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Acute Glomerulonephritis Medication

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

Medication Summary

The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to eradicate the infection. Agents used include antibiotics, loop diuretics, vasodilators, and calcium channel blockers.

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Antimicrobials (Antibiotics)

Class Summary

In streptococcal infections, early antibiotic therapy may prevent antibody response to exoenzymes and render throat cultures negative, but may not prevent the development of PSGN.

Penicillin V

 

Penicillin V is more resistant than penicillin G to hydrolysis by acidic gastric secretions and is absorbed rapidly after oral administration. 250 mg of penicillin V = 400,000 U of penicillin.

Cephalexin (Keflex)

 

Cephalexin is a first-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. It is bactericidal and effective against rapidly growing organisms forming cell walls.

Resistance occurs by alteration of penicillin-binding proteins. It is effective for the treatment of infections caused by streptococci or staphylococci, including penicillinase-producing staphylococci. It may bed used to initiate therapy when streptococcal or staphylococcal infection is suspected.

Cephalexin is used orally when outpatient management is indicated. It is at least as effective as erythromycin in eradicating GABHS infection.

Erythromycin (E.E.S., Ery-Tab, Erythrocin)

 

The recommended dosing schedule of erythromycin may result in GI upset, causing one to prescribe an alternative macrolide or to change to thrice-daily dosing. Erythromycin covers most potential etiologic agents, including mycoplasmal species.

Erythromycin is less active against H influenzae. Although 10 days seems to be a standard course of treatment, treating until the patient has been afebrile for 3-5 days seems to be a more rational approach. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is indicated for staphylococcal and streptococcal infections.

In children, age, weight, and severity of infection determine the proper dosage. When twice-daily dosing is desired, half the total daily dose may be taken every 12 hours. For more severe infections, double the dose.

Erythromycin has the added advantage of being a good anti-inflammatory agent by inhibiting the migration of polymorphonuclear leukocytes.

Oral erythromycin is an acceptable alternative for patients allergic to penicillin or cephalosporin antibiotics and is effective in the treatment of streptococcal pharyngitis. Erythromycin estolate and erythromycin ethylsuccinate are both effective, although note local antibiotic resistant rates because up to 5% of isolates of S pyogenes may be resistant to erythromycin.

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Loop Diuretics

Class Summary

Loop diuretics decrease plasma volume and edema by causing diuresis. The reductions in plasma volume and stroke volume associated with diuresis decrease cardiac output and, consequently, blood pressure.

Furosemide (Lasix)

 

Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, inhibiting sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.

Furosemide is rapidly absorbed from the gastrointestinal (GI) tract. The diuretic effect is apparent within 1 hour of oral (PO) administration, peaks by the second hour, and lasts for 4-6 hours. After intravenous (IV) administration, diuresis occurs within 30 minutes; the duration of action is about 2 hours; 66% of the dose is excreted in the urine.

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Vasodilators

Class Summary

These agents reduce systemic vascular resistance, which, in turn, may allow forward flow, improving cardiac output.

Sodium nitroprusside (Nitropress)

 

Sodium nitroprusside is a potent, rapidly acting IV antihypertensive agent. Its effect is immediate and usually ends as soon as infusion is stopped because of its rapid biotransformation. Sodium nitroprusside produces vasodilation and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing heart rate. Use this agent only for treatment of acute severe hypertension or malignant hypertension that is refractory to standard therapy.

Hydralazine

 

Hydralazine lowers blood pressure by exerting a peripheral vasodilating effect through direct relaxation of vascular smooth muscle. Sodium retention and excessive sympathetic stimulation of the heart may be precluded by coadministration of a thiazide diuretic and a beta-blocker.

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Calcium Channel Blockers

Class Summary

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit the movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Nifedipine (Afeditab CR, Nifediac, Adalat CC, Procardia, Procardia XL)

 

Nifedipine is a dihydropyridine calcium channel blocker. The specific mechanisms by which nifedipine reduces blood pressure have not been fully determined but are believed to be brought about largely by its vasodilatory action on peripheral blood vessels. Nifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery.

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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. 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].

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  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].

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  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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