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Journal Article
Research Support, Non-U.S. Gov't
Analysis of the effects of increasing delivered dialysis treatment to malnourished peritoneal dialysis patients.
Kidney International 2000 April
BACKGROUND: Poor nutrition is associated with a loss of residual renal function and inferior clinical outcome in peritoneal dialysis (PD) patients. The value of increasing the PD dose in these individuals is unclear.
METHODS: An open, prospective, longitudinal, "intention to treat" study was performed on a whole PD population. All patients treated during an 18-month recruitment period underwent nutritional assessment and were defined as malnourished if they had a subjective global assessment (SGA) of B or C and were 5% or more below their desirable body weight. These patients received an intended dialysis dose increase of 25% and were reassessed after six months. Dialysis was not increased in the remaining patients, unless dictated by uremic symptoms.
RESULTS: Forty-eight of 153 patients were malnourished by the previously mentioned criteria. When compared with well-nourished PD patients, they had evidence of declining nutrition over the previous 12 months, as judged by a loss in body weight and mid-arm circumference (MAC), a reduced creatinine appearance, a reduced appetite for protein and calories, and low plasma albumin. They had been on treatment longer and had less residual renal function, resulting in significantly poorer solute clearances. Their peritoneal membrane function, plasma bicarbonate, comorbid, Karnofsky, Hospital Anxiety and Depression (HAD) scores were not different. Following intervention, their peritoneal Kt/Vurea was increased by 22.5%, and their total Kt/Vurea by 18%, because of a continued loss of residual function. There was also an increase in dialysis-derived calories. Weight and MAC stabilized after an initial deterioration, and creatinine appearance increased. There was no increase in protein intake, as judged by dietetic interview or protein nitrogen appearance. Oral calorie intake improved, as did plasma albumin after an initial decline. Both of these improvements were correlated with the achieved increase in Kt/Vurea. Objective measures of improvement (plasma albumin and protein nitrogen appearance) were significant in those patients without comorbid disease.
CONCLUSIONS: These results support the existing evidence that malnutrition is acquired on PD in those patients who lose residual renal function. It is feasible to increase the dialysis dose in these individuals without a detrimental effect, and there is evidence of a modest benefit in patients without comorbidity.
METHODS: An open, prospective, longitudinal, "intention to treat" study was performed on a whole PD population. All patients treated during an 18-month recruitment period underwent nutritional assessment and were defined as malnourished if they had a subjective global assessment (SGA) of B or C and were 5% or more below their desirable body weight. These patients received an intended dialysis dose increase of 25% and were reassessed after six months. Dialysis was not increased in the remaining patients, unless dictated by uremic symptoms.
RESULTS: Forty-eight of 153 patients were malnourished by the previously mentioned criteria. When compared with well-nourished PD patients, they had evidence of declining nutrition over the previous 12 months, as judged by a loss in body weight and mid-arm circumference (MAC), a reduced creatinine appearance, a reduced appetite for protein and calories, and low plasma albumin. They had been on treatment longer and had less residual renal function, resulting in significantly poorer solute clearances. Their peritoneal membrane function, plasma bicarbonate, comorbid, Karnofsky, Hospital Anxiety and Depression (HAD) scores were not different. Following intervention, their peritoneal Kt/Vurea was increased by 22.5%, and their total Kt/Vurea by 18%, because of a continued loss of residual function. There was also an increase in dialysis-derived calories. Weight and MAC stabilized after an initial deterioration, and creatinine appearance increased. There was no increase in protein intake, as judged by dietetic interview or protein nitrogen appearance. Oral calorie intake improved, as did plasma albumin after an initial decline. Both of these improvements were correlated with the achieved increase in Kt/Vurea. Objective measures of improvement (plasma albumin and protein nitrogen appearance) were significant in those patients without comorbid disease.
CONCLUSIONS: These results support the existing evidence that malnutrition is acquired on PD in those patients who lose residual renal function. It is feasible to increase the dialysis dose in these individuals without a detrimental effect, and there is evidence of a modest benefit in patients without comorbidity.
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