Acute Glomerulonephritis Clinical Presentation

A thorough history should be obtained, focusing on the identification of an underlying systemic disease (if any) or recent infection. Most often, the patient is a boy, aged 2-14 years, who suddenly develops puffiness of the eyelids and facial edema in the setting of a poststreptococcal infection. The urine is dark and scanty, and the blood pressure may be elevated. Nonspecific symptoms include weakness, fever, abdominal pain, and malaise.

Ask the patient about the onset and duration of the illness. Symptom onset is usually abrupt. In the setting of acute postinfectious glomerulonephritis (GN), a latent period of up to 3 weeks occurs before onset of symptoms. However, the latent period may vary; it is typically 1-2 weeks for postpharyngitis cases and 2-4 weeks for cases of postdermal infection (ie, pyoderma). The onset of nephritis within 1-4 days of streptococcal infection suggests preexisting renal disease.

Identify a possible etiologic agent (eg, streptococcal throat infection [pharyngitis], skin infection [pyoderma]). Recent fever, sore throat, joint pains, hepatitis, travel, valve replacement, and/or intravenous drug use may be causative factors. Rheumatic fever rarely coexists with acute PSGN.

Assess the consequences of the disease process (eg, uremic symptoms). Inquire about loss of appetite, generalized itching, tiredness, listlessness, nausea, easy bruising, nosebleeds, facial swelling, leg edema, and shortness of breath.

Inquire about symptoms of acute glomerulonephritis, including the following:

• Hematuria - This is a universal finding, even if it is microscopic. Gross hematuria is reported in 30% of pediatric patients, often manifesting as smoky-, coffee-, or cola-colored urine.
• Oliguria
• Edema (peripheral or periorbital) - This is reported in approximately 85% of pediatric patients; edema may be mild (involving only the face) to severe, bordering on a nephrotic appearance.
• Headache - This may occur secondary to hypertension; confusion secondary to malignant hypertension may be seen in as many as 5% of patients.
• Shortness of breath or dyspnea on exertion - This may occur secondary to heart failure or pulmonary edema; it is usually uncommon, particularly in children.
• Possible flank pain secondary to stretching of the renal capsule

Ask about symptoms specific to an underlying systemic disease that can precipitate acute GN (see Etiology). Classic presentations include the following:

• Triad of sinusitis, pulmonary infiltrates, and nephritis, suggesting Wegener granulomatosis
• Nausea and vomiting, abdominal pain, and purpura, observed with Henoch-Schönlein purpura
• Arthralgias, associated with systemic lupus erythematosus (SLE)
• Hemoptysis, occurring with Goodpasture syndrome or idiopathic progressive glomerulonephritis
• Skin rashes, observed with hypersensitivity vasculitis or SLE; also possibly due to the purpura that can occur in hypersensitivity vasculitis, cryoglobulinemia, and Henoch-Schönlein purpura

The following description does not address all of the physical findings that can be associated with the nonnephrotic features of an infectious process, renal disorder, or systemic disease that causes acute GN; to do so would be beyond the scope of this article.

Patients often have a normal physical examination and blood pressure; most frequently, however, patients present with a combination of edema, hypertension, and oliguria.

The physician should look for the following signs of fluid overload:

• Periorbital and/or pedal edema
• Edema and hypertension due to fluid overload (in 75% of patients)
• Crackles (ie, if pulmonary edema)
• Elevated jugular venous pressure
• Ascites and pleural effusion (possible)

The physician should also look for the following:

• Rash (as with vasculitis, Henoch-Schönlein purpura, or lupus nephritis)
• Pallor
• Renal angle (ie, costovertebral) fullness or tenderness, joint swelling, or tenderness
• Hematuria, either macroscopic (gross) or microscopic
• Abnormal neurologic examination or altered level of consciousness (from malignant hypertension or hypertensive encephalopathy)
• Arthritis

Other signs include the following:

• Pharyngitis
• Impetigo
• Respiratory infection
• Pulmonary hemorrhage
• Heart murmur (possibly indicative of endocarditis)
• Scarlet fever
• Weight gain
• Abdominal pain
• Anorexia
• Back pain
• Oral ulcers

Progression to sclerosis is rare in the typical patient; however, in 0.5-2% of patients with acute GN, the course progresses toward renal failure, resulting in kidney death in a short period.

Abnormal urinalysis (ie, microhematuria) may persist for years. A marked decline in the glomerular filtration rate (GFR) is rare.

Pulmonary edema and hypertension may develop. Generalized anasarca and hypoalbuminemia may develop secondary to severe proteinuria.

A number of complications that result in relevant end-organ damage in the central nervous system (CNS) or the cardiopulmonary system can develop in patients who present with severe hypertension, encephalopathy, and pulmonary edema. Those complications include the following:

• Hypertensive retinopathy
• Hypertensive encephalopathy
• Rapidly progressive GN
• Chronic renal failure
• Nephrotic syndrome