Definition

Acute Kidney Injury (AKI) is defined as a rapid decline in kidney function over a period ranging from a few hours to several weeks. AKI is typically identified by:

• Increase in serum creatinine >26.5 µmol/L (0.3 mg/dL) within 48 hours.
• 1.5-fold increase in baseline serum creatinine within 7 days.
• Urine volume

Reversible changes leading to kidney dysfunction or the need for renal replacement therapy (RRT) are included under AKI ¹. The assessment of AKI severity is recommended according to KDIGO (Kidney Disease Improving Global Outcomes) guidelines ¹.

Impact on Nutritional Status

The nutritional requirements for AKI patients are comparable to those of other critically ill individuals. Additional adjustments are necessary to address the specific consequences of kidney dysfunction, as well as the method and intensity of renal replacement therapy ^{2, 3}.

Nutrient Requirements for Patients with AKI or Chronic Kidney Disease in a Catabolic State 
Adjustments are necessary for malnourished patients, physical activity, and age. The adjusted body weight (ADJ) should be used for patients with a BMI ≥28; otherwise, use the body weight prior to hospital admission. BW = Body weight; d = Tag

Goals of Nutritional Therapy

• Maintain or improve nutritional status.
• Prevent malnutrition and nutrient deficiencies.
• Suppress hyper-/hypoglycemia.
• Prevent deterioration of kidney function: maintain electrolyte balance, avoid overhydration, and prevent malnutrition.

Energy and protein requirements should, whenever possible, be met through oral nutrition. If less than 75% of the requirements are met with enrichment, snacks, or oral supplements within five days, enteral nutrition should be added. Complementary parenteral nutrition is indicated if less than 75% of requirements are met through oral and/or enteral nutrition. Nutritional management should be individualized and evaluated by the medical team.

General Dietary Recommendations

Protein restriction should only be considered for metabolically stable patients without renal replacement therapy ⁶.

During the first 48 hours after the onset of a catabolic state, hypocaloric nutrition (≤70% of energy requirements) should be targeted. For specific comorbidities such as uncontrolled shock or life-threatening hypoxemia, nutrition therapy should be delayed by 48 hours ⁷. After three days, energy intake can be increased to 80-100% of energy requirements depending on the risk of complications, acute illness status, and nutritional condition ⁶. Excessive nutrient intake (>100% of energy requirements) increases the risk of complications and should be avoided. For severely malnourished patients or those with fasting periods of more than seven days, food should be introduced slowly and gradually to prevent Refeeding Syndrome.

Enteral Nutrition

The infusion rate of enteral nutrition should start at only 20% of the target/end goal and be increased gradually to improve gastrointestinal tolerance and prevent metabolic complications. Prokinetics can improve the tolerance of nutrition therapy.

For dialysis-dependent patients, select a formula with moderately increased protein content and reduced electrolyte concentration. For non-dialysis patients, a protein- and electrolyte-reduced formulation is indicated ^{2, 5}.

Parenteral Nutrition

Parenteral nutrition should start at a low rate (20% of the target rate) and be increased progressively over several days. This allows close monitoring of nutrient utilization and helps prevent metabolic complications.

The use of commercially available nutrient solutions (all-in-one) is recommended. If needed, water- and fat-soluble vitamins, trace elements, and possibly electrolytes should be added. Alternatively, amino acid solutions, such as specific 'nephro' solutions with additional tyrosine and an adjusted electrolyte profile (P, K) to address the metabolic changes of kidney disease, and/or modern lipid emulsions, may be used. The amount of triglycerides administered must be adjusted to the patient's lipid utilization capacity, as lipolysis is reduced in patients with renal failure. Often, the daily lipid dose must be reduced to 1 g/kg body weight ⁵.

Monitoring

• Monitor lipid clearance (via triglyceride concentration) and glucose concentration in patients on parenteral nutrition ⁵.
  • Manage hyperglycemia by adjusting nutrient intake, reducing glucose intake to a maximum of 2 - 4 g/kg body weight, and administering insulin ⁵. Maintain strict plasma glucose levels between 6.1–8.3 mmol/L (110–149 mg/dL) ⁸.
  • Closely control lipid administration (lipid clearance may be reduced by up to 50%). Administering 1 g of lipids per kg of body weight per day usually does not increase serum triglyceride levels ⁵.
• Substitute protein during catabolism (protein loss of 1.3 to 1.8 g/kg body weight/day) ⁵.
• Avoid toxic serum vitamin A concentrations through strict monitoring ⁹.
• Monitor potassium and phosphate levels: nutrition therapy or continuous renal replacement therapy with low-dose or electrolyte-free solutions may result in hypokalemia and hypophosphatemia (comparable to Refeeding Syndrome).

Products/Medications

• Phosphate Binders: e.g., Calcium Carbonate, Calcium Acetate, Alucol®, Phosphonorm®, Renagel®, Renvela®, Fosrenol®, Velphoro®. Timing and dosage should align with phosphorus intake during meals.
• Potassium Ion Exchangers: e.g., Resonium®, Veltassa®, Sorbisterit®. Regular administration as per medical guidance is crucial and does not need to be taken directly with meals.
• Vitamin D Analogues: ViDe Drops, Rocaltrol®, Zemplar®.
• Calcimimetics: Cinacalcet (Mimpara®), Etelcalcetide (Parsabiv®).
• Fat- and Water-Soluble Vitamins: provided as part of a multivitamin supplement.