ACUTE RENAL FAILURE

    DEFINITION 

    Acute renal failure is characterized by a rapid decrease of glomerular
    filtration and, in consequence, reduced clearance of products of
    metabolism and other substances. This is usually accompanied by
    oliguria or anuria, but sometimes polyuria, with a progressive rise of
    serum creatinine and blood urea nitrogen (BUN), electrolyte imbalance
    and the development of metabolic acidosis.

    TOXIC CAUSES

    Aminoglycosides (e.g.: gentamycin, kanamycin).
    Carbon tetrachloride
    Polymycin
    Ethylene glycol
    Heavy metals
    Myoglobin and haemoglobin 

    NON-TOXIC CAUSES

    May be classified as pre-renal, renal and post-renal in origin.

    The principal causes are:     Acute tubular necrosis
                                  Acute glomerulonephritis
                                  Renal artery obstruction
                                  Acute interstitial nephritis
                                  Obstructive uropathy

    CLINICAL FEATURES

    The main sign is oliguria or anuria, occurring over several hours or a
    few days. Sometimes, however, renal failure occurs without oliguria,
    with normal or increased excretion of water and electrolytes.

    Accompanying signs and symptoms of acute renal failure include:
    weakness, apathy, loss of appetite, nausea, vomiting, increasing
    metabolic acidosis, deep, frequent respiration (Kussmaul type),
    pulmonary oedema, peripheral oedema, ascites, and coma. Cardiac
    dysrhythmia and extreme muscular weakness may be due to electrolyte
    imbalance (hyperkalaemia, hypercalcaemia).

    DIFFERENTIAL DIAGNOSIS

    Acute urinary retention
    Pre-renal uraemia (dehydration, hypotension).

    RELEVANT INVESTIGATIONS

    Biochemically, acute renal failure is characterized by elevated blood
    urea concentration and an increasing serum creatinine concentration.
    Serum potassium concentration usually rises above 6.5 mmol/L.
    Arterial blood gases indicate metabolic acidosis.
    The ECG may be helpful to assess hyperkalaemia.

    TREATMENT

    Carefully monitor clinical condition, ideally in a specialized ward.
    Control fluid balance and serum electrolyte levels, especially
    hyperkalaemia and hyponatremia.
    Correct contributing factors such as hypovolaemia and hypertension.
    Stop exposure to the offending agent(s).
    Carefully monitor dosage of potentially nephrotoxic drugs, if they are
    absolutely necessary.
    Administer  furosemide in doses of 250 mg (up to 1 g/day)
    intravenously; in children, 2 to 5 mg/kg (up to 15 mg/kg/ day).
    Start  dopamine in continuous intravenous infusion (up to 3
    µg/kg/minute).
    Control fluid intake.
    Control calorie intake.
    Hemodialysis or peritoneal dialysis should be instituted urgently in
    the following instances:
         a.   Hyperkalaemia with cardiac dysrrhythmias;
         b.   Hyperhydration in the anuric patient
         c.   Refractory metabolic acidosis.

    CLINICAL COURSE AND MONITORING

    Monitor fluid balance, electrolytes, cardiac status, acid-base
    balance, and infections.  Particular care should be taken with fluid
    balance during the polyuric phase.

    Most patients recover.  Renal function should be monitored until
    normalized.

    LONG-TERM COMPLICATIONS

    Chronic renal dysfunction.

    AUTHOR(S)/PEER REVIEW

    Author:        Dr. C. Bismuth, HÔpital Fernand Widal, Paris, France.
    Peer Review:   Cardiff, March 1995.
                   Berlin, October 1995: V. Danel, T. Meredith, J.
                   Szajewski, A. Wong, J. Pronczuk.