Treatment for
acute kidney Injury (AKI) primarily relies on treating the underlying cause and maintaining the patient until kidney function has recovered. Enteral and
parenteral nutrition are commonly used to treat
nutritional disorders in AKI patients, however their efficacy in treating AKI are still debated. This review was first published in 2010.
OBJECTIVES: We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, Chinese Biomedical Disc, VIP and China National Knowledge Infrastructure (CNKI).Date of last search: 4 July 2012
SELECTION CRITERIA: All randomised controlled trials (RCTs) reported for AKI and nutrition were included.
DATA COLLECTION AND ANALYSIS: Authors independently assessed study quality and extracted data. Results were expressed as risk ratio (RR) with 95% confidence intervals (CI) or mean difference (MD).
MAIN RESULTS: Eight studies (257 participants) were included. An overall pooled analysis was not performed due to the different interventions used and different outcomes measured. Selection bias was not reported (unclear) in six studies and was adequately reported (low) for random sequence generation in two studies. Participant/personnel blinding was adequately reported in one study and unclear in seven. Incomplete outcome reporting bias was low in six studies and high in two. Selective reporting was low in six studies, unclear in one study, and high in one study. No other biases were detected. There was a significant increase in recovery rate for AKI (RR 1.70, 95% CI 1.70 to 2.79) and survival in dialysed patients (RR 3.56, 95% CI 0.97 to 13.08) for intravenous essential L-
amino acids (EAA) compared to hypertonic
glucose alone. Compared to lower calorie-
total parenteral nutrition (TPN), higher calorie-TPN did not improve estimated
nitrogen balance,
protein catabolic rate, or
urea generation rate; but increased serum
triglycerides,
glucose,
insulin need and nutritional fluid administration. There was no difference between groups in estimated
nitrogen balance, but there were differences between
urea nitrogen appearance (MD 0.98, 95% CI 0.25 to 1.71) and net
protein utilisation (MD 21.50%, 95% CI 0.39 to 42.61).
Urea nitrogen appearance was lower in the low
nitrogen intake group than in the high
nitrogen intake group. There was no significant difference in death between EAA and general
amino acids (GAA) (RR 1.52, 95% CI 0.63 to 3.68). High dose
amino acids did not improve cumulative water excretion,
furosemide requirement,
nitrogen balance or death compared to normal dose
amino acids.
Glucose+EAA+histidin had better
nitrogen balance than glucose+GAA;
glucose+
nitrogen+fat significantly increased serum
creatinine compared with glucose+GAA;
glucose+EAA+histidin significantly improved
nitrogen balance, U/P
urea and serum
creatinine, but increased plasma
urea compared to
glucose+
nitrogen+fat.
AUTHORS' CONCLUSIONS: