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Acute Glomerulonephritis Workup

  • Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Aug 03, 2015
 

Approach Considerations

Urinalysis and sediment examination are crucial in the evaluation of patients with acute nephritic syndrome. Look for the following:

  • Protein
  • Blood
  • Red blood cells (RBCs)
  • White blood cells (WBCs)
  • Dysmorphic RBCs
  • Acanthocytes
  • Cellular (ie, RBC, WBC) casts
  • Granular casts
  • Oval fat bodies

In some instances, marked sterile pyuria is present. The presence of RBC casts is almost pathognomonic of glomerulonephritis (GN). Urine electrolyte, urine sodium, and fractional excretion of sodium (FENa) assays are needed to assess salt avidity.

Blood tests should include the following:

  • Complete blood count (CBC)
  • Blood urea nitrogen (BUN), serum creatinine, and serum electrolytes (especially serum potassium)
  • Erythrocyte sedimentation rate (ESR)
  • Complement levels (C3, C4, CH50)

Streptozyme testing may be useful. Imaging studies are helpful in some patients, for assessment of clinical signs suggesting extrarenal involvement or for structural evaluation of the kidneys.

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Initial Blood Tests

A CBC is performed. A decrease in the hematocrit may demonstrate a dilutional anemia. In the setting of an infectious etiology, pleocytosis may be evident.

Electrolyte levels are measured (particularly the serum potassium), along with BUN and creatinine (to allow estimation of the glomerular filtration rate [GFR]). The BUN and creatinine levels will exhibit a degree of renal compromise.

The ESR is usually increased.

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Complement Levels

Differentiation of low and normal serum complement levels may allow the physician to narrow the differential diagnosis. Results are not readily available to the emergency physician but may be useful to the consultant.

Low serum complement levels suggest the following systemic diseases: cryoglobulinemia, systemic lupus erythematosus (SLE), bacterial endocarditis, and shunt nephritis. Under the same conditions, renal diseases characteristic of membranoproliferative GN (MPGN) or poststreptococcal GN (PSGN) also may be considered.

Normal serum complement levels suggest a visceral abscess, polyarteritis nodosa, Goodpasture syndrome, or Henoch-Schönlein purpura. In addition, normal complement levels suggest renal diseases such as immune complex disease, idiopathic rapidly progressive GN, and immunoglobulin G (IgG) or immunoglobulin A (IgA) nephropathy.

Low C3 levels are found in almost all patients with acute poststreptococcal nephritis; C4 levels may be slightly low. Hypocomplementemia is noted in 73.9% of adult patients. Type III cryoglobulinemia may be present.

If methicillin-resistant Staphylococcus aureus (MRSA) is the inciting agent, then hypocomplementemia is usually not present, but plasma immunoglobulins, especially IgA, are markedly elevated.

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Urinalysis and 24-Hour Urine Study

The urine is dark. Its specific gravity is greater than 1.020. RBCs and RBC casts are present.

Proteinuria is observed. With the qualitative estimation of proteinuria, determination of high-molecular-weight (HMW) protein (eg, fractional excretion of IgG [FEIgG]) and low-molecular-weight (LMW) protein (eg, alpha-1-microglobulin), may help predict the clinical outcome and may help in guiding steroid and immunosuppressive therapy, especially in patients with primary glomerular diseases with nephrotic syndrome.

The 24-hour urine protein excretion and creatinine clearance, though not indicated in the emergency department (ED) setting, may be helpful to document the degree of renal dysfunction and proteinuria. With this test, it is important to remember that creatinine clearance is a “steady-state” measurement. Because of rapidly changing renal function, the creatinine clearance may not reveal the true picture; therefore, it is better to wait until renal function has stabilized before performing creatinine clearance.

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Streptozyme Test

The streptozyme tests test includes many streptococcal antigens that are sensitive for screening but are not quantitative, such as DNAase, streptokinase, streptolysin O, and hyaluronidase.

The antistreptolysin O (ASO) titer is increased in 60-80% of patients. The increase begins in 1-3 weeks, peaks in 3-5 weeks, and returns to normal in 6 months. ASO titer is unrelated to severity, duration, or prognosis of renal disease.

Increasing ASO titers or streptozyme titers confirm recent infection. In patients with skin infection, anti-DNAase B (ADB) titers are more sensitive than ASO titers for infection with Streptococcus.

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Blood and Tissue Culture

Blood culture is indicated in patients with fever, immunosuppression, intravenous (IV) drug use history, indwelling shunts, or catheters. Blood culture may indicate hypertriglyceridemia, decreased glomerular filtration rate, or anemia.

Cultures of throat and skin lesions to rule out Streptococcus species may be obtained.

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Other Laboratory Tests

Levels of antibody to nephritis-associated protease (NAPR) are elevated in streptococcal infections with GN but not in streptococcal infections without GN.

The antinuclear antibody test is useful for patients with acute GN and symptoms of underlying systemic illness, such as systemic lupus erythematosus and polyarteritis nodosa.

Other tests include the following:

A nti-DNA antibodies, triglyceride levels, hepatitis B and C serologies, antineutrophil cytoplasmic antibody (ANCA), c-ANCA (ie, if Wegener granulomatosis is suspected).

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Radiography and Computed Tomography

Chest radiography is needed in patients with a cough, with or without hemoptysis (eg, granulomatosis with polyangiitis [Wegener granulomatosis], Goodpasture syndrome, pulmonary congestion). Abdominal radiographic imaging (ie, computed tomography [CT]) is needed if visceral abscesses are suspected; also look for chest abscesses.

CT scan of the head without contrast may be necessary in any patient with malignant hypertension or altered mental status.

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Ultrasonography and Echocardiography

Bedside renal ultrasonography may be appropriate to evaluate kidney size, as well as to assess the echogenicity of the renal cortex, exclude obstruction, and determine the extent of fibrosis. A kidney size of less than 9 cm is suggestive of extensive scarring and a low likelihood of reversibility.

Echocardiography may be performed in patients with a new cardiac murmur or a positive blood culture to rule out endocarditis or a pericardial effusion.

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Renal Biopsy

Generally, a renal biopsy is not necessary for a diagnosis of acute PSGN; however, in most cases, it is important because histology guides both prognosis and therapy. Renal biopsy may be required for definitive diagnosis, particularly in primary renal diseases. Renal biopsy is not indicated as an ED procedure.

Candidates for biopsy are patients with an individual or family history of renal disease and patients with an atypical presentation, including massive proteinuria, nephrotic syndrome, or a rapid rise in creatinine level without resolution.

In a study of the types and characteristics of GN found in patients with HIV infection, Nebuloni et al reviewed 73 renal biopsies and found that immune complex GNs predominated in the biopsied patients (40 cases), with mesangial proliferative and MPGN being the most common of these (10 and 8 cases, respectively).[13] The authors also reported unusual characteristics in the immune complex GNs, including multiple-site deposits and frequent sclerotic tendencies.

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Histologic Findings

Diffuse endocapillary proliferative changes are found. The most common histologic patterns are diffuse (72.1%), focal (12.8%), and mesangial (8.1%) proliferative GN in adults.[3] In postinfectious GN, the glomerulus is hypercellular with marked cellular infiltration (ie, polymorphonuclear neutrophils, monocytes) (see the images below).

Light microscopy (hematoxylin and eosin stain X 25Light 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)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 may show fine, granular deposits of IgG in a “starry sky” appearance (see the first image below). Large subepithelial deposits may be observed on electron microscopy (see the second image below). Crescents may be observed.

Immunofluorescence (X25): Fine granular deposits oImmunofluorescence (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 sUltrastructure (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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Contributor Information and Disclosures
Author

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.

References
  1. Wen YK, Chen ML. The significance of atypical morphology in the changes of spectrum of postinfectious glomerulonephritis. Clin Nephrol. 2010 Mar. 73(3):173-9. [Medline].

  2. Oda T, Yoshizawa N, Yamakami K, Sakurai Y, Takechi H, Yamamoto K, et al. The role of nephritis-associated plasmin receptor (NAPlr) in glomerulonephritis associated with streptococcal infection. J Biomed Biotechnol. 2012. 2012:417675. [Medline]. [Full Text].

  3. Nasr SH, Markowitz GS, Stokes MB, et al. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore). 2008 Jan. 87(1):21-32. [Medline].

  4. Safadi R, Almog Y, Dranitzki-Elhalel M, Rosenmann E, Tur-Kaspa R. Glomerulonephritis associated with acute hepatitis B. Am J Gastroenterol. 1996 Jan. 91(1):138-9. [Medline].

  5. Aggarwal A, Kumar D, Kumar R. Acute glomerulonephritis in hepatitis A virus infection: a rare presentation. Trop Doct. 2009 Jul. 39(3):186-7. [Medline].

  6. Tang J, Liu N, Zhuang S. Role of epidermal growth factor receptor in acute and chronic kidney injury. Kidney Int. 2013 Jan 16. [Medline].

  7. Sasaki K, Anderson E, Shankland SJ, Nicosia RF. Diffuse Proliferative Glomerulonephritis Associated With Cetuximab, an Epidermal Growth Factor Receptor Inhibitor. Am J Kidney Dis. 2013 Mar 6. [Medline].

  8. Anochie I, Eke F, Okpere A. Childhood acute glomerulonephritis in Port Harcourt, Rivers State, Nigeria. Niger J Med. 2009 Apr-Jun. 18(2):162-7. [Medline].

  9. Wong W, Morris MC, Zwi J. Outcome of severe acute post-streptococcal glomerulonephritis in New Zealand children. Pediatr Nephrol. 2009 May. 24(5):1021-6. [Medline].

  10. Becquet O, Pasche J, Gatti H, et al. Acute post-streptococcal glomerulonephritis in children of French Polynesia: a 3-year retrospective study. Pediatr Nephrol. 2010 Feb. 25(2):275-80. [Medline].

  11. Murakami CA, Attia D, Carter-Monroe N, Lucas GM, Estrella MM, Fine DM, et al. The clinical characteristics and pathological patterns of postinfectious glomerulonephritis in HIV-infected patients. PLoS One. 2014. 9(10):e108398. [Medline]. [Full Text].

  12. Chen S, Chen H, Liu Z, Zhang H, Hu W, Tang Z, et al. Pathological spectrums and renal prognosis of severe lupus patients with rapidly progressive glomerulonephritis. Rheumatol Int. 2015 Apr. 35 (4):709-17. [Medline].

  13. Nebuloni M, Barbiano di Belgiojoso G, Genderini A, et al. Glomerular lesions in HIV-positive patients: a 20-year biopsy experience from Northern Italy. Clin Nephrol. 2009 Jul. 72(1):38-45. [Medline].

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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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