Acute Kidney Injury: A Clinical Guide

Written By Danial Mirza

Definition

Acute Kidney Injury (AKI) is a clinical syndrome defined by an abrupt and rapid decline in kidney function, occurring over hours to days. This deterioration leads to the accumulation of nitrogenous waste products like urea and creatinine, and the dysregulation of extracellular fluid volume, electrolytes, and acid-base balance (2, 3). The term AKI has critically replaced the older term "Acute Renal Failure" (ARF) to emphasize that the spectrum of injury is broad and that even minor degrees of renal dysfunction, well short of complete failure, have significant prognostic implications, including increased mortality and risk of future chronic kidney disease (3).

The diagnosis is formally established using the Kidney Disease: Improving Global Outcomes (KDIGO) 2012 criteria, which provide a standardized framework for identification and staging. AKI is diagnosed if any one of the following criteria is met:

  • An absolute increase in serum creatinine (sCr) by ≥26.5 µmol/L within a 48-hour period; OR

  • An increase in sCr to ≥1.5 times a known or presumed baseline level, which is known or presumed to have occurred within the prior 7 days; OR

  • A reduction in urine volume to <0.5 mL/kg/h for a duration of 6 hours or more (1).

For a houseman, understanding the nuance of a "presumed baseline" is vital, as many patients are admitted acutely without recent blood tests. In such cases, the lowest creatinine value during the hospital stay can be used retrospectively as an estimated baseline, or clinical judgement must be applied. It is also crucial to recognise the limitations of these markers: serum creatinine levels lag behind the actual fall in GFR by 24-48 hours and can be influenced by factors like muscle mass, age, and sex. Similarly, urine output can be a sensitive early marker but is difficult to measure accurately in non-catheterized patients (3).

Epidemiology

In Malaysia, AKI represents a major public health challenge. The landmark Malaysian AKI (My-AKI) study, a prospective multicenter analysis, revealed an overall incidence of 7.18% among hospitalized adults, confirming AKI as a common and serious complication in our wards (12). The burden is disproportionately concentrated in critically ill patients, with sepsis standing out as the predominant cause, accounting for a staggering 41.7% of all cases (12, 13). This is frequently driven by common infections like pneumonia and diabetic foot ulcers. Furthermore, Malaysia's tropical climate contributes a unique etiological profile, with infections like dengue fever (7.1%), leptospirosis, and melioidosis being significant triggers for AKI (13).

The typical Malaysian patient developing AKI is a male (60.2%) with a mean age of 57.8 years, who carries a heavy burden of pre-existing non-communicable diseases. Hypertension (55.0%) and diabetes mellitus (46.6%) are the most common comorbidities, a direct reflection of their high prevalence in the general population (12). This creates a "perfect storm" scenario where a patient with underlying diabetic or hypertensive nephropathy suffers a "second hit" from a septic insult, leading to a precipitous decline in renal function. Globally, AKI affects up to 1 in 5 hospitalized adults and is a major driver of morbidity, mortality, and healthcare costs, with particularly poor outcomes in low- and middle-income countries where access to diagnostics and renal replacement therapy may be limited (3).

Pathophysiology

The pathophysiology of AKI is traditionally and most usefully classified into three categories based on the anatomical location of the primary insult: prerenal, intrinsic, and postrenal. This framework is the cornerstone of the diagnostic workup.

  • Prerenal AKI stems from reduced renal blood flow (hypoperfusion) without initial structural damage. The kidneys, which receive 25% of cardiac output, are exquisitely sensitive to any drop in perfusion. This can be due to true volume depletion (e.g., hemorrhage, gastroenteritis) or a decrease in "effective circulating volume," where total body fluid is normal or high but organ perfusion is low (e.g., the systemic vasodilation of sepsis, cardiogenic shock, or the third-spacing of fluid in pancreatitis) (6). In response, the kidney activates powerful compensatory neurohormonal mechanisms, including the sympathetic nervous system and the Renin-Angiotensin-Aldosterone System (RAAS). Angiotensin II preferentially constricts the efferent arteriole while local prostaglandins dilate the afferent arteriole, a crucial pairing to maintain pressure within the glomerulus. This delicate balance is easily disrupted by common drugs; NSAIDs block afferent dilation and ACE inhibitors block efferent constriction, which can precipitate a sharp fall in GFR in a vulnerable, dehydrated patient (6).

  • Intrinsic AKI involves direct, structural damage to the kidney parenchyma. The most common form is Acute Tubular Necrosis (ATN), which accounts for the majority of intrinsic cases. ATN is caused either by prolonged ischemia (e.g., septic shock) where hypoperfusion overwhelms compensatory mechanisms, or by direct nephrotoxicity. Exogenous toxins include drugs like aminoglycosides and amphotericin B, and iodinated contrast media. Endogenous toxins include myoglobin released during rhabdomyolysis, which causes direct tubular injury and cast formation, and light chains in multiple myeloma (7). Other intrinsic causes include Acute Interstitial Nephritis (AIN), an allergic inflammatory reaction in the interstitium most commonly triggered by drugs (penicillins, PPIs, NSAIDs), and Acute Glomerulonephritis (GN), an immune-mediated inflammation of the glomeruli, often presenting as part of a systemic disease like lupus or ANCA-associated vasculitis (1).

  • Postrenal AKI results from a physical obstruction to urine flow. For creatinine to rise significantly, the obstruction must be bilateral, affect a solitary functioning kidney, or occur at the level of the bladder outlet or urethra (e.g., in benign prostatic hyperplasia). The blockage causes pressure to build up in the urinary tract, which is transmitted back to the Bowman's space, directly opposing the force of glomerular filtration and causing GFR to plummet (2). If not relieved promptly, this sustained pressure and resultant ischemia lead to irreversible tubular atrophy and interstitial fibrosis, transitioning a reversible problem into permanent kidney damage.

Clinical Presentation

The initial presentation of AKI is often clinically silent, with the only evidence being a rising serum creatinine or falling urine output on a chart. When symptoms and signs do manifest, they are frequently non-specific and can be attributed either to the underlying precipitating illness or to the consequences of uremia.

  • Diagnostic Clues: The presence of muddy brown granular casts in urine microscopy is pathognomonic for ATN, representing sloughed, dead tubular cells. Red blood cell casts are pathognomonic for glomerulonephritis, as they confirm that red cells have passed through a damaged glomerulus to enter the tubule (1). A clinical history of alternating periods of oliguria and polyuria is highly suggestive of a partial or intermittent urinary tract obstruction (38).

  • Common Symptoms (>50%): Reduced urine output (oliguria) is a cardinal sign, though it is crucial to remember that a significant number of patients have non-oliguric AKI, where urine output remains normal (7). Symptoms of fluid overload are very common and include pitting peripheral edema, shortness of breath on exertion (progressing to orthopnea and paroxysmal nocturnal dyspnea), and bibasal crackles on auscultation, all signs of developing pulmonary edema (34).

  • Less Common Symptoms (10-50%): As uremia worsens, patients develop systemic symptoms including persistent fatigue, loss of appetite (anorexia), a metallic taste in the mouth, nausea, and vomiting. Pruritus (itching) due to the deposition of uremic toxins in the skin is also common (2).

  • ⚠️ Red Flag Signs & Symptoms: Sudden anuria (complete cessation of urine) is a medical emergency suggesting a catastrophic vascular event (e.g., bilateral renal artery occlusion), complete urinary tract obstruction, or a rapidly progressive glomerulonephritis. Hemoptysis (coughing up blood) combined with AKI is a classic sign of pulmonary-renal syndromes like Goodpasture's or ANCA-associated vasculitis and requires immediate specialist consultation. Neurological signs such as confusion, drowsiness, asterixis (a "flapping tremor"), or seizures indicate severe uremic encephalopathy and are an absolute indication for urgent dialysis (2, 38).

Complications

The failure of kidney function leads to a cascade of life-threatening systemic complications.

  • Cardiovascular: Hyperkalemia is the most immediate life-threatening complication due to its effect on cardiac membrane potential, leading to arrhythmias and cardiac arrest. Fluid overload causes hypertension and pulmonary edema. Uremic pericarditis, an inflammation of the pericardial sac, can present with chest pain and a friction rub on auscultation and is an absolute indication for dialysis (41).

  • Metabolic: High anion gap metabolic acidosis occurs because the failing kidneys cannot excrete metabolic acids (like sulfates and phosphates) or regenerate bicarbonate. Other common electrolyte disturbances include hyponatremia (due to fluid overload), hyperphosphatemia, and hypocalcemia (43).

  • Neurological: Uremic encephalopathy results from the accumulation of neurotoxins, causing a spectrum of dysfunction from mild confusion and concentration difficulties to asterixis, seizures, and coma (2).

  • Hematological: Anemia is common and multifactorial, caused by decreased erythropoietin production, shortened red cell survival, and bleeding diathesis from uremia-induced platelet dysfunction (39).

  • Gastrointestinal: Nausea, vomiting, and anorexia are driven by high levels of uremic toxins, contributing to malnutrition and catabolism (2).

Prognosis

The prognosis of AKI in Malaysia is sobering and extends far beyond the hospital admission. The My-AKI study reported a significant in-hospital mortality rate of 16.4% (12). However, the long-term outlook for survivors is even more concerning. The post-discharge mortality rate is a staggering 30.2% at a mean follow-up of just 13.7 months, highlighting that an episode of AKI is a sentinel event that heralds a period of extreme vulnerability (12).

This high mortality is driven by the incomplete recovery of kidney function and an increased risk of cardiovascular events. In the My-AKI cohort, 16.4% of survivors had only partial renal recovery and 8.9% had no recovery at all at discharge (12). This AKI-to-CKD transition places them on a trajectory towards end-stage kidney disease and the need for chronic dialysis. The houseman's role at discharge is therefore a critical intervention point. A comprehensive discharge summary, clear patient education about the risks, and a scheduled follow-up are not administrative tasks but essential measures to mitigate this grim long-term prognosis.

Differential Diagnosis

  • Prerenal Azotemia: This is the most common differential and often the precursor to intrinsic AKI. It is considered in any patient with a history of volume loss (e.g., vomiting, diarrhea) or decreased effective circulating volume (e.g., heart failure). It is distinguished by a rapid improvement in urine output and creatinine following a fluid challenge, and by laboratory findings indicating intact tubular function: a bland urine sediment, a high urine osmolality (>500 mOsm/kg), and a low fractional excretion of sodium (FeNa <1%) (39).

  • Acute Tubular Necrosis (ATN): This should be suspected in any patient with a history of prolonged hypotension (ischemia) or exposure to nephrotoxins. The key distinguishing feature is the presence of muddy brown granular casts on urine microscopy (the action), which confirms tubular cell death and sloughing (the rationale). The tubules are damaged and cannot concentrate urine or conserve sodium, leading to a low urine osmolality and a high FeNa (>2%) (1).

  • Acute Interstitial Nephritis (AIN): Consider this in a patient with unexplained AKI who was recently started on a new drug, especially antibiotics or proton pump inhibitors. While the classic triad of fever, rash, and eosinophilia is present in only a minority of cases, the presence of white blood cell casts and eosinophils in the urine is highly suggestive, pointing to an inflammatory infiltrate in the kidney interstitium. Sterile pyuria (white cells in the urine without bacterial growth) is another important clue (39).

  • Acute Glomerulonephritis: This is a key differential when the urinalysis shows significant hematuria and proteinuria. The presence of dysmorphic red blood cells and red blood cell casts is the critical finding that localizes the bleeding to the glomerulus. This indicates an inflammatory process that requires a specific immunological workup (e.g., ANCA, anti-GBM, complement levels) and often urgent immunosuppressive therapy (1).

  • Urinary Tract Obstruction: This must be ruled out in every patient with AKI, particularly older men with prostatism or any patient with a pelvic malignancy. It is suspected with symptoms like flank pain, anuria, or urinary hesitancy. The diagnosis is confirmed by demonstrating hydronephrosis on a renal ultrasound, which visualizes the dilated collecting system caused by the blockage and necessitates an urgent urology consultation (39).

Investigations

Immediate & Bedside Tests

  • Venous/Arterial Blood Gas: This is mandatory to immediately assess for severe metabolic acidosis and hyperkalemia (the action), which are the most urgent life-threatening metabolic derangements in AKI that require immediate correction (the rationale) (43).

  • Electrocardiogram (ECG): An urgent ECG is essential to screen for the cardiotoxic effects of hyperkalemia (the action). The progression of ECG changes—from peaked T-waves to PR prolongation, QRS widening, and ultimately a sine wave pattern—signals impending cardiac arrest and dictates the urgency of treatment (the rationale) (38).

  • Urine Dipstick: This simple, inexpensive test is crucial for detecting hematuria and proteinuria (the action). Their presence is a major red flag that points away from a simple prerenal cause or ATN and towards an intrinsic glomerular disease that requires a different diagnostic and therapeutic pathway (the rationale) (41).

Diagnostic Workup

  • First-Line Investigations: A Renal Profile (Urea, Sodium, Potassium, Creatinine) is the fundamental blood test to confirm and stage the diagnosis and quantify the severity of electrolyte disturbances (2). A Renal Tract Ultrasound is the most important initial imaging modality. Its primary role is to rapidly rule out postrenal obstruction (the action) by visualizing hydronephrosis, which would necessitate urgent urological intervention (the rationale). It also provides valuable information on kidney size and echogenicity, which helps differentiate acute from chronic disease (small, shrunken kidneys suggest pre-existing CKD) (39).

  • Gold Standard: A Kidney Biopsy is the definitive gold standard for diagnosing an unknown cause of intrinsic AKI. It is an invasive procedure reserved for cases where non-invasive tests are inconclusive and a specific histological diagnosis (e.g., a rapidly progressive glomerulonephritis vs. AIN) would fundamentally alter management, for instance, by mandating the use of steroids or other immunosuppressive agents (2).

Monitoring & Staging

  • Urine Microscopy: A formal microscopic examination of the centrifuged urine sediment is performed to identify casts, cells, and crystals (the action). This provides a "liquid biopsy" that can definitively pinpoint the etiology as ATN (muddy brown casts), GN (RBC casts), or AIN (WBC casts, eosinophils), thus guiding further management (the rationale) (1).

  • Fractional Excretion of Sodium (FeNa): This calculated index is used to differentiate prerenal states from ATN. A FeNa <1% suggests the tubules are intact and avidly reabsorbing sodium in response to hypoperfusion, whereas a FeNa >2% indicates damaged tubules are unable to conserve sodium. It is important to note that FeNa is unreliable in patients who have recently received diuretics. In such cases, the Fractional Excretion of Urea (FeUrea) is a more useful alternative (38).

Management

Management Principles

The management of AKI is dynamic and revolves around three core tenets: treating the underlying cause, providing meticulous supportive care to prevent and manage complications, and recognizing the clear indications for escalation to renal replacement therapy.

Acute Stabilisation (The First Hour)

  • Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action). This is crucial not only for systemic oxygenation but also to prevent tissue hypoxia that can exacerbate renal ischemic injury in the already vulnerable kidney (the rationale) (51).

  • Circulation: For hypovolemic or septic patients, the immediate priority is restoring perfusion. Secure two large-bore IV cannulas and administer a stat fluid challenge of an isotonic crystalloid (e.g., Normal Saline or a balanced solution like Ringer's Lactate) at 20-30mL/kg over 30-60 minutes (the action). The response—an increase in urine output and improvement in heart rate and blood pressure—must be assessed promptly to guide further fluid therapy (the rationale). In patients with persistent hypotension despite adequate fluid resuscitation (vasodilatory shock), start vasopressors like noradrenaline to maintain a mean arterial pressure >65 mmHg (50).

  • Disability/Exposure: Perform a thorough and immediate medication review. Stop all potentially nephrotoxic drugs (e.g., NSAIDs, ACE inhibitors/ARBs, aminoglycosides, certain diuretics) to prevent further iatrogenic injury. This simple act is one of the most critical interventions a houseman can perform (1).

Definitive Therapy

  • First-Line Treatment: The primary treatment is always to correct the underlying cause. This means administering appropriate antibiotics within the first hour for sepsis (as per the National Antibiotic Guideline), arranging for urgent surgical or radiological relief of a urinary obstruction, or optimizing therapy for the primary cardiac or liver disease driving the AKI (9).

  • Second-Line/Escalation: For severe AKI with life-threatening complications that are refractory to medical management, the definitive therapy is Renal Replacement Therapy (RRT). The indications are classically remembered by the mnemonic AEIOU: Acidosis (severe, refractory), Electrolytes (severe, refractory hyperkalemia), Intoxications (certain dialyzable toxins like lithium or methanol), Overload (refractory pulmonary edema), and Uremia (symptomatic, e.g., pericarditis or encephalopathy) (2).

Supportive & Symptomatic Care

  • Fluid Management: Meticulous fluid balance is paramount. In fluid-overloaded patients, restrict daily fluid intake and administer loop diuretics like IV Furosemide to promote salt and water excretion. A lack of response to diuretics is a strong indicator for RRT (1).

  • Hyperkalemia Management: The emergency treatment of hyperkalemia is a stepwise process based on the 2024 Malaysian Consensus guidelines. First, stabilize the cardiac membrane with IV Calcium Gluconate 10% 10mL. Second, shift potassium into cells using IV insulin/dextrose and/or nebulized salbutamol. Third, remove potassium from the body with diuretics, potassium-binding resins, or definitive removal with dialysis (44).

  • Nutrition: Ensure adequate caloric intake (25-30 kcal/kg/day) to prevent catabolism, which worsens azotemia. Protein intake should be adjusted based on the stage of AKI and whether the patient is on dialysis (9).

Key Nursing & Monitoring Instructions

  • Strict hourly input/output chart monitoring for all critically ill or unstable patients.

  • Daily weights, performed at the same time each day with the same scale, to objectively assess net fluid balance.

  • Hourly vital signs and neurological observations (GCS, pupil checks) for the first 6 hours in unwell patients.

  • Inform the medical officer immediately if systolic BP drops below 90 mmHg, urine output is <0.5mL/kg/hr for more than 2 consecutive hours, or the patient develops any new confusion, shortness of breath, or chest pain.

Long-Term Plan & Patient Education

The discharge plan is a critical intervention to reduce the high post-AKI mortality. The houseman must educate the patient and family about what AKI is, the increased risk of future kidney problems, and the importance of follow-up. Provide clear instructions on "sick day rules": to temporarily stop taking certain medications (like ACE inhibitors, ARBs, and diuretics) during episodes of vomiting, diarrhea, or fever. Ensure all medications are reconciled, nephrotoxins remain discontinued, and a clear follow-up appointment is arranged with a primary care physician or nephrology clinic, typically within 1-2 weeks, to monitor renal function and blood pressure.

When to Escalate

Call Your Senior (MO/Specialist) if:

  • The patient develops any life-threatening complication (e.g., severe hyperkalemia [K+ >6.5] with ECG changes, severe metabolic acidosis [pH <7.15], or respiratory distress from pulmonary edema).

  • The patient becomes oliguric or anuric and does not respond to an initial fluid challenge.

  • The cause of the AKI remains unclear after initial investigations, especially if there are features of glomerulonephritis or vasculitis.

  • The patient meets any of the "AEIOU" criteria for initiating renal replacement therapy.

Referral Criteria

  • Refer to the Nephrology team for any patient with AKI Stage 3, AKI of unknown etiology, complications refractory to medical management, or suspected glomerulonephritis/vasculitis requiring a kidney biopsy (17).

  • Refer to the Urology team urgently for any patient with confirmed obstructive uropathy on ultrasound, as they may require catheterization, nephrostomy, or stenting (39).

References

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Danial Mirza
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