Kishore D. Phadke*
Prof. of Pediatric Nephrology, Children's Kidney Care Center,St. John's Medical College Hospital, Bangalore. *
Kidneys regulate volume and composition of internal fluid environment, excretory function is incidental to their regulatory function. Retention of uremic toxins and acidosis in patients with acute renal failure (ARF) leads to dysregulation of the inflammatory response, decreased immunity and impaired hemodynamics. This causes multiple adverse effects including increased risk for infection and multiple organ dysfunction. Acute renal failure is not necessarily a consequence but in fact may be an important etiological factor of multi organ failure. Hence early recognition and appropriate aggressive management of ARF has an important bearing on the outcome of a critically ill child. In the ICU, the best time to treat renal failure is before it occurs.

To prevent ARF, the most important preventive measure is optimization of intravascular volume and cardiovascular function. Aggressive restoration of intravascular volume has been shown to reduce the incidence of acute tubular necrosis (ATN) especially in postoperative cases, trauma and patients with burns. Volume depletion is a risk factor for radiocontrast nephropathy, acyclovir, aminoglycoside, amphotericin, cisplatinum, cyclosporine toxicities, urate nephropathy, hypercalcemia etc. The drugs like diuretics, ACE inhibitors, NSAID, vasodilators should be used with caution in patients with volume depletion. Daily dosing of aminoglycosides may be less nephrotoxic. Drug level monitoring should be done whenever possible.

The following measures have been found to be useful in some specific clinical situations:
  • Forced alkaline diuresis hyperuricemia, methotrexate, rhabdomyolysis.
  • N-acetyl-cystein radiocontrast injury, acetaminophen toxicity.
  • Allupurinol, rasburicase hyperuricemia, tumour lysis syndrome.
  • Leucovorin methotrexate.
  • Ethanol Ethylene glycol poisoning.
  • Dimercaprol heavy metal poisoning.
  • Immunosuppressants rapidly progressive glomerulonephritis, vasculitis.
  • Plasmapheresis HUS, TTP.
  • Early dialysis HUS, hypercatabolic states.

The following have been tried as 'renal protective measures1. Many of these, although promising in an experimental scenario, have not been proven to be useful in clinical situations:
  • Vasoactive drugs nifedipine, low dose dopamine (controlled studies have shown no benefit), ANP, anti endothelin antibody.
  • Adenosine antagonists - theophylline.
  • Diuretics mannitol, furosemide (no proven benefit may convert oliguric to non-oliguric state, fluid management becomes easier),
  • Scavengers of ROS allopurinol, desferoxamine, dimethyl thiourea, dimethyl sulfoxide, glutathione, superoxide dismutase./li>
  • Neutrophil inhibitors anti-CD 18, anti ICAM-1 antibody.
  • Agents to restore cell energetics - ATP- MgC12, thyroxin, glycine.
  • Anticoagulants PENTOXIFYLLINE, dipyridamole, heparin
  • Growth factors EGF, IGF-1
  • HE-Inhibitors of casts RGD peptides.
  • Colloids albumin (no proven benefit over crystalloids except in cirrhosis of liver, nephritic syndrome).
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Phadke D K.. Available From : Conference_abstracts/report.aspx?reportid=296
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