Chapter 4: Acute Kidney Injury

📚 CONTENT

Learning Objectives

By the end of this chapter, learners will be able to:

1.Define Acute Kidney Injury (AKI) and its diagnostic criteria.

2.Classify AKI into pre-renal, intrinsic, and post-renal causes.

3.Understand the pathophysiology of different types of AKI.

4.Outline the diagnostic approach and workup for AKI.

5.Describe the management strategies for AKI, including prevention and renal replacement therapy.

4.1 Introduction to Acute Kidney Injury

Acute Kidney Injury (AKI), formerly known as acute renal failure (ARF), is a common and serious clinical syndrome characterized by a sudden decrease in kidney function. It can range from a mild elevation in serum creatinine to severe kidney failure requiring renal replacement therapy (RRT). AKI is associated with increased morbidity and mortality in hospitalized patients.

4.2 Definition and Diagnostic Criteria

The Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline defines AKI based on changes in serum creatinine or urine output:

KDIGO AKI Staging Criteria

Stage	Serum Creatinine Criteria	Urine Output Criteria
1	Increase in SCr by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours OR Increase in SCr to 1.5-1.9 times baseline within 7 days	<0.5 mL/kg/hr for 6-12 hours
2	Increase in SCr to 2.0-2.9 times baseline within 7 days	<0.5 mL/kg/hr for ≥12 hours
3	Increase in SCr to ≥3.0 times baseline OR Increase in SCr to ≥4.0 mg/dL (≥353.6 µmol/L) OR Initiation of RRT OR, in patients <18 years, decrease in eGFR to <35 mL/min/1.73 m²	<0.3 mL/kg/hr for ≥24 hours OR Anuria for ≥12 hours

4.3 Classification of AKI

AKI is broadly classified into three main categories based on the location of the injury:

1. Pre-renal AKI (60-70% of cases)

•Cause: Decreased renal perfusion (blood flow to the kidneys) without intrinsic kidney damage.

•Pathophysiology: Reduced GFR due to inadequate blood volume (e.g., dehydration, hemorrhage), decreased effective circulating volume (e.g., heart failure, cirrhosis), or impaired renal autoregulation (e.g., NSAIDs, ACE inhibitors).

•Clinical Features: Oliguria, increased BUN/creatinine ratio (>20:1), concentrated urine (high urine osmolality, low urine sodium, FENa <1%).

2. Intrinsic Renal AKI (25-40% of cases)

•Cause: Direct damage to the kidney structures (glomeruli, tubules, interstitium, or renal vasculature).

•Subtypes:

•Acute Tubular Necrosis (ATN): Most common cause of intrinsic AKI. Caused by ischemia (prolonged pre-renal AKI) or nephrotoxins (e.g., aminoglycosides, contrast media).

•Acute Interstitial Nephritis (AIN): Inflammatory reaction in the renal interstitium, often drug-induced (e.g., penicillin, NSAIDs, PPIs) or due to infection.

•Acute Glomerulonephritis (AGN): Inflammation of the glomeruli (discussed in detail in Chapter 5).

•Vascular AKI: Conditions affecting renal arteries or veins (e.g., renal artery stenosis, renal vein thrombosis).

•Clinical Features: Variable, often associated with muddy brown granular casts (ATN), white blood cell casts (AIN), red blood cell casts (AGN), and less concentrated urine (low urine osmolality, high urine sodium, FENa >2%).

3. Post-renal AKI (5-10% of cases)

•Cause: Obstruction to urine flow anywhere from the renal pelvis to the urethra.

•Pathophysiology: Increased pressure in Bowman’s capsule opposes glomerular filtration, leading to reduced GFR.

•Common Causes: Benign prostatic hyperplasia (BPH), kidney stones, tumors, neurogenic bladder, strictures.

•Clinical Features: Anuria or oliguria, suprapubic pain, hydronephrosis on imaging. Early stages may have normal urine output.

4.4 Diagnostic Approach and Workup

1. History and Physical Examination

•History: Medications (NSAIDs, ACEIs, diuretics), recent illness (diarrhea, vomiting), pre-existing conditions (diabetes, heart failure), symptoms of obstruction.

•Physical Exam: Volume status (hypotension, orthostasis, edema), signs of systemic disease.

2. Laboratory Tests

•Serum Creatinine and BUN: Monitor trends, calculate BUN/creatinine ratio.

•Electrolytes: K+, Na+, HCO3- (to assess for hyperkalemia, hyponatremia, acidosis).

•Urinalysis: Crucial for differentiating AKI types.

•Pre-renal: High specific gravity, low urine Na+, FENa <1%, bland urine sediment.

•ATN: Isosthenuria (specific gravity ~1.010), high urine Na+, FENa >2%, muddy brown granular casts.

•AIN: White blood cells, eosinophils, white blood cell casts.

•AGN: Red blood cells, dysmorphic RBCs, red blood cell casts.

3. Imaging

•Renal Ultrasound: First-line to rule out post-renal obstruction (hydronephrosis) and assess kidney size (small, echogenic kidneys suggest CKD).

•CT/MRI: May be used for further evaluation of masses, stones, or vascular issues.

4. Renal Biopsy

•Indicated in specific cases of intrinsic AKI where the cause is unclear and potentially treatable (e.g., rapidly progressive glomerulonephritis, AIN).

4.5 Management Strategies

1. General Principles

•Identify and Treat Underlying Cause: Crucial for recovery.

•Optimize Hemodynamics: Restore adequate renal perfusion (e.g., fluid resuscitation in pre-renal AKI).

•Discontinue Nephrotoxic Agents: Avoid NSAIDs, ACEIs/ARBs (temporarily), certain antibiotics, contrast media.

•Manage Complications: Hyperkalemia, metabolic acidosis, fluid overload.

2. Fluid Management

•Fluid Resuscitation: For hypovolemic pre-renal AKI (e.g., normal saline).

•Fluid Restriction/Diuretics: For fluid overload (e.g., loop diuretics).

3. Electrolyte and Acid-Base Management

•Hyperkalemia: IV calcium gluconate (cardiac stabilization), insulin/glucose, beta-agonists (shift K+ intracellularly), diuretics, K+ binders, dialysis.

•Metabolic Acidosis: Sodium bicarbonate if severe (pH <7.1).

4. Renal Replacement Therapy (RRT)

•Indications (AEIOU mnemonic):

•Acidosis (severe, refractory metabolic acidosis)

•Electrolyte abnormalities (severe, refractory hyperkalemia)

•Intoxications (certain dialyzable toxins, e.g., lithium, salicylates)

•Overload (refractory fluid overload)

•Uremia (uremic encephalopathy, pericarditis, coagulopathy)

•Modalities: Intermittent hemodialysis (IHD), continuous renal replacement therapy (CRRT), peritoneal dialysis (PD).

5. Prevention of AKI

•Identify High-Risk Patients: Elderly, CKD, diabetes, heart failure, sepsis.

•Avoid Nephrotoxins: Judicious use of NSAIDs, contrast media, aminoglycosides.

•Optimize Volume Status: Maintain euvolemia.

•Monitor Kidney Function: Regular creatinine and urine output checks in at-risk patients.

📊 SUMMARY

Key Points on AKI

1.Definition: Acute decrease in kidney function based on KDIGO criteria (SCr or urine output).

2.Classification: Pre-renal (perfusion), Intrinsic (kidney damage), Post-renal (obstruction).

3.Pathophysiology: Varies by type; ATN is most common intrinsic cause.

4.Diagnosis: History, physical, labs (SCr, BUN, electrolytes, urinalysis), imaging (ultrasound).

5.Management: Treat cause, optimize hemodynamics, avoid nephrotoxins, manage complications, RRT if indicated.

KDIGO Staging Overview

•Stage 1: Minor SCr increase or mild oliguria.

•Stage 2: Moderate SCr increase or prolonged oliguria.

•Stage 3: Significant SCr increase, anuria, or need for RRT.

AKI Etiology Quick Guide

•Pre-renal: Dehydration, heart failure, shock.

•Intrinsic: ATN (ischemia, toxins), AIN (drugs), GN (inflammation).

•Post-renal: BPH, stones, tumors.

💎 CLINICAL PEARLS

Diagnostic Pearls

1.FENa in AKI: FENa <1% suggests pre-renal AKI; FENa >2% suggests ATN (unless diuretics are used).

2.Urine Sediment: Muddy brown granular casts are highly suggestive of ATN.

3.BUN/Creatinine Ratio: A ratio >20:1 often indicates pre-renal AKI.

Management Pearls

1.Fluid Challenge: In suspected pre-renal AKI, a fluid challenge (e.g., 250-500 mL saline over 15-30 min) can help differentiate from ATN.

2.Avoid Nephrotoxins: Always review medication list for potential nephrotoxic drugs in AKI patients.

3.Hyperkalemia Management: Prioritize cardiac stabilization with calcium gluconate in severe hyperkalemia with ECG changes.

Prevention Pearls

1.Contrast-Induced AKI: Hydration with normal saline is key for prevention in high-risk patients.

2.Sepsis and AKI: Early recognition and aggressive management of sepsis are crucial to prevent AKI.

3.AKI in CKD Patients: Patients with pre-existing CKD are at higher risk for AKI and often have worse outcomes.

Prognostic Pearls

1.AKI Recovery: Not all patients fully recover kidney function after AKI; many progress to CKD or ESRD.

2.Long-term Follow-up: Patients with AKI require long-term follow-up for monitoring of kidney function and cardiovascular risk.

3.Early Nephrology Consult: Consider early nephrology consultation for complex AKI cases, especially those requiring RRT.

🖼️ VISUAL MATERIALS

🎯 MULTIPLE CHOICE QUESTIONS

Question 1

According to KDIGO criteria, an increase in serum creatinine by ≥0.3 mg/dL within 48 hours indicates which stage of AKI?

A) Stage 1

B) Stage 2

C) Stage 3

D) Not considered AKI

Answer: A) Stage 1

Explanation: A sudden increase in serum creatinine by at least 0.3 mg/dL within 48 hours is a key criterion for KDIGO AKI Stage 1.

Question 2

Which of the following is the most common cause of intrinsic renal AKI?

A) Acute Glomerulonephritis

B) Acute Interstitial Nephritis

C) Acute Tubular Necrosis (ATN)

D) Renal artery stenosis

Answer: C) Acute Tubular Necrosis (ATN)

Explanation: ATN, often caused by ischemia or nephrotoxins, is the most frequent cause of intrinsic renal AKI.

Question 3

A patient with AKI presents with a BUN/creatinine ratio of 25:1, bland urine sediment, and a FENa of 0.5%. What is the most likely cause of their AKI?

A) Acute Tubular Necrosis

B) Acute Interstitial Nephritis

C) Pre-renal AKI

D) Post-renal obstruction

Answer: C) Pre-renal AKI

Explanation: A high BUN/creatinine ratio (>20:1), bland urine sediment, and a low FENa (<1%) are classic indicators of pre-renal AKI.

Question 4

Which of the following is a direct indication for initiating renal replacement therapy (RRT) in a patient with AKI?

A) Mild hyperkalemia (K+ 5.5 mEq/L)

B) Fluid overload responsive to diuretics

C) Uremic pericarditis

D) Serum creatinine of 3.0 mg/dL

Answer: C) Uremic pericarditis

Explanation: Uremic complications like pericarditis, encephalopathy, or severe coagulopathy are absolute indications for RRT