Acute Glomerulonephritis Overview

Glomerulonephritis

• Membranous Glomerulonephritis: characterized by pronounced thickening of the glomerular basement membrane due to IgG immune complex deposition
• Associated disorders: systemic lupus erythematosus, Sjögren syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy
• Disease progression: slow, with possible remission, and frequent development of nephrotic syndrome symptoms

Membranoproliferative Glomerulonephritis

• Type 1: increased cellularity in the subendothelial cells of the mesangium, causing thickening of the capillary walls
• Type 2: extremely dense deposits in the glomerular basement membrane
• Laboratory findings: hematuria, proteinuria, decreased serum complement levels
• Associated with autoimmune disorders, infections, and malignancies

Chronic Glomerulonephritis

• Examination of the urine reveals: hematuria, proteinuria, glucosuria, and various casts
• Markedly decreased glomerular filtration rate, increased BUN and creatinine levels, and electrolyte imbalance

Acute Glomerulonephritis

• Sterile, inflammatory process affecting the glomerulus
• Associated with blood, protein, and casts in the urine
• Multiple types, which may change over time and become chronic

Acute Poststreptococcal Glomerulonephritis

• Caused by infection with group A streptococcus
• Symptoms: fever, edema, fatigue, hypertension
• Laboratory diagnosis: urinalysis findings include hematuria, proteinuria, oliguria, and elevated ASOT

Rapidly Progressive Glomerulonephritis (RPGN)

• Aka Crescentic Glomerulonephritis
• Accumulation of cells in Bowman's space, forming "crescents"
• Initiated by deposition of immune complexes
• Complication of another form of glomerulonephritis or immunologic disorder
• Lab results similar to acute glomerulonephritis, but becomes more abnormal as it progresses

Goodpasture's Syndrome

• Presence of antiglomerular basement membrane antibody (anti-GBM)
• Attachment of autoantibody to basement membrane, followed by complement activation, producing capillary destruction
• More likely in young males between 18-35 years old
• Rapidly progresses to renal failure, with a mortality rate of up to 50%

Wegener's Granulomatosis

• A small-vessel vasculitis
• Granuloma-producing inflammation of the small blood vessels of the kidney and respiratory system
• Laboratory diagnosis: serum antineutrophilic cytoplasmic antibody (ANCA), hematuria, proteinuria, RBC casts, elevated serum creatinine and BUN

Henoch-Schönlein Purpura

• A small-vessel vasculitis
• Vasculitis with IgA-dominant immune deposits, affecting small vessels
• Disease occurs primarily in children following upper respiratory infections
• Clinical manifestations: raised, red patches on the skin, respiratory and gastrointestinal symptoms
• Renal involvement, with complete recovery in >50% of patients

Renal Failure

• Acute Renal Failure: sudden loss of renal function, often reversible
• Primary causes: prerenal (sudden decrease in blood flow), renal (acute glomerulonephritis), postrenal (renal calculi, tumors)
• General characteristics: decreased glomerular filtration rate, oliguria, edema, and azotemia
• Telescoped urine sediment: simultaneous occurrence of elements of glomerulonephritis and nephrotic syndrome

Chronic Renal Failure

• Rate of progression varies from several months to many years
• Progression occurs in four stages:
  • Diminished renal reserve (GFR drops to 50% of normal)
  • Renal insufficiency (GFR drops from 20 to 50%, azotemia, anemia, and hypertension begin)
  • Renal failure (GFR <20%, kidneys cannot regulate volume and solute concentration)
  • End-stage renal disease