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Acute Glomerulonephritis Clinical Presentation

  • Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
Updated: Aug 04, 2016


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.

With poststaphylococcal infection, in contrast, the patient is likely to be a middle-aged man, often with diabetes mellitus, with a recent history of a visceral abscess or skin infection, possibly from methicillin-resistant Staphylococcus aureus.Hematuria is almot always present.[1]

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 granulomatosis with polyangiitis (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

Physical Examination

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
Contributor Information and Disclosures

Malvinder S Parmar, MB, MS FRCP(C), FACP, FASN, Associate Professor, Department of Internal Medicine, Northern Ontario School of Medicine; Assistant Professor, Department of Medicine, University of Ottawa Faculty of Medicine; Consulting Physician, Timmins and District Hospital, Ontario, Canada

Malvinder S Parmar, MB, MS is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ajay K Singh, MB, MRCP, MBA Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Chike Magnus Nzerue, MD, FACP Professor of Medicine, Associate Dean for Clinical Affairs, Meharry Medical College

Chike Magnus Nzerue, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

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Light microscopy (hematoxylin and eosin stain X 25): Photograph showing enlargement of glomerular tuft with marked decrease of urinary space and hypercellularity. The hypercellularity is due to proliferation of endogenous cells and polymorphonuclear leukocyte infiltrate. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Light microscopy (periodic acid-Schiff stain X 40): Photograph showing enlargement of glomerular tuft with marked decrease of urinary space and hypercellularity. The hypercellularity is due to proliferation of endogenous cells and polymorphonuclear leukocyte infiltrate. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Immunofluorescence (X25): Fine granular deposits of immunoglobulin G (IgG) along the basement membrane and mesangium, with "starry sky" appearance. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Ultrastructure (electron microscopy): Photograph showing proliferation of endothelial cells and mesangial cells and leukocyte infiltrate associated with presence of large, subepithelial, electron-dense deposits (ie, "hump") (see arrow). Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
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