L3 - 7 AKI

(AKI)

I. Introduction and Definitions

Acute Kidney Injury (AKI)—formerly known as Acute Renal Failure—is a clinical syndrome characterized by a rapid decline in Glomerular Filtration Rate (GFR) over hours to days.

• Key Pathophysiological Features:
• • Retention of nitrogenous wastes (Urea and Creatinine).
  • Retention of non-nitrogenous waste products.
  • Disordered electrolyte, acid-base, and fluid homeostasis.
• Reversibility: AKI is generally reversible if the underlying cause is treated promptly.
• Term Shift: The shift from "Failure" to "Injury" reflects that AKI is a process rather than an end-stage event.

II. The "Car Analogy" for AKI Classification (⭐️Important)

To understand AKI causes, think of the kidney as a car:

1. Pre-renal (The Fuel): The car needs gasoline to run. If there is no blood flow (fuel) reaching the kidney, it cannot function.
2. Renal/Intrinsic (The Engine): The car itself (the kidney tissue) must be in working order. Damage to the "engine" prevents function even if fuel is present.
3. Post-renal (The Road): The road ahead must be clear. If there is an obstruction (blockage) after the kidney, the "car" cannot move forward.

III. Clinical Phases of AKI

The progression of AKI typically follows three distinct stages:

1. Oliguric Phase

• Duration: Days to weeks.
• Urine Output: < 400 ml/day. Absolute anuria (< 50ml/day) often suggests a post-renal cause.
• Complications:
• • Hypervolemia: Edema, hypertension, and "water intoxication" (confusion/coma).
  • Hyperkalemia: The most serious complication due to failure of tubular secretion. (⭐️Important)
  • Metabolic Acidosis: Failure to excrete H+ or reabsorb HCO3.
  • Uremic Syndrome: GI symptoms (nausea, vomiting, hiccoughs), neurological signs (asterixis, fits), and systemic issues (pericarditis, bleeding).

2. Diuretic (Polyuric) Phase

• Mechanism: Occurs during recovery as tubular obstruction is relieved and tubules regenerate. However, new tubules cannot yet concentrate urine effectively.
• Manifestations: Urine output increases dramatically (3–10 L/day).
• Risks: Hypotension, dehydration, and severe electrolyte loss (Na, K, Mg).

3. Recovery Phase

• Urine volume and kidney function tests return to normal.

V. Detailed Clinical Workup .... approchسؤال امتحان

1. History and Physical Examination

• Assess for volume loss (vomiting, diarrhea, hemorrhage).
• Review medications (NSAIDs, ACE-I, Aminoglycosides).
• Check for signs of systemic illness (SLE, vasculitis).
• Evaluate volume status (JVP, skin turgor, lung crackles).

2. Laboratory Investigations (📝MCQ)

• BUN:Creatinine Ratio:
• • Pre-renal: > 20:1 (Urea is reabsorbed with water, Creatinine is not).
  • Intrinsic (ATN): < 10-15:1.
• Fractional Excretion of Sodium (FENa):
• • Pre-renal: < 1% (Kidney is conserving salt).
  • Intrinsic (ATN): > 1% (Tubules are damaged and cannot reabsorb salt).
• Urinalysis ("The Poor Man's Biopsy"):
• • Hyaline casts: Pre-renal.
  • Muddy brown/granular casts: ATN.
  • RBC casts: Glomerulonephritis (Active sediment).
  • WBC casts: Pyelonephritis or AIN.
  • Eosinophiluria: Acute Interstitial Nephritis (AIN).

3. Imaging

• Ultrasound (US): Essential to rule out obstruction (Post-renal).
• • Large/Normal kidneys: Suggest AKI.
  • Small, hyperechoic kidneys: Suggest Chronic Kidney Disease (CKD). (📝MCQ)

4. ECG Changes in Hyperkalemia (📝MCQ)

Changes occur in a sequential (sequential) order:

1. Tall, peaked T waves.
2. Prolonged PR interval.
3. Flattened P waves.
4. Widened QRS complex.
5. Sine wave pattern.
6. VF/Asystole.

VI. Management Strategies

1. Emergency Management

• Hyperkalemia: (⭐️Important)
• • Calcium gluconate: Stabilizes the cardiac membrane (does not lower K).
  • Insulin + Glucose: Shifts K into cells.
  • Resins (Sorbisterit): Removes K from the body.
• Acidosis: Sodium Bicarbonate (NaHCO3).
• Volume Overload: Diuretics or Dialysis.

2. General Measures

• Stop all nephrotoxic drugs.
• Adjust doses of renally cleared drugs.
• Maintain fluid balance (Intake = Output + 500ml insensible loss).

3. Indications for Urgent Dialysis (⭐️Important)

The decision is clinical, not just based on numbers:

• A - Acidosis: Refractory metabolic acidosis.
• E - Electrolytes: Refractory hyperkalemia.
• I - Intoxication: Certain drug overdoses.
• O - Overload: Refractory pulmonary edema.
• U - Uremia: Encephalopathy, Pericarditis, or Neuropathy.

VII. Liver and Kidney Interaction

• Hepatorenal Syndrome (HRS): Functional renal failure in advanced liver disease. Diagnosis of exclusion.
• Spontaneous Bacterial Peritonitis (SBP): Can trigger septic shock and AKI. Renal failure is the leading cause of death in SBP.
• Viral Hepatitis:
• • HCV: Associated with MPGN and Cryoglobulinemia (Purpuric rash + Low C4).
  • HBV: Associated with Membranous GN.