Glomerulonephritis (Acute)

White blood cell cast from patient with chronic glomerulonephritis– A primary or secondary autoimmune renal disease involving the glomerulus in the kidney and classified as postinfectious, rapidly progressive (crescentic), or IgA neuropathy. (See also Nephrotic Syndrome.)

Causes and Incidence

Postinfectious glomerulonephritis is caused by a bacterial, viral, or parasitic pathogen. Poststreptococcal glomerulonephritis (PSGN), the prototypic postinfectious disease, is caused by a streptococcal infection that occurs elsewhere in the body, such as in the respiratory tract or skin. The incidence of acute PSGN is dropping rapidly in developed countries. It is most common in boys 3 to 7 years of age but can occur at any age. It has a rapid onset and usually resolves spontaneously.

Rapidly progressive (crescentic) glomerulonephritis is either idiopathic, related to the production and deposition of the antiglomerular basement membrane antibody, or occurs as part of multisystem disease. This type of glomerulonephritis is rare and is most often seen in men. IgA neuropathy is idiopathic and is usually a primary disease, although it can be secondary. It is common in children and young adults and affects males six times as often as females. It is particularly prevalent in Asia.

Disease Process

Acute glomerulonephritis (AGN) occurs when antigens from the etiologic agent provoke an antibody response, which results in antigen-antibody complexes that are deposited in the glomerular capillary walls. The deposits can be the continuous type or the more common discontinuous granular form. They cause a cascade of inflammatory changes in the glomeruli, resulting in vasoconstriction, a marked decrease in plasma flow, and a decrease in the filtering surface; this in turn reduces the glomerular filtration rate. A compensatory mechanism increases the synthesis of prostaglandins and the hydrostatic pressure in other glomeruli to increase flow and maintain the filtration rate. If the AGN is progressive, the compensatory mechanisms eventually induce glomerular damage through thickening and scarring of the filtration membrane.

Symptoms

PSGN
Onset of symptoms occurs 1 to 6 weeks after infection; symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and vomiting; about half of cases are asymptomatic

Crescentic type
Similar to PSGN, but the onset is more insidious and weakness, fatigue, and fever are the predominant symptoms

IgA neuropathy
Similar to PSGN, but the onset usually occurs 1 to 2 days after upper respiratory infection or enteral illness and is often accompanied by hematuria

Potential Complications

Complications include congestive heart failure, acute or chronic renal failure, and end-stage renal disease.

Diagnostic Tests

Urinalysis
Hematuria (microscopic or gross), proteinuria, sediment, RBC casts

Blood chemistry
Increased blood urea nitrogen, serum creatinine, and serum lipid; decreased serum albumin

Renal biopsy
Obstruction of glomerular capillaries

ASO titers
Positive in PSGN

IgA serum
Elevated in 50% of IgA nephropathy cases

IgA-fibronectin
Elevated aggregates with IgA nephropathy

Treatments

Therapy focuses on treating symptoms and preventing complications.

Surgery
Renal transplantation for end-stage renal disease.

Drugs
Antihypertensives for hypertension; diuretics for edema; antiinfective drugs if infection is still present; Kayexalate for hyperkalemia; phosphatebinding agents; corticosteroids with crescentic glomerulonephritis.

General
Bed rest; fluid, potassium, and sodium restrictions; reduced protein intake if uremia is present; hemodialysis or peritoneal dialysis for renal failure.