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Acute Glomerulonephritis Treatment & Management

  • Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jul 27, 2016
 

Approach Considerations

Treatment of acute poststreptococcal glomerulonephritis (PSGN) is mainly supportive, because there is no specific therapy for renal disease. When acute glomerulonephritis (GN) is associated with chronic infections, the underlying infections must be treated.

The expertise available in the intensive care unit may be needed for management of patients with hypertensive encephalopathy or pulmonary edema. Consultation with a nephrologist may be indicated. On an outpatient basis, renal function, blood pressure, edema, serum albumin, and urine protein excretion rate should be monitored.

In a retrospective study from New Zealand, Wong et al examined the characteristics and treatment of acute PSGN in 27 pediatric patients and determined that the need for acute dialysis was most common among the 11 children in the study with crescentic GN. These authors also determined that urinary sediment abnormalities persisted in the patients with crescentic GN even after a mean follow-up period of 3.2 years and that the benefits of immunosuppressive therapy were unclear in these patients.[12]

Go to Emergent Management of Acute Glomerulonephritis and Acute Poststreptococcal Glomerulonephritis for complete information on these topics.

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Pharmacologic Therapy

Antibiotics

Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts. Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours. Antibiotic treatment of close contacts of the index case may help prevent development of PSGN.

Other agents

Loop diuretics may be required in patients who are edematous and hypertensive, in order to remove excess fluid and to correct hypertension.

Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present.

Glucocorticoids and cytotoxic agents are of no value, except in severe cases of PSGN.

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Diet and Activity

Sodium and fluid restriction should be advised for treatment of signs and symptoms of fluid retention (eg, edema, pulmonary edema). Protein restriction for patients with azotemia should be advised if there is no evidence of malnutrition.

Bed rest is recommended until signs of glomerular inflammation and circulatory congestion subside. Prolonged inactivity is of no benefit in the patient recovery process.

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Long-Term Monitoring

Long-term studies on children with PSGN have revealed few chronic sequelae. Results of such studies are controversial because homogenous populations suitable for proper epidemiologic analysis have not been assembled.

Long-term studies show higher mortality rates in elderly patients, particularly those on dialysis. Patients may be predisposed to crescent formation.

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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
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  2. 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].

  3. 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].

  4. 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].

  5. 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].

  6. 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].

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

  8. 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].

  9. Usui J, Tawara-Iida T, Takada K, Ebihara I, Ueda A, Iwabuchi S, et al. Temporal Changes in Post-Infectious Glomerulonephritis in Japan (1976-2009). PLoS One. 2016. 11 (6):e0157356. [Medline].

  10. 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].

  11. Ibrahim A, Ahmed MM, Kedir S, Bekele D. Clinical profile and outcome of patients with acute kidney injury requiring dialysis-an experience from a haemodialysis unit in a developing country. BMC Nephrol. 2016 Jul 22. 17 (1):91. [Medline].

  12. 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].

  13. 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].

  14. 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].

  15. 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].

  16. 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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