Glomerulonephritis (GN) encompasses a heterogeneous group of disease processes. It accounts for approximately 20% of chronic kidney disease and is the second most common cause of kidney failure worldwide. A study of a cohort of Medicare patients found that approximately 1.2% were affected. GN should be suspected in patients with unexplained hematuria, particularly with persistent hematuria with red blood cell casts and/or acanthocytes, and proteinuria. Other presenting features include purpura (in children) and hypertension. When GN is suspected based on test results, patients should be referred to a nephrologist for further evaluation and consideration of kidney biopsy, which is the gold standard diagnostic test. GN is categorized as acute (sudden onset of hematuria and proteinuria) or chronic (with irreversible scarring on biopsy). Acute GN is more likely to be reversible. Initial management consists of supportive and protective measures, including blood pressure control, drugs to block the renin-angiotensin system, and lifestyle modifications to minimize cardiovascular risk. The underlying cause should be treated when possible. Subsequent management depends on the specific type of GN and might include antimicrobial therapy and/or immunosuppressive therapy when appropriate.
Case 1. RZ is a 27-year-old patient who comes to your office with a 2-day history of a sore throat and fever of 38 °C (100.4 °F). The physical examination is notable for hypertension, oropharyngeal erythema, and minimal cervical lymphadenopathy. A rapid streptococcal antigen test has a positive result and a urinalysis dipstick result shows 3+ blood and 1+ protein.
Pathophysiology
Glomerulonephritis (GN) encompasses a heterogeneous group of disease processes. The pathologic mechanism of GN is related to immune-mediated kidney damage, although it is not completely understood.1,2
A common inciting factor is antibody deposition in a glomerular layer, such as immunoglobulin (Ig) G deposition in the glomerular basement membrane (anti-glomerular basement membrane GN) or IgA deposition in the mesangial cells (IgA nephropathy). This antibody deposition can provoke an inflammatory immune response with subsequent glomerular damage.2
Another mechanism is dysregulation of complement pathways leading to deposition of complement in the glomeruli (C3 GN). A similar mechanism is seen in lupus nephritis (LN) and acute poststreptococcal GN.2,3
Epidemiology
PREVALENCE
Given the variability in causes of GN, there is a paucity of epidemiologic information and its prevalence is unknown. It is known that GN accounts for approximately 20% of chronic kidney disease and is the second most common cause of kidney failure worldwide.2,4 In the United States, GN is the third most common cause of kidney failure, after diabetic nephropathy and hypertension, and is more likely to affect younger and healthier patients.4,5 A study of a cohort of Medicare patients found that approximately 1.2% were affected by GN.5
Kidney failure is more common in primary GN (originating in or confined to the kidney) than secondary GN (caused by systemic or immunologic conditions). Among Medicare enrollees, mortality rates are higher in patients with secondary GN than primary GN.5
SEX AND AGE DIFFERENCES
Males are more likely than females to develop GN. The only exception is autoimmune causes of GN, such as LN.2
Children and adults can be affected by GN. However, the underlying causes differ. Children between ages 3 and 12 years are more likely to develop acute poststreptococcal GN, which is a common form of childhood GN.6 Another common cause in children is IgA vasculitis, also known as Henoch-Schönlein purpura.7
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