Pathogenesis (disease development)
Rapid (fast) progressive glomerulonephritis (RPGN) can be classified immunohistologically into three types:
- Type 1 (12%) is due to antibodies against the glomerular basement membrane (e.g., in anti-GBM (glomerular basement membrane) disease (synonym: Goodpasture’s syndrome)). Antibasement membrane antibodies are diagnostically groundbreaking.
- Type 2 (44%) is caused by deposition of immune complexes. This type occurs, for example, in the presence of lupus erythematosus (autoimmune disease; lupus nephritis) or other immune complex-related pathogenesis.
- Type 3 (44%) is characterized by the absence of immune complexes and antibasement membrane antibodies on immunohistology and electron microscopy.
Common to all three of the above forms of RPGN is that a large number of cases must be designated as idiopathic (disease that arose independently without an identifiable cause), because even in the presence of one of the three immunohistologic forms, there is no link between the renal disease and an etiology.
Etiology (Causes)
Biographic Causes
- Genetic burden from parents, grandparents.
Disease-related causes
- Autoimmune diseases such as systemic lupus erythematosus (SLE), vasculitides (e.g. granulomatosis with polyangiitis (GPA), formerly Wegener’s granulomatosis or microscopic polyangiitis (MPA)).
- Endocarditis (meningitis of the heart).
- Hepatitis B or C (inflammation of the liver)
- Infectious diseases, for example, caused by streptococci.
Medication
- Amoxicillin – antibiotic (drug against bacterial inflammation).
- Carbimazole – thyrostatic (drug against hyperthyroidism / hyperthyroidism).
- Penicillamine (rheumatism drug)
- Rifampicin – antibiotic (drug against bacterial inflammation).
- Warfarin – drug to inhibit blood clotting.
