Protein restriction in children with chronic renal failure

The progressive nature of renal functional impairment has been recognized for a long time (Mitch 1976, Rutherford 1977). Once glomerularfiltration rate has decreased to 25 ml!min/1.73m' progression to end stage renal disease is inevitable and independent of the primary renal disease (Leumann 1978, Arbus 1981, Warshaw 1982, Warshaw 1985, Claris-Appiani 1986, Fine 1991, Norwick 1991). Based on the assumption that renal functional deterioration is related to renal workload, Addis suggested in 1948 to decrease protein intake in patients with chronic renal failure (Addis 1917, Addis 1948). His aim was not to reduce uremic symptoms (fatigue, thirst, stunted growth, itching) but rather to prevent an increase in the "workload" of surviving nephrons of diseased kidneys in order to prevent further loss of renal function. This concept was supported by the early finding in rats that renal mass increases with long-term feeding of protein (MacKay 1928). This interesting idea lead to widespread advocation of protein restricted diets for children with chronic renal failure. Notwithstanding theoretical ideas and evidence from animal studies there are no prospective randomized controlled studies in children

Absence of tolerance and toxicity to high-dose continuous intravenous furosemide in haemodynamically unstable infants after cardiac surgery

What is already known about this subjectContinous i.v. infusion of furosemide is superior to intermittent administrations, especially in haemodynamically unstable infants, because it results in a more controlled diuresis (although doses are generally chosen rather low).What this study addsHigh-dose continuous furosemide infusion is an effective treatment for volume overload in haemodynamically unstable infants.Development of tolerance to furosemide was not observed despite high doses and prolonged exposure.Maximum serum furosemide concentrations remained well below the presumed toxic concentration