ACUTE GLOMERULONEPHRITIS (GN)

Historically called the “nephritic syndrome.” Characterized by development, over days, of azotemia, hypertension, edema, hematuria, proteinuria, and sometimes oliguria. Salt and water retention are due to reduced glomerular filtration rate (GFR) and may result in circulatory congestion. Red blood cell (RBC) casts on urinalysis confirm diagnosis. Proteinuria is usually <3 g/d. Most forms of acute GN are mediated by humoral immune mechanisms. Clinical course depends on underlying lesion (Table 145-1).

TABLE 145-1: Causes of Acute Glomerulonephritis
Infectious diseases Poststreptococcal glomerulonephritis^a Nonstreptococcal postinfectious glomerulonephritis Bacterial: infective endocarditis, “shunt nephritis,” sepsis, pneumococcal pneumonia, typhoid fever, secondary syphilis, meningococcemia Viral: hepatitis B, infectious mononucleosis, mumps, measles, varicella, vaccinia, echovirus, and coxsackievirus Parasitic: malaria, toxoplasmosis IgA dominant postinfectious glomerulonephritis—usually poststaphylococcal Multisystem diseases: SLE, vasculitis, Henoch-Schönlein purpura, Goodpasture’s syndrome Primary glomerular diseases: mesangiocapillary glomerulonephritis, Berger’s disease (IgA nephropathy), “pure” mesangial proliferative glomerulonephritis Miscellaneous: Guillain-Barré syndrome, irradiation of Wilms’ tumor, self-administered diphtheria-pertussis-tetanus vaccine, serum sickness

^aMost common cause.

Source: Glassock RJ, Brenner BM: Harrison’s Principles of Internal Medicine, 13th ed, 1995.

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