Acute Interstitial Nephritis Overview

Acute Interstitial Nephritis (AIN)

• Characterized by inflammation of the renal interstitium and tubules
• Mostly due to immune-mediated response

Etiologies of AIN

• Drugs (most frequent cause)
  • Antibiotics (penicillins, cephalosporins, sulfonamides)
  • NSAIDs
  • Proton pump inhibitors
  • Diuretics (furosemide, thiazides)
• Infections
  • Bacterial (e.g., pyelonephritis)
  • Viral (CMV, HIV, hepatitis)
  • Tuberculosis
• Systemic diseases
  • Sarcoidosis
  • Sjögren's syndrome
  • Systemic lupus erythematosus (SLE)
• Idiopathic causes: Unknown or autoimmune-related triggers

Pathogenesis of AIN

• Hypersensitivity reaction leading to interstitial inflammation
• Infiltrating T cells and macrophages cause tubular damage
• Impairment of renal function

Acute Kidney Injury (AKI)

• Rapid loss of kidney function associated with tubular and interstitial injury

Underlying Mechanisms of AKI

• Ischemic injury, hypoperfusion of kidneys leading to ischemic damage in the tubular epithelium
• Nephrotoxic injury, toxic substances directly damage the renal tubular cells
• Inflammatory response, infections or systemic diseases causing damage to tubules and interstitium
• Obstruction, blockages leading to back-pressure and interstitial damage

Clinical Manifestations of Tubulointerstitial Nephritis (TIN)

• Non-specific symptoms
  • Fever
  • Rash
  • Malaise
  • Flank pain
• Renal symptoms
  • Oliguria (low urine output)
  • Hematuria
  • Proteinuria
  • Pyuria (presence of white blood cells in urine)

Diagnostic Criteria for TIN

• Laboratory findings
  • Elevated serum creatinine
  • Eosinophilia and eosinophiluria (especially drug-induced AIN)
  • Urinalysis showing WBCs, RBCs, and white cell casts
• Imaging
  • Ultrasound or CT scan may show enlarged kidneys or signs of inflammation
• Kidney biopsy
  • Infiltration of interstitial spaces with lymphocytes, eosinophils, and plasma cells, along with tubular injury

Treatment Options for TIN

• Drug-Induced AIN: Discontinuation of the offending drug, corticosteroids (prednisone)
• Infection-Related AIN: Treatment of underlying infection with appropriate antibiotics
• Autoimmune-related AIN: Immunosuppressive therapy (e.g., corticosteroids, azathioprine)
• Supportive care: Maintaining hydration, correcting electrolyte imbalances, and monitoring renal function

Renal Tubular Acidosis (RTA)

• Group of disorders characterized by defects in renal acid-base handling

Types of RTA

• Type 1 (Distal RTA): Impaired hydrogen ion secretion in the distal tubule, leading to metabolic acidosis, hypokalemia, and kidney stones
• Type 2 (Proximal RTA): Impaired bicarbonate reabsorption in the proximal tubule, results in metabolic acidosis and often occurs with other tubular dysfunctions
• Type 4 (Hyperkalemic RTA): Deficiency or resistance to aldosterone, leading to impaired potassium excretion and acidosis, often associated with diabetic nephropathy or chronic kidney disease

Inherited Tubulopathies

• Bartter Syndrome: Genetic disorder affecting the thick ascending limb of the loop of Henle leading to defective reabsorption of sodium, potassium, and chloride
• Gitelman Syndrome: Milder genetic disorder affecting the distal convoluted tubule

Symptoms of Bartter Syndrome

• Hypokalemia
• Metabolic alkalosis
• Polyuria
• Hypercalciuria

Treatment of Bartter Syndrome

• Potassium supplements
• Aldosterone antagonists (e.g., spironolactone)
• NSAIDs to reduce polyuria

Symptoms of Gitelman Syndrome

• Hypokalemia
• Hypomagnesemia
• Hypocalciuria

Treatment of Gitelman Syndrome

• Potassium and magnesium supplements
• Aldosterone antagonists to manage symptoms

This quiz covers Acute Interstitial Nephritis (AIN), detailing its causes, including drugs, infections, and systemic diseases. Understand the pathogenesis and mechanisms of Acute Kidney Injury (AKI) associated with AIN. Test your knowledge on this important renal pathology.