Low-dose dopamine infusion (1-3 g/kg/min) has been used for more than 25 years as part of the management of oliguria. The renal actions of dopamine include renal arteriolar vasodilatation and a diuretic effect at the proximal tubule ( Duke and B.e.rs.t.e.Q 1992). However, dopamine has a significant inotropic effect even at so-called
'renal-dose' infusion rates, and it has not been possible to separate any specific renal increase in glomerular filtration rate from that due to an increase in cardiac output. In a number of studies dopamine has been shown to increase glomerular filtration rate, urine output, and induce natriuresis. However, there have been no prospective randomized controlled studies to determine whether administration of low-dose dopamine to oliguric patients reduces the requirement for renal support.
There is experimental evidence that furosemide has renoprotective properties by improving tubular oxygen balance. This is thought to be due to a reduction for the requirement of Na+,K+-ATPase and an increase in vasodilatory prostaglandin E 2 concentrations which combine to improve oxygen balance in the medullary tubule.
Furosemide has traditionally been used in large bolus doses (up to 1 g) in the management of oliguria when other measures have failed. This approach may increase urine output but has not been shown to reduce the time course or mortality of renal failure. Indeed, large doses of furosemide can be nephrotoxic with concurrent use of aminoglycosides or cephalosporins.
It is notable that intravenous infusion of furosemide has a greater diuretic effect than intravenous bolus administration ( v§.D...Me.y®!eLal 1992).
Boluses of mannitol are also commonly used in oliguric patients and frequently result in increased urine output. Mannitol is an osmotic diuretic but is also an oxygen free-radical scavenger, increases renal tubular flow, causes a rise in renal prostaglandin E 2 concentrations, and reduces cell swelling following ischemia.
It is important that intravascular volume should be optimized prior to the use of any diuretic agents as further depletion may worsen renal perfusion. Natriuretic peptides
Natriuretic peptides (atrial natriuretic peptide (ANP), ANP analogs, and urodilatin) increase glomerular filtration pressure by renal afferent arteriolar dilatation and efferent arteriolar constriction. They also increase glomerular permeability and enhance sodium and water excretion. ANP infusion reverses the antinatriuretic and antidiuretic effects of positive pressure ventilation in intensive care patients ( Andrivet eLaL 19.9.1).
ANP infusion can result in systemic hypotension but this is less likely with urodilatin, a natriuretic peptide produced in the kidney.
Further studies in general intensive care patients are required to explore the potential of these agents to reduce the incidence of acute tubular necrosis. It is worth noting that aggressive intravascular fluid loading will also increase ANP production and may achieve similar effects. The potential advantage of ANP is that it may be given instead of volume and therefore may minimize other risks of volume loading.
Although there have been no prophylactic studies with calcium antagonists among critical care patients, they have been found to reduce the incidence of post-transplant acute tubular necrosis.
Theophylline and related drugs have a number of potentially beneficial effects in maintaining renal function. These include an inotropic action, a proximal tubular diuretic effect, and antagonism of adenosine. In the kidney, adenosine production is increased under hypoxic conditions and reduces glomerular filtration rate as part of the tubuloglomerular feedback mechanism.
Animal models of ARF have demonstrated a potential protective effect of theophylline and other adenosine antagonists. In the clinical setting administration of theophylline prior to radiocontrast media has been shown to prevent a reduction in glomerular filtration rate.
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