Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (529 page)

   Immune complex–mediated diseases (typically show hypocomplementemia): for example, IgA nephropathy, systemic lupus erythematosus (SLE), acute postinfectious GN, membranoproliferative GN

Cell Mediated

   Examples include Wegener granulomatosis, polyarteritis.

Infectious

   Acute poststreptococcal (group A beta-hemolytic GN)

   Non-poststreptococcal: bacterial (e.g., infective endocarditis, bacteremia), viral (e.g., HBV, HCV, CMV infections), parasitic (e.g., trichinosis, toxoplasmosis, malaria), or fungal

Noninfectious

   Multisystem (e.g., SLE, Henoch-Schönlein purpura, Goodpasture syndrome, Alport syndrome)

   Primary glomerular disease (e.g., IgA nephropathy, membranoproliferative GN)

Hypocomplementemic

   Intrinsic renal diseases (especially poststreptococcal, membranoproliferative GN)

   Systemic (e.g., SLE, cryoglobulinemia)

Normocomplementemic

   Intrinsic renal diseases (e.g., IgA nephropathy, idiopathic rapidly progressive GN)

   Systemic (e.g., polyarteritis nodosa, Wegener granulomatosis)

   See Table
12-4
.

TABLE 12–4. Serum Complement in Acute Nephritis

   Various Clinical Courses of GN