acute renal failure easy notes pathophysiology, Study notes of Pathophysiology

Subject - pathophysiology. Topic - acute renal failure. course - Pharm D, B pharma, M pharma, MBBS, all medical field. Notes made by ROHIT KUMAR SINGH.

Typology: Study notes

2025/2026

Available from 06/05/2026

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ACUTE RENAL FAILURE
Acute Renal Failure (AKI) – Introduction
Acute Renal Failure (ARF), now called Acute Kidney Injury (AKI), is a sudden
and rapid decline in kidney function occurring within hours to days. It results in
decreased glomerular filtration rate (GFR), leading to accumulation of
nitrogenous waste products such as urea and creatinine (azotemia). It also
causes imbalance of fluids, electrolytes, and acid-base status. AKI is potentially
reversible if detected and treated early, but if severe or prolonged, it can
progress to chronic kidney disease or cause death.
Types of Acute Renal Failure
1. Prerenal AKI
Prerenal AKI is caused by decreased renal blood flow without structural damage
to kidneys. It accounts for most cases of AKI. Causes include dehydration,
hemorrhage, burns, shock, heart failure, and sepsis. Reduced perfusion leads to
decreased GFR. If prolonged, it may progress to intrinsic renal damage (acute
tubular necrosis).
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ACUTE RENAL FAILURE

Acute Renal Failure (AKI) – Introduction

Acute Renal Failure (ARF), now called Acute Kidney Injury (AKI), is a sudden and rapid decline in kidney function occurring within hours to days. It results in decreased glomerular filtration rate (GFR), leading to accumulation of nitrogenous waste products such as urea and creatinine (azotemia). It also causes imbalance of fluids, electrolytes, and acid-base status. AKI is potentially reversible if detected and treated early, but if severe or prolonged, it can progress to chronic kidney disease or cause death.

Types of Acute Renal Failure

  1. Prerenal AKI Prerenal AKI is caused by decreased renal blood flow without structural damage to kidneys. It accounts for most cases of AKI. Causes include dehydration, hemorrhage, burns, shock, heart failure, and sepsis. Reduced perfusion leads to decreased GFR. If prolonged, it may progress to intrinsic renal damage (acute tubular necrosis).
  1. Intrarenal (Intrinsic) AKI This occurs due to direct damage to kidney tissues such as glomeruli, tubules, interstitium, or blood vessels. The most common cause is acute tubular necrosis (ATN), usually due to ischemia or nephrotoxic drugs (e.g., aminoglycosides, contrast agents). Other causes include glomerulonephritis, acute interstitial nephritis, and vasculitis.
  2. Postrenal AKI Postrenal AKI is caused by obstruction of urine flow anywhere in the urinary tract. Common causes include kidney stones, tumors, enlarged prostate (BPH), and urethral strictures. The obstruction leads to increased pressure in kidneys, reducing GFR and causing damage.

Clinical Phases of AKI

  1. Initiation Phase
    • Begins with the initial injury (ischemia or toxin exposure)
    • Mild decrease in urine output and GFR
  2. Oliguric Phase
    • Urine output <400 mL/day
    • Accumulation of waste products (uremia)
    • Electrolyte imbalance (hyperkalemia, acidosis)
    • Fluid overload → edema, hypertension
  3. Diuretic Phase
    • Increased urine output (polyuria)
    • Loss of electrolytes and water
    • Risk of dehydration and hypokalemia
  4. Recovery Phase

Pathophysiology

  • Reduced renal perfusion or direct injury → decreased GFR
  • Tubular cell damage → impaired reabsorption and secretion
  • Backflow of filtrate due to tubular obstruction
  • Accumulation of urea, creatinine → uremia
  • Fluid retention → edema and hypertension
  • Electrolyte imbalance: o Hyperkalemia (life-threatening) o Metabolic acidosis (↓ bicarbonate)
  • Inflammatory mediators worsen kidney damage
  • Severe cases → multi-organ dysfunction

Diagnosis

  1. Clinical Diagnosis Based on sudden reduction in urine output and symptoms of fluid overload or uremia.
  2. Blood Tests
    • ↑ Serum creatinine and BUN (azotemia)
    • Electrolyte imbalance (↑ potassium, ↓ bicarbonate)
    • CBC may show infection or anemia
  3. Urine Tests
  • Urinalysis: protein, blood, casts
  • Urine sodium and osmolality help differentiate types
  1. Imaging Studies
  • Ultrasound: Detect obstruction, kidney size
  • CT scan: In selected cases
  1. Special Tests
  • Fractional excretion of sodium (FENa) to differentiate prerenal vs intrinsic AKI

Pharmacological Treatment

  1. Fluid Therapy (Most Important in Prerenal AKI)
    • IV fluids (normal saline) restore blood volume
    • Improves renal perfusion and GFR
  2. Diuretics
    • Example: Furosemide (loop diuretic)
    • Mechanism: Inhibits Na⁺-K⁺-2Cl⁻ transporter in loop of Henle → increases urine output
    • Used in fluid overload, not for prevention
  3. Management of Hyperkalemia (Emergency)
    • Calcium gluconate: stabilizes cardiac membrane
    • Insulin + glucose: shifts potassium into cells
    • Sodium bicarbonate: corrects acidosis
    • Beta-agonists: promote intracellular K⁺ shift
  4. Management of Metabolic Acidosis
  • Acidosis → bicarbonate Step 5: Stop nephrotoxic drugs Step 6: Start dialysis if severe Step 7: Monitor urine output, electrolytes, and renal function