ACUTE RENAL FAILURE is an uncommon emergency which faces pediatricians. It is usually easy to recognize. The management in the early phase is critical to the survival potential of the patient. The purpose of this review is to cite the causes, characteristics, and principally the management of acute renal failure.
Renal failure is defined as a state in which there is not sufficient kidney function to prevent the development of severe uremia or to maintain plasma electrolyte values in a range compatible with ordinary activities. Clinically the condition is associated with mental confusion, stupor, and frequently convulsions. Persistent hiccoughs, irregular respirations, and muscle cramps also may occur. Usually though not always, there is obvious oliguria. Since urine flow is ordinarily but 0.2-2,0% of glomerular filtration rate, and since glomerular filtration rate reduction to 5-10% may be associated with uremia, it is possible to have renal failure without oliguria. It is also possible to have physiological oliguria (< 300 ml per square meter) in response to rigid water restriction that is not related to renal failure. Hence, the term must be defined in terms of its effect on plasma composition rather than in terms of urine flow.
The presence of certain clinical conditions known to result in acute renal failure should alert the physician. These include: nephrotoxie agents; hemoglobinuria or myoglobinuria; shock with anoxic damage; acute, diffuse renal disease; acute dehydration in patients with chronic advanced renal disease; and acute obstructive uropathy. Nephrotoxic agents, hemoglobinuria, and shock all result in acute tubular necrosis, and recovery depends upon the capacity of the nephron to regenerate on an intact basement membrane.
Dissociation of glomerular filtration and renal blood flow in HgCl2-induced acute renal failure