10.5 · Glomerular disorders

Glomerulonephritis

Inflammation of the glomerulus

Glomerulonephritis risk factors

Hypertension, immunologic responses, infection, and diabetes mellitus

Type II hypersensitivity glomerular injury

Antibody reacting against antigen within the glomerulus, for example Goodpasture syndrome

Type III hypersensitivity glomerular injury

Deposition of circulating antibody-antigen complexes into the glomerulus, for example post-streptococcal glomerulonephritis

Mechanism of glomerulonephritis damage

Immune activation damages glomerular cells, increasing glomerular permeability and allowing proteins and RBCs to escape into the filtrate

Result of increased glomerular permeability

Proteinuria and/or hematuria

Nephritic syndrome

Sudden excretion of blood cells and protein, diminished GFR, and oliguria

Cause of nephritic syndrome

Inflammation with leukocyte invasion and swelling that blocks the glomerular capillary lumen and damages the capillary wall, typically postinfectious glomerulonephritis

Nephrotic syndrome

Massive proteinuria and lipiduria but no RBCs, with hypoalbuminemia, edema, and hyperlipidemia

Hallmark manifestation of nephrotic syndrome

Edema

Cause of nephrotic syndrome

Increased glomerular permeability from blood vessel damage, for example diabetes mellitus or SLE

Additional risks in nephrotic syndrome

Thrombotic complications and increased risk of infection