoDialysis
–
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
Access
Access
Return
Return
Dialysate
Access
SCUF
Effluent
CVVH
Access
Return
Return
Replacement
Replacement
(pre or post
dilution)
Effluent
Dialysate
(pre or
post dilution)
I
Effluent
CVVHD
Effluent
CVVHDF
Complication: Vascular access
 Monitor for complications
 Subclavian or jugular vein
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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 dialysisCAPD
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
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
COMPLICATIONS OF PERMANENT
DIALYSIS
 CARDIOVASCULAR

Accelerated
Atherosclerosis
Coronary calcification
Ischemic heart disease
Peripheral vascular
disease
Left ventricular
hypertrophy- HTN,
Anemia
Valvular calcification

Heart failure





 BONE and JOINTS
disease
 secunder
hyperparathyroidism
 b 2 microglobuline
amyloidosis
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 overloadpossible
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