AETIOPATHOGENESIS & MANAGEMENT OF ACUTE RENAL FAILURE

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Human beings are essentially big bags of water, the volume of which must be kept under tight control, to prevent us from either drying out or drowning…..

DEFINITION

Acute renal failure (ARF) or acute kidney injury (AKI), as it is now referred to in the literature, is defined as an abrupt or rapid decline in renal filtration function. This condition is usually marked by a rise in serum creatinine concentration or azotemia (a rise in blood urea nitrogen [BUN] concentration). However, immediately after a kidney injury, BUN or creatinine levels may be normal, and the only sign of a kidney injury may be decreased urine production

‘ACUTE KIDNEY INJURY’

Abrupt reduction [<48 hrs] in kidney function, defined as an absolute increase in S creatinine of ≥0.3 mg/dLA percentage increase in S creatinine of ≥ 50% [1.5 fold from baseline] or a reduction in urine output-- documented oliguria of < 0.5 ml/kg/hr, for more than six hours.

STAGING SYSTEM FOR A.K.I.STAGE S.CREATININE

CRITERIAURINE OUTPUT CRITERIA

1 INCREASE IN S.CREATININE ≥0.3mg/dL OR INCREASE TO ≥ 150-200% FROM BASELINE

<0.5 ml/kg/hr FOR >6HRS

2 INCREASE IN S.CREATININE TO >200-300%[2-3 FOLD] FROM BASELINE

<0.5 ml/kg/hr FOR >12 HRS

3 INCREASE IN S. CREATININE TO >300%[>3 FOLD] FROM BASELINE OR S.CREATININE OF ≥4mg/dL WITH AN ACUTE INCREASE OF ATLEAST 0.5 mg/dL

<0.3ml/kg/hr FOR 24 HRS OR ANURIA FOR 12 HRS

RIFLE Classification System

CLASSIFICATION

PRERENAL ARF

as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons

GFR is reduced as a result of hemodynamic disturbances that decrease glomerular perfusion.

. CAUSES-PRERENAL ARF

HYPOVOLEMIA>HEMORRHAGE>G-I LOSSES>DECREASED INTAKE>URINARY LOSSES>SKIN LOSSES>OTHERS:BURNS,PANCREATITIS,SEVERE HYPOALBUMINEMIA

INTRINSIC ARF

• The so called diuretic phase…• Recovery phase• Filtration recovers early• Recovery of epithelial function lags behind

CAUSES

ISCHEMIAISCHEMIA>MAJOR CARDIOVASCULAR >TRAUMA >HEMORRHAGE >HYPOVOLEMIA

TOXINSTOXINSExogenous: Antibiotics-Aminoglycosides,Chemotherapeutic agents-Cisplatin, Endogenous: myoglobin,hemoglobin,calcium,bilirubinSEPSISSEPSIS

INTERSTITIUMINTERSTITIUMAllergic: Antibiotics : b-lactam ,quinolone , rifampin NSAIDs B/L pyelonephritis

INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir, methotrexate , indinavir , myeloma proteins

POSTRENAL ARF

Obstruction is always the most likely cause when there is anuriaBladder neck obstruction

When the insult cross the limits….

Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall

Decreased O2 delivery needs to decrease its work decrease filtration oliguria

Increased Na reabsorption = more work by medulla blood flow towards medulla ,i.e. away from cortex GFR decrease oliguria

“acute renal success”

Clinical features

Pre renal

vomiting , diarrhoea Intestinal obstruction….

Look forThirstReduced JVPDecreased skin turgorDry mucus membrane

Intrinsic renal

oliguria,edema,hypertensionIntake of nephrotoxic drugsatrial fibrillation

Post renal

AnuriaFlank pain

INVESTIGATIONS

Laboratorium

Urine microscopicAssessment GFRRadiology (Abdominal USG, Pyelography, MRA)

Assessment of GFR

Blood urea

15-40mg/dL

Increased in dehydration , post G-I bleed

Serum creatinine

Normal: <1.5 mg/dL

Rise by 1-2 mg/dL in ARF

Creatinine clearance

Volume of plasma cleared off creatinine per unit timeEarlier warnings, 2hr samples[140-age] x body wt / / S.Creatinine x 7291-130 ml / min

INTERVENTION

• Hemodynamic &urinary output monitoring• Aggressive fluid loading• Adequate oxygenation• Pharmacologic strategies• Renal replacement therapy

Hemodynamic &urinary output monitoring

Blood pressureCVPPAWPUrine output ensure catheter is not compressed ensure good urine flow from start monitor output hourly ensure output >1ml/kg/hr

Aggressive fluid loading

TraumaCompartment syndromeLimb revascularization

….high chance for rhabdomyolysis

Pharmacologic strategies

Mannitol

Improve urinary flowPulmonary edema, intra renal vasoconstriction, Aortic surgeries, Renal transplantation, CABG6.25-12.5g is given 15 mins prior to the defined insult / repeated 4-6 hrs24 hr cumulative dose not >1.5 mg/kg

Furosemide

Renal vasodilationShouldn’t be given if pt is not adequately fluid loaded2-10 mg/kg for converting oliguric to non oliguric renal failureContinuous infusion 1-10mg/hr after a LD of 10-20mg

othersMetabolic acidosis: NaHCO3 to keep its level >15mmol/L or pH >7.2Hyperphosphatemia :Ca carbonate, Al(OH)3Hypocalcemia :Ca gluconate , CaCl2Nutrition : Because potassium and phosphorus are not excreted optimally in patients with AKI, blood levels of these electrolytes tend to be high. Frequent measurements are mandatory to initiate early treatment and avoid complications.In the polyuric phase of AKI, potassium and phosphorus may be depleted and patients require dietary supplementation and intravenous replacement.Calculation of the nitrogen balance can be challenging, especially in the presence of volume contraction, hypercatabolic states, gastrointestinal bleeding, and diarrheal disease. Critically ill patients should receive at least 1 g/kg/day protein intake but should avoid hyperalimentation, which can lead to elevated BUN level and water loss resulting in hypernatremia.

Renal replacement therapy

Criteria for initiation of RRT

Anuria Oliguria Pulmonary edemaHyperkalemia >6.5mmol/LUreum > 200 mg %Overhydrasi

hemodialysis

• Intermittent HD: 3-4hrs per day,3-4 times per week

• Slow Low Efficiency Dialysis ^-12 hrs per day

peritoneal dialysis

Less effective than HDUseful if HD not availableImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed

Peritoneal dialysis

Access via a peritoneal catheterAllowed to dwell for a short period of time [2-4hrs]

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