eMedicine Specialties > Pediatrics: General Medicine > Nephrology

Acute Poststreptococcal Glomerulonephritis: Differential Diagnoses & Workup

Author: Robert G Schacht, MD, Professor, Department of Pediatrics, New York University Medical Center
Coauthor(s): Yang Sun Kim, MD, Assistant Professor, Department of Pediatrics, Division of Neonatology, New York University Medical Center; Clinical Director, Neonatology Intensive Care Unit, Bellevue Hospital; Luther Travis, MD, William W Glauser Professor of Pediatrics and Pediatric Nephrology, Department of Pediatrics, Divisions of Nephrology and Diabetes, University of Texas Medical Branch and Children's Hospital
Contributor Information and Disclosures

Updated: Jun 18, 2009

Differential Diagnoses

Hematuria
Nephritis

Other Problems to Be Considered

A number of disorders can produce an acute proliferative glomerulonephritis (GN). Any of these disorders may be confused with poststreptococcal acute glomerulonephritis (PSAGN). The following are the most common diseases that may present as acute nephritic syndrome (see Physical):

  • Mesangiocapillary and/or membranoproliferative glomerulonephritis (MPGN)
  • Postinfectious glomerulonephritis
    • Poststreptococcal
    • After other bacterial infections
    • Postviral infections
    • Postparasitic infections
  • Immunoglobulin A (IgA)-associated glomerulonephritis
    • Henoch-Schönlein purpura (HSP) nephritis
    • Other IgA nephritis (Berger disease)
  • Others (less common)
    • Chronic glomerulonephritis (recurrence and/or relapse)
    • Shunt nephritis
    • Familial nephritis
    • Rapidly progressive (crescentic) glomerulonephritis
    • Systemic lupus erythematosus (SLE) nephritis

Workup

Laboratory Studies

  • Urine
    • Urine output most is often reduced in acute glomerulonephritis (AGN), and urine is concentrated and acidic.
    • Glucosuria occurs occasionally, and proteinuria is commonly present.
    • The urine reaction for protein rarely exceeds 3+ by dipstick, corresponding to fewer than 2 g/m2/d when assessed quantitatively.
    • Approximately 2-5% of children with poststreptococcal acute glomerulonephritis  (PSAGN) have massive proteinuria and a nephrotic picture.
    • Hematuria is the most consistent urinary abnormality, although histologic findings consistent with poststreptococcal acute glomerulonephritis have been reported in children who had no or minimal urinary abnormalities.
    • Polymorphonuclear leukocytes and renal epithelial cells are common in the urine of patients with poststreptococcal acute glomerulonephritis, particularly during the early phase of the disease.
    • Hyaline and/or cellular casts are almost always present.
    • RBC casts have been found in 60-85% of hospitalized children with poststreptococcal acute glomerulonephritis. RBC casts, although characteristic of a glomerular lesion, are often not detected because the urine is not fresh or is examined by an inexperienced person.
  • Streptococcal infection
    • Look for evidence of streptococcal infection in all patients.
    • Cultures from either the pharynx or skin may be positive; however, high streptococcal antibody titers are more compelling.
    • Numerous laboratory tests can be used to measure antibodies to various streptococcal antigens (eg, ASO, AH, anti-DNase B) or to combinations of antigens (eg, streptozyme test).
    • Whatever test is used, a rise in the titer of the antibody, measured at an interval of 2-3 weeks, is more meaningful than a single measurement. An ASO titer of 250 U or higher is highly suggestive of recent streptococcal infection.
  • Hemolytic complement
    • Total hemolytic complement and some of its components are low during poststreptococcal acute glomerulonephritis.
    • The concentration of C3 has been found to be decreased in more than 90% of patients with poststreptococcal acute glomerulonephritis when measured serially during the first 2 weeks of the illness.
    • Total hemolytic complement values are also depressed.
    • These tests help to differentiate poststreptococcal from other postinfectious forms of acute glomerulonephritis.
    • C4 levels are most often normal.
    • Serum levels of fifth component of complement (C5) and properdin are usually decreased.
    • The complement levels generally return to normal by 6-8 weeks after onset.
  • Renal
    • The extent of renal functional impairment is correlated directly to the severity of the glomerular injury.
    • The elevation in the serum concentrations of creatinine and blood urea nitrogen (BUN) is usually modest, although some patients may have severe azotemia at onset.
    • The electrolyte profile is usually normal; hyperkalemia and metabolic acidosis are only present in patients with significant renal functional impairment. The same applies to hyperphosphatemia.
    • Total serum calcium, but not ionized calcium levels, may be low in patients who have a nephrotic picture.
  • Blood
    • A mild anemia (normocytic, normochromic) is common in persons in the early phase of acute glomerulonephritis; its degree tends to parallel the degree of extracellular (ECF) volume expansion.
    • Erythropoiesis may decline in the aftermath of acute glomerulonephritis, particularly in individuals with severe cases.
    • WBC and platelet counts are usually normal, although an occasional patient exhibits a leukocytosis; rarely, a mild thrombocytopenia may be present.
    • A few patients have hypoproteinemia and hyperlipidemia. A nephrotic picture has been reported in approximately 5% of hospitalized patients with poststreptococcal acute glomerulonephritis.

Imaging Studies

  • No specific radiologic studies are particularly helpful in either the evaluation or the treatment of patients with acute glomerulonephritis.
    • Renal ultrasonography generally demonstrates normal to slightly enlarged kidneys bilaterally with some evidence of increased echogenicity.
    • Chest radiographs commonly demonstrate central venous congestion in a hilar pattern, the degree of which parallels the increase in ECF volume. Occasionally, an enlarged cardiac shadow is evident.

Other Tests

  • Currently, no other tests provide any meaningful data regarding acute glomerulonephritis.

Procedures

  • No procedures are recommended routinely in the evaluation of patients with acute glomerulonephritis.
  • The performance of a renal biopsy is indicated in patients whose clinical presentation, laboratory findings, or course is atypical. In such persons, study of the histology by light, immunofluorescent, and electron microscopy may be diagnostic.

Histologic Findings

  • Histologic findings depend on the etiology of the acute glomerulonephritis, the severity of the inflammatory process, and the stage of the disease at the time of the biopsy. The section below concentrates on the findings observed in individuals with poststreptococcal acute glomerulonephritis. The severity of the histologic process correlates with the clinical severity of the initial phase of the disease, and it may correlate with the ultimate prognosis (ie, severe lesions have worse prognoses).
  • By light microscopy, the glomerular tufts appear enlarged and swollen, often filling Bowman space. A moderate-to-marked increase in proliferation of both mesangial and epithelial cells is present. Polymorphonuclear leukocytes often are observed, and monocytes also may be present. The increased cell mass expands the central lobular area in a centrifugal pattern, leading to narrowing of the capillary lumens. When the inflammatory process is extensive, the epithelial cells of Bowman capsule proliferate, forming crescents. Few, if any, tubular changes are noted.
  • Granular deposits of immunoglobulin G (IgG) and C3 along the capillary walls generally are observed when the specimen is studied by immunofluorescent microscopy early in the course of the disease. Other immunoglobulins (eg, immunoglobulin M [IgM]), complement components (eg, C4), properdin, and fibrinogen often are observed. Later in the course of the disease, the immunoreactants are observed primarily in the mesangium. In the nonstreptococcal forms of postinfectious glomerulonephritis, no significant deposition of complement components is present, although either IgG or IgM may be observed (as may immunoglobulin A [IgA] in persons with Henoch-Schönlein purpura (HSP) or IgA nephropathy).
  • Electron microscopy of renal tissue from patients with poststreptococcal acute glomerulonephritis usually reveals electron-dense deposits (humps) in the subepithelial space. During the recovery process, these deposits rapidly disappear, although fragments still may be found in the mesangium.
  • Renal biopsy is not needed in most patients with poststreptococcal acute glomerulonephritis (see Procedures).

More on Acute Poststreptococcal Glomerulonephritis

Overview: Acute Poststreptococcal Glomerulonephritis
Differential Diagnoses & Workup: Acute Poststreptococcal Glomerulonephritis
Treatment & Medication: Acute Poststreptococcal Glomerulonephritis
Follow-up: Acute Poststreptococcal Glomerulonephritis
References
Further Reading
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References

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Keywords

acute poststreptococcal glomerulonephritis, acute glomerulonephritis, AGN, acute nephritis, acute postinfectious glomerulonephritis, poststreptococcal acute glomerulonephritis, PSAGN, acute proliferative glomerulonephritis, Bright disease, Bright's disease, acute diffuse proliferative glomerulonephritis, coxsackievirus B, echovirus type 9, influenza virus, mumps, treatment, diagnosis, hypertensive encephalopathy, CNS dysfunction, pulmonary rales, Streptococcus pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis, Rickettsia rickettsiae, Mycoplasma species, Meningococcus species, Leptospira species, IgA nephropathy, Berger disease

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Contributor Information and Disclosures

Author

Robert G Schacht, MD, Professor, Department of Pediatrics, New York University Medical Center
Robert G Schacht, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Federation for Clinical Research, American Society of Pediatric Nephrology, International Society of Nephrology, New York Academy of Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Coauthor(s)

Yang Sun Kim, MD, Assistant Professor, Department of Pediatrics, Division of Neonatology, New York University Medical Center; Clinical Director, Neonatology Intensive Care Unit, Bellevue Hospital
Yang Sun Kim, MD is a member of the following medical societies: American Academy of Pediatrics and Eastern Society for Pediatric Research
Disclosure: Nothing to disclose.

Luther Travis, MD, William W Glauser Professor of Pediatrics and Pediatric Nephrology, Department of Pediatrics, Divisions of Nephrology and Diabetes, University of Texas Medical Branch and Children's Hospital
Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, and Texas Pediatric Society
Disclosure: Nothing to disclose.

Medical Editor

Richard Neiberger, MD, PhD, Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital
Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group
Disclosure: The Osler Institute Honoraria Speaking and teaching

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Adrian Spitzer, MD, Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center
Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Howard Trachtman, MD, Program Director, Pediatrics Research, Schneider Children's Hospital, Department of Pediatrics, Division of Nephrology, Professor, Albert Einstein College of Medicine
Howard Trachtman, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD, The Isaac A Abt, MD, Professor of Kidney Diseases, Feinberg School of Medicine, Northwestern University; Division Head of Kidney Diseases, Children's Memorial Hospital, Chicago
Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology
Disclosure: Amgen Grant/research funds None; Altus Pharmaceuticals Grant/research funds None; Genzyme Grant/research funds None; Merck Grant/research funds None; NIH Grant/research funds None

 
 
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