Acute glomerulonephritis refers to a specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium. Hippocrates originally described the manifestation of back pain and hematuria, which lead to oliguria or anuria. With the development of the microscope, Langhans was later able to describe these pathophysiologic glomerular changes.
Most original research focuses on the poststreptococcal patient. Acute glomerulonephritis is defined as the sudden onset of hematuria, proteinuria, and red blood cell casts. This clinical picture is often accompanied by hypertension, edema, and impaired renal function. As will be discussed, acute glomerulonephritis can be due to a primary renal or systemic disease.
This article addresses the aspects of glomerulonephritis relevant to emergency physicians during its acute management.
Glomerular lesions in acute glomerulonephritis are the result of glomerular deposition or in situ formation of immune complexes. On gross appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocyte. Immunofluorescence reveals deposition of immunoglobulins and complement.
With the exception of poststreptococcal glomerulonephritis, the exact triggers for the formation of the immune complexes are unclear. In streptococcal infection, involvement of derivatives of streptococcal proteins has been reported. A streptococcal neuraminidase may alter host immunoglobulin G (IgG). IgG combines with host antibodies. IgG/anti-IgG immune complexes are formed and then collect in the glomeruli. In addition, elevations of antibody titers to other antigens, such as antistreptolysin O or antihyaluronidase, DNAase-B, and streptokinase, provide evidence of a recent streptococcal infection.
Glomerulonephritis represents 10-15% of glomerular diseases. Variable incidence has been reported due in part to the subclinical nature of the disease in more than one half the affected population. Despite sporadic outbreaks, incidence of poststreptococcal glomerulonephritis has fallen over the last few decades. Factors responsible for this decline may include better health care delivery and improved socioeconomic conditions.
With some exceptions, a reduction in the incidence of poststreptococcal glomerulonephritis has occurred in most western countries. It remains much more common in regions such as Africa, the Caribbean, India, Pakistan, Malaysia, Papua New Guinea, and South America. In Port Harcourt, Nigeria, the incidence of acute glomerulonephritis in children aged 3-16 years was 15.5 cases per year, with a male-to-female ratio of 1.1:1; the current incidence has not changed much over the past 14 years.1
Immunoglobulin A (IgA) nephropathy glomerulonephritis (ie, Berger disease) is the most common cause of glomerulonephritis worldwide.
Most epidemic cases follow a course ending in complete patient recovery (as many as 100%).
Sporadic cases of acute nephritis often progress to a chronic form. This progression occurs in as many as 30% of adult patients and 10% of pediatric patients.
Glomerulonephritis is the most common cause of chronic renal failure (25%).
The mortality rate of acute glomerulonephritis in the most commonly affected age group, pediatric patients, has been reported at 0-7%.
A male-to-female ratio of 2:1 has been reported.
Most cases occur in patients aged 5-15 years.
Only 10% occur in patients older than 40 years.
Acute nephritis may occur at any age, including infancy.
A thorough history should focus on the identification of an underlying systemic disease (if any) or recent infection.
Most often, the...
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