8 Acute Renal Failure Nursing Care Plans

Use this nursing care plan and management guide to help care for patients with acute renal failure. Learn about the nursing assessment, nursing interventions, goals and nursing diagnosis for acute renal failure in this guide.

What is Acute Renal Failure?

Acute renal failure (ARF), also known as acute kidney failure or acute kidney injury (AKI), is the abrupt loss of kidney function. The glomerular filtration rate (GFR) falls over a period of hours to a few days and is accompanied by a concomitant rise in serum creatinine and urea nitrogen. However, immediately after a kidney insult, BUN or serum creatinine levels may be normal. In the early phase, the only sign of a kidney injury may be decreased urine production (Workeneh & Batuman, 2022). If left untreated, acute renal failure may complicate chronic renal failure.

Traditionally, AKI may be classified into three general categories. Prerenal which occurs as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons. Intrinsic that occurs in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage. Lastly, Postrenal occurs from obstruction to the passage of urine. 

The annual incidence of acute renal failure is 100 cases for every million people in the United States. It is diagnosed in 1% of hospital admissions. AKI develops within 30 days postoperatively in approximately 1% of general surgery cases and arises in more than 50% of intensive care unit clients (Workeneh & Batuman, 2022).

Most clients with AKI have no clinical symptoms related to AKI and are diagnosed on the basis of a routine laboratory blood test. Depending on the degree of kidney function impairment and duration, however, they might have hypertension, edema, decreased urine output, shortness of breath, anorexia, nausea, sleep disturbances, and altered mental status (Workeneh & Batuman, 2022).

The prognosis for clients with AKI is directly related to the cause of the injury and, to a great extent, to the presence or absence of preexisting kidney disease, as well as to the duration of kidney dysfunction prior to therapeutic intervention (Workeneh & Batuman, 2022).

Nursing Care Plans and Management

The nursing care plan and management for clients with acute renal failure are to promote renal function, correct or eliminate any reversible causes of kidney failure, and provide supportive care. Specific interventions include monitoring and managing fluid and electrolyte imbalances, optimizing nutrition, and ensuring medication safety. Nurses also work to support the patient’s emotional well-being and provide education on self-care and prevention of future kidney damage.

Nursing Problem Priorities

The following are the nursing priorities for patients with acute renal failure (ARF):

1. Assessment and monitoring of renal function
2. Fluid and electrolyte balance management
3. Identification and treatment of the underlying cause
4. Prevention and management of complications (e.g., electrolyte imbalances, metabolic acidosis)
5. Monitoring and management of fluid overload or dehydration
6. Hemodynamic stability and blood pressure control
7. Education on self-care and compliance with treatment plans

Nursing Assessment

Assess for the following subjective and objective data:

• Decreased urine output or oliguria (reduced urine volume)
• Swelling or edema in the hands, feet, or face
• Fatigue and weakness
• Shortness of breath or difficulty breathing
• Nausea, vomiting, or loss of appetite
• Confusion or altered mental status
• Abdominal pain or discomfort
• High blood pressure
• Irregular heart rhythm or palpitations
• Signs of fluid overload

Assess for factors related to the cause of acute renal failure (ARF):

• Compromised regulatory mechanism (renal failure)
• Fluid overload (kidney dysfunction/failure, overzealous fluid replacement)
• Fluid shifts, fluid deficit (excessive losses)
• Electrolyte imbalance (potassium, calcium); severe acidosis
• Uremic effects on cardiac muscle/oxygenation
• Protein catabolism; dietary restrictions to reduce nitrogenous waste products
• Increased metabolic needs
• Anorexia, nausea/vomiting; ulcerations of oral mucosa
• Depression of immunologic defenses (secondary to uremia)
• Invasive procedures/devices (e.g., urinary catheterization)
• Changes in dietary intake/malnutrition
• Excessive loss of fluid (diuretic phase of ARF, with rising urinary volume and delayed return of tubular reabsorption capabilities)

Nursing Diagnosis

Following a thorough assessment, a nursing diagnosis is formulated to specifically address the challenges associated with acute renal failure based on the nurse’s clinical judgement and understanding of the patient’s unique health condition. While nursing diagnoses serve as a framework for organizing care, their usefulness may vary in different clinical situations. In real-life clinical settings, it is important to note that the use of specific nursing diagnostic labels may not be as prominent or commonly utilized as other components of the care plan. It is ultimately the nurse’s clinical expertise and judgment that shape the care plan to meet the unique needs of each patient, prioritizing their health concerns and priorities.

Nursing Goals

Goals and expected outcomes may include:

• The client will display appropriate urinary output with specific gravity/laboratory studies near normal; stable weight, vital signs within the client’s normal range; and absence of edema.
• The client will maintain cardiac output as evidenced by BP and HR/rhythm within the client’s normal limits; peripheral pulses are strong and equal with adequate capillary refill time.
• The client will maintain/regain the weight as indicated by the individual situation, free of edema.
• The client will experience no signs/symptoms of infection.
• The client will display I&O near balance; good skin turgor, moist mucous membranes, palpable peripheral pulses, stable weight, vital signs, and electrolytes within normal range.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with acute renal failure (ARF) may include:

1. Managing Fluid Volume and Hypervolemia

In the case of prerenal acute kidney injury (AKI), fluid resuscitation is the gold standard, but if this resuscitation continues beyond the correction of hypovolemia, then it is associated with increased morbidity, mortality, and length of hospital stay as well as increased risk of AKI. Several observational studies have demonstrated a correlation between fluid overload and mortality in critically ill clients with acute respiratory distress syndrome, acute lung injury, sepsis, and AKI (Patil & Salunke, 2020).

Assess the level of consciousness. Investigate changes in mentation and the presence of restlessness.
This may reflect fluid shifts, accumulation of toxins, acidosis, electrolyte imbalances, or developing hypoxia. Older adults with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI. Insensible fluid losses can result in severe hypovolemia in clients with restricted fluid access and should be suspected in older adult clients and in comatose or sedated clients (Workeneh & Batuman, 2022).

Assess skin, face, and dependent areas for edema. Evaluate the degree of edema (on a scale of +1–+4).
Edema occurs primarily in dependent tissues of the body, (hands, feet, lumbosacral area). The client can gain up to 10 lb (4.5 kg) of fluid before pitting edema is detected. Periorbital edema may be a presenting sign of this fluid shift because these fragile tissues are easily distended by even minimal fluid accumulation.

Monitor heart rate (HR), BP, and JVD/CVP.
Tachycardia and hypertension can occur because of: (1) failure of the kidneys to excrete urine, (2) excess fluid resuscitation during efforts to treat hypovolemia and/or hypotension or convert oliguric phase of renal failure, (3) changes in the renin-angiotensin system. Invasive monitoring may be needed for assessing intravascular volume, especially in clients with poor cardiac function. Although clients with heart failure may have low blood pressure, volume expansion is present, and effective renal perfusion is poor, which can result in AKI (Workeneh & Batuman, 2022).

Auscultate lung and heart sounds.
Fluid overload may lead to pulmonary edema and heart failure evidenced by the development of adventitious breath sounds, and extra heart sounds. The most important part of physical examination is the assessment of cardiovascular status and volume status. The cardiovascular examination may reveal murmurs, pericardial friction rub, and increased jugulovenous distention, rales, and S3 gallops (Workeneh & Batuman, 2022).

Accurately record intake and output (I&O) noting to include “hidden” fluids such as IV antibiotic additives, liquid medications, frozen treats, and ice chips. Religiously measure gastrointestinal losses and estimate insensible losses (sweating), including wound drainage, nasogastric outputs, and diarrhea.
The widely accepted Kidney Disease: Improving Global Outcome (KDIGO) definition of AKI is based on the change of serum creatinine and urine output of < 0.5 mL/kg/hour for six hours. Accurate monitoring of I&O is necessary for determining renal function and fluid replacement needs and reducing the risk of fluid overload. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction (Workeneh & Batuman, 2022).

Monitor urine-specific gravity.
This measures the kidney’s ability to concentrate urine. In intrarenal failure, specific gravity is usually equal to or less than 1.010, indicating loss of ability to concentrate the urine. Aggressive fluid resuscitation is appropriate in prerenal AKI. However, overly aggressive volume resuscitation in a client with ATN who is unable to excrete the extra fluid can result in volume overload and respiratory embarrassment. To help with the differentiation of prerenal azotemia, analysis of urine may provide important clues (Sinert & Sugalski, 2019).

Weigh daily at the same time of day, on the same scale, with the same equipment and clothing.
Daily body weight is the best monitor of fluid status. A weight gain of more than 0.5 kg/day suggests fluid retention. Over-aggressive volume resuscitation can cause tissue congestion and hypoxia and is associated with worse survival in general ICU populations and in clients with AKI (Fülöp et al., 2010).

Monitor diagnostic studies (Hgb, hct, sodium, potassium, bun, crea and urine sodium).  
See Laboratory and Diagnostic Procedures

Monitor Serial chest x-rays.
See Laboratory and Diagnostic Procedures

Monitor echocardiography results as indicated.
See Laboratory and Diagnostic Procedures

Scatter desired beverages throughout the 24-hour period and give various offerings (hot, cold, frozen).
This helps avoid periods without fluids, minimizes boredom of limited choices, and reduces the sense of deprivation and thirst. Drinking black coffee, instead of coffee with high potassium and high phosphorus milk, or high-calorie sugar drinks is best. A cup of unsweetened green tea is full of compounds called “polyphenols”, which function as antioxidants. Carbonated, or sparkling, water hydrates, as well as water, does (Shusterman, 2021).

Maintain volume homeostasis and correct biochemical abnormalities.
Kidneys may be able to return to normal functioning, preventing or limiting residual effects. Measures include correction of fluid overload, correction of severe acidosis, and correction of hematologic abnormalities such as transfusions and administration of medications (Workeneh & Batuman, 2022).

Use appropriate safety measures (raising side rails and restraints.
Clients with CNS involvement may be dizzy and/or confused. The kidney and the brain are frequently injured during critical illness. Acute kidney injury, which affects up to half of the critically ill clients, is strongly associated with short and long-term morbidity and mortality. Similarly, acute brain dysfunction, which manifests as delirium or coma in the ICU, is common during critical illness and associated with adverse short and long-term outcomes (Siew et al., 2017).

Administer and/or restrict fluids as indicated.
Fluid management is usually calculated to replace output from all sources plus estimated insensible losses (metabolism, diaphoresis). Prerenal failure (azotemia) is treated with volume expansion and/or vasopressors. The oliguric client with adequate circulating volume or fluid overload who is unresponsive to fluid restriction and diuretics requires dialysis. During the oliguric phase, “push/pull” therapy (push IV fluids and diuresis with diuretics) may be tried to stimulate kidney function. However, a rapid fluid infusion can result in life-threatening fluid overload in clients with AKI (Sinert & Sugalski, 2019).

Assist the client in performing the passive leg-raising maneuver (PLR) or virtual fluid challenge as indicated.
PLR is a test that predicts whether cardiac output will increase with volume expansion. By transferring a volume of around 300 mL of venous blood from the lower body toward the right heart, PLR mimics a fluid challenge (Effat et al., 2021).

Promote sodium and fluid restriction as indicated.
Restriction of salt and fluid becomes crucial in the management of oliguric kidney failure, wherein the kidneys do not adequately excrete either toxins or fluids (Workeneh & Batuman, 2022). Oliguric clients should also have a fluid restriction of 400 ml plus the previous day’s urine output unless there are signs of volume depletion (Bindroo et al., 2022).

Insert indwelling catheter, as indicated.
Catheterization excludes lower tract obstruction and provides means of accurate monitoring of urine output during the acute phase; however, indwelling catheterization may be contraindicated because of the increased risk of infection. Placement of a urinary catheter in AKI not only allows diagnosis and treatment of urethral and bladder outlet urinary obstruction but also allows for accurate measurement of urine output (Sinert & Sugalski, 2019).

Administer furosemide, vasodilators, and calcium channel blockers as indicated. 
See Pharmacologic Management

Prepare for dialysis as indicated: hemodialysis, peritoneal dialysis, or continuous renal replacement therapy (CRRT).
Dialysis is done to correct volume overload, electrolyte, and acid-base imbalances, and to remove toxins. The type of dialysis chosen for ARF depends on the degree of hemodynamic compromise and the client’s ability to withstand the procedure. However, dialysis, especially hemodialysis, may delay the recovery of clients with AKI. Most authorities prefer using biocompatible membrane dialyzers for hemodialysis. Peritoneal dialysis is not frequently used in AKI. Nevertheless, it can technically be used in acute cases and probably is tolerated better hemodynamically than conventional hemodialysis (Workeneh & Batuman, 2022). 

Assist in renal replacement therapy.
The principal methods of renal replacement therapy (RRT) are intermittent hemodialysis, continuous venovenous hemodiafiltration, and peritoneal dialysis. Continuous RRT techniques are more expensive, associated with increased bleeding risk, and not universally available. However, in addition to avoiding hypotension, they are believed to achieve better control of uremia and clearance of solute from the extravascular compartment (Sinert & Sugalski, 2019).

2. Minimizing Risk of Cardiac Complications

In AKI, the kidneys are unable to remove excess fluid from the body, leading to fluid overload. This can increase the volume of blood that the heart has to pump leading to an increase in the workload of the heart and decreased cardiac output. AKI can also lead to electrolyte imbalances that can affect the heart’s electrical activity and reduce its ability to contract effectively.

Monitor BP and HR.
Fluid volume excess, combined with hypertension (common in renal failure) and the effects of uremia, increases cardiac workload and can lead to cardiac failure. In ARF, cardiac failure is usually reversible.  Vital signs can be considered indicators of kidney damage and therefore need to receive more attention from healthcare professionals. It was observed that temperature and breathing cycle increase as kidney damage increases, while blood pressure and pulse also undergo significant changes due to kidney damage (Sacomboio et al., 2021).

Observe ECG or telemetry for changes in rhythm.
Changes in electromechanical function may become evident in response to progressing renal failure and accumulation of toxins and electrolyte imbalance. Peaked T wave, wide QRS, and prolonged PR interval are usually associated with hyperkalemia. The flat T wave, peaked P wave, and appearance of the U waves usually indicate hypokalemia. Prolonged QT interval may reflect calcium deficit.

Auscultate heart sounds.
Development of S₃/S₄ is indicative of failure. Pericardial friction rub may be the only manifestation of uremic pericarditis, requiring prompt intervention and possibly acute dialysis (Workeneh & Batuman, 2022).

Assess the color of skin, mucous membranes, and nail beds. Note capillary refill time.
Pallor may reflect vasoconstriction or anemia. Cyanosis is a late sign and is related to pulmonary congestion and/or cardiac failure. AKI can cause a decrease in the production of RBCs, leading to anemia. Anemia can cause pallor, which is the paleness of the skin due to a decreased amount of oxygenated blood reaching the skin’s surface. AKI can also cause a build-up of fluid in the lungs, leading to respiratory distress and decreased oxygenation of the blood. This causes cyanosis.

Note the occurrence of slow pulse, hypotension, flushing, nausea and vomiting, and depressed level of consciousness.
The use of drugs (like antacids) containing magnesium can result in hypermagnesemia, potentiating neuromuscular dysfunction, and risk of respiratory or cardiac arrest. Use aluminum-hydroxide-based antacid. Hypovolemia leads to hypotension; however, hypotension may not necessarily indicate hypovolemia (Workeneh & Batuman, 2022).

Monitor for GI bleeding by guaiac testing all stools for blood.
See Laboratory and Diagnostic Procedure

Investigate reports of muscle cramps, numbness of fingers, muscle twitching, and hyperreflexia.
Neuromuscular indicators of hypocalcemia can also affect cardiac contractility and function. Hypocalcemia causes muscle spasms and cramps, especially in the hands, feet, and face. This occurs because calcium is necessary for proper muscle function. Severe hypocalcemia can cause tetany, a condition in which the muscles in the hands and feet contract involuntarily, causing muscle spasms and twitching.

Monitor laboratory studies (potassium, calcium, and magnessium). 
See Laboratory and Diagnostic Procedure

Maintain bed rest or encourage adequate rest and provide assistance with care and desired activities.
This reduces oxygen consumption and cardiac workload. During rest, the heart rate decreases, which reduces the workload on the heart and allows it to pump more efficiently. This can improve cardiac output and increase the amount of blood that is circulated throughout the body.

Encourage the client to perform relaxation techniques and improve sleep quality.
Relaxation techniques reduce stress and lower the levels o stress hormones. These hormones can increase the heart rate and blood pressure, which decreases cardiac output. Improving sleep quality allows the body to repair and regenerate cells and tissues. This improves the overall health of the heart and improves cardiac output.

Administer and/or restrict fluids as indicated.
Cardiac output depends on circulating volume (affected by both fluid excess and deficit) and myocardial muscle function. Clients with AKI represent challenging fluid management problems. Hypovolemia potentiates and exacerbates all forms of AKI. Reversal of hypovolemia by rapid fluid infusion is often sufficient to treat many forms of AKI. However, a rapid fluid infusion can result in life-threatening fluid overload (Sinert & Sugalski, 2019).

Provide supplemental oxygen if indicated.
This maximizes available oxygen for myocardial uptake to reduce cardiac workload and cellular hypoxia. The heart requires a constant supply of oxygen to function properly. Supplemental oxygen allows the heart to function more efficiently and effectively.

Administer medications (inotropic agent, calcium gluconate, aluminum hydroxide gels, insulin, sodium bicarbonate, and sodium polystyrene sulfonate with or without sorbitol as indicated.
See Pharmacologic Management

Prepare for/assist with dialysis as necessary.
This may be indicated for persistent dysrhythmias, and progressive heart failure unresponsive to other therapies. The current recommendation by KDIGO is dialysis-dependent AKI clients is to deliver a kt/v of 3.9 per week when using intermittent or extended RRT and an effluent volume of 20 to 25 mg/kg/hour when using continuous renal replacement therapy (Workeneh & Batuman, 2022).

Prepare the client for echocardiography.
Echocardiography is an essential tool for guiding resuscitation in critically ill clients. It is an evidence-based approach and ideally suited to address fluid responsiveness. Resuscitation often requires the infusion of IV fluids in an effort to reverse organ dysfunction (Effat et al., 2021).

3. Promoting Optimal Nutritional Balance

Malnutrition is highly prevalent among AKI clients and is an important independent predictor of in-hospital mortality. Nutrient requirements for clients with AKI may differ widely between individual clients and nutrition support must be coordinated with the metabolic consequences associated with renal failure, the underlying disease process, as well as the derangements in nutrient balance induced by renal replacement therapy (RRT) (Hung et al., 2022).

Assess and document dietary intake.
This aids in identifying deficiencies and dietary needs. General physical condition, uremic symptoms (nausea, anorexia), and multiple dietary restrictions affect food intake. Critically ill clients with AKI are often suffering from multiple organ failures that complicate nutritional support. The nutritional status of critically ill clients affects plans for nutritional support (Hung et al., 2022). 

Weigh daily.
The fasting or catabolic client normally loses 0.2 to 0.5 kg/day. Changes in excess of 0.5 kg may reflect shifts in fluid balance. Studies have shown that obesity was associated with an increased risk of developing AKI. Paradoxically, obese clients seem to have a survival benefit compared to underweight or normal-weight clients regardless of whether or not they required RRT. Clients with a BMI of ≥31 kg/m² had higher mortality, which was the same as those clients with a low body weight (BMI <18 kg/m²) (Hung et al., 2022).

Measure the client’s energy requirements.
The energy requirements of clients with AKI are determined by the underlying disease and not by renal failure. Studies and clinical guidelines suggest that indirect calorimetry can be used to measure indirect energy requirements when available (Hung et al., 2022). Indirect calorimetry calculates heat production by measuring gas exchange. During resting conditions, food sources are broken down to produce energy (heat or kcal). The oxygen consumed and the carbon dioxide produced are measured to provide an indirect assessment of calorie requirement at rest per day (The Medical City, 2017).

Perform a general nutritional assessment and screen for malnutrition.
Nutrition-related symptoms have been shown to have an important role in predicting malnutrition risk in kidney clients, and among those, appetite loss conveyed the highest prognostic power. Recently, a new renal inpatient nutritional screening tool (Renal iNUT) was specifically developed for hospitalized clients with AKI or CKD, showing good sensitivity, specificity, and positive predictive value. A general nutritional assessment should include client history, report of unintentional weight loss or decrease in physical performance before hospital or ICU admission, physical examination, and general assessment of body composition, muscle mass, and strength (Fiaccadori et al., 2021).

Assess lean body mass, muscle mass, and function.
Body composition assessment should be preferred to anthropometry measurements when diagnosing and monitoring malnutrition in hospitalized clients with AKI. Because critically ill clients suffer an important and accelerated skeletal muscle loss already occurring in the first few days at the ICU, body composition monitoring is of major importance. Muscle function should be assessed by hand-grip strength (Fiaccadori et al., 2021).

Monitor laboratory studies such as BUN, albumin, transferrin, sodium, potassium, and phosphorus.
These are indicators of nutritional needs, restrictions, and the necessity for and effectiveness of therapy.  Renal function is critical to maintaining internal electrolyte balance. Severe electrolyte and acid-base disorders are considered important indicators for renal replacement treatment and cause of death. One national report in the UK stated that one-fifth of in-hospital AKI could be avoidable, if only they received better monitoring of electrolytes, recognition of risk factors, and prompt management (Chen et al., 2021). 

Provide frequent, small feedings.
This minimizes anorexia and nausea associated with a uremic state and/or diminished peristalsis. Two clinical trials compared trophic feeding with full-feeding nutrition for the first six days in acute lung injury clients on ventilator support. The trophic feeding group had less gastrointestinal intolerance and insulin use and lower plasma glucose levels. The definition of trophic feeding is to give enteral nutrition at 10 to 20 kcal/hour or up to 500 kcal/day. For critically ill clients with AKI, begin feeding with a low-energy diet or full-energy diet if the effect of mortality is still controversial. However, initial trophic feeding can reduce episodes of GI intolerance (Hung et al., 2022).

Give the client or family caregiver a list of permitted foods or fluids and encourage involvement in menu choices.
This provides the client with a measure of control within dietary restrictions. Food from home may enhance appetite. Dietary changes are an important facet of AKI treatment. Restriction of salt and fluid becomes crucial in the management of oliguric kidney failure, wherein the kidneys do not adequately excrete either toxins or fluids (Workeneh & Batuman, 2022).

Offer frequent mouth care or rinse with 10% hydrogen peroxide if there is stomatitis. Give gums, hard candy, and breath mints between meals.
Xerostomia denotes the subjective sensation of dry mouth and is related to the overall volume status of clients who are discouraged from drinking excess fluids. One-third of hemodialyzed clients present a characteristic halitosis called “uremic fetor” and a metallic taste due to high urea content in saliva and its breakdown in ammonia. An important problem is also represented by uremic stomatitis, which consists of painful lesions on oral mucosal surfaces. To promote the healing of the lesions, gargling with 10% hydrogen peroxide four times a day can be recommended (Costantinides, 2018).

Consult with the dietitian support team.
This determines individual calorie and nutrient needs within the restrictions and identifies the most effective route and product (oral supplements, enteral or parenteral nutrition). The client should have a dietary consult because salt and fluid restriction is vital when managing acute kidney injury. Similarly, the client should avoid a high-potassium diet when there is renal dysfunction (Goyal et al., 2022).

Include complex carbohydrates and fat sources to meet caloric needs and essential amino acids. Avoid concentrated sugar sources.
Carbohydrates meet energy needs and limit tissue catabolism, preventing keto acid formation from protein and fat oxidation. Carbohydrate intolerance mimicking DM may occur in severe renal failure. Essential amino acids improve nitrogen balance and nutritional status, stimulate the repair of tubular epithelial cells, and enhance the client’s ability to fight systemic complications. Almost all of the standard enteral nutrition and parenteral nutrition formulas available today contain a high percentage of calories from carbohydrates, even in lipid-based all-in-one formulas. This non-protein macronutrient distribution may not be appropriate for hospitalized clients with kidney failure (Fiaccadori et al., 2021).

Provide a high-calorie, low to moderate-protein diet.
The protein requirement of clients with AKI is determined by the underlying disease causing the AKI, the extent of catabolism, and the type of treatment. Since hypoalbuminemia is associated with effective hypovolemia and increases mortality in these clients, nutritional management should aim at supplying sufficient protein to maintain the serum albumin concentration and immune function. Nutritional protein administration should not be restricted to attenuating the rise in blood urea nitrogen or delaying the initiation of dialysis. The protein intake should be increased when clients undergo RRT (Hung et al., 2022).

Maintain proper electrolyte balance by strictly monitoring levels.
Medications and a decrease in GFR can cause electrolyte imbalances and may further cause renal injury. Urine electrolyte findings can also serve as valuable indicators of functioning renal tubules. The fractional excretion of sodium (FENa) is the commonly used indicator. FENa can be a valuable test for helping to detect extreme renal avidity for sodium in conditions such as hepatorenal syndrome (Workeneh & Batuman, 2022).

Restrict potassium, sodium, and phosphorus intake as indicated.
Restriction of these electrolytes may be needed to prevent further renal damage, especially if dialysis is not part of treatment, and during the recovery phase of ARF. Because potassium and phosphorus are not excreted optimally in clients with AKI, blood levels of these electrolytes tend to be high. Restriction of these elements in the diet may be necessary, with guidance from frequent measurements (Workeneh & Batuman, 2022).

Administer medications(iron preparations, calcium carbonate, selenium, vitamin C, and folic acid as indicated.
See Pharmacologic Management

Provide enteral/parenteral nutrition as indicated.
According to 2019 guidelines of the European Society for Clinical Nutrition and Metabolism (ESPEN) and 2016 guidelines of the ASPEN for critically ill clients, those who are at high nutritional risk should be started on enteral or parenteral nutrition within 24 to 48 hours of ICU admission. AKI clients at high nutritional risk who received early enteral nutrition had a significantly lower mortality rate compared to those who received late enteral nutrition. Parenteral nutrition should be given if, after 7 to 10 days, enteral nutrition is unable to meet 60% of energy requirements (Hung et al., 2022).

Maintain serum glucose levels between 140 t0 180 mg/dL.
Clients are at increased risk of both hyper- and hypoglycemia. Insulin resistance is highly prevalent among clients with AKI and is associated with increased mortality risk. High blood glucose concentration can be considered one of the best independent predictors of mortality in this setting. Since insulin is metabolized by the kidney, renal function impairment may also act as a predisposing factor for hypoglycemia (Fiaccadori et al., 2021).

4. Promoting Infection Control and Minimizing Risk for Infection

AKI also adversely affects immune function and is widely considered an immunosuppressed state. A wealth of data has accumulated that clients with AKI have a substantially increased risk of subsequent infection and sepsis. Based on early data and the fact that sepsis is the leading cause of death in clients with AKI, it is possible that the systemic inflammatory response syndrome (SIRS) and counter anti-inflammatory response syndrome responses in AKI result in a state of persistent or prolonged immunoparalysis that increases the risk for subsequent sepsis (Gist & Faubel, 2020).

Assess skin integrity.
Excoriations from scratching may become secondarily infected. Livedo reticularis, digital ischemia, butterfly rash, and purpuras may suggest vasculitis. Some clients may have track marks to suggest endocarditis in an IV drug abuser (Workeneh & Batuman, 2022). Pruritus associated with calcium phosphate deposition and nail atrophy is common in clients with uremia (Alper, 2022).

Monitor vital signs.
Fever (higher than 100.4°F) with increased pulse and respirations is typical of an increased metabolic rate resulting from an inflammatory process, although sepsis can occur without a febrile response. Clients with a worse prognosis of kidney disease presented febrile on admission. Temperature values dropped significantly after four days of hospitalization, indicating that temperature can be a good initial indicator of renal complications (Sacomboio et al., 2021).

Monitor WBC count with differential.
See Laboratory and Diagnostic Procedure

Obtain specimen(s) for culture and sensitivity and administer appropriate antibiotics as indicated.
See Laboratory and Diagnostic Procedure

Promote good hand washing by the client and staff.
This reduces the risk of cross-contamination. One of the best preventive measures for protecting ourselves from the risk of getting infected is washing our hands properly and efficiently. Medical personnel that comes in direct contact with the clients have a high chance of spreading viruses and nosocomial infections; therefore, it is of utmost necessity that they know proper hand-washing technique and that they wash their hands regularly following standard hand-washing guidelines (Khadka & Dani, 2020).

Avoid invasive procedures, instrumentation, and manipulation of indwelling catheters whenever possible. Use an aseptic technique when caring for and manipulating IV and invasive lines. Change site dressings per protocol. Note edema, and purulent drainage.
This limits the introduction of bacteria into the body. Early detection of developing infection may prevent sepsis. Specific risk factors for the development of infection post-AKI include at least 3 days of oliguria, a higher percentage of daily fluid overload, invasive procedures post-AKI, higher severity of illness score, and dialysis requirement (Gist & Faubel, 2020).

Provide routine catheter care and promote meticulous perineal care. Keep the urinary drainage system closed and remove the indwelling catheter as soon as possible.
This reduces bacterial colonization and the risk of ascending UTIs. Placement of a urinary catheter may allow diagnosis and treatment of urethral and bladder outlet urinary obstruction and accurate measurement of urine output, but routine use must be tempered by consideration of the inherent risks of catheter-associated infections (Sinert & Sugalski, 2019).

Encourage deep breathing, coughing, and frequent position changes.
This prevents atelectasis and mobilizes secretions to reduce the risk of pulmonary infections. Deep breathing followed by a forceful cough can help clear the lungs of any trapped mucus or particles that may be harboring infection. This can prevent the build-up of harmful bacteria or viruses in the lungs, reducing the risk of infection.

Administer intravenous fluids as indicated.
Septic AKI clients tend to have lower urinary outputs, receive more fluid therapy and/or diuretics, and are more likely to develop fluid restriction than non-septic AKI clients. Crystalloids are the fluid of choice for resuscitation and hydroxyethyl starches (HES) or hyperchloremic solutions are not recommended (Godin et al., 2017).

Administer antimicrobial therapy as prescribed.
See Pharmacologic Management

Administer vasopressors as prescribed.
See Pharmacologic Management

Avoid nephrotoxic medications.
Another key element in the management of septic clients in regard to AKI prevention is the avoidance of potentially nephrotoxic medication and contrast agents when possible, especially in high-risk clients (Godin et al., 2017). 

Provide adequate nutritional support.
Nutritional support is an important but often overlooked aspect of global client care. It is especially important in septic AKI, a hypercatabolic state that requires adapted protein and caloric intake. Numerous aspects need to be considered when calculating a septic AKI client’s nutritional requirements such as their baseline characteristics, underlying conditions, volume status, and possible protein loss through RRT. For this reason, each client requires an individual approach to nutritional support (Godin et al., 2017).

5. Minimizing Risk for Hypovolemia

During the diuretic phase, daily urine output is approximately 1 to 3 liters but can reach as high as 5 liters or more. The kidneys recover their ability to excrete waste but cannot concentrate the urine. Hypovolemia and hypotension may occur due to massive volume loss. Due to the loss of large volumes of fluid and electrolytes, clients should be monitored for hyponatremia, hypokalemia, and dehydration. This phase may last 1 to 3 weeks (American Nephrology Nurses Association, 2019).

Measure I&O accurately. Weigh daily. Calculate insensible fluid losses.
Assessment can help estimate fluid replacement needs. Fluid intake should approximate losses through urine, nasogastric or wound drainage, and insensible water losses (diaphoresis, metabolism). Insensible fluid losses can result in severe hypovolemia in clients with restricted fluid access and should be suspected in older adult clients and in comatose or sedated clients (Workeneh & Batuman, 2022).

Monitor BP (noting postural changes), HR, and mean arterial pressure (MAP) if possible.
Orthostatic hypotension and tachycardia suggest hypovolemia. Hypotension below a particular threshold MAP was associated with stag 3 progression.  Surviving Sepsis Campaign Guidelines recommend maintaining MAP ≥65 mmHg in clients with sepsis, while some earlier reports indicate that maintenance of MAP ≥70 mm Hg would prevent AKI and progression to severe stage AKI (Izawa et al., 2016).

Note signs and symptoms of dehydration: dry mucous membranes, thirst, dulled sensorium, and peripheral vasoconstriction.
In the diuretic or post-obstructive phase of renal failure, urine output can exceed 3 liters/day. Extracellular fluid volume depletion activates the thirst center, and sodium depletion causes persistent thirst, unrelieved by drinking water. Continued fluid losses including inadequate replacement may lead to a hypovolemic state. Clients commonly present with symptoms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension. Older adults with vague mental status changes are commonly found to have prerenal or normotensive ischemic AKI (Workeneh & Batuman, 2022).

Measure and monitor urine output closely.
In one study designed to determine the value of monitoring urine output in detecting AKI, researchers carefully measured output in critically ill clients; they found AKI incidence rose from 24% to 52% when urine output was added as a variable and monitored hourly. This study indicates urine output directly reflects glomerular filtration rate (GFR) in the kidney and therefore is a sensitive and early AKI biomarker (Dirkes, 2015).

Monitor laboratory studies
In non-oliguric ARF or in the diuretic phase of ARF, large urine losses may result in sodium wasting while elevated urinary sodium acts osmotically to increase fluid losses. Restriction of sodium may be indicated to break the cycle. The kidneys play a role in sodium and potassium homeostasis, and their function decline leads to electrolyte disorder. Abnormal sodium levels may often be accompanied by hypokalemia or hyperkalemia (Gao et al., 2019).

Provide allowed fluids throughout the 24-hour period.
The diuretic phase of ARF may revert to the oliguric phase if fluid intake is not maintained or nocturnal dehydration occurs. The longer the oliguric phase, the poorer the prognosis for the recovery of kidney function. Reversal of hypovolemia by rapid fluid infusion is often sufficient to treat many forms of AKI. However, a rapid fluid infusion can result in life-threatening fluid overload in clients with AKI (Sinert & Sugalski, 2019).

Control environmental temperature; limit bed linens as indicated.
This may reduce diaphoresis, which contributes to overall fluid losses. The reduction of diaphoresis in response to a decrease in environmental temperature is due to several factors. One of the primary mechanisms is the constriction of blood vessels in the skin, which reduces the flow of blood to the sweat glands. This constriction of blood vessels is a part of the body’s natural response to cold temperatures, as it helps retain heat in the body’s core. This leads to a decrease in sweat production.

Administer intravenous fluids as indicated.
Clients with AKI represent challenging fluid management problems. Hypovolemia potentiates and exacerbates all forms of AKI. Vigorous fluid administration in this setting aims to reverse renal ischemia and dilute nephrotoxins to either avert the onset of acute tubular necrosis or prevent recurrent injury that might compromise renal recovery (Effat et al., 2021). 

Administer vasopressors as prescribed.
In clients with vasomotor shock at risk for or with AKI, vasopressors are used along with fluids. For persistent hypotension not responsive to fluid resuscitation, vasopressors are started with the goal of a MAP of 65 or greater (American Nephrology Nurses Association, 2019). Catecholamines, vasopressin, and angiotensin II are the current therapeutic options available for use in increasing blood pressure in septic shock (Busse & Ostermann, 2019).

Insert a urinary catheter as indicated.
Placement of a urinary catheter early in the workup of a client with AKI not only allows diagnosis and treatment of urethral and bladder outlet urinary obstruction but also allows for accurate measurement of urine output. Routine use of urinary catheters should be tempered by consideration of the inherent risks of catheter-associated infections (Sinert & Sugalski, 2019).

6. Initiating Health Teachings and Patient Education

The importance of kidney care has become evident in studies showing that individuals who survive an episode of AKI are at increased risk of adverse outcomes that include both kidney and non-kidney sequelae. Unfortunately, under-recognition of the post-discharge implications of AKI may be common and compounded by fragmentation and poor coordination of care after hospital discharge (Silver & Siew, 2017).

Review disease process, prognosis, and precipitating factors if known.
This provides a knowledge base from which the client can make informed choices. In low- and middle-income countries, although the majority of urban cases occur in the context of acute illness, usually in association with hypovolemia and sepsis, AKI occurring in the community is under-recognized. Hospital-acquired AKI develops in the intensive care unit, in the context of multiple organ failure, post-cardiovascular procedures, or sepsis as a complication of nephrotoxic medications (Lewington et al., 2013).

Identify symptoms requiring medical intervention: decreased urinary output, sudden weight gain, presence of edema, lethargy, bleeding, signs of infection, and altered mentation.
Prompt evaluation and intervention may prevent serious complications or progression to chronic renal failure. A common factor across high-income and low- to middle-income countries is that most cases of AKI are managed by non-nephrologists, who may be unfamiliar with the risk factors and early manifestations of the disease. This contributes to delayed recognition and suboptimal management (Lewington et al., 2013).

Review dietary plans and restrictions. Include a fact sheet listing food restrictions.
Adequate nutrition is necessary to promote tissue healing; adherence to restrictions may prevent complications. Because clients with AKI often have other serious diseases, nutritional support should be considered in a holistic manner. The nutritional requirements of clients with AKI are not determined by AKI per se but are related to the primary disease and any comorbidity. The severity of kidney injury affects the elimination of the daily production of metabolic wastes and nutrients lost due to dialysis treatment. Hypovolemia causing non-catabolic AKI is common in older and malnourished clients which may result from dehydration, upper gastrointestinal bleeding, congestive heart disease, and hypoalbuminemia (Hung et al., 2022).

Review the use of medication. Encourage the client to discuss all medications and herbal supplements with the healthcare provider.
Medications that are concentrated in and/or excreted by the kidneys can cause toxic cumulative reactions and/or permanent damage to the kidneys. Some supplements may interact with prescribed medications and may electrolytes. Categorizations of drug-associated AKI are made based on the underlying mechanism of renal injury. Direct nephrotoxicity occurs from tubuloepithelial injury, interstitial nephritis, glomerular injury, or obstructive nephropathy whereas indirect nephrotoxicity develops from decreased renal blood flow. (Kellum & Hall, 2018)

Establish a regular schedule for weighing.
A useful tool for monitoring fluid and dietary needs. Studies have shown that obesity was associated with an increased risk of developing AKI. Clients with a BMI of ≥ 31 kg/m² had higher mortality, which was the same as those clients with low body weight (BMI <18 kg/m² (Hung et al., 2022).

Explain the level of renal function after the acute episode is over.
The client may experience residual defects in kidney function, which may or may not be permanent. Continued nephron loss causes more hyperfiltration until complete kidney failure results. This has been termed the hyperfiltration theory of kidney failure and explains the scenario in which progressive failure is frequently observed after apparent recovery from AKI (Workeneh & Batuman, 2022).

Encourage the client to observe the characteristics of urine and the amount, and frequency of output.
Changes may reflect alterations in renal function and the need for dialysis. Findings of granular, muddy brown casts in urine sediment are highly suggestive of acute tubular necrosis (ATN). Reddish brown or cola-colored urine suggests the presence of myoglobin or hemoglobin (Workeneh & Batuman, 2022).

Provide social and emotional support to the client and family.
This will reassure them of all the procedures that the client may undergo. Social support is defined as resources provided by a network of individuals and social groups. Members of one’s social network who provide support include peers, family, religious group members, professionals, etc. The members of social networks provide emotional, tangible, informational, and companionship support. Higher levels of social support can improve one’s ability to acquire and understand medical information, and to negotiate in the healthcare system, which would be particularly important for people to facilitate the establishment of healthful attitudes and behaviors (Chen et al., 2018).

Review fluid restriction. Remind the client to spread fluids over an entire day and to include all fluids (ice) in daily fluid counts.
Depending on the cause and stage of ARF, the client may need to either restrict or increase the intake of fluids. Fluids should be considered drugs and should be used judiciously. Accurate assessment of intravascular fluid status, looking for fluid responsiveness, and planning individual targets should be followed in order to improve client outcomes (Patil & Salunke, 2020).

Discuss activity restriction and gradual resumption of desired activity. Encourage the use of energy-saving, relaxation, and diversional techniques.
The client with severe ARF may need to restrict activity and/or may feel weak for an extended period during the lengthy recovery phase, requiring measures to conserve energy and reduce boredom. A study observed an association between higher levels of physical activity and improved renal function. It is known that those with recovery following AKI have better outcomes than those with persistent renal impairment (Asad et al., 2022).

Discuss the reality of the continued presence of fatigue.
Decreased metabolic energy production, the presence of anemia, and states of discomfort commonly result in fatigue. In one study, survivors of severe AKI had a worse health-related quality of life than the general population, even after adjusting for their reduced kidney function. Both physical and mental components were affected. Increasing age and reduced kidney function were associated with poorer physical QOL (Workeneh & Batuman, 2022).

Discuss renal dialysis or transplantation if these are likely options for the future.
Although these options would have been previously presented by the healthcare provider, the client may now be at a point when options need to be considered and may desire additional input. The current recommendation by KDIGO for dialysis-dependent AKI clients is to deliver a kt/v of 3.9 per week when using intermittent or extended RRT and an effluent volume of 20 to 25 mg/kg/hour when using continuous renal replacement therapy (CRRT) (Workeneh & Batuman, 2022).

Determine ADLs and personal responsibilities. Identify available resources and support systems.
This helps the client manage lifestyle changes and meet personal needs. Several studies of social support for chronic diseases have found that social support can be instrumental in improving self-management behaviors and reducing factors affecting the progression of diseases. Social support has also been found to influence the client’s health behaviors and disease management outcomes (Chen et al., 2018).

Recommend scheduling activities with adequate rest periods.
This prevents excessive fatigue and conserves energy for healing and tissue regeneration. Exercise also has the ability to impact many of the adverse outcomes associated with an episode of AKI. Moreover, the suitability of exercise programs for individuals following a cardiac event suggests that it may also be feasible in the AKI population. This is due to the assumed similarity in the functional status of both AKI and cardiac clients (Asad, 2020).

Stress the necessity of follow-up care and laboratory studies.
Renal function may be slow to return following acute failure (up to 12 months), and deficits may persist, requiring changes in therapy to avoid recurrence. Renal recovery is usually observed within the first two weeks, and many nephrologists tend to diagnose clients with end-stage kidney failure 6 to 8 weeks after the onset of AKI. It is always better to check these clients periodically, because some clients may regain kidney function much later (Workeneh & Batuman, 2022).

Be well-informed about AKI before providing education to the client and the family.
Nursing plays a key role as an integral part of the client care team. In high-income countries, nurses play a central role in the care of hospitalized clients where standards of care are well established. Credentialing is required and ongoing educational programs are mandated to maintain nursing competence. In contrast, in low- to middle-income countries, there is a wider variation in the level of nursing care. Care is often provided in small private clinics where standards for nursing care may be highly variable and educational activities may not be as well defined (Lewington et al., 2013).

Raise awareness about AKI in the community.
There are opportunities to raise awareness of AKI as a complication of other disease processes in the developing world and mobilize local resources to manage it at an early phase. The WHO/UN UNDP Millenium Project and the Campaign to Eradicate Malaria deal with the main root causes of community disease in developing countries. The Millenium Project attempts to eradicate extreme poverty and hunger, achieve universal primary education, promote gender equality and empower women, improve maternal health and reduce child mortality, combat HIV/AIDS, malaria, and other diseases, ensure environmental sustainability, and promote a global partnership for development. All these issues are intimately related to AKI in developing countries (Lewington et al., 2013).

Arrange follow-up consultations with a nephrologist.
Previous research has demonstrated that nephrologists are more skilled at recognizing and managing CKD complications according to evidence-based guidelines than primary care providers. Some centers have started to establish outpatient care models dedicated to clients who survive an episode of AKI. Clinic visits consist of a standardized assessment by a nephrologist that highlights blood pressure and urine albumin control, a review of core laboratory studies that are obtained quarterly, cardiovascular risk modification, management of CKD complications, medication reconciliation, and specialist referrals for co-morbidity management (Silver & Siew, 2017).

7. Administering Medications and Pharmacologic Support

In the management of Acute Renal Failure (ARF), medications are primarily focused on addressing the underlying cause, managing complications, and promoting renal function recovery. Medications may include diuretics to increase urine output, electrolyte supplements to correct imbalances, medications to control blood pressure, renal vasodilators and antioxidant agents to minimize further renal damage and drugs to treat specific conditions contributing to ARF, such as antibiotics for sepsis.

Diuretics such as furosemide, bumetanide, torsemide, and mannitol
These are given early in the oliguric phase of ARF in an effort to convert to a non-oliguric phase, flush the tubular lumen of debris, reduce hyperkalemia, and promote adequate urine volume. Furosemide can be used to correct volume overload when the kidneys are still responsive; this often requires high intravenous doses. Furosemide plays no role in converting an oliguric AKI to a non-oliguric AKI or in increasing urine output when a client is not hypervolemic (Workeneh & Batuman, 2022).

Vasodilators such as fenoldopam
Fenoldopam is a selective dopamine-receptor agonist that acts as a rapid-acting vasodilator. It is six times more potent than dopamine in producing renal vasodilation. It increases renal blood flow to the cortex and medullary regions in the kidney, increases diuresis, and has minimal adrenergic effects. Fenoldopam is indicated for the treatment of severe hypertension, including for clients with renal compromise (Workeneh & Batuman, 2022).

Calcium channel blockers
These are given early in nephrotoxic acute tubular necrosis (ATN) to reduce the influx of calcium into kidney cells, thereby helping to maintain cell integrity and improve GFR. Calcium channel blockers have been shown in animal models to be protective in AKI if given before renal insult. Their only benefit in humans is preventing AKI in renal transplant clients receiving cyclosporine (Sinert & Sugalski, 2019).

Inotropic agents such as dopamine
Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect is dose-dependent. In small doses, dopamine predominantly stimulates dopaminergic receptors, which, in turn, produces vasodilation of the renal vasculature. Enhancing renal perfusion (Workeneh & Batuman, 2022).

Calcium gluconate
Serum calcium is often low but does not require specific treatment in ARF. Calcium gluconate may be given to treat hypocalcemia and to offset the effects of hyperkalemia by modifying cardiac irritability. Calcium gluconate directly antagonizes the neuromuscular and cardiovascular effects of magnesium (Fulop & Batuman, 2020).

Aluminum hydroxide gels
Increased phosphate levels may occur as a result of the failure of glomerular filtration and require the use of phosphate-binding antacids to limit phosphate absorption from the GI tract.

Glucose and/or insulin solution
A temporary measure to lower serum potassium is by driving potassium into cells when the cardiac rhythm is endangered. Glucose and insulin may help promote magnesium entry into cells. Glucose should be administered with insulin to prevent hypoglycemia (Fulop & Batuman, 2020).

Sodium bicarbonate or sodium citrate
This may be used to correct acidosis or hyperkalemia (by increasing serum pH) if the client is severely acidotic and not suffering from fluid overload. Raising bicarbonate concentration will increase the filtered bicarbonate load above the proximal tubule’s reduced absorptive capacity, resulting in a marked bicarbonate diuresis. (Najjar, 2022)

Sodium polystyrene sulfonate with or without sorbitol
Exchange resin trades sodium for potassium in the GI tract to lower serum potassium levels. Sorbitol may be included to cause osmotic diarrhea to help excrete potassium. Sodium polystyrene sulfonate helps by removing extra potassium from the body.  Due to its slow onset of action, it is a second-line agent in emergent situations (Rahman & Marathi, 2022).

Iron preparations
Iron deficiency may occur if the protein is restricted, the client is anemic, or GI function is impaired. In randomized trials, 100% of clients received oral or parenteral iron over 29 days, and this might explain the higher increase in hemoglobin in their clients (Aoun et al., 2022).

Calcium carbonate
This restores normal serum levels to improve cardiac and neuromuscular function, blood clotting, and bone metabolism. Low serum calcium is often corrected as phosphate absorption is decreased in the GI system. Calcium may be substituted as a phosphate binder (Fulop & Batuman, 2020).

Selenium, vitamin C, and folic acid
These are vital as coenzymes in cell growth and actions. Intake is decreased because of protein restrictions. During critical illnesses, vitamins, and trace elements may impact immunomodulation, and wound healing, and may have antioxidant properties. The current recommendation is that the losses of selenium and other micronutrients in the effluent fluid should be replaced. The optimal dose remains unknown, but a dosage of 100 mg/dL has been suggested for vitamin C (Fiaccadori et al., 2021).

Antibiotics
Early administration of appropriate antimicrobial therapy within six hours and ideally within one hour is the cornerstone treatment in sepsis and improves survival. In a multicenter retrospective study with hypotensive clients with septic shock, longer delays before administration of appropriate antimicrobial therapy were associated with early AKI development (Godin et al., 2017).

Vasopressors
Vasopressor support is often needed in septic shock since fluid therapy alone does not correct sepsis-induced systemic vasodilation and endothelial dysfunction. Norepinephrine is the drug of choice for septic clients requiring vasopressors (Godin et al., 2017).

8. Monitoring Laboratory and Diagnostic Procedures

Laboratory and diagnostic procedures play a crucial role in the evaluation and management of Acute Renal Failure (ARF). Common tests include blood tests to assess kidney function (such as serum creatinine and blood urea nitrogen), electrolyte levels, and acid-base balance. Urine tests, such as urinalysis and urine electrolyte measurements, can provide valuable information on kidney function and help identify the underlying cause of ARF.

Blood urea nitrogen (BUN), and creatinine (cr)
BUN assesses the management of renal dysfunction. Both values may increase but creatinine is a better indicator of renal function because it is not affected by hydration, diet, and tissue catabolism. Dialysis is usually indicated if the ratio is higher than 10:1 or if therapy fails to indicate fluid overload or metabolic acidosis. The ratio of BUN to creatinine is an important finding. The ratio can exceed 20:1 in conditions in which enhanced reabsorption of urea is favored (Workeneh & Batuman, 2022).

Urine sodium
In acute tubular necrosis, tubular functional integrity is lost and sodium resorption is impaired, resulting in increased sodium excretion. Urine electrolyte findings can also serve as valuable indicators of functioning renal tubules. The fractional excretion of sodium (FENa) is the commonly used indicator. Calculating FENa is useful in AKI only in the presence of oliguria (Workeneh & Batuman, 2022).

Serum sodium
Hyponatremia may result from fluid overload (dilutional) or the kidney’s inability to conserve sodium. Hypernatremia indicates total body water deficit. Clients suffering from AKI were associated with impaired sodium and potassium homeostasis. Hyponatremia and hypernatremia are common electrolyte abnormalities among critically ill clients. A study suggested that abnormal sodium is an important risk factor for mortality independent of potassium levels among clients with heart failure (Gao et al., 2019).

Serum potassium
Lack of renal excretion and/or selective retention of potassium to excrete excess hydrogen ions leads to hyperkalemia, requiring prompt intervention. Hyperkalemia is a common and important complication of AKI (Sinert & Sugalski, 2019).

Hemoglobin and hematocrit
Decreased values may indicate hemodilution (hypervolemia) however, during prolonged failure, anemia frequently develops as a result of RBC loss. Other possible causes (active or occult hemorrhage) should also be evaluated. Postoperative anemia and a decrease in hemoglobin levels have been reported as predictive factors for AKI and in-hospital mortality in cardiac surgery. The results of the studies emphasize the importance of detecting and correcting anemia in clients with AKI (Lombardi et al., 2021).

Calcium
In addition to its own cardiac effects, calcium deficit enhances the toxic effects of potassium. Hypocalcemia is common in AKI; marked hypocalcemia is more typical of chronic renal failure (Sinert & Sugalski, 2019).

Magnesium
Dialysis or calcium administration may be necessary to combat the CNS-depressive effects of an elevated serum magnesium level. Decreasing renal function represents a risk factor for magnesium accumulation, in the setting of exogenous supplementation. In clients with AKI, hypermagnesemia usually presents during the oliguric phase; the serum magnesium level returns to normal during the polyuric phase (Fulop & Batuman, 2020).

Serial chest X-rays
Increased cardiac size, prominent pulmonary vascular markings, pleural effusion, and congestion indicate acute responses to fluid overload or chronic changes associated with renal and heart failure. Obtain chest radiographs on a routine basis to look for evidence of volume overload (Sinert & Sugalski, 2019).

Echocardiography
Echocardiography is an essential tool for guiding resuscitation in critically ill clients. Resuscitation often requires the infusion of intravenous fluids in an effort to reverse organ dysfunction. Echocardiography is an evidence-based approach and is ideally suited to address fluid overload (Effat et al., 2021).

Stool guaiac test
Gastrointestinal bleeding is a known complication of renal failure; however, its pathogenesis remains uncertain. Some have attributed gastrointestinal bleeding to the effects of uremia on the gastrointestinal mucosa; others have suggested that uremia may affect platelet adhesiveness, which may explain the prolonged gastrointestinal bleeding seen in clients with renal failure. In addition, the role of heparinization and the widespread use of antiplatelet agents in clients on dialysis have been implicated in the etiology of gastrointestinal bleeding.

WBC count with differential.
Although elevated WBCs may indicate generalized infection, leukocytosis is commonly seen in ARF and may reflect injury within the kidney. A shifting of the differential to the left is indicative of infection. It is known that alteration in WBC counts is associated with the risk of long-term kidney outcomes. Each WBC subtype are one of the immunologic factors that play a pivotal role in most processes of organ damage. This role can apply to the issue of kidney damage. (Han et al., 2014)

Culture and sensitivity
Verification of infection and identification of specific organisms aids in the choice of the most effective treatment. Note: A number of anti-infective agents require adjustments of dose and/or time while renal clearance is impaired. The presence of eosinophils, as visualized with the Wright stain or Hansel stain, might suggest interstitial nephritis. However, it has poor sensitivity in AIN diagnosis and can also be seen in UTIs, glomerulonephritis, and atheroembolic disease (Workeneh & Batuman, 2022).

Recommended Resources

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy.

See Also

Other recommended site resources for this nursing care plan:

• Nursing Care Plans (NCP): Ultimate Guide and Database ^{MUST READ!}
  Over 150+ nursing care plans for different diseases and conditions. Includes our easy-to-follow guide on how to create nursing care plans from scratch.
• Nursing Diagnosis Guide and List: All You Need to Know to Master Diagnosing
  Our comprehensive guide on how to create and write diagnostic labels. Includes detailed nursing care plan guides for common nursing diagnostic labels.

Other care plans and nursing diagnoses related to reproductive and urinary system disorders:

• Acute Glomerulonephritis | 4 Care Plans
• Acute Renal Failure | 6 Care Plans
• Benign Prostatic Hyperplasia (BPH) | 5 Care Plans
• Chronic Renal Failure | 10 Care Plans
• Hemodialysis | 3 Care Plans
• Hysterectomy (TAHBSO) | 6 Care Plans
• Mastectomy | 15 Care Plans
• Menopause | 6 Care Plans
• Nephrotic Syndrome | 5 Care Plans
• Peritoneal Dialysis | 6 Care Plans
• Prostatectomy | 6 Care Plans
• Urolithiasis (Renal Calculi) | 4 Care Plans
• Urinary Tract Infection | 4 Care Plans
• Vesicoureteral Reflux (VUR) | 5 Care Plans

References and Sources

Resources you can use to further your research about acute kidney injury nursing care plan:

• Alper, A. B. (2022, January 6). Uremia: Practice Essentials, Pathophysiology, Etiology. Medscape Reference. Retrieved March 11, 2023.
• American Nephrology Nurses Association. (2019). Acute Kidney Injury Fact Sheet. American Nephrology Nurses Association.
• Aoun, M., Sleilaty, G., Boueri, C., Younes, E., Gabriel, K., Kahwaji, R.-M., Hilal, N., Hawi, J., Araman, R., Chelala, D., & Beaini, C. (2022). Erythropoietin in Acute Kidney Injury (EAKI): a pragmatic randomized clinical trial. BMC Nephrology, 23(100).
• Asad, A. (2020, October 23). Exercise as a therapeutic option for acute kidney injury: mechanisms and considerations for the design of future clinical studies – BMC Nephrology. BMC Nephrology. Retrieved March 13, 2023.
• Asad, A., Thomas, A., Dungey, M., Hull, K. L., March, D. S., & Burton, J. O. (2022, April 11). Associations between physical activity levels and renal recovery following acute kidney injury stage 3: a feasibility study. NCBI. Retrieved March 13, 2023.
• Bindroo, S., Quintanilla Rodriguez, B. S., & Challa, H. J. (2022, August 8). Renal Failure – StatPearls. NCBI. Retrieved March 10, 2023.
• Busse, L. W., & Ostermann, M. (2019, September). Vasopressor Therapy and Blood Pressure Management in the Setting of Acute Kidney Injury. Seminars in Nephrology, 39(5).
• Chen, X., Xu, J., Li, Y., Xu, X., Shen, B., Zou, Z., Ding, X., Teng, J., & Jiang, W. (2021, May 27). Risk Scoring Systems Including Electrolyte Disorders for Predicting the Incidence of Acute Kidney Injury in Hospitalized Patients. NCBI. Retrieved March 11, 2023.
• Chen, Y.-C., Chang, L.-C., Liu, C.-Y., Ho, Y.-F., Weng, S.-C., & Tsai, T.-I. (2018, March). The Roles of Social Support and Health Literacy in Self-Management Among Patients With Chronic Kidney Disease. Journal of Nursing Scholarship, 50(3).
• Costantinides, F. (2018, November 13). Dental Care for Patients with End-Stage Renal Disease and Undergoing Hemodialysis. NCBI. Retrieved March 11, 2023.
• Dirkes, S. M. (2015, July 13). Acute kidney injury: Causes, phases, and early detection. American Nurse. Retrieved March 13, 2023.
• Effat, H., Alsayed, I. A., Alhusseiny, R., & Farouk, W. (2021, September). Fluid Management in Critically Ill Patients with Acute Kidney Injury: Role of Noninvasive Assessment of Stroke Volume. The Egyptian Journal of Critical Care Medicine, 8(1).
• Fiaccadori, E., Sabatino, A., Barazzoni, R., Carrero, J. J., Cupisti, A., De Waele, E., Jonckheer, J., Singer, P., & Cuerda, C. (2021, April). ESPEN guideline on clinical nutrition in hospitalized patients with acute or chronic kidney disease. Clinical Nutrition, 40(4).
• Fulop, T., & Batuman, V. (2020, May 4). Hypermagnesemia: Overview, Renal Failure, Other Causes. Medscape Reference. Retrieved March 10, 2023.
• Fülöp, T., Pathak, M. B., Schmidt, D. W., Lengvarszky, Z., Juncos, J. P., Lebrun, C. J., Brar, H., & Juncos, L. A. (2010, July). Volume-Related Weight Gain and Subsequent Mortality in Acute Renal Failure Patients Treated with Continuous Renal Replacement Therapy. American Society for Artificial Internal Organs Journal, 56(4).
• Gao, X., Zheng, C., Liao, M., He, H., Liu, Y., Jing, C., Zeng, F., & Chen, Q. (2019). Admission serum sodium and potassium levels predict survival among critically ill patients with acute kidney injury: a cohort study. BMC Nephrology, 20(311).
• Gist, K. M., & Faubel, S. (2020, June). Infection Post-AKI: Should We Worry? Nephron, 144.
• Godin, M., Murray, P., & Mehta, R. L. (2017, September 27). Clinical Approach to the Patient with AKI and Sepsis. NCBI. Retrieved March 11, 2023.
• Goyal, A., Daneshpajouhnejad, P., Hashmi, M. F., & Bashir, K. (2022, August 18). Acute Kidney Injury – StatPearls. NCBI. Retrieved March 11, 2023.
• Han, S. S., Ahn, S. Y., Ryu, J., Baek, S. H., Kim, K., Chin, H. J., Na, K. Y., Chae, D.-W., & Kim, S. (2014). U-Shape Relationship of White Blood Cells with Acute Kidney Injury and Mortality in Critically Ill Patients. 232, 3.
• Hung, K.-Y., Chen, S.-T., Chu, Y.-Y., Ho, G., & Liu, W.-L. (2022, February). Nutrition support for acute kidney injury 2020-consensus of the Taiwan AKI task force. Journal of the Chinese Medical Association, 85(2).
• Izawa, J., Kitamura, T., Iwami, T., Uchino, S., Takinami, M., Kellum, J. A., & Kawamura, T. (2016). Early-phase cumulative hypotension duration and severe-stage progression in oliguric acute kidney injury with and without sepsis: an observational study. Critical Care, 20.
• Kellum, J. A., & Hall, S. (2018, February 26). Drug-Associated Acute Kidney Injury: Who’s at risk? NCBI. Retrieved March 13, 2023.
• Khadka, A., & Dani, S. (2020, December 31). Washing Hands according to the WHO Guideline since the COVID-19 Outbreak in the Context of Medical Undergraduates at a Tertiary Care Center: A Descriptive Cross-sectional Study. NCBI. Retrieved March 11, 2023.
• Lewington, A. J.P., Cerda, J., & Mehta, R. L. (2013, September). Raising awareness of acute kidney injury: a global perspective of a silent killer. Kidney International, 84(3).
• Lombardi, Y., Ridel, C., & Touzot, M. (2021, February). Anaemia and acute kidney injury: the tip of the iceberg? Clinical Kidney Journal, 14(2).
• The Medical City. (2017, January). News – Indirect Calorimetry. The Medical City. Retrieved March 11, 2023.
• Moorhouse, M. F., Doenges, M. E., & Murr, A. C. (2010). Nursing Care Plans: Guidelines for Individualizing Client Care Across the Life Span. F.A. Davis Company.
• Najjar, F. (2022, July 18). Renal Tubular Acidosis – StatPearls. NCBI. Retrieved March 10, 2023.
• Patil, V. P., & Salunke, B. G. (2020, April). Fluid Overload and Acute Kidney Injury. Indian Journal of Critical Care Medicine, 24(3).
• Rahman, S., & Marathi, R. (2022, July 4). Sodium Polystyrene Sulfonate – StatPearls. NCBI. Retrieved March 10, 2023.
• Sacomboio, E. N. M., Campos, L. H., Daniel, F. N., & Ekundi-Valentin, E. (2021, November). Can vital signs indicate acute kidney injury in patients with malaria? Results of an observational study in Angola. Scientific African, 14.
• Shusterman, B. (2021, May 19). Top 5 healthy drinks for people with kidney disease. American Kidney Fund. Retrieved March 10, 2023.
• Siew, E. D., Fissell, W. H., Tripp, C. M., Blume, J. D., Wilson, M. D., Clark, A. J., Vincz, A. J., Ely, E. W., Pandharipande, P. P., & Girard, T. D. (2017, June). Acute Kidney Injury as a Risk Factor for Delirium and Coma during Critical Illness. American Journal of Respiratory and Critical Care Medicine, 195(12).
• Silver, S. A., & Siew, E. D. (2017, July). Follow-up Care in Acute Kidney Injury: Lost in Transition. Advances in Chronic Kidney Disease, 24(4).
• Sinert, R. H., & Sugalski, G. (2019, November 20). Acute Kidney Injury (Renal Failure) in Emergency Medicine: Practice Essentials, Prognosis, Differential Diagnosis. Medscape Reference. Retrieved March 10, 2023.
• Workeneh, B. T., & Batuman, V. (2022, December 10). Acute Kidney Injury (AKI): Practice Essentials, Background, Pathophysiology. Medscape Reference. Retrieved March 10, 2023.