Nutritional Management in Acute Kidney Injury

Introduction to Nutritional Supplementation

Patients with Acute Kidney Injury (AKI) require supplementation of trace elements (selenium, zinc, copper) and water-soluble vitamins (thiamine, vitamin C, folate), with increased attention to these losses if undergoing kidney replacement therapy (KRT), while avoiding high-dose glutamine and using renal-specific rather than standard multivitamins 1, 2, 3

Monitor and supplement trace elements due to increased requirements during critical illness and large losses during KRT 1, 2
Selenium and Zinc: Serum levels decrease significantly during continuous KRT (CKRT) due to increased utilization in critical illness and dialysis losses, standard supplementation of 50 mg/day zinc and 75 mg/day selenium may not correct deficiencies in patients on chronic KRT 2, 3, 4
Copper: Large effluent losses during CKRT far exceed nutritional intakes, measure blood copper levels and consider intravenous administration of approximately 3 mg/day to prevent deficiency if CKRT is required for more than 2 weeks 1, 2, 3, 4

Water-soluble vitamins should be monitored and supplemented, with special attention to vitamin C, folate, and thiamine 2, 3, 4
Thiamine (B1): Daily losses during dialysis are approximately 4 mg/day, with deficiency documented in 24.7% of hemodialysis patients, patients on CKRT may require 100-300 mg/day 4
Vitamin C: Daily effluent losses are approximately 68 mg, supplement at least 90 mg/day for men and 75 mg/day for women, but do not greatly exceed these amounts due to oxalate accumulation risk 2, 3, 4
Folate: Daily losses during dialysis are approximately 0.3 mg 2, 3, 4
Vitamin B6: Deficiency documented in 35.1% of hemodialysis patients 2, 4, 5

Use renal-specific multivitamins rather than standard multivitamins in AKI patients, particularly those on dialysis 5
Renal vitamins contain lower or absent fat-soluble vitamins (A, E, K) to prevent toxicity, while providing adequate water-soluble vitamins to replace dialysis losses 5
Vitamin A accumulates to toxic levels in kidney disease because retinol-binding protein is normally catabolized in renal tubules; standard multivitamins containing vitamin A pose significant toxicity risk and should be avoided 5
Renal formulas have lower electrolyte content (sodium, potassium, phosphorus) to prevent hyperkalemia and hyperphosphatemia 5
Vitamin K is typically excluded from renal vitamins, which is particularly important for patients on anticoagulants like warfarin 5

Enteral supplementation of amino acids is recommended to achieve protein goals, with patients on KRT requiring at least 1.5 g/kg/day plus an additional 0.2 g/kg/day to compensate for amino acid losses during dialysis 1
Moderately restricted protein regimens may be considered ONLY in metabolically stable AKI patients without catabolic conditions and not undergoing KRT 1, 3, 4

In critically ill patients with AKI, additional high-dose parenteral glutamine shall NOT be administered 6, 7
The REDOX study demonstrated that high doses of intravenous or enteral alanyl-glutamine are harmful in the subgroup of critically ill patients with kidney failure 6, 7
There is insufficient evidence to support routine use of omega-3 PUFA supplements or parenteral nutrition solutions enriched with omega-3 in hospitalized AKI patients 6, 7

Electrolyte abnormalities are common in AKI patients receiving KRT and must be closely monitored 2, 6, 7
Hypophosphatemia (prevalence 60-80% in ICU) is associated with respiratory failure, cardiac arrhythmias, and prolonged hospitalization 2, 7
Hypokalemia and hypomagnesemia are common with intensive/prolonged KRT 2, 7
The initiation of KRT is a major risk factor for development of hypophosphatemia 2