eMedicine Specialties > Emergency Medicine > Genitourinary

Glomerulonephritis, Acute

Author: Dimitrios Papanagnou, MD, MPH, Staff Physician, Department of Emergency Medicine, Bellevue Hospital Center
Coauthor(s): Nancy S Kwon, MD, MPA, Assistant Professor of Clinical Surgery, Consulting Staff, Department of Emergency Medicine, New York University School of Medicine and Bellevue Hospital Center
Contributor Information and Disclosures

Updated: Oct 2, 2009

Introduction

Background

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.

Pathophysiology

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.

Frequency

United States

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.

International

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.

Mortality/Morbidity

• 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%.

Sex

• A male-to-female ratio of 2:1 has been reported.

Age

• 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.

Clinical

History

• A thorough history should focus 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.
• Onset of symptoms is usually abrupt.
• Nonspecific symptoms include weakness, fever, abdominal pain, and malaise.
• In the setting of a postinfectious acute nephritis, a latent period of up to 3 weeks occurs before onset of symptoms. However, the latent period may vary; typically 1-2 weeks for postpharyngitis cases and 2-4 weeks for cases of postdermal infection (ie, pyoderma).
• Onset of nephritis within 1-4 days of streptococcal infection suggests preexisting renal disease.
• Symptoms of acute glomerulonephritis include the following:
  • Hematuria is a universal finding, even if it is microscopic. Gross hematuria is reported in 30% of pediatric patients.
  • Oliguria
  • Edema (peripheral or periorbital) is reported in approximately 85% of pediatric patients; edema may be mild (involving only the face) to severe, bordering on a nephrotic appearance.
  • Headache 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 secondary to heart failure or pulmonary edema; usually uncommon, particularly in children.
  • Possible flank pain secondary to stretching of the renal capsule.
• Patients may also present with symptoms specific to an underlying systemic disease that can precipitate an acute glomerulonephritis. These disease entities are briefly described in Causes. Classic presentations include the following:
  • Triad of sinusitis, pulmonary infiltrates, and nephritis suggesting Wegener granulomatosis
  • Nausea/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 a hypersensitivity vasculitis or systemic lupus erythematosus; also possibly due to the purpura that can occur in hypersensitivity vasculitis, cryoglobulinemia, and Henoch-Schönlein purpura

Physical

This description does not include all the physical findings that can be associated with the nonnephritic features of an infectious process (eg, fever), renal etiology, or systemic etiology, as such a description is 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.

• Edema frequently involves the face, specifically the periorbital area.
• Hypertension is seen in as many as 80% of affected patients.
• Hematuria, either macroscopic (gross) or microscopic, may be noted.
• Skin rashes (ie, malar rash frequently seen with lupus nephritis) may be observed.
• Abnormal neurologic examination or altered level of consciousness occurring because of malignant hypertension or hypertensive encephalopathy.
• Arthritis may be noted.
• Other signs 
  • Pharyngitis
  • Impetigo
  • Respiratory infection
  • Pulmonary hemorrhage
  • Heart murmur may indicate endocarditis
  • Scarlet fever
  • Weight gain
  • Abdominal pain
  • Anorexia
  • Back pain
  • Skin pallor
  • Palpable purpura in patients with Henoch-Schönlein purpura
  • Oral ulcers

Causes

• Postinfectious etiologies
  • The most common cause is postinfectious Streptococcus species (ie, group A, beta-hemolytic). Two types have been described as (1) attributed to serotype 12, poststreptococcal nephritis due to an upper respiratory infection occurring primarily in the winter months, and (2) attributed to serotype 49, poststreptococcal nephritis due to a skin infection usually observed in the summer and fall and more prevalent in southern regions of the United States.
  • Other specific agents include viruses and parasites, systemic and renal disease, visceral abscesses, endocarditis, infected grafts or shunts, and pneumonia.
  • Bacterial causes other than group A streptococci may be diplococcal, streptococcal, staphylococcal, or mycobacterial. Salmonella typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, and actinobacilli have also been identified.
  • Cytomegalovirus, coxsackievirus, Epstein-Barr virus, hepatitis B,² rubella, rickettsial scrub typhus, and mumps are accepted as viral causes only if it can be documented that a recent group A beta-hemolytic streptococcal infection did not occur. Acute glomerulonephritis has been documented as a rare complication of hepatitis A.³
  • Fungal and parasitic: Attributing glomerulonephritis to a parasitic or fungal etiology requires the exclusion of a streptococcal infection. Identified organisms include Coccidioides immitis and the following parasites: Plasmodium malariae, Plasmodium falciparum, Schistosoma mansoni, Toxoplasma gondii, filariasis, trichinosis, and trypanosomes.
• Systemic causes
  • Vasculitis (ie, Wegener granulomatosis causes glomerulonephritis that combines upper and lower granulomatous nephritides).
  • Collagen vascular diseases (ie, systemic lupus erythematosus causes glomerulonephritis through renal deposition of immune complexes).
  • Hypersensitivity vasculitis encompasses a heterogeneous group of disorders featuring small vessel and skin disease.
  • Cryoglobulinemia causes abnormal quantities of cryoglobulin in plasma that result in repeated episodes of widespread purpura and cutaneous ulcerations upon crystallization.
  • Polyarteritis nodosa causes nephritis from a vasculitis involving the renal arteries.
  • Henoch-Schönlein purpura causes a generalized vasculitis resulting in glomerulonephritis.
  • Goodpasture syndrome causes circulating antibodies to type IV collagen and often results in a rapidly progressive oliguric renal failure (weeks to months).
  • Drug-induced (ie, gold, penicillamine)
• Renal diseases
  • Membranoproliferative glomerulonephritis is due to the expansion and proliferation of mesangial cells as a consequence of the deposition of complements.
  • Type I refers to the granular deposition of C3; type II refers to an irregular process.
  • Berger disease (IgG-immunoglobulin A [IgA] nephropathy) glomerulonephritis results from a diffuse mesangial deposition of IgA and IgG.
  • Idiopathic rapidly progressive glomerulonephritis is a form of glomerulonephritis characterized by the presence of glomerular crescents. Three types have been distinguished. Type I is an antiglomerular basement membrane disease, type II is mediated by immune complexes, and type III is identified by antineutrophil cytoplasmic antibody.

• Search for CME/CE on This Topic »

• Glomerulonephritis, Acute (Nephrology)
• Acute Poststreptococcal Glomerulonephritis (Pediatrics: General Medicine)
• Glomerulonephritis, Poststreptococcal (Nephrology)
• Glomerulonephritis, Chronic (Nephrology)

• Causes of Blood in Urine
• Blood in Urine Symptoms
• Blood in Urine Treatment
• Kidneys and Urinary System Center
• Blood in Urine Overview

• TAVI Has Low Acute Renal Injury Rate, Compares Favorably With Surgical Valve Replacement
• T-Cell Depletion Improves Transplant Outcomes in Adults With Acute Myeloid Leukemia
• Higher-Intensity Continuous Renal Replacement May Not Reduce Mortality Risk From Acute Kidney Injury

• Angiotensin II Receptor Blockade Inhibits Acute Glomerular Injuries With the Alteration of Receptor Expression
• Acute Phase Reaction to Gadolinium-DTPA in Dialysis Patients
• Acute Interstitial Nephritis Due to Deferasirox: A Case Report

• Acute Leukemia Resource Center
• Pediatrics/Neonatal Care Nursing Resource Center
• Pancreatitis Resource Center