Nephritic syndrome indicates glomerular Inflammation.

Aetiology

• Poststreptococcal glomerulonephritis
• IgA nephropathy (Berger disease)
• Goodpasture syndrome (anti-GBM disease)
• alports
• HSP
• HUS
• Lupus nephritis
• Small vessel vasculitis
• Rapidly progressive glomerulonephritis (RPGN)

Pathophysiology

inflammation → cytokine release → glomerular cap damage → porous glomerular basement membrane → leakage of proteins and RBCs and inflammatory infiltrates reduces fluid movement across the membrane

Clinical Features

• Proteinuria (< 3.5 g/24h): leakage of proteins
• Haematuria: leakage of RBCs--> Intermittent gross haematuria (red or brown urine, i.e., cola-coloured urine)
• Oliguria: inflammatory infiltrates reduce fluid movement across the membrane ( ↓ GFR)
• Azotemia (An increase in the level of nitrogenous waste): inflammation prevents sufficient filtering and excretion of urea
• Salt retention → hypertension and Edema. The mechanisms that induce salt retention in nephritic syndrome are not clear

Investigation Findings

• Urinalysis: nephritic sediment
  • Haematuria (either microhematuria or intermittent macrohematuria)
  • Acanthocytes (a type of irregular red blood cell)
  • Red blood cell casts: RBC casts form through the congregation of proteins and RBCs inside the tubules.
  • Mild to moderate proteinuria of > 150 mg/24 h but < 3.5 g/24 h
  • Sterile pyuria and sometimes WBC casts
• Blood tests
  • ↑ Creatinine, ↓ GFR
  • Azotemia (increased ↑ BUN)

Other tests for specific aetiologies

• Poststreptococcal glomerulonephritis
  • Positive antistreptococcal antibodies (ASO, ADB)
  • ↓ Serum C3 complement levels (due to consumption)