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Year : 2019  |  Volume : 5  |  Issue : 4  |  Page : 93-96

Practical approach to a patient with acute kidney injury

Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Submission29-Apr-2020
Date of Acceptance30-Apr-2020
Date of Web Publication09-Jun-2020

Correspondence Address:
Dr. Anita Saxena
Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_7_20

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How to cite this article:
Saxena A. Practical approach to a patient with acute kidney injury. J Renal Nutr Metab 2019;5:93-6

How to cite this URL:
Saxena A. Practical approach to a patient with acute kidney injury. J Renal Nutr Metab [serial online] 2019 [cited 2023 Oct 4];5:93-6. Available from: http://www.jrnm.in/text.asp?2019/5/4/93/286280

Acute kidney injury (AKI) is a common complication affecting approximately 5% of hospitalized patients and 10%–30% of patients managed in intensive care units (ICUs).[1] High prevalence of malnutrition in AKI is associated with morbidity and mortality (mild malnutrition mortality is 20%, moderate malnutrition mortality is 60%, while hypercatabolic patients mortality is reported to be 80%).[1]

The initial workup for a patient with AKI includes capturing detailed patient history on probable cause (s) of AKI, which can span from prerenal to intrarenal to extrarenal. Physical examination can reveal intravascular volume status, reveal alterations in the skin, if present, and indicate the presence of systemic illness. The initial workup includes biochemical evaluation and ultrasonography of the kidneys. Urine output is a good indicator of severity of renal damage. Laboratory investigations normally include serum creatinine, complete blood count, urinalysis, and fractional excretion of sodium.

In AKI patients admitted in the ICU, attaining a positive nitrogen balance with gain in lean mass is like aiming for nearly unrealistic goal; however, a more near-satisfactory, realistic approach helps to minimize muscle wasting and to preserve lean mass as much as possible with nutritional support.[2] Nutritional strategies aim at avoiding the development of deficiency states, “hospital-acquired malnutrition,” and progression from oliguric to anuric state. Depending upon the severity of associated illnesses, nutrient requirements differ among patients during the course of disease. Issues that require immediate attention are volume overload, metabolic acidosis, hyperkalemia, hypocalcemia, hypoalbuminemia, hyperphosphatemia, anorexia, poor nutritional intake, oral ulcers, hyperglycemia, gastrointestinal (GI) complications, infection, and sepsis.[2],[3],[4]

Management of AKI involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. The key steps in the nutritional management of AKI are given in [Figure 1]. Renal replacement therapy (RRT – dialysis) is indicated for refractory hyperkalemia; volume overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Team-based approaches for prevention, early diagnosis, and aggressive management are critical for improving outcomes.[5],[6]
Figure 1: Nutritional management in acute kidney injury

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  Fluid Balance Top

Key aspect of the treatment of AKI is the fluid balance to restore cardiac output, blood pressure, and glomerular filtration rate (GFR), increase urine output, dilute tubular toxins and attenuate tubular obstructions from casts, and counteract negative effects of both catabolism and hypermetabolism associated with critical illness on lean body mass to support immune function to minimize inflammation. Oliguria is related to reduced GFR and increased salt and water retention. Restriction of sodium and water is the first step as fluid overload can cause intra-abdominal hypertension, cerebral edema, pulmonary edema, gut edema, and hepatic congestion and can worsen AKI.[5] Initiation of RRT when life-threatening changes in the fluid, electrolyte, and acid–base balance exist is warranted. Advantage of early initiation of CRRT is that it permits nutritional support without worsening fluid balance. CRRT allows time for vascular refilling and effective control of fluid balance while maintaining hemodynamic stability (because of constant slow rate of ultrafiltration). Intensive (daily) RRT can readily correct metabolic abnormalities by appropriate regulation of the composition of hemodialysis (HD)/hemofiltration fluids and of the intensity of RRT. Optimization of the hemodynamic status and correction of any volume deficit have salutary effects on kidney function. One can plan the measurement of extracellular and intracellular volume expansion using bioimpedance technique.

Correct interstitial edema by correcting plasma colloid osmotic pressure to prevent hypotension during HD. Resuscitation fluids can be divided into colloids (e.g. 6% hydroxyethyl starch [130/0.4]) and crystalloids (e.g. saline). Frequent administration 0.9% saline (154 mmol/l of chloride) for drugs causes hyperchloremia, which is associated with reduced renal blood flow and impaired sodium excretion causing edema.[6],[7],[8],[9],[10] Adverse effects of fluid overload are pronounced in systemic sepsis, major surgery, or trauma, which predispose to acquired AKI. Positive fluid balance in the order of 5%–10% of body weight (BW) is associated with worsening organ dysfunction in the critically ill patients.[11],[12],[13] Once fluid overload is established, it is often difficult to resolve. Positive fluid balance is associated with worsening organ dysfunction; it may impede renal recovery (AKI) and can lead to worst postoperative outcome.[11],[12],[13],[14],[15]

  Twenty-Four-Hour Fluid Prescription Top

It is mandatory to monitor changes in BW and fluid intake daily. Use actual weight before illness as target dry weight. Restrict fluid intake according to 24-h urine output presence of edema and intravenous (IV) infusions. Oral fluid intake should include 24-h intake of water, milk, tea, curd, or any other liquid. In anuric and oliguric patients, fluid intake equals 24-h urine output and additional 500 mL or less depending.upon presence of edema. Weight status is frequently altered by changes in volume status and dialysis. Use current weight as the dosing weight as caloric intake based on ideal BW (IBW) can lead intake of excess calories and metabolic imbalance, leading to refeeding syndrome. Use edema-free BW.

  Correct Electrolyte and Mineral Imbalance Top

Aggressive use of loop diuretics for the removal of fluid can cause electrolyte imbalance. Replace electrolytes as and when required. Treat hypokalemia with either oral potassium chloride (KCl, 1 tea spoon = 6 mEq K) or IV KCL (60–80 mEql/day). Fruits and fruit juices can be prescribed if the patient is taking orally. Hypokalemia and hypomagnesemia play a role in the pathogenesis of gastroparesis. Hyperkalemia can be due to nondietary causes. In severe cases, HD (K ≥6.5 mmol/l) may be appropriate. To correct hyperkalemia, check inadequacy of dialysis and use potassium-free dialysate. If dialysis is not indicated, use antihyperkalemic measures such as IV calcium gluconate + dextrose + insulin or bicarbonate therapy (e.g., 1 ampule [50 mEq] infused over 5 min), which is effective in shifting potassium into the cell or potassium-binding resins along with laxatives.[2] Restrict fruits and fruit juices. Remove offending medication and control consumption of nonrenal-specific nutritional supplements. Treat chronic constipation by increasing fiber in diet to promote gut motility and by changing phosphate-binding agents to reduce constipation effect. High-efficient modalities of RRT often remove phosphates and magnesium and induce hypophosphatemia and hypomagnesemia. To correct hypophosphatemia, supplement phosphorus and/or prescribe foods with high phosphorus content and phosphorus-based additives such as milk products, frozen meals, dry fruits chocolate, spreadable cheeses, cereals, and legumes.

Correct hypocalcemia with oral calcium carbonate or with 10% calcium gluconate 0.5–1.0 mL/kg infused over 5–10 min with cardiac monitoring.

Hyponatremia can be nutritional because of long-standing inadequate intake which can be corrected with the supplementation of sodium by salt or salt capsules. If hyponatremia is dilutional, diuretic therapy is advisable.

  Approach to Feeding Patient With Acute Kidney Injury Top

AKI is a hypercatabolic state.[16] Patient with AKI can present with sudden onset (days) of anorexia, lethargy, depression, vomiting, and diarrhea. Since nausea and vomiting can affect dietary intake, therefore, antiemetics can be prescribed ½ h before meals. Reverse underlying cause or causes of anorexia and on-going risk factors (drugs, hemodynamic instability, and concurrent diseases) and provide nutritional support until renal function is returned.

Recommend nutrition support within 24–48 h of ICU admission (or once hemodynamically stable).[17] For patients with underlying diseases associated with excess protein catabolism, nutritional support should be initiated early regardless of whether the patient is likely to eat before 5 days. Decision for nutritional support in AKI patients with protein–energy wasting (PEW) or at risk of PEW is made based on whether the gut is functioning or not. If oral feeding is not possible, but the gut is functioning, then enteral feeding (tube feeding) should be initiated within 24 h. If nutrient delivery goals are not achieved, then parenteral support should be initiated. Enteral feeding may be more difficult in patients with AKI because of impaired GI motility and decreased absorption of nutrients secondary to bowel edema. Avoid hyperosmolar enteral nutrition as it predisposes patients to diarrhea or symptoms similar to dumping syndrome if it is infused rapidly. If spontaneous intake of energy is >20 kcal/kg/ Ideal body weight (IBW) and of protein is 0.8 g/kg/IBW, then intradialytic parenteral nutrition (IDPN) should be initiated (tube feeding + IDPN). If gut is not functioning, then parenteral feeding from peripheral or central route should be started. If spontaneous energy intake is <20 kcal/kg IBW and protein <0.8 g/kg/Bw despite oral and IDPN, then total parenteral nutrition should be initiated. Dumping syndrome is characterized by symptoms of nausea, shaking, diaphoresis, and diarrhea shortly after eating foods containing high amounts of refined sugars. Use renal formulae with high energy (2 kcal/mL) and high protein content (70 g/L) and low electrolyte levels. Metabolic acidosis (nonnutritional) causes protein catabolism. To prevent protein catabolism, correct metabolic acidosis.

Patients can be classified according to substrate requirement and extent of catabolism.[2],[17] Patients can be mildly catabolic if nitrogen losses are <6 g/day of the ingested food or moderately catabolic if nitrogen losses are 6–12 g/day or severe catabolism if nitrogen losses are >12.0 g/day. Patients in AKI Stage I are mildly catabolic and rarely require dialysis; patients in AKI Stage 2 can overlap with patients in AKI Stage 3. However, patients in AKI Stage 2 are moderately catabolic as they require dialysis, but patients in AKI Stage 3 are severely catabolic as they require frequent dialysis. In all the studies in AKI patients on RRT, protein catabolic rate has been shown to be 1.5.[2],[17]

Mildly catabolic patients normally do not require nutritional support, and they do very well with 0.8 g/kg/day of protein while patients who are moderately to severely catabolic require 1.0–1.5 g/kg/day of protein. These patients can require both enteral and parenteral nutritional support. Patients who are severely catabolic protein intake can be increased up to 1.7 g/kg/g. Patients should be started with 25 kcal/kg/day, but energy intake should not exceed 30 kcal/kg/day in AKI patients. Source of energy substrate should be glucose (3.0–5.0 day/kg) in mildly catabolic patients and glucose along with fat in moderately to severely catabolic patients. Patients can require essential amino acids (EAA) and non-EAA which can be given during dialysis (IDPN). Plan administering lipids during HD or hemofiltration as lipids are not lost through the filters. Administer 0.8–1.2 g/kg/day of lipids from 10% to 30% lipid emulsions once or twice a week, or as a part of the commercially available three-in-one total nutrient admixtures.

People who have not eaten for more than 5 days should have nutrition support introduced at no more than 20 kcal/kg/24 h initially.[2] For patients at risk of developing refeeding syndrome, nutritional support should be started at ≤10 kcal/kg/day, which can be increased slowly to meet full requirements by day 4–7. Avoid overfeeding patients with raised or increasing inotropic requirements. It is advisable to use the NICE 2006 criteria for determining which patient is at high risk of developing refeeding problems. Dosing weight can be calculated as IBW + 0.25 (actual body weight – IBW).[17]

In polyuric phase, patients require protein 0.97–1.3 g/kg BW/day protein, and it is important to maintain intravascular volume as diuresis can exceed 150–200 mL/h and kidneys regaining function are unable to produce a concentrated urine, risking volume depletion, and recurrent AKI.[2],[16] Renal-specific oral nutrition supplements can be prescribed if protein and energy intake is not adequate. Prescribe protein of high biological value such as milk and milk products, poultry, and soya bean products. Patients should be supplemented with folic acid (losses up to 600 nmol/day), thiamin (3 mg/day as losses >1.5 times daily provision), pyridoxine, and Vitamin C 60 mg (CRRT 150–200 mg).

Patients with AKI are at risk of trace element depletion zinc, selenium (50–100 mcg), chromium, and copper. The standard multiple trace element preparation delivers 1000 mcg/day, which takes care of additional losses attributed to CRRT. Low antioxidants, Vitamin E, selenium, and glutathione reductase exacerbate ischemic renal injury and worsen the course and increase mortality. Antioxidants administered along with omega-3 fatty acids in a feeding product may have an anti-inflammatory effect. Although controversies surround the role of glutamine in boosting recovery in critically ill, yet if desired, glutamine powder can be mixed with water 2–3 doses to provide 0.3–0.5 g glutamine/kg/day and given to the patient.

Special attention should be paid both to the impact of RRT on macronutrient and micronutrient losses. Risk of complications includes hypoglycemia and hyperglycemia, hypertriglyceridemia, fluid balance alterations, electrolyte, and acid–base derangement.

  Contraindications to Enteral Nutrition Top

Critically ill patients who are hemodynamically unstable, and who have not had their intravascular volume fully resuscitated, may be predisposed to bowel ischemia. Bowel obstruction, severe and protracted ileus, upper GI bleed, intractable vomiting or diarrhea, severe acute pancreatitis or shock, GI ischemia or high-output fistula, and a new GI anastomosis contraindicate enteral nutrition. Enteral nutrition is best avoided when prognosis does not warrant aggressive nutritional support.

For malnourished patients who have contraindications to enteral nutrition, initiate parenteral nutrition. Alterations in lipid metabolism are characterized by hypertriglyceridemia due to inhibition of lipolysis. Exogenous fat clearance after enteral or parenteral delivery of lipids can, therefore, be reduced. Lipids account for <30%–35% of total nonprotein energy and should be infused over 18–24 h. Serum triglycerides should be monitored, and if triglycerides exceed 400 mg/dL, stop lipid administration.

  Common Complications of Parenteral Nutrition Top

These include increased bloodstream infectious complications, metabolic abnormalities such as hyperglycemia hypertriglyceridemia, refeeding syndrome, and problems related to venous access. Tolerance to volume load is limited. These preparations are more expensive than enteral feedings.

  Contraindications to Parenteral Nutrition Top

i) Volume overload, hyperosmolarity, and decreased fat clearance can cause severe hyperglycemia and hypertriglyceridemia and severe electrolyte abnormalities. ii) Inadequate attempts to feed enterally. iii) Sepsis or systemic inflammatory response syndrome.

  Conclusion Top

Nutritional support should be initiated within 24–48 h to correct deficits if the patient is hemodynamically stable. Patients can require enteral and parenteral support depending upon the extent of catabolism. High-efficient modalities of RRT often remove phosphates and magnesium and induce hypophosphatemia and hypomagnesemia. Continuous hemofiltration induces considerable heat loss. Caloric loss can be up to 1500 kcal/day and can result in a fall in body temperature. Caloric loss during CRRTs should be considered when calculating the energy balance of a patient. Correct deficiencies. Control blood sugar as normoglycemia is renoprotective and reduces incidence of AKI (some random controlled trials suggest intensive insulin therapy, but this is debatable).[18] Minimize inflammation with inflammatory mediators such as omega-3 fatty acids (EPA and DHA) or antioxidants.

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Conflicts of interest

There are no conflicts of interest.

Additional reading

NKF KDOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure

Guideline 19. Indications for Nutritional Support

Guideline 20. Protein Intake during Acute Illness

Guideline 21. Energy Intake during Acute Illness 2000. AJKD Suppl June Vol 2.

  References Top

Susantitaphong P, Cruz DN, Cerda J, Abulfaraj M, Alqahtani F, Koulouridis I, et al. World incidence of AKI: A meta-analysis. Clin J Am Soc Nephrol 2013;8:1482-93.  Back to cited text no. 1
Druml W. Nutritional management of acute renal failure. J Ren Nutr 2005;15:63–70.  Back to cited text no. 2
Fiaccadori E, Regolisti G, Cabassi A. Specific nutritional problems in acute kidney injury, treated with non-dialysis and dialytic modalities. NDT Plus 2010;3:1-7.  Back to cited text no. 3
Kellum JA, Cerda J, Kaplan LJ, Nadim MK, Palevsky PM. Fluids for prevention and management of acute kidney injury. Int J Artif Organs 2008;31:96-110.  Back to cited text no. 4
Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004;350:2247-56.  Back to cited text no. 5
Estrada CA, Murugan R. Hydroxyethyl starch in severe sepsis: End of starch era? Crit Care 2013;17:310.  Back to cited text no. 6
Gervasio JM, Cotton AB. Nutrition support therapy in acute kidney injury: Distinguishing dogma from good practice. Curr Gastroenterol Rep 2009;11:325-31.  Back to cited text no. 7
Leblanc M, Kellum JK, Gibney RT, Lieberthal W, Tumlin J, Mehta R. Risk Factors for Acute Renal Failure: Inherent and Modifiable Risks Curr Opin Crit Care. 2005;11:533-6.  Back to cited text no. 8
Payen D, de Pont AC, Sakr Y, Spies C, Reinhart K, Vincent JL, et al. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care 2008;12:R74.  Back to cited text no. 9
Bouchard J, Soroko SB, Chertow GM, Himmelfarb J, Ikizler TA, Paganini EP, et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int 2009;76:422-7.  Back to cited text no. 10
Brandstrup B, Tønnesen H, Beier-Holgersen R, Hjortsø E. Danish study group on perioperative fluid therapy effects of intravenous fluid restriction on postoperative complications effects of intravenous fluid restriction on postoperative complications: Comparison of two perioperative fluid regimens: A randomized assessor-blinded multicenter trial. Ann Surg 2003;238:641-8.  Back to cited text no. 11
Payen D, de Pont AC, Sakr Y, Spies C, Reinhart K, Vincent JL, et al. Apositive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care 2008;12:R74.  Back to cited text no. 12
Bouchard J, Soroko SB, Chertow GM, Himmelfarb J, Ikizler TA, Paganini EP, et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int 2009;76:422-7.  Back to cited text no. 13
Prowle JR, Echeverri JE, Ligabo EV, Ronco C, Bellomo R. Fluid balance and acute kidney injury. Nat Rev Nephrol 2010;6:107-15.  Back to cited text no. 14
Guidet B, Martinet O, Boulain T, Philippart F, Poussel JF, Maizel J, et al. Assessment of hemodynamic efficacy and safety of 6% hydroxyethylstarch 130/0.4 vs. 0.9% NaCl fluid replacement in patients with severe sepsis: The CRYSTMAS study. Crit Care 2012;16:R94.  Back to cited text no. 15
Flügel-Link RM, Salusky IB, Jones MR, Kopple JD. Protein and amino acid metabolism in posterior hemicorpus of acutely uremic rats. Am J Physiol 1983;244:E615-23.  Back to cited text no. 16
Irish Society of Clinical Nutrition and Metabolism Critical Care Programme Reference Document for Nutrition Support Guideline; 2012.  Back to cited text no. 17
Brunkhorst FM, Engel C, Bloos F, Meier-Hellmann A, Ragaller M. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008;358:125-39.  Back to cited text no. 18


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