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Acute Renal Failure
Dr:Sahar K. Attia - Pediatric Specialist King Khaled Hospital
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.
Structure and Function of the Kidney
• 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
Renal blood flow
Glomerular Filtration Rate
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
Glomerular Filtration Rate 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
Tubular Function
Tubular Function
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
Tubular Function 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
Tubular Function
Tubular Function
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
Acute Renal Failure - DefinitionsRenal 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.
Acute Renal Failure - Definitions
• 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.!!!
Acute Renal Failure - Definitions
Acute Renal Failure - Definitions
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
ARF- Pathogenesis
“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
ARF- Pathogenesis
• 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.
ARF- Pathogenesis
ARF- Classifications
ARF- Classifications
• 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 outflowcheck bladder, catheter & ultrasound
ARF- Causes
ARF- Diagnosis 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
ARF- Diagnosis
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
Acute Renal Failure - Intrinsic
Pre-Renal vs. Renal Failure
Prerenal RenalBUN/Cr >20 <20FENa <1% >2%Renal Failure Index UNa UCr/PCr
<1% >1%
UNa <20 mEq/L >40 mEq/LSpecific Gravity >1.020 <1.010Uosm >500 mOsm/L <350 mOsm/LUosm/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)
ARF- Post renal
Urinary sediment.
Urinary indices:•Urine volume•Urine electrolytes
Radiologic studies
Acute Renal FailureDiagnostic Tools
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
Urinary Sediment (Cast)
Anuria (< 100 ml/24h)• Acute bilateral arterial or venous
occlusion• Bilateral cortical necrosis• Acute necrotizing
glomerulonephritis• Obstruction (complete)• ATN (very rare)
Acute Renal FailureUrine Volume (1)
Oliguria (<500 ml/24h)
• Pre-renal azotemia
• ATN
Non-Oliguria (> 500 ml/24h)
• ATN
• Obstruction (partial)
Acute Renal FailureUrine Volume (1)
Urinary Indices:
FeNa =
FeNa <1%
FeNa 1%-2%
FeNa >2%
ARF Urine indices
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
ARF Urine indices
FeNa <1%
1. Prerenal: sometimes2. ATN: sometimes3. AIN-higher FeNa due to tubular
damage
1. ATN - Damaged tubules can't reabsorb Na
ARF Urine indices
FeNa 1%-2%
FeNa >2%
Other helpful indices:
1.Fractional Excretion of Lithium.
2. Fractional Excretion of Uric Acid.
3. Fractional Excretion of Urea
ARF Urine indices
Ultrasound•Structural anomalies – polycystic, obstruction, etc.•ATN –
- poor corticomedullary differentiation- Increased Doppler resistive index- (Systolic Peak – Diastolic peak) / systolic
peakNuclear medicine scans
-DMSA – Static - anatomy and scarring
- DTPA/MAG3 – Dynamic – renal function, urinary excretion, and upper tract outflow
Acute Renal Failure -Diagnosis
ARF- ManagementImmediate treatment of pulmonary edema and
hyperkalaemiaRemove offending cause or treat offending causeDialysis as needed to control hyperkalaemia,
pulmonary edema, metabolic acidosis, and uremic symptoms
Adjustment of drug regimenUsually restriction of water, Na, and K intake, but
provision of adequate proteinPossibly phosphate binders and Na polystyrene
sulfonate
ARF- Management
Nutrition management
- Initially very catabolic
Goals:Adequate calories
Low protein
Low K and Phos
Decreased fluid intake
Peritoneal Dialysis
Acute Intermittent Hemodialysis
Continuous Hemofiltration
CAVHSCUFCVVH, CVVHDAnd others….
Renal Replacement Therapy
Peritoneal dialysisAdvantages Disadvantages
• Simple to set up & perform
o Unreliable ultrafiltrationo Slow fluid & solute removal
• Easy to use in infants o Drainage failure & leakage• Hemodynamic
stabilityo Catheter obstruction
• No anti-coagulation o Respiratory compromiseo Hyperglycemia
• Bedside peritoneal access
o Peritonitis
• Treat severe hypothermia or hyperthermia
o Not good for hyperammonemia or intoxication with dialyzable poisons
Intermittent HemodialysisAdvantages 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
Continuous Hemofiltration
Advantages DisadvantagesEasy to use in PICU Systemic
anticoagulation (except citrate)Rapid electrolyte correction
Excellent solute clearancesFrequent filter
clottingRapid acid/base correction
Tolerated by unstable ptsVascular access in
infantsControllable fluid balanceEarly use of TPN
Oliguria/AnuriaHyperammonemiaHyperkalemiaSevere acidemiaSevere azotemiaPulmonary EdemaUremic complicationsSevere electrolyte abnormalitiesDrug overdose with a filterable
toxinAnasarcaRhabdomyolysis
Indications for RRTStill 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
BEFORE WE SAY GOOD BYE
THANK YOU FOR YOUR
ATTENTION