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ARF- acute renal failure

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Acute Renal Failure

Dr:Sahar K. Attia - Pediatric Specialist King Khaled Hospital

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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

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• 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

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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.

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• 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

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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

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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

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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

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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

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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

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• 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

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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

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• 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

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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.

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Usual causes

• Hypo-perfusion and ischemia

• Toxin mediated

• Inflammation

ARF- Pathogenesis

“Damage is caused mostly by renal perfusion problems and tubular dysfunction”

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• 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

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• 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

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ARF- Classifications

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ARF- Classifications

• Pre-renal (functional)

• Renal-intrinsic (structural)

• Post-renal (obstruction)

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• 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

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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

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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

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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

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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

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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

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Urinary sediment.

Urinary indices:•Urine volume•Urine electrolytes

Radiologic studies

Acute Renal FailureDiagnostic Tools

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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)

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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)

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Oliguria (<500 ml/24h)

• Pre-renal azotemia

• ATN

Non-Oliguria (> 500 ml/24h)

• ATN

• Obstruction (partial)

Acute Renal FailureUrine Volume (1)

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Urinary Indices:

FeNa =

FeNa <1%

FeNa 1%-2%

FeNa >2%

ARF Urine indices

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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%

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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%

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Other helpful indices:

1.Fractional Excretion of Lithium.

2. Fractional Excretion of Uric Acid.

3. Fractional Excretion of Urea

ARF Urine indices

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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

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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

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ARF- Management

Nutrition management

- Initially very catabolic

Goals:Adequate calories

Low protein

Low K and Phos

Decreased fluid intake

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Peritoneal Dialysis

Acute Intermittent Hemodialysis

Continuous Hemofiltration

CAVHSCUFCVVH, CVVHDAnd others….

Renal Replacement Therapy

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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

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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

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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

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Oliguria/AnuriaHyperammonemiaHyperkalemiaSevere acidemiaSevere azotemiaPulmonary EdemaUremic complicationsSevere electrolyte abnormalitiesDrug overdose with a filterable

toxinAnasarcaRhabdomyolysis

Indications for RRTStill evolving….Generally accepted

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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

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THANK YOU FOR YOUR

ATTENTION