Address For Correspondence:
R Bhimma, Department of Paediatrics & Child Health, Nelson R Mandela School of Medicine, University of Kwazulu-Natal, Private Bag 7, Congella, 4013, South Africa.
Email: bhimma@ukzn.ac.za

Management of Acute Kidney Injury

Aggressive treatment should begin at the easiest indication of renal dysfunction. Recognising the presence of AKI and promptly initiating therapy is aimed at minimizing damage to the remaining functional renal mass. Reversing renal damage can only be accomplished by identifying the underlying cause and directing appropriate therapy.

Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment. Furosemide can be used to correct volume overload when patients are still responsive to it. Response to furosemide often portends a good progress. However furosemide plays no role in converting an oliguric AKI to a non oliguric AKI or to increase urine output when a patient is not hypervolemic.

The accompanying metabolic acidosis is corrected by bicarbonate administration. Hyperkalaemia can be life threatening and must be treated urgently. Treatment is aimed at decreasing the intake of potassium, delaying the absorption of potassium, exchanging potassium across the gut lumen using potassium-binding resins, controlling intracellular shifts and if these measures fail, by instituting dialysis.

Correcting haematological abnormalities (e.g. anaemia, platelet dysfunction) warrants appropriate measures, including blood transfusion and administration of desmopressin or oestrogens.

Dietary modulations to correct electrolytes imbalances particularly potassium and phosphate, and restricting fluids are crucial in the management of oliguric renal failure. During the recovery phase of AKI, patients are usually polyuric and may require dietary supplementation and increased intravenous fluids.

Future therapies in AKI
The future management of AKI may also include antioxidant; anti adhesion molecular therapy and the administration of vascular mediators or mesenchymal stem cells to prevent injury and/or promote recovery [67-70]. Despite promising animal models of intervention in AKI, clinical studies in humans have been largely disappointing, including studies that utilized anaritide (atrial natriuretic peptide) and 1GF-1 [71,72].

Prognosis of AKI
The progress of AKI is highly dependent on the underlying aetiology of the AKI. Progress is worse in children who developed AKI as a component of multisystem organ failure. Children with nephrotoxic AKI and hypoxic/ischemic AKI usually recover normal renal failure function. AKI is likely to be especially deleterious when the kidney has not yet grown to adult size and/or before the full complement of nephrons have developed [73].

Acknowledgements

I will like to thank Ms Slindile Phakati for her assistance in typing the manuscript, the authors and publishers to reproduce some of the published work that has been duly referenced.

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Last Updated: 1^st November 2009 Volume 6 Issue 11 Art # 57

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Bhimma R. Newer Insights into Acute Renal Failure in Children. Pediatric Oncall (Serial Online] 2009 [cited 2009 November 1]1 Art # 57. Available From: