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Acute Renal Failure

Definition

  • Severe clinical syndrome as a result of sudden fast reduction of intact renal function
  • Rapid decline of GFR, retention of nitrogenous waste products and perturbation of extracellular fluid volume, of electrolytes and acid-base balance

Epidemiology

  • 5% of admitted pts in surgical wards have increased serum creatinine
  • 5-15% of pts in ICU
  • Assoc with high morbidity and mortality
    • 50-80% MR with oliguric ARF
    • 15-40% for non-oliguric ARF

Etiology

  • EXTRA RENAL CAUSES – etiological agent acts on tissues other than kidneys
    • Hypovolemic shock
      • hypotension, trauma with blood loss, myocardial dysfunction, vol depletion (burns, D, V), sepsis
    • Severe hemolysis + myolysis
      • Incomplete hemotransfusion, bact HL, immune/drug HL, traumatic HL (MVA)
    • Endogenous intoxication
      • Peritonitis, volvulus, Hepatorenal syndrome
  • INTRA RENAL CAUSES – etiological agent acts on kidneys
    • 1o/2o bilateral diffuse nephropathies
      • Acute GLN, rapidly progressive GLN, severe suppurative acute PLN, acute interstitial nephritis, multiple myeloma, nephropathy in pregnancy
    • Bilateral disorders of renal vascular system
      • Multiple renal infarcts, thrombosis of renal artery
    • Exogenous intoxicants
      • Heavy metals (Hg), hydrocarbons (petrol, benzol, chloroform, anti-freeze), mushrooms
    • Drugs – AGs, methicillin, cefamandole, sulphonamide, XR contrast, vaccine
    • Severe infections – Sepsis, leptospirosis, hemorrhagic fever
  • There are no post-renal causes of ARF
    • Obstruction can cause severe azotemia + anuria – e.g. benign prostatic hyperplasia, nephrolithiasis, neoplasm
    • Removal of etio agent leads to fast improvement of clinical pic of pt
    • No disturbance of renal parenchyma (in contrast to ARF)

Pathogenesis

  • Theory for tubular dystrophic-necrotizing changes
    • In hypovolemia – ischemia + hypoxia
    • In intoxication – blockage of cell enzyme systems
  • Homeostatic deviations
    • Disturbance of depurating function
      • Azotemia + uremia >> endointoxication (urea, guanidine, indoles)
    • Disturbance of water balance
      • Hyper-hydration
        • EC syndrome/ hypertonic – sc edema, LHF
        • IC syndrome/hypotonic – brain edema
      • Dehydration
        • EC syndrome/hypertonic
        • IC syndrome/hypotonic
    • Disturbance of ionic balance – K, Na, Ca, Mg, Cl
    • Disturbance of acid base state – metabolic alk/ac
    • Endocrine dysfunction

Clinical Presentation

  • Initial stage – clinical picture of causative disease e.g. shock, abortion, trauma
  • Oligo/anuric stage – CP of ARF, sudden onset (Oligouria <500ml; Anuria <100ml)
    • Symptoms
      • General status – changes from mild to severe
      • GI – no appetite, N, V, constipation, paralytic ileus
      • Resp – dysp/tachy –pnea
      • CDV – tachy/bradycardia, arrhythmia, HTN, LVHF
      • Nervous system – headache, vision loss, tremor, convulsions
      • Edema of face and extremities
    • Symptoms are due to
      • Azotemia , hyper-hydration, metabolic acidosis, hyperkalemia, uremia
    • Lab results
      • Urine – oligo/anuria, low urine weight
      • Blood – high BUN, creatinine, uric acid, K, Na, change pH of blood
    • Imaging
      • ECG – hyperkalemia (increased T wave, widened PQ interval, change in QRS)
      • XR – fluid lungs
  • Polyruic stage (>2L per day) – 2-3 weeks
    • Dehydration
    • Hypokalemia
    • Metabolic acidosis
    • Inflammatory complications – pneumonia etc
  • Restoration stage – 1-12 months

Diagnosis

  • Basic dx criteria
    • Oligo/anuria, low SG (isosthenuria), rapidly progressive azotemia, proved etio agent
  • Normal kidney size (CRF has small kidneys)
  • Serology – ANA, RF, anti-GBM, IgG/M/A, anti-PL
  • Electrophoresis
  • Fractional Na exretion best indicator (<1 pre renal, >2 intrinsic)

Treatment

  • No specific etiological/PG treatment for ARF – because changes are intracellular
  • Avoidance of etiological agent
  • Normalise CDV function in pts with heart disease
  • Prescribe safe doses of nephrotoxic drugs
  • Supportive treatment
    • Restrict Na and water to manage hypervolemia
    • Dopamine (1-5mg/kg/min) – promotes Na + water excretion
    • Severe hyperkalemia
      • Calcium gluconate – 10ml of a 10% soln infused over 2-3 mins
      • 10 units of insulin + 50g of glucose – shifts K into cells
      • NaHCO3 – also shifts K into cells
  • Indicators of dialysis (hemodialysis preferred)
    • Symptoms of uremic syndrome and management of hypervol, hyperkal, acidosis
    • Creatinine >600-700μmol/l
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