Estimation of Nutritional Requirements in AKI

AKI itself has no effect on the patient’s energy requirements. Even in individuals with AKI and multiorgan failure, measured energy requirements are only 20%-30% above the estimated basal metabolic rate values (KDIGO 2012). KDIGO guidelines for AKI (2012) suggest achieving a total energy intake of 20–30 kcal/kg/day in patients with any stage of AKI.

Within ICU settings indirect calorimetry is considered the gold standard to estimate energy requirements. It can be used for those undergoing CRRT (Johnkheer et al, 2020) but has not been studied for patients undergoing SLED or those receiving IHD who are not in a clinically ‘steady state’.

An alternative approach to estimating energy requirements on ICU is to use critical care specific equations that aim to avoid risks of over and underfeeding (Fiaccadori et al 2021). These include weight based equations (20-25kcal/kg/day) (Singer et al, 2019) or the PENN state equation (Frankenfield et al 2009). Whilst these are the most widely available options in the absence of indirect calorimetry, predictive formulas may frequently lead to incorrect energy need estimation and close monitoring to avoid underfeeding and overfeeding is needed (Sabatino et al, 2017). Energy intake should be based on Ideal Body Weight for those with a BMI over 26 kg/m2 (Singer et al, 2019). In acutely unwell patients with AKI on ICU, hypocaloric feeding (not exceeding 70% of energy expenditure) should be administered for the first 3 days of ICU admission (Singer et al, 2019). After day 3, caloric delivery can be increased up to 80-100% of measured REE (Singer et al, 2019, Fiaccadori et al, 2021).

In those receiving CRRT, the energy contribution from solutions that use lactate as a substrate or citrate as an anticoagulant should be considered, as previously discussed.

Protein requirements are influenced by the patient’s clinical condition, severity of AKI, presence or absence of a catabolic state and any RRT they may receive (Table 2). Recommendations for protein requirements vary in the literature. It is essential that attention is given to individual patient condition and treatment goals, when considering the protein requirements as suggested in Table 1.

For stable patients who are not receiving RRT, protein turnover is not increased; a protein intake of 0.8–1.0 g/kg/day has been suggested (Gervaso et al, 2011; KDIGO 2012; Fiaccadori et al 2021). In contrast, patients receiving RRT may require a higher protein intake, with a suggested range from 1.5-1.7g/kg/day, depending on RRT treatment (McClave et al, 2016; Patel et al, 2017; Singer et al 2019; Meyer et al 2020; Fiaccadori et al, 2021). Recently, the EFFORT trial (Hayland et al 2023) showed that patients who were mechanically ventilated, critically unwell, with AKI and high SOFA score at baseline, not on RRT and receiving high protein dose (prescribed 2.0g/kg; on average received 1.6g/kg) were associated with higher harm than those having less protein 1.2 or less (Heyland et al 2023; Stoppe et al 2023). The subgroup analysis suggested an interaction between protein dose and ventilated unwell patients with an AKI (Stage 1-3) and a high sequential organ failure assessment (SOFA) score (>/=9) on both time to discharge alive and 60 day mortality (Hayland et al 2023; Stoppe et al 2023). A secondary analysis indicated that mechanically ventilated patients with AKI are harmed by higher protein dosing, particularly in patients who did not receive RRT (Stoppe et al 2023). As a result a more cautious approach has been suggested in ventilated patients
with AKI not on RRT, see Table 2 (Heyland et al 2023; Stoppe et al 2023).

For patients receiving CRRT who are metabolically stressed 1.5- 1.7g/kg/BW (with caution) is a realistic target (KDIGO 2012; Patel et al, 2017; Singer et al, 2020; Fiaccadori et al, 2021) (Stoppe et. al 2023).

Ideal body weight should be used for patients who are obese with a BMI over 26kg/m2
in critical care (Singer et al, 2019).

AKI may be associated with significant electrolyte changes such as elevated potassium and phosphate levels. Electrolyte intake should be individualised according to the patient’s blood biochemistry, clinical condition and dietary provision. Frequent monitoring of blood biochemistry is essential. Patients requiring dietary electrolyte manipulation should be referred to the Dietitian regardless of their risk of malnutrition. Low potassium and low phosphate diets can be implemented where serum levels are high.

Avoidance of hyperkalaemia is a clinical priority in AKI, however not all patients with AKI and hyperkalaemia require dietary potassium restriction. Health care professionals should consider the cause of hyperkalaemia; the presence of metabolic acidosis and other non-dietary related causes as well as the contribution of potassium from dietary intake and provision via enteral and parenteral solutions where applicable. Recently, there has been an increased use of gastrointestinal cation exchange resins to support in the emergency management of acute life-threatening hyperkalaemia (Meyer et al, 2020; Selby et al. 2020).

Dietary restriction of phosphate may limit an individual’s food choice. Allowing more liberal phosphate consumption to help promote food intake is a better approach. In the short-term, maintaining a good nutritional intake is of greater priority than achieving phosphate control. If and when kidney function recovers and serum potassium and phosphate levels normalise any restrictions can be relaxed.

In the polyuric phase if low electrolyte levels occur, oral or intravenous supplementation may be required.

Persistent hypophosphatemia may present in critically ill patients and has been correlated with increased mortality (Meyer et al, 2020). Hypophosphatemia may be an effect of the RRT employed, particularly in CRRT in which case the treatment is likely to be pharmacological. The nutritional intake of patients with hypophosphatemia, particularly in those who are not undergoing RRT, should be scrutinised to ensure that a deficiency in protein intake is not present.

The medical team should advise on fluid provision taking into account clinical condition, stage of AKI and current treatment. Equations to estimate fluid requirements may be not useful in AKI. Instead, a multidisciplinary team approach is needed to establish the optimal fluid intake for the patient as well as the volume within which nutrition support can be given if required. Daily weights, strict fluid balance and medical assessment are key tools to assess optimal fluid requirements. In oliguric and fluid overloaded patients, fluid intake may be restricted. Limiting sodium intake will help control thirst and aid adherence with fluid restriction. During recovery patients may become polyuric. An increased fluid intake (adequate to cover the large urine volumes and insensible losses) must then be maintained.

Requirements for micronutrients are not well defined. Caution should be taken when interpreting serum micronutrient levels; many patients with AKI present in the acute phase response, which will itself alter blood levels (Gervasio et al, 2011). Plasma levels of vitamins A, D, E (Druml et al, 1998) and vitamin C (Story et al 1999) together with selenium and zinc (Story et al, 1999; Berger et al, 2004; Oh WC et al, 2019) are lower in AKI than in normal subjects. However, this may be related to inflammatory processes, RRT or medication rather than true nutritional deficiencies.

Micronutrient losses on CRRT may also be significant. Documented daily ultrafiltrate losses include 100mg vitamin C (Bellomo & Boyce 1993), 290g folate (Fortin et al, 1999) and 4mg thiamine (Berger et al, 2004), with some authors suggesting supplementation (Gervaso et al, 2011). Mega doses of vitamin C (>250mg/day) are potentially toxic due to the risk of secondary oxalosis in kidney failure, although ensuring adequate ascorbic acid status may confer some benefit (Honore et al, 2020). Vitamin A toxicity has been reported in patients with AKI receiving parenteral nutrition; some authors suggest monitoring Vitamin A levels (Gervasio et al, 2011).

Trace elements circulate mainly bound to protein and therefore are generally unaffected by CRRT but may be affected by the acute phase response. Selenium is affected by CRRT with reported daily losses of 0.97μmol (Berger et al, 2004) some authors suggest a need for its supplementation
(Gervaso et al, 2011).

Since the provision of micronutrients from commonly used parenteral sources and enteral feeds may be insufficient to replace some of these losses to meet requirements, there is some suggestion that selective supplementation should be considered (Gervasio et al, 2011). However, demonstrating deficiency of micronutrients in patients with AKI does not equate to demonstrating a clinical benefit from supplementation; it is not known whether micronutrient supplementation to compensate for RRT losses improves outcomes (Oh et al, 2019; Meyer et al, 2020). Current guidelines lack specific recommendations on specific micronutrient doses and duration.