Nephrology

516 Acute renal failure

  • Acute  Renal Failure 

    Definition

    Acute changes in glomerular filtration such that the renal solute load (electrolytes, other ions, and nitrogenous wastes) cannot be excreted.

    There are two main forms:

    Oliguric: acute reduction in urine output to 0.5 ml/kg/h.  This form is more complex to manage

    Polyuric: often subacute and clinically inapparent, until fluid intake is reduced and the patient becomes dehydrated due to an inappropriately high urine output.

    Causes

    • Pre-Renal 
    • Dehydration (eg. gastroenteritis)
    • Shock (blood loss)
    • Sepsis
    • Nephrotic Syndrome

    Renal

    • Crescentic glomerulonephritis: acute post-infections; membranoproliferative; Henoch-Schoenlein purpura; antineutrophil cytoplasmic antibody-associated haemolytic uraemic syndrome
    • Acute tubular necrosis
    •  Crush injury (myoglobinuria)
    • UTI with septicaemia

    Nephrotoxin (eg. gentamicin)

    • Post-Renal
      Obstruction, especially to a single kidney.

    Management  Principles

    Immediate Management

    1. Ascertain and Treat the Cause of the renal failure.  Infuse blood, plasma, albumin, or saline for pre-renal conditions.   Obtain a Renal Ultrasound to exclude post-renal obstruction
    2. Give IV Frusemide, 4 mg/kg, to oliguric patients with renal disorders. If no response to frusemide in 1 hour, institute water and electrolyte restriction to the estimated urine plus insensible output. Urine flow may be estimated from measurement of previous day's urine output. Insensible losses are 350 ml/M2/day (more if febrile). Less fluid is given if fluid overloaded or hypertensive. Give no salt or potassium if anuric, and only small amounts to replace losses if oliguric (measure urine electrolytes). Give extra energy as Polyjoule or Calogen (see Dietary Guidelines).
    3. Dialysis will be required if serum potassium is raised or symptomatic fluid overload is present and urine output is not IMMEDIATELY increased by frusemide. Usually dialysis will be required after 24 hours of anuria.

    Management of established acute renal failure

    Water

    • Limit to insensible losses (300 ml/m2) plus urine losses

    Sodium

    • Principle: intake = urine sodium + other sodium losses
    • Oliguric: minimal Na+ intake
    • Polyuric: need to measure urine [Na]+ volume of urine.  Generally about 75 mmol/l required

    Potassium

    • No intravenous or oral intake until losses of K+ established.

    Hyperkalaemia

    • Repeat venous or arterial serum K+ urgently. 
    • Arrange haemofiltration or dialysis with patient in established renal failure
    • Salbutamol (inhaled, may be given to induce K+ temporary shits (ECT fo ICF)

    ECG:  peaked T waves, wide QRS, increased PR interval, decreased P and R waves, ST segment depression, prolonged QT interval

    If K+ >7 mmol/l with ECG changes:
    Salbutomol
    10% calcium gluconate 0.5 ml/kg, IV over 3-5 min (do not mix with bicarbonate).  Works in seconds

    Glucose and Insulin infusions

    • Glucose infusion 2 ml/kg 50% dextrose. 
    • Insulin infusion is often not required.  If necessary commence 0.1U/kg rapid acting insulin.  Works in minutes.
    • Arrange dialysis urgently
    •  If K+ >7 mmol/l, no ECG changes:
      •  Salbutomol NaHCO3 1-3 mmol/kg (shirts K+ intracellularly); risk of hypocalcaemic tetany with decreased pH.  Works within hour
      • Dextrose 0.5 g/kjg per h (10% dextrose at 5 ml/kg per h) until blood glucose reaches 14 mmol/l (shifts K+ intracellularly).   Works within hour
      •  Arrange dialysis urgently
    • If K+ >6 mmol/ Na+-K+ exchange resin, eg. Resonium A, 1 g/kg, p.o. (action within 6-12 h) or p.r. (action within 30 min; may repeat Q1-2h)
      •  Arrange dialysis. 

    Acidosis

    May be corrected with sodium bicarbonate (mmol = base deficit x weight (kg) x 1/3) over 4 hr should be avoided if:

    • Patient is hypocalcaemic (HCO3 may lower Ca2+ and cause convulsions)
    • Accompanying Na load likely to cause fluid overload (hypertension, pulmonary oedema)

    Hypocalcaemia

    This is usually due to increased serum phosphate

    1.  Low phosphate diet
    2. Calcium carbonate (phosphate binder)
    3. Symptomatic hypocalcaemia may require intravenous calcium gluconate
    4. Danger of metastitic calcification if Ca x PO4 product is >5-6
    5. If increased phosphate, consider dialysis.

    Uraemia
    1. Acute rise in serum urea to >30 mmol/L may cause CNS symptoms
    2. Protein restriction and high-quality protein food
    3. High carbohydrate diet

    Indications for dialysis/haemofiltration

    1. Fluid overload (hypertension or pulmonary oedema) not responding to frusemide)
    2. Hyperkalaemia
    3. Severe metabolic acidosis
    4. Progressive uraemia
    5. Dialysable nephrotoxin
    6. Hyperammonaemia
    7. Reduction of intravascular volume of facilitate total parenteral nutrition or blood transfusion
       

    The cause is usually apparent from the clinical context of the illness.