Acute Kidney Injury

Overview

Acute Kidney Injury (AKI) is a sudden, typically reversible decline in renal function that develops over hours to days and results in the accumulation of nitrogenous waste products, dysregulation of fluid and electrolyte balance, and impaired acid-base homeostasis. AKI has largely replaced the older term “acute renal failure” in clinical and educational literature, reflecting recognition that clinically significant kidney impairment occurs across a continuum of severity — not only at end-stage functional loss.

AKI is one of the most common and serious complications encountered in hospitalized patients. According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, AKI affects approximately 10–15% of all hospitalized adults and up to 50% of patients admitted to the intensive care unit (ICU). It is independently associated with increased morbidity, prolonged hospital length of stay, progression to chronic kidney disease (CKD), and mortality. Even a modest, transient rise in serum creatinine during hospitalization significantly worsens patient outcomes.

For the BSN-prepared nurse, AKI represents a high-priority clinical judgment challenge. The nurse is uniquely positioned to identify early warning signs, initiate protective measures, collaborate with the interprofessional team, monitor for deterioration, and provide individualized patient and family education. Mastery of AKI pathophysiology, staging criteria, and nursing management is therefore an essential component of medical-surgical nursing competency and is consistently tested on the NCLEX-NG.

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Pathophysiology

The kidney performs four interrelated functions that are disrupted in AKI: filtration of metabolic waste products from the blood (glomerular filtration), regulation of fluid volume and electrolyte composition, maintenance of acid-base balance, and hormonal functions including erythropoietin production and renin release. Understanding how each category of AKI disrupts these functions provides the physiological foundation for nursing assessment and intervention.

AKI is classified into three etiological categories based on the anatomical location of the primary insult: prerenal, intrarenal (also called intrinsic renal), and postrenal. These categories are not mutually exclusive — a patient may develop intrarenal injury secondary to a prolonged prerenal insult, and postrenal obstruction can trigger secondary intrarenal damage if left unrelieved.

Prerenal AKI

Prerenal AKI is the most common form, accounting for approximately 40–70% of all cases. It results from decreased renal perfusion pressure that reduces glomerular filtration without causing direct structural damage to the nephron. Because the renal parenchyma itself is initially intact, prerenal AKI is rapidly reversible when the underlying cause is identified and corrected promptly.

The common causes of reduced renal perfusion include:

• Hypovolemia: Hemorrhage, severe dehydration, gastrointestinal losses (vomiting, diarrhea), diuretic overuse, burns, and third-spacing (e.g., pancreatitis, sepsis-related capillary leak).
• Reduced cardiac output: Heart failure, cardiogenic shock, massive pulmonary embolism, and cardiac tamponade reduce the forward flow of blood delivered to the kidneys.
• Systemic vasodilation: Sepsis and anaphylaxis produce profound vasodilation that lowers mean arterial pressure below the renal autoregulatory threshold.
• Altered renal hemodynamics: NSAIDs inhibit prostaglandin-mediated afferent arteriolar dilation; ACE inhibitors and ARBs inhibit angiotensin II–mediated efferent arteriolar constriction. Either mechanism can precipitate AKI, particularly in patients already reliant on these compensatory vascular adjustments.

In response to hypoperfusion, the kidney activates the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, resulting in sodium and water retention, increased urine osmolality, and oliguria. Urine sodium is typically low (< 20 mEq/L) and the fractional excretion of sodium (FENa) is less than 1%, reflecting intact tubular function and avid sodium reabsorption.

Intrarenal (Intrinsic) AKI

Intrarenal AKI results from direct structural damage to the kidney itself — the glomeruli, renal tubules, interstitium, or renal vasculature. The most common and clinically significant form is acute tubular necrosis (ATN), which accounts for approximately 85% of intrinsic AKI cases. ATN may result from ischemic injury (prolonged prerenal hypoperfusion), nephrotoxic injury, or both.

Key causes of intrarenal AKI include:

• Ischemic ATN: The proximal tubule and thick ascending loop of Henle are the renal segments most vulnerable to ischemia because of their high metabolic demand and poor collateral perfusion. Ischemic tubular epithelial cell death leads to sloughing of cellular debris, cast formation, tubular obstruction, and backleak of filtrate through denuded basement membranes.
• Nephrotoxic ATN: Exogenous nephrotoxins include aminoglycoside antibiotics, contrast media (particularly iodinated CT contrast in patients with pre-existing CKD or diabetes), cisplatin and other chemotherapy agents, amphotericin B, and NSAIDs. Endogenous nephrotoxins include myoglobin (released from rhabdomyolysis) and free hemoglobin (released in hemolysis).
• Acute glomerulonephritis: Immune-mediated inflammatory injury to the glomerular capillary tuft, associated with conditions such as anti-GBM disease (Goodpasture syndrome), ANCA-associated vasculitis, and IgA nephropathy.
• Acute interstitial nephritis (AIN): Inflammatory infiltration of the renal interstitium, most commonly triggered by drug hypersensitivity (penicillins, cephalosporins, sulfonamides, PPIs, NSAIDs) or infection. Classic AIN presents with the triad of fever, rash, and eosinophilia, though this triad is present in fewer than 30% of cases.
• Renal vascular injury: Renal artery thrombosis or embolism, renal vein thrombosis, thrombotic microangiopathy (HUS/TTP), and severe hypertensive crisis.

In intrinsic AKI, the FENa is typically greater than 2% because tubular damage impairs sodium reabsorption, resulting in inappropriately high urinary sodium concentrations.

Postrenal AKI

Postrenal AKI results from obstruction to urinary outflow at any level distal to the renal pelvis. Obstruction causes a rise in intratubular pressure that is transmitted retrograde to Bowman’s space, opposing glomerular filtration pressure and reducing GFR. Bilateral obstruction (or unilateral obstruction in a solitary functioning kidney) is required to cause clinically significant AKI.

Common causes of postrenal AKI include:

• Bladder outlet obstruction: Benign prostatic hyperplasia (BPH) is the most common cause in older male patients. Neurogenic bladder, urethral stricture, and anticholinergic-induced urinary retention are also frequently encountered.
• Ureteral obstruction: Nephrolithiasis, ureteral or retroperitoneal malignancy, retroperitoneal fibrosis, and iatrogenic ureteral ligation during pelvic surgery.
• Intrarenal obstruction: Cast nephropathy (e.g., myeloma kidney) and crystal nephropathy (e.g., uric acid or acyclovir crystals).

Postrenal AKI is potentially the most rapidly reversible form — prompt relief of obstruction (e.g., urethral catheterization for BPH-related retention, ureteral stenting for obstructing calculus) can restore GFR substantially. However, prolonged obstruction causes tubular atrophy and progressive irreversible damage.

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Staging and Classification

The current standard for AKI staging is the KDIGO (Kidney Disease: Improving Global Outcomes) criteria, which define AKI as any of the following:

• Serum creatinine increase of ≥ 0.3 mg/dL within 48 hours, OR
• Serum creatinine increase to ≥ 1.5 times baseline within 7 days, OR
• Urine output < 0.5 mL/kg/hour for ≥ 6 hours.

KDIGO Stage	Serum Creatinine Criteria	Urine Output Criteria
Stage 1	1.5–1.9× baseline, OR ≥ 0.3 mg/dL increase	< 0.5 mL/kg/hr for 6–12 hours
Stage 2	2.0–2.9× baseline	< 0.5 mL/kg/hr for ≥ 12 hours
Stage 3	≥ 3.0× baseline, OR ≥ 4.0 mg/dL absolute, OR initiation of renal replacement therapy	< 0.3 mL/kg/hr for ≥ 24 hours, OR anuria for ≥ 12 hours

AKI may also be described according to its urine output pattern. Oliguric AKI (urine output < 400 mL/24 hours) is associated with more severe injury and worse prognosis than non-oliguric AKI (urine output > 400 mL/24 hours). A small proportion of patients develop anuric AKI (urine output < 100 mL/24 hours), which indicates near-complete loss of filtration and typically requires renal replacement therapy.

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Clinical Presentation

The clinical presentation of AKI varies with severity, duration, and etiology. In early or mild AKI, patients may be asymptomatic, with the diagnosis established only through laboratory findings. In more severe or prolonged AKI, a constellation of systemic manifestations reflects the kidney’s failure to maintain homeostasis.

Fluid and Hemodynamic Findings

• Oliguria or anuria in most patients (though non-oliguric AKI is common with nephrotoxic ATN)
• Signs of volume overload in oliguric AKI: peripheral edema, pulmonary crackles, jugular venous distension (JVD), hypertension
• Signs of volume depletion in prerenal AKI: hypotension, tachycardia, dry mucous membranes, decreased skin turgor, orthostatic changes

Laboratory and Diagnostic Findings

• Elevated blood urea nitrogen (BUN) and serum creatinine — rising creatinine is the primary diagnostic marker; BUN rises in parallel but is less specific (elevated BUN with normal or mildly elevated creatinine and a BUN:creatinine ratio > 20:1 suggests prerenal etiology)
• Hyperkalemia — impaired potassium excretion; levels > 6.0 mEq/L carry risk of fatal dysrhythmia
• Metabolic acidosis — impaired acid excretion leads to anion gap or non-anion gap metabolic acidosis; bicarbonate is typically low
• Hyperphosphatemia and hypocalcemia — impaired phosphate excretion with reciprocal depression of calcium
• Hyponatremia — from dilution in volume-overloaded states
• Elevated uric acid and magnesium
• Urinalysis — muddy brown granular casts are pathognomonic of ATN; red cell casts indicate glomerulonephritis; white cell casts and eosinophiluria suggest interstitial nephritis; proteinuria may be present

Systemic Manifestations

Uremic syndrome develops as nitrogenous waste products accumulate, typically when GFR falls below 10–15 mL/min/1.73 m²:

• Neurological: Uremic encephalopathy (confusion, somnolence, asterixis, seizures), peripheral neuropathy
• Cardiovascular: Pericarditis (uremic pericarditis), dysrhythmias from electrolyte disturbances (particularly hyperkalemia), accelerated hypertension
• Gastrointestinal: Nausea, vomiting, anorexia, metallic taste, uremic fetor (ammonia-like breath odor), GI bleeding (from uremic platelet dysfunction)
• Hematological: Normocytic normochromic anemia (decreased erythropoietin production), prolonged bleeding time (uremic platelet dysfunction)
• Integumentary: Pruritus, uremic frost (rare, seen in severe chronic uremia)

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Nursing Assessment

Comprehensive nursing assessment is the foundation of AKI management. Because the early clinical signs of AKI are often subtle and the window for reversing prerenal injury is narrow, systematic and vigilant monitoring is essential.

History and Risk Factor Identification

The nursing history should identify established risk factors for AKI, including:

• Pre-existing CKD, diabetes mellitus, hypertension, heart failure, liver disease, and vascular disease
• Age ≥ 65 years (reduced renal reserve and diminished autoregulatory capacity)
• Recent nephrotoxin exposure: contrast dye, aminoglycosides, NSAIDs, ACE inhibitors/ARBs in the setting of hemodynamic instability, chemotherapy
• Recent surgery, trauma, burns, or sepsis
• Recent history of reduced oral intake, diarrhea, vomiting, or excessive diuresis
• Symptoms of urinary obstruction: difficulty initiating urination, incomplete emptying, urinary frequency, or sudden cessation of urine output

Fluid and Hemodynamic Assessment

• Accurate intake and output (I&O) measurement, including all sources of fluid gain and loss — IV fluids, oral intake, urine, emesis, wound drainage, insensible losses
• Daily weights (same scale, same time, same clothing) — a weight gain of 1 kg corresponds to approximately 1 L of fluid retention
• Vital signs with attention to blood pressure trends, mean arterial pressure, heart rate, and respiratory rate
• Assessment for signs of volume excess: peripheral edema, crackles on auscultation, elevated jugular venous pressure, dyspnea, decreased SpO₂
• Assessment for signs of volume depletion: hypotension, orthostatic blood pressure changes, tachycardia, flat neck veins, dry mucous membranes, decreased skin turgor, concentrated urine

Laboratory Monitoring

Trending laboratory values over time is more informative than single point-in-time values. Priority labs to monitor include:

• Serum creatinine and BUN (trend over 24–48 hours)
• Serum electrolytes: potassium, sodium, bicarbonate, phosphorus, calcium, magnesium
• Complete blood count (CBC) for anemia
• Arterial blood gas (ABG) or venous blood gas for acid-base status
• Urinalysis with microscopy
• Urine electrolytes (sodium, creatinine) for FENa calculation when etiology is unclear

Physical Assessment Priorities

• Cardiovascular: Auscultate heart sounds for pericardial friction rub (uremic pericarditis); assess peripheral pulses and capillary refill; monitor cardiac rhythm continuously for hyperkalemia-associated changes (peaked T waves, widened QRS, sine wave pattern)
• Respiratory: Auscultate lungs for crackles (pulmonary edema); assess respiratory rate and effort (Kussmaul respirations in severe metabolic acidosis)
• Neurological: Assess level of consciousness and orientation; test for asterixis (flapping tremor) by asking patient to dorsiflex wrists with arms extended — a positive sign suggests uremic encephalopathy
• Gastrointestinal: Assess for nausea, vomiting, GI bleeding; note any guaiac-positive stools
• Integumentary: Inspect skin for edema, pruritus, and uremic frost

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Nursing Interventions

Nursing management of AKI is directed toward four overarching goals: identifying and eliminating the underlying cause, restoring and maintaining hemodynamic stability, preventing and managing complications, and supporting recovery of renal function.

Fluid Management

Fluid management is highly individualized and depends on the AKI etiology, current volume status, and cardiac and pulmonary reserve.

• In prerenal AKI due to volume depletion, IV fluid resuscitation with isotonic crystalloid (typically 0.9% normal saline or balanced crystalloid such as lactated Ringer’s or PlasmaLyte) is the cornerstone of treatment. Reassess response by trending urine output, blood pressure, and serum creatinine after each fluid challenge.
• In oliguric AKI with volume overload, restrict oral and IV fluid intake; loop diuretics (furosemide) may be prescribed to promote diuresis and manage hypervolemia, though they do not alter the course of AKI or reduce mortality — their role is symptomatic management.
• Avoid fluid overload in any AKI patient: cumulative positive fluid balance is independently associated with worse outcomes, including prolonged mechanical ventilation, increased ICU days, and higher mortality.

Electrolyte and Acid-Base Management

• Hyperkalemia is the most immediately life-threatening complication of AKI. Nursing priorities include: continuous cardiac monitoring, prompt provider notification when K⁺ > 5.5 mEq/L or when ECG changes appear, preparation and administration of prescribed interventions (calcium gluconate for cardiac stabilization, sodium bicarbonate or insulin/dextrose to shift potassium intracellularly, sodium polystyrene sulfonate or patiromer to promote GI elimination, dialysis for severe or refractory hyperkalemia).
• Dietary potassium restriction is initiated and reinforced with the patient and family.
• Metabolic acidosis is managed with sodium bicarbonate supplementation when pH < 7.2 and/or bicarbonate < 15 mEq/L, pending resolution of the underlying cause or initiation of dialysis.
• Phosphate binders (calcium carbonate, sevelamer) are administered with meals to manage hyperphosphatemia. Calcium supplementation or active vitamin D analogs may be prescribed for symptomatic hypocalcemia.

Medication Management and Nephroprotective Practices

The nurse plays a central role in preventing medication-related harm to the kidneys:

• Avoid or dose-adjust nephrotoxic medications: Aminoglycosides require careful dosing (extended-interval regimens preferred), peak and trough monitoring, and duration minimization. NSAIDs should be withheld. Contrast-based imaging studies should be flagged and alternatives considered.
• Dose-adjust renally cleared medications: Many common medications — including antibiotics, antivirals, anticoagulants, and analgesics — require dose reduction or interval extension in AKI. Review the medication administration record with pharmacy and the provider to ensure appropriate renal dosing.
• Avoid volume depletion before procedures: Intravenous pre-hydration is commonly prescribed before iodinated contrast administration in high-risk patients.
• Maintain accurate medication reconciliation: Polypharmacy is a major nephrotoxin risk. Conduct thorough medication reconciliation on admission and at each transition of care.

Nutritional Support

• AKI increases catabolism, necessitating adequate protein and caloric intake to support healing.
• In non-dialyzed patients with AKI: protein intake of 0.8–1.0 g/kg/day is generally recommended; excessive protein restriction worsens outcomes and is no longer advocated.
• In patients receiving continuous renal replacement therapy (CRRT): protein needs increase to 1.5–1.7 g/kg/day due to losses during filtration.
• Collaborate with dietitian for individualized nutrition assessment and planning. Dietary restrictions commonly include potassium, phosphorus, and sodium (tailored to laboratory values and urine output).

Renal Replacement Therapy (RRT)

When AKI progresses to the point that medical management cannot control the metabolic consequences, renal replacement therapy (RRT) is initiated. Common indications (the mnemonic AEIOU is widely used):

• A — Acidosis (severe metabolic acidosis refractory to bicarbonate therapy)
• E — Electrolytes (life-threatening hyperkalemia refractory to medical management)
• I — Ingestion (toxic ingestion of dialyzable substance)
• O — Overload (volume overload refractory to diuretic therapy)
• U — Uremia (uremic encephalopathy, pericarditis, or bleeding)

RRT modalities used in AKI include:

• Intermittent hemodialysis (IHD): Most efficient solute clearance; best tolerated in hemodynamically stable patients; typically performed 3–4 times per week.
• Continuous renal replacement therapy (CRRT): Preferred in hemodynamically unstable patients (ICU setting); slower, continuous solute and fluid removal minimizes cardiovascular stress; requires continuous anticoagulation and specialized nursing monitoring.
• Peritoneal dialysis (PD): Less commonly used for AKI in adults; may be appropriate in resource-limited settings or when vascular access is unavailable.

Nursing responsibilities during RRT include: monitoring vascular access patency, assessing for catheter-related complications, maintaining anticoagulation protocols, documenting accurate fluid balance, monitoring for dialysis disequilibrium syndrome (headache, nausea, altered mental status during or after IHD), and providing patient and family education about the purpose and process of therapy.

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Complications

AKI is associated with significant local and systemic complications that the nurse must proactively monitor and manage:

• Hyperkalemia and cardiac dysrhythmia — most immediately life-threatening complication
• Pulmonary edema — from volume overload; may require emergent dialysis
• Uremic pericarditis — presents with pleuritic chest pain, pericardial friction rub, and ECG changes; risk of cardiac tamponade
• Uremic encephalopathy — confusion, asterixis, myoclonus, seizures; impairs patient’s ability to participate in care and education
• Anemia — from reduced erythropoietin and blood loss; may require packed red blood cell transfusion
• Infection — AKI patients are highly susceptible to nosocomial infections, particularly catheter-associated UTI and central line-associated bloodstream infection; meticulous aseptic technique and prompt removal of unnecessary catheters are essential
• Progression to CKD — even patients who appear to recover from AKI are at significantly elevated lifetime risk of CKD, end-stage renal disease (ESRD), and cardiovascular mortality; long-term nephrology follow-up is strongly recommended

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Patient and Family Education

Patient and family education in AKI must begin as early as the patient’s condition allows and should be ongoing throughout the hospitalization and at discharge. Key education topics include:

• Understanding the diagnosis: Explain AKI in accessible language — “the kidneys are temporarily having trouble filtering the blood” — and differentiate it from permanent kidney failure when appropriate and accurate.
• Fluid and dietary restrictions: Explain the rationale for fluid intake limits (typically 1–1.5 L/day in oliguric AKI), low-potassium diet, low-phosphorus diet, and sodium restriction. Provide written materials and involve the dietitian.
• Medication safety: Instruct the patient to inform all healthcare providers (including dentists and pharmacists) about their AKI history; avoid OTC NSAIDs and nephrotoxic supplements. Advise caution with ACE inhibitors/ARBs pending nephrology evaluation.
• Signs of recurrence or progression: Decreased urine output, weight gain of more than 2–3 lbs in a day, increased swelling, shortness of breath, confusion — seek medical attention promptly.
• Follow-up care: Emphasize the importance of nephrology and primary care follow-up, including repeat renal function testing at 3 months post-discharge. Patients with a history of AKI are at high risk for CKD and benefit from long-term renal health monitoring.
• Hydration: In the recovery phase and after discharge, maintain adequate hydration (unless contraindicated by cardiac or renal status) to support renal perfusion.

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Nursing Diagnoses and Care Planning

Priority nursing diagnoses commonly associated with AKI include:

• Excess Fluid Volume related to decreased glomerular filtration rate and impaired urinary elimination, evidenced by oliguria, edema, weight gain, and elevated BUN/creatinine.
• Risk for Electrolyte Imbalance related to impaired renal regulation of potassium, sodium, phosphorus, and bicarbonate.
• Risk for Infection related to invasive lines and catheters, immunosuppression, and uremic immune dysfunction.
• Imbalanced Nutrition: Less Than Body Requirements related to nausea, vomiting, dietary restrictions, and catabolism.
• Deficient Knowledge related to AKI diagnosis, treatment, dietary and fluid restrictions, medication safety, and follow-up care.
• Anxiety related to acute illness, potential for dialysis, and uncertainty about recovery.

Expected outcomes and nursing interventions should be individualized, measurable, and time-limited, consistent with current evidence-based practice and institutional guidelines.

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Standards Alignment Summary

This entry directly supports the following accreditation and professional standards:

• AACN Essentials (2021): Domain 1 (Knowledge for Nursing Practice), Domain 2 (Person-Centered Care), Domain 3 (Population Health), Domain 4 (Scholarship for Nursing Practice), Domain 9 (Professionalism)
• NCLEX-NG Clinical Judgment Measurement Model: Recognize Cues, Analyze Cues, Prioritize Hypotheses, Generate Solutions, Take Action, Evaluate Outcomes
• QSEN Competencies: Patient-Centered Care (PCC), Evidence-Based Practice (EBP), Safety (S), Quality Improvement (QI)
• CCNE Standards: I, II, III (program quality, curriculum, faculty and student resources)
• ACEN Standards: 3 (curriculum), 4 (faculty and staff)

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References

Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements, 2(1), 1–138. https://doi.org/10.1038/kisup.2012.1

Makris, K., & Spanou, L. (2016). Acute kidney injury: Definition, pathophysiology and clinical phenotypes. The Clinical Biochemist Reviews, 37(2), 85–98.

Ronco, C., Bellomo, R., & Kellum, J. A. (2019). Acute kidney injury. The Lancet, 394(10212), 1949–1964. https://doi.org/10.1016/S0140-6736(19)32563-2

Silbernagel, S., & Floege, J. (2021). Acute kidney injury. In Comprehensive Clinical Nephrology (6th ed., pp. 787–812). Elsevier.

American Association of Colleges of Nursing. (2021). The essentials: Core competencies for professional nursing education. AACN. https://www.aacnnursing.org/Portals/0/PDFs/Publications/Essentials-2021.pdf

National Council of State Boards of Nursing. (2023). NCLEX-RN examination: Test plan for the national council licensure examination for registered nurses. NCSBN.