Acute Renal Failure Nursing Diagnosis Care Plan: Comprehensive Guide

Acute Renal Failure (ARF), also known as Acute Kidney Injury (AKI), represents a sudden decline in kidney function, significantly impacting overall health. This condition leads to a rapid decrease in the glomerular filtration rate (GFR) over hours to days, resulting in an increase in serum creatinine and urea nitrogen levels. Early detection can be challenging as initial signs may be subtle, often presenting only as reduced urine production following a kidney insult (Workeneh & Batuman, 2022). Untreated ARF can severely complicate pre-existing chronic renal failure.

AKI is traditionally categorized into three types based on the location of the issue: Prerenal, Intrinsic, and Postrenal. Prerenal AKI is often a physiological response to conditions like severe volume depletion and hypotension, where the kidney structure is still intact. Intrinsic AKI involves direct damage to the kidney tissues from cytotoxic, ischemic, or inflammatory insults, causing structural and functional impairment. Postrenal AKI arises from obstructions in the urinary tract that prevent urine outflow.

Acute renal failure is a significant health concern, with an annual incidence of approximately 100 cases per million people in the US and affecting about 1% of hospital admissions. Post-surgical AKI occurs in roughly 1% of general surgeries, but the incidence dramatically increases to over 50% in intensive care unit patients (Workeneh & Batuman, 2022).

Many patients with AKI may not exhibit obvious clinical symptoms, and the condition is frequently diagnosed through routine blood tests. However, depending on the severity and duration of kidney function loss, symptoms can manifest as hypertension, edema, decreased urine output, shortness of breath, anorexia, nausea, sleep disturbances, and altered mental status (Workeneh & Batuman, 2022).

The prognosis for AKI is heavily influenced by the underlying cause of the kidney injury, the presence of pre-existing kidney disease, and the duration of kidney dysfunction before medical intervention (Workeneh & Batuman, 2022). Effective nursing care is crucial in managing ARF, focusing on supporting renal function, addressing reversible causes, and providing comprehensive supportive treatment to improve patient outcomes.

Nursing Care Plans and Management for Acute Renal Failure

Nursing care for acute renal failure focuses on several key objectives: promoting kidney function, identifying and treating reversible causes of kidney failure, and providing comprehensive supportive care. Essential nursing interventions include vigilant monitoring and management of fluid and electrolyte imbalances, optimizing nutritional support, and ensuring medication safety. Additionally, nurses play a vital role in supporting the patient’s emotional and psychological well-being, as well as educating patients on self-care strategies and preventive measures to avoid future kidney damage. This holistic approach is crucial for effective acute renal failure management.

Prioritized Nursing Problems for Acute Renal Failure

Effective management of acute renal failure requires addressing several critical nursing priorities:

Renal Function Assessment and Continuous Monitoring: Regularly evaluate kidney function through lab results, urine output, and physical assessments to detect changes and guide interventions.
Fluid and Electrolyte Balance Management: Carefully manage fluid intake and output, monitor electrolyte levels, and correct imbalances to prevent complications like hyperkalemia and fluid overload.
Identification and Treatment of Underlying Cause: Determine the root cause of ARF (prerenal, intrinsic, or postrenal) to direct specific treatments and improve outcomes.
Prevention and Management of Complications: Proactively prevent and manage potential complications such as electrolyte abnormalities, metabolic acidosis, and infections that can arise from kidney dysfunction.
Fluid Overload and Dehydration Management: Balance fluid replacement to avoid both dehydration and fluid overload, monitoring closely for signs of each condition.
Hemodynamic Stability and Blood Pressure Control: Maintain stable blood pressure and hemodynamic status to ensure adequate renal perfusion and prevent further kidney damage.
Patient Education on Self-Care and Treatment Adherence: Educate patients and families about ARF, treatment plans, dietary and fluid restrictions, medication management, and the importance of follow-up care to promote compliance and better long-term outcomes.

Nursing Assessment for Acute Renal Failure

A comprehensive nursing assessment is crucial for patients with acute renal failure. This involves gathering both subjective and objective data to understand the patient’s condition and needs.

Subjective and Objective Data to Assess:

Changes in Urinary Output: Monitor for oliguria (decreased urine output) or anuria, which are key indicators of kidney dysfunction. Assess urine volume and frequency.
Fluid Retention: Observe for edema in extremities (hands, feet), face, and periorbital areas, which indicates fluid overload due to impaired kidney function.
Fatigue and Weakness: Patients may report increased fatigue and generalized weakness due to uremia and electrolyte imbalances.
Respiratory Distress: Assess for shortness of breath, dyspnea, or labored breathing, which can result from fluid overload and pulmonary edema.
Gastrointestinal Symptoms: Inquire about nausea, vomiting, loss of appetite, or changes in taste, common symptoms of uremia.
Neurological Changes: Assess for confusion, altered mental status, lethargy, or seizures, which can occur due to electrolyte imbalances and uremic encephalopathy.
Pain and Discomfort: Evaluate for abdominal pain, flank pain, or discomfort, which may indicate kidney-related issues or complications.
Cardiovascular Changes: Monitor for hypertension, irregular heart rhythms, or palpitations, as kidney dysfunction affects blood pressure and cardiac function.
Fluid Overload Signs: Look for signs of fluid overload such as jugular venous distension (JVD), crackles in lungs, and rapid weight gain.

Assessment of Factors Related to Acute Renal Failure Etiology:

Regulatory Mechanism Compromise: Evaluate the extent of renal failure and its impact on the body’s regulatory functions.
Fluid Imbalance: Differentiate between fluid overload (from kidney dysfunction or excessive IV fluids) and fluid deficit (from excessive losses).
Electrolyte Imbalances: Assess for imbalances in electrolytes, particularly potassium and calcium, and for severe acidosis, all common in ARF.
Uremic Impact on Cardiac Function: Evaluate for uremic effects on cardiac muscle and oxygenation, which can lead to cardiac complications.
Metabolic Changes: Consider protein catabolism and dietary restrictions needed to manage nitrogenous waste products. Assess increased metabolic needs due to illness.
Gastrointestinal Disturbances: Assess anorexia, nausea, vomiting, and oral mucosa ulcerations, which can affect nutritional intake.
Immunological Depression: Recognize potential depression of immune defenses secondary to uremia, increasing infection risk.
Invasive Procedures/Devices: Note any invasive procedures like urinary catheterization, which can introduce infection.
Dietary and Nutritional Status: Evaluate changes in dietary intake and potential malnutrition, which can impact recovery.
Fluid Loss Patterns: Assess for excessive fluid loss, especially during the diuretic phase of ARF, where high urine output can lead to dehydration if not managed properly.

Alt text: Nursing assessment for edema in feet of patient with acute renal failure, focusing on fluid retention.

Nursing Diagnosis for Acute Renal Failure

Following a thorough assessment, a nursing diagnosis is formulated to specifically address the health challenges associated with acute renal failure. This diagnosis is based on the nurse’s clinical judgment and comprehensive understanding of the patient’s unique health condition. Nursing diagnoses provide a structured framework for organizing care, though their specific use can vary in clinical practice. Ultimately, the nurse’s expertise and clinical judgment are paramount in tailoring the care plan to meet each patient’s individual needs and health priorities.

Nursing Goals for Acute Renal Failure

Establishing clear goals and expected outcomes is essential in the nursing care plan for acute renal failure. These goals are patient-centered and focused on recovery and stabilization:

Optimal Fluid Balance: The patient will demonstrate appropriate urinary output, with urine specific gravity and laboratory values approaching normal ranges. They will maintain a stable weight, exhibit vital signs within their normal limits, and show no signs of edema.
Stable Cardiac Output: The patient will maintain adequate cardiac output, evidenced by blood pressure and heart rate/rhythm within their normal limits, strong and equal peripheral pulses, and adequate capillary refill time.
Nutritional Maintenance: The patient will maintain or regain weight appropriate to their individual situation, remaining free from edema, indicating proper nutritional balance and fluid management.
Absence of Infection: The patient will exhibit no signs or symptoms of infection, reflecting effective infection prevention and control measures.
Electrolyte Balance: The patient will demonstrate intake and output balance, good skin turgor, moist mucous membranes, palpable peripheral pulses, stable weight, and vital signs, with electrolytes within normal ranges, indicating effective management of fluid and electrolyte balance.

Nursing Interventions and Actions for Acute Renal Failure

Therapeutic nursing interventions and actions are critical in managing patients with acute renal failure (ARF). These interventions are designed to address the prioritized nursing problems and achieve the established patient goals.

1. Managing Fluid Volume and Hypervolemia

In prerenal acute kidney injury (AKI), fluid resuscitation is the primary treatment. However, it’s crucial to manage fluid administration carefully; excessive fluid beyond what’s needed to correct hypovolemia can lead to increased morbidity, mortality, prolonged hospital stays, and a higher risk of AKI. Studies have shown a link between fluid overload and adverse outcomes in critically ill patients with conditions like acute respiratory distress syndrome, acute lung injury, sepsis, and AKI (Patil & Salunke, 2020).

Nursing Actions:

Assess Level of Consciousness: Monitor for changes in mentation, restlessness, or confusion, which may indicate fluid shifts, toxin accumulation, acidosis, electrolyte imbalances, or hypoxia. In older adults, subtle mental status changes can be an early sign of prerenal or normotensive ischemic AKI. Suspect insensible fluid losses in older, comatose, or sedated patients with restricted fluid access (Workeneh & Batuman, 2022).
Evaluate Edema: Assess skin, face, and dependent areas for edema, grading its severity from +1 to +4. Edema typically occurs in dependent tissues (hands, feet, lumbosacral area). Patients can retain up to 10 lbs (4.5 kg) of fluid before pitting edema becomes noticeable. Periorbital edema can be an early indicator due to the sensitivity of these tissues to fluid accumulation.
Monitor Vital Signs: Track heart rate (HR), blood pressure (BP), jugular venous distension (JVD), and central venous pressure (CVP). Tachycardia and hypertension can result from the kidneys’ inability to excrete urine, excessive fluid resuscitation, or changes in the renin-angiotensin system. Invasive monitoring may be necessary to assess intravascular volume, especially in patients with poor cardiac function. Even in heart failure patients with low blood pressure, volume expansion can be present, leading to poor renal perfusion and AKI (Workeneh & Batuman, 2022).
Auscultate Lung and Heart Sounds: Listen for adventitious breath sounds and extra heart sounds, which can indicate fluid overload, pulmonary edema, or heart failure. Cardiovascular examination can reveal murmurs, pericardial friction rub, increased JVD, rales, and S3 gallops (Workeneh & Batuman, 2022).
Accurate Intake and Output (I&O) Recording: Meticulously record all fluid intake and output, including “hidden” fluids like IV antibiotic additives, liquid medications, and ice chips. Measure gastrointestinal losses and estimate insensible losses (sweating, wound drainage, NG output, diarrhea). The Kidney Disease: Improving Global Outcome (KDIGO) definition of AKI includes changes in serum creatinine and urine output. Decreasing urine output may suggest urethral stricture or bladder outlet obstruction (Workeneh & Batuman, 2022).
Monitor Urine Specific Gravity: This test assesses the kidney’s ability to concentrate urine. In intrarenal failure, specific gravity is often ≤1.010, indicating impaired urine concentration. While aggressive fluid resuscitation is appropriate for prerenal AKI, in patients with acute tubular necrosis (ATN), it can lead to volume overload and respiratory distress. Urine analysis aids in differentiating prerenal azotemia (Sinert & Sugalski, 2019).
Daily Weight Monitoring: Weigh the patient daily at the same time, using the same scale and clothing. Daily weight is a sensitive indicator of fluid status. A gain of >0.5 kg/day suggests fluid retention. Overly aggressive fluid resuscitation can cause tissue congestion, hypoxia, and worsen outcomes in ICU patients and those with AKI (Fülöp et al., 2010).
Monitor Diagnostic Studies: Regularly check hemoglobin (Hgb), hematocrit (Hct), serum sodium, potassium, BUN, creatinine, and urine sodium levels.
Serial Chest X-rays: Monitor for pulmonary congestion and fluid overload.
Echocardiography: Assess cardiac function and guide fluid management.
Beverage Distribution: Distribute desired beverages throughout the day, offering variety (hot, cold, frozen) to prevent dehydration and reduce thirst without excessive fluid intake. Recommend healthier choices like black coffee or unsweetened green tea over high-potassium/phosphorus or sugary drinks (Shusterman, 2021).
Maintain Volume Homeostasis: Correct fluid overload and biochemical abnormalities to support kidney function recovery and prevent residual effects. This includes managing acidosis and hematologic abnormalities (Workeneh & Batuman, 2022).
Implement Safety Measures: Use side rails and restraints as needed for patients with CNS involvement who may be dizzy or confused. AKI and acute brain dysfunction (delirium/coma) are common in critically ill patients and associated with adverse outcomes (Siew et al., 2017).
Fluid Administration and Restriction: Administer or restrict fluids as prescribed, typically replacing output plus insensible losses. Prerenal failure is treated with volume expansion and/or vasopressors. Oliguric patients unresponsive to fluid restriction and diuretics may require dialysis. “Push/pull” therapy (IV fluids and diuretics) may be used cautiously to stimulate kidney function, but rapid fluid infusion can be dangerous in AKI (Sinert & Sugalski, 2019).
Passive Leg-Raising Maneuver (PLR): Assist with PLR or virtual fluid challenge to predict cardiac output response to volume expansion. PLR mimics a fluid challenge by shifting about 300 mL of venous blood from the lower body to the heart (Effat et al., 2021).
Sodium and Fluid Restriction: Implement sodium and fluid restrictions, especially in oliguric kidney failure, to manage toxin and fluid accumulation (Workeneh & Batuman, 2022). Oliguric patients typically need fluid restriction to 400 mL plus the previous day’s urine output unless volume depletion is evident (Bindroo et al., 2022).
Indwelling Catheter Insertion: Insert a catheter if necessary to rule out lower urinary tract obstruction and accurately monitor urine output, but be mindful of infection risks (Sinert & Sugalski, 2019).
Administer Medications: Give furosemide, vasodilators, and calcium channel blockers as prescribed.
Prepare for Dialysis: Prepare for hemodialysis, peritoneal dialysis, or continuous renal replacement therapy (CRRT) as indicated to manage volume overload, electrolyte and acid-base imbalances, and remove toxins. Dialysis type depends on hemodynamic stability. Peritoneal dialysis is less common in AKI but may be better tolerated hemodynamically than hemodialysis (Workeneh & Batuman, 2022).
Assist with Renal Replacement Therapy (RRT): Support intermittent hemodialysis, continuous venovenous hemodiafiltration, or peritoneal dialysis. Continuous RRT is more expensive and carries bleeding risks but may offer better uremia and solute control (Sinert & Sugalski, 2019).

2. Minimizing Risk of Cardiac Complications

Acute kidney injury (AKI) can significantly strain the cardiovascular system. The kidneys’ inability to eliminate excess fluid leads to fluid overload, increasing the heart’s workload and potentially decreasing cardiac output. Electrolyte imbalances from AKI can also disrupt the heart’s electrical activity and contractility.

Nursing Actions:

Monitor Blood Pressure and Heart Rate: Closely track BP and HR. Fluid volume excess, hypertension (common in renal failure), and uremia increase cardiac workload, potentially leading to cardiac failure. In ARF, cardiac failure is often reversible. Vital signs are key indicators of kidney damage and require careful attention. Increased temperature and breathing rate, along with changes in blood pressure and pulse, correlate with worsening kidney damage (Sacomboio et al., 2021).
ECG/Telemetry Monitoring: Observe ECG or telemetry for rhythm changes. Electromechanical function changes can occur due to progressing renal failure, toxin accumulation, and electrolyte imbalances. Hyperkalemia is associated with peaked T waves, widened QRS complexes, and prolonged PR intervals. Hypokalemia may show flat T waves, peaked P waves, and U waves. Prolonged QT intervals can indicate calcium deficiency.
Auscultate Heart Sounds: Listen for the development of S3 or S4 heart sounds, which can indicate heart failure. A pericardial friction rub may be the only sign of uremic pericarditis, requiring prompt intervention and possible acute dialysis (Workeneh & Batuman, 2022).
Assess Skin, Mucous Membranes, and Nail Beds: Evaluate color and capillary refill time. Pallor may indicate vasoconstriction or anemia. Cyanosis is a late sign of pulmonary congestion and/or cardiac failure. AKI can reduce RBC production, causing anemia and pallor. Fluid buildup in the lungs due to AKI can lead to respiratory distress and cyanosis due to decreased blood oxygenation.
Monitor for Hypermagnesemia Signs: Note slow pulse, hypotension, flushing, nausea, vomiting, and depressed level of consciousness. Magnesium-containing drugs like antacids can cause hypermagnesemia, worsening neuromuscular dysfunction and increasing the risk of respiratory or cardiac arrest. Use aluminum-hydroxide-based antacids instead. Hypovolemia can cause hypotension, but hypotension doesn’t always mean hypovolemia (Workeneh & Batuman, 2022).
Guaiac Stool Testing: Monitor for gastrointestinal bleeding by testing stools for blood using guaiac tests.
Assess Neuromuscular Irritability: Investigate reports of muscle cramps, finger numbness, muscle twitching, and hyperreflexia, which are neuromuscular indicators of hypocalcemia. Hypocalcemia can affect cardiac contractility and function, causing muscle spasms and cramps due to the necessity of calcium for muscle function. Severe hypocalcemia can lead to tetany.
Monitor Electrolyte Levels: Regularly monitor laboratory studies for potassium, calcium, and magnesium levels.
Promote Rest: Encourage bed rest or adequate rest, and assist with care and activities to reduce oxygen consumption and cardiac workload. Rest decreases heart rate, reducing cardiac workload and improving pumping efficiency, which can enhance cardiac output.
Encourage Relaxation and Improve Sleep Quality: Promote relaxation techniques and improve sleep quality to reduce stress hormones, which can increase heart rate and blood pressure, thereby decreasing cardiac output. Improved sleep aids in body repair and regeneration, benefiting heart health and cardiac output.
Fluid Management: Administer or restrict fluids as indicated, as cardiac output is affected by circulating volume and myocardial function. AKI patients pose complex fluid management challenges. Hypovolemia worsens AKI, and rapid fluid infusion to reverse hypovolemia can cause life-threatening fluid overload (Sinert & Sugalski, 2019).
Supplemental Oxygen: Provide supplemental oxygen if indicated to maximize oxygen availability for myocardial uptake, reducing cardiac workload and cellular hypoxia. The heart requires constant oxygen supply; supplemental oxygen helps it function more efficiently.
Administer Medications: Administer inotropic agents, calcium gluconate, aluminum hydroxide gels, insulin, sodium bicarbonate, and sodium polystyrene sulfonate as prescribed.
Prepare for Dialysis: Prepare for or assist with dialysis for persistent dysrhythmias and progressive heart failure unresponsive to other treatments. KDIGO recommends a kt/v of 3.9 per week for dialysis-dependent AKI patients on intermittent or extended RRT and an effluent volume of 20-25 mg/kg/hour for continuous renal replacement therapy (Workeneh & Batuman, 2022).
Echocardiography Preparation: Prepare the patient for echocardiography, a vital tool for guiding resuscitation in critically ill patients and assessing fluid responsiveness (Effat et al., 2021).

3. Promoting Optimal Nutritional Balance

Malnutrition is common in AKI patients and is a significant predictor of in-hospital mortality. Nutritional needs vary greatly among AKI patients and must be tailored to metabolic consequences of renal failure, underlying conditions, and effects of renal replacement therapy (RRT) (Hung et al., 2022).

Nursing Actions:

Assess Dietary Intake: Document dietary intake to identify deficiencies and needs. Uremic symptoms (nausea, anorexia), physical condition, and dietary restrictions impact food intake. Critically ill AKI patients often have multiple organ failures, complicating nutritional support (Hung et al., 2022).
Daily Weighing: Weigh patients daily. Normal catabolic loss is 0.2-0.5 kg/day. Changes >0.5 kg may indicate fluid shifts. Obesity is associated with increased AKI risk, but obese patients may paradoxically have better survival than underweight or normal-weight patients, even with RRT. BMI ≥31 kg/m² is linked to higher mortality, similar to low BMI (<22 kg/m²) (Hung et al., 2022).
Measure Energy Requirements: Determine energy needs, which depend on the underlying disease, not renal failure itself. Indirect calorimetry is recommended when available to measure energy expenditure (Hung et al., 2022). Indirect calorimetry measures gas exchange to calculate heat production and calorie needs (The Medical City, 2017).
Nutritional Assessment and Malnutrition Screening: Perform a general nutritional assessment and screen for malnutrition risk, especially appetite loss, a strong predictor. The Renal inpatient Nutritional Screening Tool (Renal iNUT) is designed for hospitalized AKI/CKD patients and shows good sensitivity and specificity. Assessment includes patient history, unintentional weight loss, physical exam, and body composition analysis (Fiaccadori et al., 2021).
Assess Body Composition: Evaluate lean body mass, muscle mass, and function. Body composition assessment is preferred over anthropometry for diagnosing and monitoring malnutrition in AKI patients. Critically ill patients experience rapid muscle loss early in ICU stay. Assess muscle function with hand-grip strength (Fiaccadori et al., 2021).
Monitor Laboratory Studies: Monitor BUN, albumin, transferrin, sodium, potassium, and phosphorus levels to assess nutritional status, guide dietary adjustments, and evaluate therapy effectiveness. Electrolyte and acid-base imbalances are major indicators for RRT and mortality in AKI (Chen et al., 2021).
Frequent Small Feedings: Provide frequent, small meals to minimize anorexia and nausea from uremia and reduced peristalsis. Trophic feeding (10-20 kcal/hour or ≤500 kcal/day) may be better tolerated initially, reducing GI intolerance and insulin use compared to full feeding in acute lung injury patients on ventilators. Start with a low-energy or full-energy diet, but initial trophic feeding can reduce GI issues (Hung et al., 2022).
Dietary Preferences: Give patients/families a list of allowed foods and involve them in menu choices to increase control and appetite. Home food may improve intake. Dietary changes are vital in AKI treatment, especially salt and fluid restriction in oliguric failure (Workeneh & Batuman, 2022).
Oral Care: Offer frequent mouth care or 10% hydrogen peroxide rinses for stomatitis. Provide gum, hard candy, and breath mints for dry mouth (xerostomia) and uremic fetor (halitosis) caused by high urea in saliva. Uremic stomatitis can cause painful oral lesions, treatable with 10% hydrogen peroxide gargles four times daily (Costantinides, 2018).
Dietitian Consultation: Consult a dietitian for individualized calorie and nutrient needs within restrictions, and to determine the best feeding route (oral supplements, enteral, or parenteral nutrition). Dietary consult is crucial for salt and fluid restriction, and to avoid high-potassium diets in renal dysfunction (Goyal et al., 2022).
Nutrient Composition: Include complex carbohydrates and fats for calories and essential amino acids. Avoid concentrated sugars. Carbohydrates provide energy and limit tissue catabolism. Carbohydrate intolerance may occur in renal failure. Essential amino acids improve nitrogen balance and aid in tubular cell repair. Standard enteral and parenteral formulas are often high in carbohydrates, which may not be ideal for kidney failure patients (Fiaccadori et al., 2021).
High-Calorie, Protein-Adjusted Diet: Provide a high-calorie, low to moderate-protein diet. Protein needs depend on AKI cause, catabolism, and treatment. Aim for sufficient protein to maintain serum albumin and immune function. Protein intake should be increased during RRT (Hung et al., 2022).
Electrolyte Balance: Maintain electrolyte balance by closely monitoring levels. Medications and decreased GFR can cause imbalances. Urine electrolyte findings, like fractional excretion of sodium (FENa), help assess renal tubule function (Workeneh & Batuman, 2022).
Electrolyte Restrictions: Restrict potassium, sodium, and phosphorus intake to prevent further renal damage, especially if dialysis is not used and during recovery (Workeneh & Batuman, 2022).
Administer Supplements: Administer iron preparations, calcium carbonate, selenium, vitamin C, and folic acid as indicated.
Enteral/Parenteral Nutrition: Provide enteral or parenteral nutrition if needed. ESPEN and ASPEN guidelines recommend starting nutrition within 24-48 hours of ICU admission for high nutritional risk AKI patients. Early enteral nutrition is linked to lower mortality compared to late initiation. Parenteral nutrition is used if enteral feeding doesn’t meet 60% of energy needs after 7-10 days (Hung et al., 2022).
Glucose Control: Maintain serum glucose between 140-180 mg/dL. AKI patients are at risk for both hyper- and hypoglycemia. Insulin resistance is common and linked to higher mortality. Hyperglycemia is a predictor of mortality. Renal impairment can predispose to hypoglycemia as insulin is metabolized by the kidneys (Fiaccadori et al., 2021).

4. Promoting Infection Control and Minimizing Risk for Infection

AKI impairs immune function, making patients immunosuppressed and increasing their risk of infection and sepsis. Sepsis is a leading cause of death in AKI patients. Systemic inflammatory response syndrome (SIRS) and counter anti-inflammatory response syndrome in AKI may lead to prolonged immunoparalysis, increasing sepsis risk (Gist & Faubel, 2020).

Nursing Actions:

Assess Skin Integrity: Check skin for excoriations from scratching, which can become infected. Look for livedo reticularis, digital ischemia, butterfly rash, and purpuras, which may suggest vasculitis. Track marks may indicate endocarditis in IV drug users (Workeneh & Batuman, 2022). Pruritus and nail atrophy are common in uremia (Alper, 2022).
Monitor Vital Signs: Monitor for fever (>100.4°F), increased pulse and respirations, indicating metabolic rate increase from inflammation. Sepsis can occur without fever. Febrile status on admission may indicate worse kidney disease prognosis (Sacomboio et al., 2021).
Monitor WBC Count: Monitor white blood cell (WBC) count with differential.
Obtain Cultures: Obtain specimens for culture and sensitivity and administer antibiotics as indicated.
Promote Hand Hygiene: Emphasize good hand washing for both patient and staff to reduce cross-contamination. Proper hand hygiene is crucial for preventing infections (Khadka & Dani, 2020).
Minimize Invasive Procedures: Avoid unnecessary invasive procedures, instrumentation, and manipulation of indwelling catheters. Use aseptic technique for IV and invasive lines. Change dressings per protocol. Monitor insertion sites for edema and purulent drainage to detect infection early and prevent sepsis. Risk factors for infection post-AKI include oliguria ≥3 days, fluid overload, invasive procedures, illness severity, and dialysis need (Gist & Faubel, 2020).
Catheter Care: Provide routine catheter care and meticulous perineal care. Keep urinary drainage systems closed and remove catheters as soon as possible to reduce bacterial colonization and UTI risk. Catheters help diagnose and treat urinary obstruction and monitor output, but routine use increases infection risk (Sinert & Sugalski, 2019).
Encourage Respiratory Exercises: Encourage deep breathing, coughing, and frequent position changes to prevent atelectasis and mobilize secretions, reducing pulmonary infection risk. Deep breathing and coughing help clear lungs of mucus and particles that can harbor infection.
Administer IV Fluids: Administer intravenous fluids as indicated. Septic AKI patients often have lower urine output, receive more fluids/diuretics, and are more likely to need fluid restriction than non-septic AKI patients. Crystalloids are preferred for resuscitation; avoid hydroxyethyl starches (HES) and hyperchloremic solutions (Godin et al., 2017).
Antimicrobial Therapy: Administer antimicrobial therapy as prescribed.
Vasopressors: Administer vasopressors as prescribed.
Avoid Nephrotoxic Medications: Avoid nephrotoxic medications and contrast agents when possible, especially in high-risk patients, to prevent further kidney damage (Godin et al., 2017).
Adequate Nutritional Support: Provide adequate nutritional support, crucial for septic AKI patients in a hypercatabolic state, requiring adjusted protein and calorie intake. Nutritional needs are individualized based on baseline characteristics, conditions, volume status, and protein loss through RRT (Godin et al., 2017).

5. Minimizing Risk for Hypovolemia

During the diuretic phase of ARF, urine output can dramatically increase to 1-3 liters daily, sometimes reaching 5 liters or more. Although the kidneys regain waste excretion ability, they cannot yet concentrate urine effectively. This massive fluid loss can lead to hypovolemia and hypotension. Patients in this phase are at risk of hyponatremia, hypokalemia, and dehydration due to significant fluid and electrolyte losses. This phase may last 1-3 weeks (American Nephrology Nurses Association, 2019).

Nursing Actions:

Accurate I&O and Daily Weight: Measure intake and output accurately, weigh daily, and calculate insensible fluid losses to estimate fluid replacement needs. Intake should balance urine, NG/wound drainage, and insensible losses. Insensible losses can cause severe hypovolemia in fluid-restricted patients, especially older, comatose, or sedated individuals (Workeneh & Batuman, 2022).
Monitor Vital Signs: Monitor blood pressure (and for postural changes), heart rate, and mean arterial pressure (MAP). Orthostatic hypotension and tachycardia suggest hypovolemia. Hypotension below a MAP threshold is linked to AKI progression. Surviving Sepsis Campaign recommends MAP ≥65 mmHg in sepsis, while some suggest ≥70 mmHg to prevent AKI and severe AKI progression (Izawa et al., 2016).
Assess Dehydration Signs: Note signs of dehydration: dry mucous membranes, thirst, dulled sensorium, peripheral vasoconstriction. In the diuretic phase, urine output >3 liters/day can occur. Extracellular fluid depletion triggers thirst, and sodium loss causes persistent thirst. Continued fluid losses without replacement lead to hypovolemia. Symptoms include thirst, decreased urine output, dizziness, and orthostatic hypotension. Older adults with vague mental status changes may have prerenal or normotensive ischemic AKI (Workeneh & Batuman, 2022).
Closely Monitor Urine Output: Measure and monitor urine output closely. Hourly urine output monitoring can improve AKI detection, as it directly reflects glomerular filtration rate (GFR) and is an early AKI biomarker (Dirkes, 2015).
Monitor Laboratory Studies: Monitor lab results. In non-oliguric ARF or the diuretic phase, large urine losses can cause sodium wasting. Elevated urinary sodium increases fluid loss osmotically. Sodium restriction may be needed. Kidney dysfunction disrupts sodium and potassium homeostasis, leading to electrolyte disorders (Gao et al., 2019).
Fluid Administration: Provide allowed fluids throughout the day to prevent oliguric phase recurrence due to inadequate intake or nocturnal dehydration. Prolonged oliguria worsens kidney function recovery prognosis. Rapid fluid infusion to reverse hypovolemia can treat AKI, but can also cause fluid overload (Sinert & Sugalski, 2019).
Environmental Temperature Control: Control room temperature and limit bed linens to reduce diaphoresis and fluid losses. Lowering environmental temperature reduces sweating by constricting skin blood vessels, part of the body’s heat retention response.
Administer IV Fluids: Administer IV fluids as indicated. AKI patients require careful fluid management. Hypovolemia exacerbates AKI. Vigorous fluid administration aims to reverse renal ischemia and dilute nephrotoxins, preventing tubular necrosis or recurrent injury (Effat et al., 2021).
Administer Vasopressors: Administer vasopressors as prescribed. Vasopressors are used with fluids for vasomotor shock and AKI risk or presence. For hypotension unresponsive to fluids, vasopressors are started aiming for MAP ≥65 mmHg (American Nephrology Nurses Association, 2019). Norepinephrine is the vasopressor of choice in septic shock (Busse & Ostermann, 2019).
Urinary Catheter Insertion: Insert a urinary catheter if indicated for early AKI workup to diagnose and treat urinary obstruction and accurately measure urine output. However, consider catheter-associated infection risks (Sinert & Sugalski, 2019).

6. Initiating Health Teachings and Patient Education

Post-AKI care is crucial as survivors face increased risks of kidney and non-kidney related complications. Under-recognition of these post-discharge risks and fragmented care are common (Silver & Siew, 2017).

Nursing Actions:

Disease Process Review: Review the disease process, prognosis, and known precipitating factors to provide a knowledge base for informed patient choices. AKI in low- and middle-income countries often occurs with acute illness, hypovolemia, and sepsis, but community-acquired AKI is under-recognized. Hospital-acquired AKI is common in ICUs, post-cardiovascular procedures, or due to nephrotoxic medications (Lewington et al., 2013).
Symptom Identification: Identify symptoms requiring medical attention: decreased urine output, sudden weight gain, edema, lethargy, bleeding, infection signs, and altered mentation. Prompt intervention can prevent serious complications or progression to chronic renal failure. Non-nephrologists often manage AKI, potentially leading to delayed recognition and suboptimal management due to unfamiliarity with risk factors and early signs (Lewington et al., 2013).
Dietary Education: Review dietary plans and restrictions, providing a fact sheet of restricted foods. Proper nutrition is essential for tissue healing; dietary adherence prevents complications. Nutritional support should be holistic due to comorbidities. Nutritional needs in AKI relate to the primary disease and comorbidities, not AKI itself. Kidney injury severity affects waste elimination and nutrient loss from dialysis. Hypovolemia-induced non-catabolic AKI is common in older and malnourished patients from dehydration, GI bleeding, heart failure, and hypoalbuminemia (Hung et al., 2022).
Medication Review: Review medication use. Advise patients to discuss all medications and herbal supplements with healthcare providers. Kidney-concentrated/excreted medications can cause toxic reactions or kidney damage. Some supplements interact with prescribed drugs and electrolytes. Drug-associated AKI mechanisms include direct nephrotoxicity (tubular, interstitial, glomerular, obstructive) and indirect nephrotoxicity (decreased renal blood flow) (Kellum & Hall, 2018).
Weight Monitoring Schedule: Establish a regular weighing schedule for monitoring fluid and dietary needs. Obesity increases AKI risk, with BMI ≥ 31 kg/m² associated with higher mortality, similar to low BMI (<22 kg/m²) (Hung et al., 2022).
Renal Function Explanation: Explain the level of renal function expected post-acute episode. Patients may have residual kidney function defects, possibly permanent. Continued nephron loss leads to hyperfiltration and eventual kidney failure, explaining progressive failure post-AKI recovery (Workeneh & Batuman, 2022).
Urine Observation: Encourage patients to observe urine characteristics, amount, and frequency. Changes may indicate renal function alterations and dialysis needs. Granular, muddy brown casts suggest acute tubular necrosis (ATN). Reddish-brown urine may indicate myoglobin or hemoglobin (Workeneh & Batuman, 2022).
Social and Emotional Support: Provide social and emotional support to patients and families to reassure them about procedures. Social support enhances medical information understanding and healthcare system navigation, improving health attitudes and behaviors (Chen et al., 2018).
Fluid Restriction Review: Review fluid restriction, emphasizing spreading fluids throughout the day and including all fluids (ice) in daily counts. Fluid management depends on ARF cause and stage. Fluids are like drugs and should be used judiciously. Accurate fluid status assessment and individual targets are crucial for better outcomes (Patil & Salunke, 2020).
Activity and Rest: Discuss activity restrictions and gradual resumption of activities. Encourage energy-saving, relaxation, and diversional techniques. Severe ARF may necessitate activity restriction and extended weakness during recovery. Higher physical activity levels are linked to improved renal function in AKI recovery (Asad et al., 2022).
Fatigue Management: Discuss the reality of continued fatigue due to decreased metabolic energy, anemia, and discomfort. Severe AKI survivors may have worse health-related quality of life, affecting both physical and mental components, especially with increased age and reduced kidney function (Workeneh & Batuman, 2022).
Dialysis and Transplant Discussion: Discuss renal dialysis or transplantation if likely future options. Reiterate information about dialysis options, KDIGO recommends kt/v of 3.9 per week for dialysis-dependent AKI on intermittent/extended RRT and effluent volume of 20-25 mg/kg/hour for CRRT (Workeneh & Batuman, 2022).
ADLs and Support Systems: Determine ADLs and personal responsibilities. Identify available resources and support systems to help manage lifestyle changes and needs. Social support improves self-management and reduces disease progression factors, positively influencing health behaviors and outcomes (Chen et al., 2018).
Activity Scheduling: Recommend scheduling activities with rest periods to prevent fatigue and conserve energy for healing and regeneration. Exercise can improve outcomes post-AKI, similar to cardiac patients (Asad, 2020).
Follow-Up Care: Stress the necessity of follow-up care and lab studies. Renal function recovery can be slow (up to 12 months), and deficits may persist, requiring therapy adjustments. Renal recovery is often seen in the first two weeks, but some patients recover later, necessitating periodic checks (Workeneh & Batuman, 2022).
Nurse Education: Be well-informed about AKI to educate patients and families effectively. Nurses play a key role in client care teams, especially in high-income countries with established care standards. In low- to middle-income countries, nursing care varies, and education may be less structured (Lewington et al., 2013).
Community Awareness: Raise community awareness about AKI as a complication of other diseases and mobilize resources for early management. WHO/UN initiatives address root causes of community diseases in developing countries, all related to AKI (Lewington et al., 2013).
Nephrologist Consultations: Arrange follow-up nephrologist consultations. Nephrologists are more skilled in managing CKD complications. Some centers have dedicated outpatient care models for AKI survivors, focusing on blood pressure, urine albumin control, lab reviews, cardiovascular risk modification, CKD management, and medication reconciliation (Silver & Siew, 2017).

7. Administering Medications and Pharmacologic Support

Medications for Acute Renal Failure (ARF) aim to treat the underlying cause, manage complications, and support kidney function recovery. Common medications include diuretics to increase urine output, electrolyte supplements to correct imbalances, blood pressure control drugs, renal vasodilators, antioxidants to minimize further kidney damage, and antibiotics for sepsis-related ARF.

Medications:

Diuretics (Furosemide, Bumetanide, Torsemide, Mannitol): Used early in the oliguric phase to convert to non-oliguric phase, flush tubules, reduce hyperkalemia, and promote urine volume. Furosemide corrects volume overload if kidneys respond, often requiring high IV doses. It does not convert oliguric AKI to non-oliguric AKI or increase urine output if the patient is not hypervolemic (Workeneh & Batuman, 2022).
Vasodilators (Fenoldopam): Selective dopamine-receptor agonist, rapid vasodilator, more potent than dopamine for renal vasodilation. Increases renal blood flow, diuresis, minimal adrenergic effects. Treats severe hypertension, including in renal compromise (Workeneh & Batuman, 2022).
Calcium Channel Blockers: Given early in nephrotoxic acute tubular necrosis (ATN) to reduce calcium influx into kidney cells, maintaining cell integrity and improving GFR. Protective in animal AKI models if given pre-insult. In humans, benefit is mainly AKI prevention in renal transplant recipients on cyclosporine (Sinert & Sugalski, 2019).
Inotropic Agents (Dopamine): Stimulates adrenergic and dopaminergic receptors. Low doses stimulate dopaminergic receptors, causing renal vasodilation and enhancing renal perfusion (Workeneh & Batuman, 2022).
Calcium Gluconate: Treats hypocalcemia and counters hyperkalemia’s cardiac effects by reducing cardiac irritability. Antagonizes neuromuscular and cardiovascular effects of magnesium (Fulop & Batuman, 2020).
Aluminum Hydroxide Gels: Phosphate-binding antacids to limit phosphate absorption from GI tract due to increased phosphate levels from glomerular filtration failure.
Glucose and/or Insulin Solution: Temporarily lowers serum potassium by shifting potassium into cells in hyperkalemia emergencies. Glucose with insulin prevents hypoglycemia (Fulop & Batuman, 2020).
Sodium Bicarbonate or Sodium Citrate: Corrects acidosis or hyperkalemia (by increasing pH) if not fluid overloaded. Increases filtered bicarbonate, causing bicarbonate diuresis (Najjar, 2022).
Sodium Polystyrene Sulfonate (with/without Sorbitol): Exchange resin to lower serum potassium by trading sodium for potassium in the GI tract. Sorbitol induces osmotic diarrhea to excrete potassium. Slow onset, second-line for hyperkalemia emergencies (Rahman & Marathi, 2022).
Iron Preparations: For iron deficiency from protein restriction, anemia, or impaired GI function. Iron supplementation can improve hemoglobin levels (Aoun et al., 2022).
Calcium Carbonate: Restores serum calcium to improve cardiac and neuromuscular function, blood clotting, and bone metabolism. Low serum calcium is often corrected as phosphate absorption decreases. Can be used as a phosphate binder (Fulop & Batuman, 2020).
Selenium, Vitamin C, Folic Acid: Vital coenzymes for cell growth and action. Intake is often reduced due to protein restrictions. May improve immunomodulation and wound healing with antioxidant properties. Replace losses during critical illness. Vitamin C dosage of 100 mg/dL suggested (Fiaccadori et al., 2021).
Antibiotics: Early antibiotics within 6 hours (ideally 1 hour) are crucial in sepsis to improve survival and prevent AKI. Delays in antibiotics in septic shock increase early AKI risk (Godin et al., 2017).
Vasopressors (Norepinephrine): Needed in septic shock to counter vasodilation and endothelial dysfunction. Norepinephrine is the preferred vasopressor in sepsis (Godin et al., 2017).

8. Monitoring Laboratory and Diagnostic Procedures

Laboratory and diagnostic procedures are essential for evaluating and managing Acute Renal Failure (ARF). Common tests include blood tests to assess kidney function (serum creatinine, BUN), electrolyte levels, and acid-base balance. Urine tests (urinalysis, urine electrolytes) provide insights into kidney function and ARF causes.

Diagnostic Procedures:

Blood Urea Nitrogen (BUN) and Creatinine (Cr): BUN assesses renal dysfunction management. Both may increase, but creatinine is a better renal function indicator as it’s less affected by hydration, diet, and catabolism. Dialysis is considered if BUN:creatinine ratio >20:1 or if therapy fails to resolve fluid overload or acidosis (Workeneh & Batuman, 2022).
Urine Sodium: In acute tubular necrosis, impaired sodium resorption leads to increased urine sodium excretion. Fractional excretion of sodium (FENa) is useful in oliguric AKI (Workeneh & Batuman, 2022).
Serum Sodium: Hyponatremia can result from fluid overload or kidney’s inability to conserve sodium. Hypernatremia indicates total body water deficit. Abnormal sodium levels are common in AKI and linked to mortality in heart failure patients (Gao et al., 2019).
Serum Potassium: Hyperkalemia is a common and serious AKI complication due to impaired renal excretion and potassium retention to excrete hydrogen ions (Sinert & Sugalski, 2019).
Hemoglobin (Hgb) and Hematocrit (Hct): Decreased values may indicate hemodilution (hypervolemia). Anemia often develops in prolonged failure from RBC loss. Postoperative anemia is a predictor of AKI and in-hospital mortality in cardiac surgery (Lombardi et al., 2021).
Calcium: Hypocalcemia is common in AKI and enhances potassium’s cardiac toxicity (Sinert & Sugalski, 2019).
Magnesium: Hypermagnesemia can occur in AKI, especially during oliguric phase. Dialysis or calcium may be needed for CNS depression (Fulop & Batuman, 2020).
Serial Chest X-rays: Detect fluid overload, pulmonary edema, and cardiac changes associated with renal and heart failure (Sinert & Sugalski, 2019).
Echocardiography: Guides resuscitation in critically ill patients and assesses fluid overload (Effat et al., 2021).
Stool Guaiac Test: Detects gastrointestinal bleeding, a renal failure complication possibly due to uremia effects on mucosa or platelet function.
WBC Count with Differential: Elevated WBCs may indicate infection or kidney injury. Leukocytosis is common in ARF. A left shift suggests infection. WBC count changes are linked to long-term kidney outcomes (Han et al., 2014).
Culture and Sensitivity: Identifies infections and organisms for targeted treatment. Dose adjustments of anti-infectives may be needed in renal impairment. Eosinophils in urine may suggest interstitial nephritis, but sensitivity is poor (Workeneh & Batuman, 2022).