Acute Poststreptococcal Glomerulonephritis Workup

  • Author: Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal); Chief Editor: Craig B Langman, MD   more...
 
Updated: Sep 21, 2011
 

Approach Considerations

As noted earlier, consider the possibility of acute poststreptococcal glomerulonephritis (ASPGN) in children with symptoms that may be secondary to hypertension or congestive heart failure, even in the absence of visible hematuria or a history of a preceding streptococcal infection. A urinalysis is helpful as microscopic hematuria is typically present in children with APSGN.

Streptococcal antibodies

Recent poststreptococcal infection is most commonly demonstrated by serological markers for elevated antibodies to extracellular streptococcal antigens. The streptozyme test, which measures 5 different streptococcal antibodies, is positive in more than 95% of patients with APSGN due to pharyngitis. However, sensitivity drops to 80% if APSGN follows pyoderma. The streptococcal antibodies measured include the following:

  • Antistreptolysin (ASO)
  • Antihyaluronidase (AHase)
  • Antistreptokinase (ASKase)
  • Antinicotinamide-adenine dinucleotidase (anti-NAD)
  • Anti-DNAse B antibodies

Apart from antistreptokinase (ASKase), all other streptococcal antibodies are commonly elevated after a pharyngitis, whereas only anti-DNAase B and AHase titers are typically increased after pyoderma. Thus, if only an ASO titer is used to screen for APSGN after skin infections, it may be falsely low or negative, and if the patient has received prior antibiotic treatment for a pharyngitis, this may blunt the rise in ASO titer.

Complement profiles

Theoretically, the complement (or C3) levels should be decreased in all such patients; however, the duration of low values may be quite brief and, therefore, missed, even when examined serially. When the serum level is low in individuals with APSGN, a depressed level for longer than 6-8 weeks is unusual. Thus, if the value remains low after this period of time, thinking of some other nephritic process, such as membranoproliferative glomerulonephritis (MPGN), is wise.

Kidney biopsy

Kidney biopsy is generally not recommended in the evaluation of patients with APSGN since the clinical history is usually highly suggestive and resolution of APSGN typically begins within 1 week of presentation. However, the performance of a renal biopsy is indicated in patients whose clinical presentation, laboratory findings, or disease course is atypical. In such persons, study of the histology by light, immunofluorescent, and electron microscopy may be diagnostic. Indications for kidney biopsy include the following:

  • Failure to document a recent streptococcal infection by a rise in ASO or streptozyme titer
  • Normocomplementemia
  • Renal insufficiency, especially if the glomerular filtration rate remains less than 30 mL/min/1.73 m2 for more than 1 week
  • Persistently low complement (C3) levels beyond 6-8 weeks, without resolution of features of acute glomerulonephritis.
  • Recurrent episodes of hematuria, especially frank hematuria

The typical light microscopy findings are that of diffuse hypercellularity of endothelial and mesangial cells and infiltration of the glomerular tuft with polymorphonuclear cells.[55] In more severe cases, epithelial crescents may form during the course of APSGN. In a small percentage of patients, crescentic involvement may be present in over 50% of glomeruli, leading to the clinical picture of rapidly progressive glomerulonephritis.[56, 57, 58]

Immunofluorescence performed on biopsy specimens taken during the acute phase of the illness shows discrete granular deposits of IgG and C3 in a capillary loop and mesangial distribution[59, 60] However, IgG deposits may be absent in about a third of biopsy samples. The presence of heavy and sometimes confluent capillary loop deposits with the total absence of mesangial deposits leads to the starry-sky appearance described in these biopsy reports.

The presence of subepithelial humps on electron microscopy is the hallmark finding in biopsy specimens from patients with APSGN. These electron-dense deposits may also occur in subendothelial and intramembranous locations.

Imaging studies

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

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Hematologic and Blood Chemistry Studies

Erythropoiesis may decline in the aftermath of acute glomerulonephritis, particularly in individuals with severe cases.

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 fluid (ECF) volume expansion. White blood cell (WBC) and platelet counts are usually normal, although an occasional patient exhibits a leukocytosis; rarely, a mild thrombocytopenia may be present.

The extent of renal functional impairment is correlated directly to the severity of the glomerular injury. A few patients have hypoproteinemia and hyperlipidemia. A nephrotic picture has been reported in approximately 5% of hospitalized patients with poststreptococcal acute glomerulonephritis (APSGN).

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.

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Urine Studies

Urine output is most often reduced in acute glomerulonephritis, and the urine is concentrated and acidic. Glucosuria occurs occasionally, and proteinuria is commonly present.

Proteinuria rarely exceeds 3+ by dipstick, corresponding to fewer than 2 g/m2/d when assessed quantitatively. Approximately 2-5% of children with acute poststreptococcal glomerulonephritis (APSGN) have massive proteinuria and a nephrotic picture.

Hematuria is the most consistent urinary abnormality, although histologic findings consistent with acute poststreptococcal glomerulonephritis (APSGN) 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. In addition, hyaline and/or cellular casts are almost always present.

Red blood cell casts have been found in 60-85% of hospitalized children with APSGN. These casts, although characteristic of a glomerular lesion, are often not detected, because the urine is not fresh or is examined by an inexperienced person.

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Streptococcal Studies

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, antistreptolysin O [ASO], antihyaluronidase [AH], anti-DNase B) or to combinations of antigens (eg, streptozyme test). Whichever 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.

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Hemolytic Complement Levels

Total hemolytic complement and some of its components are low during acute poststreptococcal glomerulonephritis (APSGN). The concentration of C3 has been found to be decreased in more than 90% of patients with this disease 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. The complement levels generally return to normal by 6-8 weeks after onset.

C3 levels

The differential diagnosis of acute glomerulonephritis can be divided as follows (percentages indicate approximate frequency of C3 or hemolytic complement).[61]

Low serum complement level may indicate the following systemic diseases:

  • Systemic lupus erythematosus (SLE) (focal, 75%; diffuse, 90%)
  • Subacute bacterial endocarditis (90%)
  • Visceral abscess
  • "Shunt" nephritis (90%)
  • Cryoglobulinemia (58%)

Low serum complement level may indicate the following renal diseases:

  • Acute postinfectious glomerulonephritis (>90%)
  • MPGN: Type I (50-80%), type 2 (80-90%)

A normal serum complement level may indicate the following systemic diseases:

  • Polyarteritis nodosa group
  • Hypersensitivity vasculitis
  • Wegener granulomatosis
  • Henoch-Schönlein purpura
  • Goodpasture syndrome

A normal serum complement level may indicate the following renal diseases:

  • Immunoglobulin (Ig) A (or IgG-IgA) nephropathy
  • Idiopathic rapidly progressive glomerulonephritis (RPGN)
  • Anti-glomerular basement membrane (GBM) disease
  • Negative immunofluorescence findings
  • Immune complex disease

C4 and C5 levels

C4 levels are most often normal. Serum levels of fifth component of complement (C5) and properdin are usually decreased.

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Histology

Renal biopsy is not usually indicated in the person who presents with relatively typical acute poststreptococcal glomerulonephritis (APSGN). However, in individuals whose initial presentation or early course is atypical, an examination of renal tissue may be indicated. Irrespective of the degree of severity of the initial inflammatory response, the histologic picture is consistent and specific.

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. This section 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).

Light microscopy

As observed by light microscopy, glomerular changes are generalized and diffuse. The glomerular tufts usually appear enlarged and swollen, often filling the Bowman space, and a moderate to marked increase in proliferation of mesangial and epithelial cells is present.

Polymorphonuclear leukocytes are also often observed as part of the inflammatory process, and monocytes may also be present. In persons with the most severe disease, the glomeruli appear bloodless because of the associated edema of the capillary walls, which impedes glomerular perfusion. 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 (Ig) G and C3 along the capillary walls are typically found when the specimen is studied by immunofluorescent microscopy early in the course of the disease; other immunoglobulins (eg, IgM), complement components (eg, C4), properdin, and fibrinogen are often 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 IgA in persons with Henoch-Schönlein purpura or IgA nephropathy).

Electron microscopy

Electron microscopy of renal tissue from patients with APSGN 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.

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Contributor Information and Disclosures
Author

Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal)  Associate Professor of Pediatrics, Principal Specialist, Department of Pediatrics and Child Health, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa

Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal) is a member of the following medical societies: American Association for the Advancement of Science, International Pediatric Transplant Association, International Society of Nephrology, South African Medical Association, South African Paediatric Association, and South African Transplant Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Adrian Spitzer, MD  Clinical Professor Emeritus, Department of Pediatrics, Albert Einstein College of Medicine

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.

Chief Editor

Craig B Langman, MD  The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, Children's Memorial Hospital

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: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Robert G Schacht, MD, Yang Sun Kim, MD, and Luther Travis, MD,to the development and writing of the source article.

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A schematic representation of the proposed mechanism for acute poststreptococcal glomerulonephritis (APSGN). C = Activated complement; Pl = Plasmin; NAPlr = Nephritis-associated plasmin receptor; SK = Streptokinase; CIC = Circulating immune complex.
 
 
 
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