Medical Nutrition Therapy in Acute Kidney Injury

Ann Beemer Cotton

Acute kidney injury (AKI) occurs across a spectrum, varying by underlying cause and severity. The cause of AKI has less impact on medical nutrition therapy (MNT) decisions compared to the level of AKI severity and presence of co-morbidities. Supportive care working towards the resolution of AKI is essential. This often involves renal replacement therapy (RRT) and ventilator dependency. The MNT should avoid stressing the patient further and control doses of specific nutrients so that additional kidney injury is not incurred. A collaborative approach is needed among the dietitian, nurse, physician, and other ancillary staff to maximize the effects of all therapies aimed at the resolution of AKI.

Nutrition Assessment in AKI

Organ failure, including AKI, is an inflammatory state. Albumin and prealbumin synthesis is depressed by inflammatory cytokines rendering these visceral proteins as poor markers of nutritional status (Fuhrman, Charney, & Mueller, 2004; Steinman, 2000). Weight history and review of usual dietary intake can, however, provide some insight into nutritional risk. The immediate pre-AKI weight or edema free weight should be identified and used to estimate energy and protein needs. In moderate and severe AKI, volume overload can increase weight by 10 to 20 kg, leading to overfeeding if current weight is utilized (Manning & Shenkin, 1995; Marin & Hardy, 2001). Physical assessment to evaluate muscle wasting and subcutaneous fat would be helpful, but these parameters are also masked by volume overload until kidney function returns and adequate diuresis has occurred(Manning & Shenkin, 1995; Marin & Hardy, 2001).

The development of the MNT plan in AKI requires a review of past medical history to identify co-morbidities that can impact nutritional status. Diabetes mellitus, vascular disease, and hypertension are commonly present. These co-morbidities can lead to chronic kidney disease (CKD). Baseline pre-AKI creatinine, therefore, should be identified and trended over the course of AKI and MNT adjusted accordingly. Gastrointestinal disorders including related symptoms such as nausea, vomiting, and diarrhea will indicate the most feasible feeding route and contribute to diet or enteral formula selection. Recent surgeries and/or the presence of other wounds as well as any pre-existing malnutrition require feeding be initiated by the most appropriate route as early as possible.

MNT and Mild AKI

In its mildest form, AKI exhibits only an elevated BUN and creatinine without electrolyte abnormalities and normal urine output. There is no need for RRT. An oral diet is usually tolerated without electrolyte or phosphorus restrictions. Oral supplements may be necessary if pre-AKI nutritional status is marginal to poor and/or current oral intake is inadequate. Providing 30 to 35 kcal/kg and 0.8 to 1.0 gm protein/kg of desirable weight are the goals of MNT (Druml, 2005). An adequate caloric intake controls the generation of more urea from the breakdown of somatic protein for energy purposes. These patients have often experienced volume depletion, a drug nephrotoxicity or post-renal obstruction as the cause of AKI.

TMNT and Moderate AKI

In moderate AKI, oliguria or urine volume less than 400 mL/day is often noted with retention of BUN, creatinine, electrolytes, and phosphorus. Moderate AKI is more catabolic than mild AKI, often occurring after abdominal vascular surgery or with a combination of simultaneous injuries such as volume depletion, drug toxicity, and hypotension. Pre-existing nondialysis-dependent CKD is also frequently present.

Intermittent hemodialysis (IHD) is provided as needed to correct volume overload and remove accumulated nitrogenous wastes and electrolytes. Energy needs can be met with 25 to 35 kcals/kg of edema-free weight. If respiratory distress develops necessitating ventilator support, energy intake should be limited to 25 kcal/kg. This avoids overfeeding and facilitates ventilator weaning (Talpers, Romberger, Bunce, & Pingleton, 1992). Protein intake should be 0.8 to 1.2 gm/kg without IHD and a minimum of 1.2 gm/kg with IHD (Druml, 2005).

The feeding route may be oral, enteral, and/or parenteral as indicated. Enteral nutrition should utilize a renal formula to avoid excesses of vitamins C and A that are found in wound healing and critical care-specific enteral formulas. Currently available renal formulas do not, however, provide adequate protein, especially with IHD. Modular protein should be given to meet protein needs. If less than 1 L of a renal formula is used, a renal-specific vitamin also should be provided to adequately correct for water soluble vitamin losses.

Careful attention should be given to the cumulative dose of vitamins A and C from any combination of oral, enteral, and/or parenteral feeding routes. Vitamin C intake should not exceed 200 mg/day or twice the recommended dietary allowance (RDA) (Marin & Hardy, 2001). Approximately 40% of vitamin C is converted to oxalate. At low glomerular filtration rates, as occur with oliguria, oxalate accumulates in the renal tubules. Oxalate is an oxidant to renal tubular cells. Following oxalate exposure, renal tubular cells show an increase in plasma membrane permeability and DNA fragmentation (Khan et al., 1999; Ono & Kikawa, 1989; Swartz, Wesley, Somermeyer, & Lau, 1984; Thamilselvan, Hackett, & Khan, 1999). This loss of cellular integrity from oxalate exposure represents another AKI that can prolong the initial AKI insult or potentially lead to irreversible renal failure.

Vitamin A should be limited to 1 mg/day or less in AKI or CKD. At doses greater than this, toxicity symptoms of hypercalcemia with an elevated alkaline phosphatase and hypertriglyceridemia have been observed (Farrington, Miller, Varghese, Baillod, & Moorhead, 1981; Fishbane, Frei, Finger, Dressler, & Silbiger, 1995; Gleghorn, Eisenberg, Hack, Parton, & Merritt, 1986).

MNT and Severe AKI

Severe AKI is a state of hypercatabolism and hemodynamic instability. Severe trauma, sepsis-related multi-system organ dysfunction, or extensive thermal injury commonly cause severe AKI. Patients are anuric and volume overloaded from fluid resuscitation. Multiple intravenous (IV) infusions are necessary to control the hemodynamic instability but add to the volume overload. The nitrogenous wastes and electrolyte abnormalities from hypercatabolism, as well as the volume overload and hemodynamic instability,often require continuous renal replacement therapy (CRRT). Slow, steady state solute and fluid removal from CRRT protects injured kidneys from hypotensive events that may lead to ischemic reperfusion injury and irreversible kidney failure.

The convective and diffusive clearances utilized by CRRT permits the loss of significant quantities of proteins and amino acids. Protein intakes of 2.0 to 2.5 gm/kg of edema-free body weight are required to correct for these losses and those of hypercatabolism (Druml, 2005; Marin & Hardy, 2001; Wooley, Btaiche, & Good, 2005). Providing 20 to 25 kcal/kg may improve outcome by avoiding any additional stress from overfeeding with concurrent hypercatabolism (Jeejeebhoy, 2004; McCowen et al., 2000). Nutrition support should account for the caloric contribution from dextrose and lipid contained in IV infusions use to provide hemodynamic stability and sedation.

In severe AKI, patients are frequently ventilator dependent and require enteral or parenteral nutrition according to the degree of gut dysfunction. Early enteral nutrition initiated within 48 hours of ventilator dependency is preferable, at least in the form of trophic feeds to maintain gut integrity and avoid bacterial translocation. Trophic feeding involves providing low rates of enteral formula at 5 to 10 mL/hour. As discussed above, a renal enteral formula with modular protein as indicated should be given to meet energy and protein requirements.

Parenteral nutrition should be maximally concentrated to avoid further contribution to volume overload. Lipid may be omitted for the initial 7 to 10 days in severe sepsis to avoid the inflammatory effects of the omega-6 fatty acids (Battistella et al., 1997; Hamawy et al., 1985). With CRRT, vitamin C is limited to 200 mg/day, which is the dose contained in the standard IV multivitamin added to parenteral nutrition. The vitamin A content of this multivitamin is also appropriate at 1 mg. An additional 10 mg of pyridoxine and 1 mg of folate should be added to adequately correct for water soluble vitamin losses with IHD or CRRT(Marin & Hardy, 2001).

References
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