SlideShare ist ein Scribd-Unternehmen logo
1 von 48
 Primary unit of the kidney is the nephron
 1 million nephrons per kidney
 Composed of a glomerulus and a tubule
 Kidneys receive 20% of cardiac output.
• Aorta  Renal artery  interlobar
arteries  interlobular arteries 
afferent arterioles  glomerulus 
efferent arterioles
• In the cortex  peritubular
capillaries
• In the juxtamedullary region vasa
recta
• Back to the heart through the
interlobular  intralobar  renal
veins
Hydrostatic pressure in the glomerulus
is higher than in the tubule, so you get a
net outflow of filtrate into the tubule.
Oncotic pressure in the glomerulus is
the result of non-filterable proteins.
Greater oncotic pressure as you
progress through the glomerulus
GFR =
Kf (hydrostatic – oncotic pressure)
Determined by:
the hydrostatic and oncotic pressure within the
nephron.
• Foot processes of the podocytes
form filtration slits that :
 Allow for ultrafiltrate passage
 Limit filtration of large negatively charged
particles
►Less than 5,000 daltons = freely filtered
►Large particles (albumin 69,000 daltons)
not filtered
 The capillary endothelium is surrounded by
a basement membrane and podocytes
Proximal
• Most of reabsorption occurs here
• Fluid is isotonic with plasma
• 66-70% of sodium presented is
reabsorbed
• Glucose and amino acids are
completely reabsorbed
Loop of Henle
• Urine concentration and dilution
via changes in oncotic pressure in
the vasa recta
• Descending tubule – permeable to
water, impermeable to sodium
• Ascending tubule – actively
reabsorbs sodium, impermeable to
water
 Medullary thick ascending limb – critical for
urinary dilution and most often damaged in ARF
• ADH stimulates Na re-absorption in
this area
• Most sensitive to ischemia
• Low oxygen tension, high oxygen
consumption
• Lasix use here inhibits the Na-K-2Cl
ATPase which in the face of ARF,
may decrease oxygen consumption
and ameliorate the severity of the
ARF
Distal Tubule
• Re-absorption of another ~12% of
NaCl
• Proximal segment – impermeable
to water
• Distal segment is the cortical
collecting duct and secretes K and
HCO3
Collecting Duct
• Aldosterone acts here to increase
Na reuptake and K wasting
• ADH enhances water re-absorption
• Urea re-absorption to maintain the
medullary interstitial concentration
gradient
• Inability of kidney to maintain
homeostasis leading to a buildup of
nitrogenous wastes
• Different to renal insufficiency
where kidney function is deranged
but can still support life
Renal failure
is defined as the cessation of kidney function with
or without changes in urine volume
Anuria – no urine output or less
than 100mls/24 hours or UOP <
0.5 cc/kg/hour
Oliguria - <500mls urine output/24
hours or <20mls/hour or UOP
“more than 1 cc/kg/hour
Polyuria - >2.5L/24 hours.
• 70% Non-oliguric , 30% Oliguric
• Non-oliguric associated with better
prognosis and outcome
• “Overall, the critical issue is
maintenance of adequate urine
output and prevention of further
renal injury.”
Our main role here as doctors
is not to convert non-oliguric
ARF to oliguric.!!!
Lab definition
• Increase in baseline creatinine of
more than 50%.
• Decrease in creatinine clearance of
more than 50%.
• Deterioration in renal function
requiring dialysis.
Usual causes
• Hypo-perfusion and ischemia
• Toxin mediated
• Inflammation
“Damage is caused mostly by renal
perfusion problems and tubular
dysfunction”
• Renal vasoconstriction is a well
documented cause of ARF.
• Renal vasodilation does not
consistently reduce ARF once
established
• Although renal hemodynamic
factors play a large role in initiating
ARF, they are not the dominant
determinants of cell damage
• Overall, renal vasoconstriction is
the major cause of the problems
in ARF
►Suggested ARF be replaced
with vasomotor nephropathy
• Insult to tubular epithelium
causes release of vasoactive
agents which cause the
constriction.
• Angiotensin II, endothelin, NO,
adenosine, prostaglandins, etc.
• Pre-renal (functional)
• Renal-intrinsic (structural)
• Post-renal (obstruction)
• Pre-renal:
- Inadequate perfusion
►check volume status
• Renal:
- ARF despite perfusion & excretion
►check urinalysis, CBC &
autoimmune screen
• Post-renal:
- Blocked outflow
►check bladder, catheter &
ultrasound
 Pre-renal:
• Decrease in RBF constriction
of afferent arteriole which serves
to increase systemic blood
pressure by reducing the “shunt”
through the kidney, but does so
at a cost of decreased RBF.
• At the same time, efferent
arteriole constricts to attempt to
maintain GFR
 Pre-renal (cont.):
•As GFR decreases, amount of filtrate
decreases. Urea is reabsorbed in the
distal tubule, leading to increased
tubular urea concentration and thus
greater re-absorption of urea into the
blood.
•Creatinine cannot be reabsorbed,
thus leading to a BUN/Cr ratio of > 20
 Acute tubular necrosis (ATN)
• Ischaemia
• Toxin
• Tubular factors
 Acute interstitial Necrosis (AIN)
• Inflammation
• oedema
 Glomerulonephritis (GN)
• Damage to filtering mechanisms
• Multiple causes as per previous
presentation
BUN/Cr >20 <20
FENa <1% >2%
Renal Failure Index
UNa UCr/PCr
<1% >1%
UNa <20 mEq/L >40 mEq/L
Specific Gravity >1.020 <1.010
Uosm >500 mOsm/L <350 mOsm/L
Uosm/Posm >1.3 <1.3
Intra-renal Obstruction
• Acute uric acid nephropathy
• Drugs (e.g., acyclovir)
Extra-renal Obstruction
-Renal pelvis or ureter
(e.g., stones, clots, tumors, papillary
necrosis, retroperitoneal fibrosis)
-Bladder (e.g.,neuropathic bladder)
-Urethra (e.g., stricture)
Urinary sediment.
Urinary indices:
•Urine volume
•Urine electrolytes
Radiologic studies
Bland
• Pre-renal azotaemia.
• Urinary outlet obstruction
RBC casts or dysmorphic RBCs
• Acute glomerulonephritis.
• Small vessel vasculitis.
WBC Cells and WBC Casts
•Acute interstitial nephritis
•Acute pyelonephritis
Anuria (< 100 ml/24h)
• Acute bilateral arterial or venous
occlusion
• Bilateral cortical necrosis
• Acute necrotizing
glomerulonephritis
• Obstruction (complete)
• ATN (very rare)
Oliguria (<500 ml/24h)
• Pre-renal azotemia
• ATN
Non-Oliguria (> 500 ml/24h)
• ATN
• Obstruction (partial)
Urinary Indices:
FeNa =
urine Na x plasma Cr
𝒑𝒍𝒂𝒔𝒎𝒂 𝑵𝒂 𝒙 𝒖𝒓𝒊𝒏𝒆 𝑪𝒓
FeNa <1%
FeNa 1%-2%
FeNa >2%
1. PRERENAL
- Urine Na < 20. Functioning tubules
reabsorb lots of filtered Na
2. ATN (unusual)
- Postischemic dz: most of UOP comes
from few normal nephrons, which
handle Na appropriately
- ATN + chronic prerenal dz (cirrhosis,
CHF)
3. Glomerular or vascular injury
-Despite glomerular or vascular injury, pt
may still have well-preserved tubular
function and be able to concentrate Na
FeNa <1%
FeNa 1%-2%
FeNa >2%
Other helpful indices:
Ultrasound
•Structural anomalies – polycystic,
obstruction, etc.
•ATN –
- poor corticomedullary differentiation
- Increased Doppler resistive index
- (Systolic Peak – Diastolic peak) / systolic
peak
Nuclear medicine scans
-DMSA – Static - anatomy and scarring
- DTPA/MAG3 – Dynamic – renal function,
urinary excretion, and upper tract
outflow
Immediate treatment of pulmonary edema and
hyperkalaemia
Remove offending cause or treat offending
cause
Dialysis as needed to control hyperkalaemia,
pulmonary edema, metabolic acidosis, and
uremic symptoms
Adjustment of drug regimen
Usually restriction of water, Na, and K intake, but
provision of adequate protein
Possibly phosphate binders and Na polystyrene
sulfonate
Nutrition management
- Initially very catabolic
Goals:
 Adequate calories
 Low protein
 Low K and Phos
 Decreased fluid intake
Peritoneal Dialysis
Acute Intermittent Hemodialysis
Continuous Hemofiltration
CAVH
SCUF
CVVH, CVVHD
And others….
Advantages Disadvantages
• Simple to set up &
perform
o Unreliable ultrafiltration
o Slow fluid & solute removal
• Easy to use in infants o Drainage failure & leakage
• Hemodynamic
stability
o Catheter obstruction
• No anti-coagulation o Respiratory compromise
o Hyperglycemia
• Bedside peritoneal
access
o Peritonitis
• Treat severe
hypothermia or
hyperthermia
o Not good for hyperammonemia
or intoxication with dialyzable
poisons
Advantages Disadvantages
• Maximum solute clearance of 3
modalities
o Hemodynamic
instability
• Best therapy for severe
hyperkalemia
o Hypoxemia
• Limited anti-coagulation time o Rapid fluid and
electrolyte shifts
o Complex equipment
• Bedside vascular access can
be used
o Specialized personnel
o Difficult in small
infants
Advantages Disadvantages
Easy to use in PICU Systemic
anticoagulation
(except citrate)Rapid electrolyte correction
Excellent solute clearances
Frequent filter
clottingRapid acid/base correction
Tolerated by unstable pts
Vascular access in
infants
Controllable fluid balance
Early use of TPN
Oliguria/Anuria
Hyperammonemia
Hyperkalemia
Severe acidemia
Severe azotemia
Pulmonary Edema
Uremic complications
Severe electrolyte abnormalities
Drug overdose with a filterable
toxin
Anasarca
Rhabdomyolysis
Still evolving….Generally accepted
Remember to:
 Think about who might be
vulnerable to acute renal failure.
 Think twice before initiating
therapy that may cause ARF.
 Think about it as a diagnosis –> it
happens rapidly, you won’t see/
find signs
ARF- acute renal failure

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (20)

Chronic Kidney Disease
Chronic Kidney Disease Chronic Kidney Disease
Chronic Kidney Disease
 
Adequacy of Hemodialysis
Adequacy of HemodialysisAdequacy of Hemodialysis
Adequacy of Hemodialysis
 
Acute kidney injury
Acute kidney injuryAcute kidney injury
Acute kidney injury
 
Anuria & acute retention
Anuria & acute retentionAnuria & acute retention
Anuria & acute retention
 
Approach to CKD
Approach to CKDApproach to CKD
Approach to CKD
 
Nephrolithiasis
NephrolithiasisNephrolithiasis
Nephrolithiasis
 
Chronic Kidney Disease
Chronic Kidney Disease Chronic Kidney Disease
Chronic Kidney Disease
 
pyelonephirits
pyelonephiritspyelonephirits
pyelonephirits
 
Urolithiasis
UrolithiasisUrolithiasis
Urolithiasis
 
AKI
AKIAKI
AKI
 
Aki
AkiAki
Aki
 
Metabolic acidosis by akram
Metabolic acidosis by akramMetabolic acidosis by akram
Metabolic acidosis by akram
 
Chronic hepatitis
Chronic hepatitisChronic hepatitis
Chronic hepatitis
 
Acute Kidney Injury
Acute Kidney InjuryAcute Kidney Injury
Acute Kidney Injury
 
Cystitis INFLAMMATION OF URINARY BLADDER
Cystitis INFLAMMATION OF URINARY BLADDERCystitis INFLAMMATION OF URINARY BLADDER
Cystitis INFLAMMATION OF URINARY BLADDER
 
Anemia in ckd
Anemia in ckd Anemia in ckd
Anemia in ckd
 
Acute kidney injury defnition, causes,
Acute kidney injury   defnition, causes,Acute kidney injury   defnition, causes,
Acute kidney injury defnition, causes,
 
Kidney failure in hypertension
Kidney failure in hypertensionKidney failure in hypertension
Kidney failure in hypertension
 
Glumeronephritis
GlumeronephritisGlumeronephritis
Glumeronephritis
 
Acute kidney injury
Acute kidney injuryAcute kidney injury
Acute kidney injury
 

Andere mochten auch

05 Goldstein Acute Renal Failure
05 Goldstein   Acute Renal Failure05 Goldstein   Acute Renal Failure
05 Goldstein Acute Renal Failure
guest2379201
 
PHOTOFOLIO2016_AGUM KURNIAWAN
PHOTOFOLIO2016_AGUM KURNIAWANPHOTOFOLIO2016_AGUM KURNIAWAN
PHOTOFOLIO2016_AGUM KURNIAWAN
jarikurakura
 
Trabajo Final Integrador-Formación y Práctica de Tutores
Trabajo Final Integrador-Formación y Práctica de TutoresTrabajo Final Integrador-Formación y Práctica de Tutores
Trabajo Final Integrador-Formación y Práctica de Tutores
Claudia Alejandra Serrano
 

Andere mochten auch (17)

05 Goldstein Acute Renal Failure
05 Goldstein   Acute Renal Failure05 Goldstein   Acute Renal Failure
05 Goldstein Acute Renal Failure
 
Diptico b
Diptico bDiptico b
Diptico b
 
Xdin - Sebastien Rassinoux
Xdin - Sebastien RassinouxXdin - Sebastien Rassinoux
Xdin - Sebastien Rassinoux
 
Salto condicional
Salto condicionalSalto condicional
Salto condicional
 
Bài tập luyện nghe amazing you
Bài tập luyện nghe amazing youBài tập luyện nghe amazing you
Bài tập luyện nghe amazing you
 
PHOTOFOLIO2016_AGUM KURNIAWAN
PHOTOFOLIO2016_AGUM KURNIAWANPHOTOFOLIO2016_AGUM KURNIAWAN
PHOTOFOLIO2016_AGUM KURNIAWAN
 
Microprocesadores
MicroprocesadoresMicroprocesadores
Microprocesadores
 
Trabajo Final Integrador-Formación y Práctica de Tutores
Trabajo Final Integrador-Formación y Práctica de TutoresTrabajo Final Integrador-Formación y Práctica de Tutores
Trabajo Final Integrador-Formación y Práctica de Tutores
 
Higiene bucal
Higiene bucalHigiene bucal
Higiene bucal
 
Check Out FAAIF News for October, 2016! (Camille Paldi)
Check Out FAAIF News for October, 2016! (Camille Paldi)Check Out FAAIF News for October, 2016! (Camille Paldi)
Check Out FAAIF News for October, 2016! (Camille Paldi)
 
Agenda Programme 3rd ISRA Colloquium 2013
Agenda Programme 3rd  ISRA Colloquium 2013Agenda Programme 3rd  ISRA Colloquium 2013
Agenda Programme 3rd ISRA Colloquium 2013
 
Introducing Takaful into the United States: Prospects and Possibilities
Introducing Takaful into the United States: Prospects and PossibilitiesIntroducing Takaful into the United States: Prospects and Possibilities
Introducing Takaful into the United States: Prospects and Possibilities
 
La tecnologia y sus multiples relaciones
La tecnologia y sus multiples relacionesLa tecnologia y sus multiples relaciones
La tecnologia y sus multiples relaciones
 
zero day exploits
zero day exploitszero day exploits
zero day exploits
 
Acute renal failure (2)
Acute renal failure (2)Acute renal failure (2)
Acute renal failure (2)
 
Gatos
GatosGatos
Gatos
 
Enfoque cualitativo cuantitativo
Enfoque cualitativo cuantitativoEnfoque cualitativo cuantitativo
Enfoque cualitativo cuantitativo
 

Ähnlich wie ARF- acute renal failure

01 Graciano Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano Acute Renal Failure In The Intensive Care Unit
Dang Thanh Tuan
 
Acute Renal Failure
Acute Renal FailureAcute Renal Failure
Acute Renal Failure
Jaymax13
 
01 Graciano Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano Acute Renal Failure In The Intensive Care Unit
guest2379201
 
ACUTE RENAL FAILURE_FINAL PRESENTATION.pptx
ACUTE RENAL FAILURE_FINAL PRESENTATION.pptxACUTE RENAL FAILURE_FINAL PRESENTATION.pptx
ACUTE RENAL FAILURE_FINAL PRESENTATION.pptx
Aditya Sinha
 

Ähnlich wie ARF- acute renal failure (20)

ACUTE RENAL FAILURE
ACUTE RENAL FAILUREACUTE RENAL FAILURE
ACUTE RENAL FAILURE
 
RENAL FUNCTION TEST.pptx
RENAL FUNCTION TEST.pptxRENAL FUNCTION TEST.pptx
RENAL FUNCTION TEST.pptx
 
Acute kidney injury
Acute kidney injuryAcute kidney injury
Acute kidney injury
 
01 Graciano Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano Acute Renal Failure In The Intensive Care Unit
 
Acute Renal Failure
Acute Renal FailureAcute Renal Failure
Acute Renal Failure
 
01 Graciano Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano Acute Renal Failure In The Intensive Care Unit
 
Acute Kidney Injury
Acute Kidney InjuryAcute Kidney Injury
Acute Kidney Injury
 
Aki
AkiAki
Aki
 
Renal function test
Renal function testRenal function test
Renal function test
 
Acute kidney injury (aki)
Acute kidney injury (aki)Acute kidney injury (aki)
Acute kidney injury (aki)
 
ACUTE RENAL FAILURE_FINAL PRESENTATION.pptx
ACUTE RENAL FAILURE_FINAL PRESENTATION.pptxACUTE RENAL FAILURE_FINAL PRESENTATION.pptx
ACUTE RENAL FAILURE_FINAL PRESENTATION.pptx
 
RENAL-DISEASE small animal medicine -I.pptx
RENAL-DISEASE small animal medicine -I.pptxRENAL-DISEASE small animal medicine -I.pptx
RENAL-DISEASE small animal medicine -I.pptx
 
Renal Failure
Renal FailureRenal Failure
Renal Failure
 
Physiology of urine formation and kidney function test swati mam
Physiology of urine formation and kidney function test  swati mamPhysiology of urine formation and kidney function test  swati mam
Physiology of urine formation and kidney function test swati mam
 
ARF final.ppt
ARF final.pptARF final.ppt
ARF final.ppt
 
Acute and chronic renal failure
Acute and chronic renal failureAcute and chronic renal failure
Acute and chronic renal failure
 
Post obstructive diuresis
Post obstructive diuresisPost obstructive diuresis
Post obstructive diuresis
 
RENAL ANATOMY , PHYSIOLOGY AND ANESTHESIA
RENAL ANATOMY , PHYSIOLOGY AND ANESTHESIARENAL ANATOMY , PHYSIOLOGY AND ANESTHESIA
RENAL ANATOMY , PHYSIOLOGY AND ANESTHESIA
 
1 Acute Kidney Injury.pptx
1 Acute Kidney Injury.pptx1 Acute Kidney Injury.pptx
1 Acute Kidney Injury.pptx
 
acute-renal-failure.ppt
acute-renal-failure.pptacute-renal-failure.ppt
acute-renal-failure.ppt
 

Kürzlich hochgeladen

🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...
🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...
🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...
Call Girls In Delhi Whatsup 9873940964 Enjoy Unlimited Pleasure
 

Kürzlich hochgeladen (20)

Call Girls Service Jaipur {8445551418} ❤️VVIP BHAWNA Call Girl in Jaipur Raja...
Call Girls Service Jaipur {8445551418} ❤️VVIP BHAWNA Call Girl in Jaipur Raja...Call Girls Service Jaipur {8445551418} ❤️VVIP BHAWNA Call Girl in Jaipur Raja...
Call Girls Service Jaipur {8445551418} ❤️VVIP BHAWNA Call Girl in Jaipur Raja...
 
Saket * Call Girls in Delhi - Phone 9711199012 Escorts Service at 6k to 50k a...
Saket * Call Girls in Delhi - Phone 9711199012 Escorts Service at 6k to 50k a...Saket * Call Girls in Delhi - Phone 9711199012 Escorts Service at 6k to 50k a...
Saket * Call Girls in Delhi - Phone 9711199012 Escorts Service at 6k to 50k a...
 
Independent Call Girls Service Mohali Sector 116 | 6367187148 | Call Girl Ser...
Independent Call Girls Service Mohali Sector 116 | 6367187148 | Call Girl Ser...Independent Call Girls Service Mohali Sector 116 | 6367187148 | Call Girl Ser...
Independent Call Girls Service Mohali Sector 116 | 6367187148 | Call Girl Ser...
 
Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...
Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...
Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...
 
Pondicherry Call Girls Book Now 9630942363 Top Class Pondicherry Escort Servi...
Pondicherry Call Girls Book Now 9630942363 Top Class Pondicherry Escort Servi...Pondicherry Call Girls Book Now 9630942363 Top Class Pondicherry Escort Servi...
Pondicherry Call Girls Book Now 9630942363 Top Class Pondicherry Escort Servi...
 
Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...
Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...
Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...
 
Independent Call Girls In Jaipur { 8445551418 } ✔ ANIKA MEHTA ✔ Get High Prof...
Independent Call Girls In Jaipur { 8445551418 } ✔ ANIKA MEHTA ✔ Get High Prof...Independent Call Girls In Jaipur { 8445551418 } ✔ ANIKA MEHTA ✔ Get High Prof...
Independent Call Girls In Jaipur { 8445551418 } ✔ ANIKA MEHTA ✔ Get High Prof...
 
Andheri East ) Call Girls in Mumbai Phone No 9004268417 Elite Escort Service ...
Andheri East ) Call Girls in Mumbai Phone No 9004268417 Elite Escort Service ...Andheri East ) Call Girls in Mumbai Phone No 9004268417 Elite Escort Service ...
Andheri East ) Call Girls in Mumbai Phone No 9004268417 Elite Escort Service ...
 
Mumbai ] (Call Girls) in Mumbai 10k @ I'm VIP Independent Escorts Girls 98333...
Mumbai ] (Call Girls) in Mumbai 10k @ I'm VIP Independent Escorts Girls 98333...Mumbai ] (Call Girls) in Mumbai 10k @ I'm VIP Independent Escorts Girls 98333...
Mumbai ] (Call Girls) in Mumbai 10k @ I'm VIP Independent Escorts Girls 98333...
 
Premium Call Girls In Jaipur {8445551418} ❤️VVIP SEEMA Call Girl in Jaipur Ra...
Premium Call Girls In Jaipur {8445551418} ❤️VVIP SEEMA Call Girl in Jaipur Ra...Premium Call Girls In Jaipur {8445551418} ❤️VVIP SEEMA Call Girl in Jaipur Ra...
Premium Call Girls In Jaipur {8445551418} ❤️VVIP SEEMA Call Girl in Jaipur Ra...
 
🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...
🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...
🌹Attapur⬅️ Vip Call Girls Hyderabad 📱9352852248 Book Well Trand Call Girls In...
 
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service AvailableCall Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
 
Jogeshwari ! Call Girls Service Mumbai - 450+ Call Girl Cash Payment 90042684...
Jogeshwari ! Call Girls Service Mumbai - 450+ Call Girl Cash Payment 90042684...Jogeshwari ! Call Girls Service Mumbai - 450+ Call Girl Cash Payment 90042684...
Jogeshwari ! Call Girls Service Mumbai - 450+ Call Girl Cash Payment 90042684...
 
Call Girls Madurai Just Call 9630942363 Top Class Call Girl Service Available
Call Girls Madurai Just Call 9630942363 Top Class Call Girl Service AvailableCall Girls Madurai Just Call 9630942363 Top Class Call Girl Service Available
Call Girls Madurai Just Call 9630942363 Top Class Call Girl Service Available
 
Most Beautiful Call Girl in Bangalore Contact on Whatsapp
Most Beautiful Call Girl in Bangalore Contact on WhatsappMost Beautiful Call Girl in Bangalore Contact on Whatsapp
Most Beautiful Call Girl in Bangalore Contact on Whatsapp
 
Coimbatore Call Girls in Coimbatore 7427069034 genuine Escort Service Girl 10...
Coimbatore Call Girls in Coimbatore 7427069034 genuine Escort Service Girl 10...Coimbatore Call Girls in Coimbatore 7427069034 genuine Escort Service Girl 10...
Coimbatore Call Girls in Coimbatore 7427069034 genuine Escort Service Girl 10...
 
Call Girls Vasai Virar Just Call 9630942363 Top Class Call Girl Service Avail...
Call Girls Vasai Virar Just Call 9630942363 Top Class Call Girl Service Avail...Call Girls Vasai Virar Just Call 9630942363 Top Class Call Girl Service Avail...
Call Girls Vasai Virar Just Call 9630942363 Top Class Call Girl Service Avail...
 
Call Girls Service Jaipur {9521753030 } ❤️VVIP BHAWNA Call Girl in Jaipur Raj...
Call Girls Service Jaipur {9521753030 } ❤️VVIP BHAWNA Call Girl in Jaipur Raj...Call Girls Service Jaipur {9521753030 } ❤️VVIP BHAWNA Call Girl in Jaipur Raj...
Call Girls Service Jaipur {9521753030 } ❤️VVIP BHAWNA Call Girl in Jaipur Raj...
 
Russian Call Girls Service Jaipur {8445551418} ❤️PALLAVI VIP Jaipur Call Gir...
Russian Call Girls Service  Jaipur {8445551418} ❤️PALLAVI VIP Jaipur Call Gir...Russian Call Girls Service  Jaipur {8445551418} ❤️PALLAVI VIP Jaipur Call Gir...
Russian Call Girls Service Jaipur {8445551418} ❤️PALLAVI VIP Jaipur Call Gir...
 
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
 

ARF- acute renal failure

  • 1.
  • 2.
  • 3.  Primary unit of the kidney is the nephron  1 million nephrons per kidney  Composed of a glomerulus and a tubule  Kidneys receive 20% of cardiac output.
  • 4. • Aorta  Renal artery  interlobar arteries  interlobular arteries  afferent arterioles  glomerulus  efferent arterioles • In the cortex  peritubular capillaries • In the juxtamedullary region vasa recta • Back to the heart through the interlobular  intralobar  renal veins
  • 5. Hydrostatic pressure in the glomerulus is higher than in the tubule, so you get a net outflow of filtrate into the tubule. Oncotic pressure in the glomerulus is the result of non-filterable proteins. Greater oncotic pressure as you progress through the glomerulus GFR = Kf (hydrostatic – oncotic pressure) Determined by: the hydrostatic and oncotic pressure within the nephron.
  • 6.
  • 7. • Foot processes of the podocytes form filtration slits that :  Allow for ultrafiltrate passage  Limit filtration of large negatively charged particles ►Less than 5,000 daltons = freely filtered ►Large particles (albumin 69,000 daltons) not filtered  The capillary endothelium is surrounded by a basement membrane and podocytes
  • 8. Proximal • Most of reabsorption occurs here • Fluid is isotonic with plasma • 66-70% of sodium presented is reabsorbed • Glucose and amino acids are completely reabsorbed
  • 9. Loop of Henle • Urine concentration and dilution via changes in oncotic pressure in the vasa recta • Descending tubule – permeable to water, impermeable to sodium • Ascending tubule – actively reabsorbs sodium, impermeable to water
  • 10.  Medullary thick ascending limb – critical for urinary dilution and most often damaged in ARF • ADH stimulates Na re-absorption in this area • Most sensitive to ischemia • Low oxygen tension, high oxygen consumption • Lasix use here inhibits the Na-K-2Cl ATPase which in the face of ARF, may decrease oxygen consumption and ameliorate the severity of the ARF
  • 11. Distal Tubule • Re-absorption of another ~12% of NaCl • Proximal segment – impermeable to water • Distal segment is the cortical collecting duct and secretes K and HCO3
  • 12. Collecting Duct • Aldosterone acts here to increase Na reuptake and K wasting • ADH enhances water re-absorption • Urea re-absorption to maintain the medullary interstitial concentration gradient
  • 13. • Inability of kidney to maintain homeostasis leading to a buildup of nitrogenous wastes • Different to renal insufficiency where kidney function is deranged but can still support life Renal failure is defined as the cessation of kidney function with or without changes in urine volume
  • 14. Anuria – no urine output or less than 100mls/24 hours or UOP < 0.5 cc/kg/hour Oliguria - <500mls urine output/24 hours or <20mls/hour or UOP “more than 1 cc/kg/hour Polyuria - >2.5L/24 hours.
  • 15. • 70% Non-oliguric , 30% Oliguric • Non-oliguric associated with better prognosis and outcome • “Overall, the critical issue is maintenance of adequate urine output and prevention of further renal injury.” Our main role here as doctors is not to convert non-oliguric ARF to oliguric.!!!
  • 16. Lab definition • Increase in baseline creatinine of more than 50%. • Decrease in creatinine clearance of more than 50%. • Deterioration in renal function requiring dialysis.
  • 17. Usual causes • Hypo-perfusion and ischemia • Toxin mediated • Inflammation “Damage is caused mostly by renal perfusion problems and tubular dysfunction”
  • 18. • Renal vasoconstriction is a well documented cause of ARF. • Renal vasodilation does not consistently reduce ARF once established • Although renal hemodynamic factors play a large role in initiating ARF, they are not the dominant determinants of cell damage
  • 19. • Overall, renal vasoconstriction is the major cause of the problems in ARF ►Suggested ARF be replaced with vasomotor nephropathy • Insult to tubular epithelium causes release of vasoactive agents which cause the constriction. • Angiotensin II, endothelin, NO, adenosine, prostaglandins, etc.
  • 20.
  • 21.
  • 22. • Pre-renal (functional) • Renal-intrinsic (structural) • Post-renal (obstruction)
  • 23. • Pre-renal: - Inadequate perfusion ►check volume status • Renal: - ARF despite perfusion & excretion ►check urinalysis, CBC & autoimmune screen • Post-renal: - Blocked outflow ►check bladder, catheter & ultrasound
  • 24.
  • 25.
  • 26.  Pre-renal: • Decrease in RBF constriction of afferent arteriole which serves to increase systemic blood pressure by reducing the “shunt” through the kidney, but does so at a cost of decreased RBF. • At the same time, efferent arteriole constricts to attempt to maintain GFR
  • 27.  Pre-renal (cont.): •As GFR decreases, amount of filtrate decreases. Urea is reabsorbed in the distal tubule, leading to increased tubular urea concentration and thus greater re-absorption of urea into the blood. •Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20
  • 28.  Acute tubular necrosis (ATN) • Ischaemia • Toxin • Tubular factors  Acute interstitial Necrosis (AIN) • Inflammation • oedema  Glomerulonephritis (GN) • Damage to filtering mechanisms • Multiple causes as per previous presentation
  • 29. BUN/Cr >20 <20 FENa <1% >2% Renal Failure Index UNa UCr/PCr <1% >1% UNa <20 mEq/L >40 mEq/L Specific Gravity >1.020 <1.010 Uosm >500 mOsm/L <350 mOsm/L Uosm/Posm >1.3 <1.3
  • 30. Intra-renal Obstruction • Acute uric acid nephropathy • Drugs (e.g., acyclovir) Extra-renal Obstruction -Renal pelvis or ureter (e.g., stones, clots, tumors, papillary necrosis, retroperitoneal fibrosis) -Bladder (e.g.,neuropathic bladder) -Urethra (e.g., stricture)
  • 31. Urinary sediment. Urinary indices: •Urine volume •Urine electrolytes Radiologic studies
  • 32. Bland • Pre-renal azotaemia. • Urinary outlet obstruction RBC casts or dysmorphic RBCs • Acute glomerulonephritis. • Small vessel vasculitis. WBC Cells and WBC Casts •Acute interstitial nephritis •Acute pyelonephritis
  • 33. Anuria (< 100 ml/24h) • Acute bilateral arterial or venous occlusion • Bilateral cortical necrosis • Acute necrotizing glomerulonephritis • Obstruction (complete) • ATN (very rare)
  • 34. Oliguria (<500 ml/24h) • Pre-renal azotemia • ATN Non-Oliguria (> 500 ml/24h) • ATN • Obstruction (partial)
  • 35. Urinary Indices: FeNa = urine Na x plasma Cr 𝒑𝒍𝒂𝒔𝒎𝒂 𝑵𝒂 𝒙 𝒖𝒓𝒊𝒏𝒆 𝑪𝒓 FeNa <1% FeNa 1%-2% FeNa >2%
  • 36. 1. PRERENAL - Urine Na < 20. Functioning tubules reabsorb lots of filtered Na 2. ATN (unusual) - Postischemic dz: most of UOP comes from few normal nephrons, which handle Na appropriately - ATN + chronic prerenal dz (cirrhosis, CHF) 3. Glomerular or vascular injury -Despite glomerular or vascular injury, pt may still have well-preserved tubular function and be able to concentrate Na FeNa <1%
  • 39. Ultrasound •Structural anomalies – polycystic, obstruction, etc. •ATN – - poor corticomedullary differentiation - Increased Doppler resistive index - (Systolic Peak – Diastolic peak) / systolic peak Nuclear medicine scans -DMSA – Static - anatomy and scarring - DTPA/MAG3 – Dynamic – renal function, urinary excretion, and upper tract outflow
  • 40. Immediate treatment of pulmonary edema and hyperkalaemia Remove offending cause or treat offending cause Dialysis as needed to control hyperkalaemia, pulmonary edema, metabolic acidosis, and uremic symptoms Adjustment of drug regimen Usually restriction of water, Na, and K intake, but provision of adequate protein Possibly phosphate binders and Na polystyrene sulfonate
  • 41. Nutrition management - Initially very catabolic Goals:  Adequate calories  Low protein  Low K and Phos  Decreased fluid intake
  • 42. Peritoneal Dialysis Acute Intermittent Hemodialysis Continuous Hemofiltration CAVH SCUF CVVH, CVVHD And others….
  • 43. Advantages Disadvantages • Simple to set up & perform o Unreliable ultrafiltration o Slow fluid & solute removal • Easy to use in infants o Drainage failure & leakage • Hemodynamic stability o Catheter obstruction • No anti-coagulation o Respiratory compromise o Hyperglycemia • Bedside peritoneal access o Peritonitis • Treat severe hypothermia or hyperthermia o Not good for hyperammonemia or intoxication with dialyzable poisons
  • 44. Advantages Disadvantages • Maximum solute clearance of 3 modalities o Hemodynamic instability • Best therapy for severe hyperkalemia o Hypoxemia • Limited anti-coagulation time o Rapid fluid and electrolyte shifts o Complex equipment • Bedside vascular access can be used o Specialized personnel o Difficult in small infants
  • 45. Advantages Disadvantages Easy to use in PICU Systemic anticoagulation (except citrate)Rapid electrolyte correction Excellent solute clearances Frequent filter clottingRapid acid/base correction Tolerated by unstable pts Vascular access in infants Controllable fluid balance Early use of TPN
  • 46. Oliguria/Anuria Hyperammonemia Hyperkalemia Severe acidemia Severe azotemia Pulmonary Edema Uremic complications Severe electrolyte abnormalities Drug overdose with a filterable toxin Anasarca Rhabdomyolysis Still evolving….Generally accepted
  • 47. Remember to:  Think about who might be vulnerable to acute renal failure.  Think twice before initiating therapy that may cause ARF.  Think about it as a diagnosis –> it happens rapidly, you won’t see/ find signs