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Acute Poststreptococcal Glomerulonephritis Clinical Presentation

  • Author: Rajendra Bhimma, MB, MD, ChB, PhD, DCH (SA), FCP(Paeds)(SA), MMed(Natal); Chief Editor: Craig B Langman, MD  more...
 
Updated: May 27, 2015
 

History and Physical Assessment

A delay in the diagnosis of acute poststreptococcal glomerulonephritis (APSGN) is sometimes related to the absence of a clear history of a preceding documented streptococcal infections.[44] This may be due to more stringent definition criteria that require documented evidence of past infection by streptococci. Typically, an acute nephritic syndrome develops 1-2 weeks after an antecedent streptococcal pharyngitis, whereas a lapse of 3-6 weeks is common before a nephritic syndrome develops following streptococcal pyoderma.

Other factors contributing to a delay in the diagnosis of acute poststreptococcal glomerulonephritis include the sporadic occurrence of disease, because this often requires a high index of suspicion, as opposed to epidemics; the history of an upper respiratory tract infection alone during the preceding month, which may not be diagnostically helpful, because upper respiratory tract infections are common during winter; the misdiagnosis of severe volume overload in a child as primarily due to a cardiac cause, because volume overload in children is relatively rare; and the absence of visible hematuria (a presentation that is relatively common).

Physicians must consider the possibility of acute poststreptococcal glomerulonephritis 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.

Most patients with acute glomerulonephritis exhibit milder symptoms and/or signs somewhere between the extremes described below.

Asymptomatic versus symptomatic presentation

At one extreme is the asymptomatic child whose disease is discovered only by examination of the urine. Based on surveillance studies of the siblings and/or household contacts of children affected with acute poststreptococcal glomerulonephritis (APSGN), at least 50% of persons with laboratory evidence of nephritis (ie, abnormal urinalysis) appear to have no symptoms or signs of clinical illness.

At the other extreme is the child who presents with severe disease manifested by oliguria, edema, hypertension, and azotemia and with proteinuria, hematuria, and urinary casts (cylindruria).

Typical postinfectious presentation

In those patients whose acute glomerulonephritis is the result of a postinfectious cause (ie, poststreptococcal acute glomerulonephritis being the most common), a latent period of 7-21 days between onset of the streptococcal infection and development of clinical glomerulonephritis is characteristic.[45] This latent period, more clearly defined after pharyngeal infections than after pyoderma, averages approximately 10 days.

Almost characteristic by their absence are arthralgia, arthritis, carditis, hepatic involvement, and gastrointestinal bleeding. Pallor is common at onset and is not explained entirely by the presence of anemia.

The median age of presentation in childhood is age 6-8 years, with the condition being extremely rare prior to age 2 years.[46, 47, 48, 49, 50] In very young children, it is postulated that APSGN is rare because of the low rate of streptococcal pharyngitis in this age group and an immature immune response.[49] Males are 2 times more likely to have this condition compared with females; the reason this difference in sex prevalence is not known.[46, 49, 50] However, the site of streptococcal infection (pyoderma or pharyngitis) does not influence the sex difference.

Edema and/or hematuria

Edema and/or gross hematuria represent the most common clinical presentation resulting in patients seeking medical attention. One or both findings usually appear abruptly and may be associated with various degrees of malaise, lethargy, anorexia, fever, abdominal pain, and headache. The classic description of tea- or cola-colored urine occurs in approximately 25-60% of patients.

Edema is the most frequent and sometimes the only clinical finding. According to some investigators, edema is found in approximately 85% of patients. Edema usually appears abruptly and first involves the periorbital area, but it may be generalized. The degree of edema widely varies and depends on a number of factors, including the severity of glomerular involvement, the fluid intake, and the degree of hypoalbuminemia. The triad of edema, hematuria, and hypertension is classic for APSGN. Three phases of the disease can be identified: the latent phase, the acute phase, and the recovery phase.

Gross hematuria occurs at onset in 30-50% of children with poststreptococcal acute glomerulonephritis who require hospitalization. The urine is usually described as being smoky, cola colored, tea colored, or rusty. The color is usually dependent on the amount of blood present and the pH of the urine. Observant parents may note oliguria. Clots are exceedingly rare in persons with acute glomerulonephritis.

Proteinuria

Varying degrees of proteinuria are also typically present, but nephrotic syndrome is rare, occurring in 2-4% of cases.[46] . Both microscopic proteinuria and mild proteinuria may persist for several months after the acute presentation.

Hypertension

Hypertension is the third cardinal feature of poststreptococcal acute glomerulonephritis and is reported in 50-90% of children who are hospitalized with acute glomerulonephritis. The magnitude of the increase in blood pressure widely varies; however, systolic pressures greater than 200 mm Hg and diastolic pressures greater than 120 mm Hg are not unusual. Hypertension usually resolves in 1-2 weeks and rarely requires long-term treatment.[51, 52]

Hypertensive encephalopathy

Hypertensive encephalopathy can be the presenting feature of postinfectious glomerulonephritis. This condition has been reported in approximately 5% of hospitalized children and is the most serious early complication of this disease. In these patients, hypertension is usually severe and is accompanied by signs of central nervous system (CNS) dysfunction such as headache, vomiting, depressed sensorium, confusion, visual disturbances, aphasia, memory loss, coma, and convulsions. The mechanism of hypertension is most likely retention of sodium and water with resulting expansion of the extracellular space.[51]

Hypertensive encephalopathy has been reported in the occasional individual with minimal or no edema and with minimal urinary abnormalities. Since the urinalysis in such patients exhibits minimal abnormalities, the underlying cause may not be readily apparent. A high index of suspicion is required to make an appropriate diagnosis.

Circulatory congestion

Circulatory congestion is apparent in most children admitted to the hospital but is responsible only rarely for significant early symptoms. Dyspnea, orthopnea, and cough may be present. Both systolic and diastolic hypertension may be present to a varying degree. Either bradycardia or tachycardia may be observed.

Pulmonary rales are often audible. At times, the only evidence of congestion is detected on chest radiograph. A prominent cardiac shadow may be present until the onset of diuresis. In the patient with an otherwise normal cardiovascular system, cardiac failure is unusual.

Uncommon/atypical presentation suggesting alternative diagnosis

The development of clinical nephritis (ie, hematuria and/or edema) either during or within 2-5 days after the onset of a respiratory tract infection is atypical and suggests the possibility of some other form of glomerulonephritis. Subclinical cases may be missed and are sometimes identified based on knowledge of the affected family or contacts. One report found APSGN in 20% of asymptomatic family members with the condition.[34, 53] Numerous case reports describe children who present with extreme manifestations, usually hypertensive encephalopathy, who do not display the typical urinary findings at presentation.[54] Serial examination of the urine after presentation may eventually confirm the suspicion of acute glomerulonephritis.

An insidious onset of edema is more indicative of other forms of renal disease.

An occasional child may have a scarlatiniform rash or evidence of a viral exanthema, but petechial or purpuric rashes suggest other conditions.

Typical physical findings

The most frequent findings on clinical examination are features of an acute nephritic syndrome such as edema with mild hypertension, and there may be evidence of healed or healing impetigo.

Urine dipsticks analysis usually shows blood and mild proteinuria. Hematuria is rarely gross, and nephrotic-range proteinuria is seen in 5-10% of cases. Red blood cells casts are detected in urine sediment. Often, patients have oliguria that resolves within a week. Microscopic hematuria and mild proteinuria may persist for several months after the acute presentation.

In cases complicated by acute kidney injury or hypertensive crises, the physical findings vary with the severity of the complications seen.

See Differentials.

 
 
Contributor Information and Disclosures
Author

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, 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, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

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 and Dental Associations, 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, Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

Acknowledgements

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

Disclosure: Nothing to disclose.

Robert G Schacht, MD, Professor, Vice-Chair of Pediatrics, Department of Pediatrics, Division of Nephrology, New York University Medical Center.

Disclosure: Nothing to disclose.

Luther Travis, MD Professor Emeritus, Departments of Pediatrics, Nephrology and Diabetes, University of Texas Medical Branch School of Medicine

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.

References
  1. Avner ED, Davis ID. Acute poststreptococcal glomerulonephritis. Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: Elsevier Science; 2004. 1740-41.

  2. Rodríguez-Iturbe B, Batsford S. Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. Kidney Int. 2007 Jun. 71(11):1094-104. [Medline].

  3. Blyth CC, Robertson PW, Rosenberg AR. Post-streptococcal glomerulonephritis in Sydney: a 16-year retrospective review. J Paediatr Child Health. 2007 Jun. 43(6):446-50. [Medline].

  4. Sanjad S, Tolaymat A, Whitworth J, Levin S. Acute glomerulonephritis in children: a review of 153 cases. South Med J. 1977 Oct. 70(10):1202-6. [Medline].

  5. Sagel I, Treser G, Ty A, et al. Occurrence and nature of glomerular lesions after group A streptococci infections in children. Ann Intern Med. 1973 Oct. 79(4):492-9. [Medline].

  6. Kimmelstiel P. The hump-a lesion of glomerulonephritis. Bull Pathol. 1965. 6:187.

  7. Nissenson AR, Baraff LJ, Fine RN, Knutson DW. Poststreptococcal acute glomerulonephritis: fact and controversy. Ann Intern Med. 1979 Jul. 91(1):76-86. [Medline].

  8. Yoshizawa N, Yamakami K, Fujino M, et al. Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response. J Am Soc Nephrol. 2004 Jul. 15(7):1785-93. [Medline].

  9. Oda T, Yamakami K, Omasu F, et al. Glomerular plasmin-like activity in relation to nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis. J Am Soc Nephrol. 2005 Jan. 16(1):247-54. [Medline].

  10. Poon-King R, Bannan J, Viteri A, Cu G, Zabriskie JB. Identification of an extracellular plasmin binding protein from nephritogenic streptococci. J Exp Med. 1993 Aug 1. 178(2):759-63. [Medline]. [Full Text].

  11. Parra G, Rodríguez-Iturbe B, Batsford S, et al. Antibody to streptococcal zymogen in the serum of patients with acute glomerulonephritis: a multicentric study. Kidney Int. 1998 Aug. 54(2):509-17. [Medline].

  12. Cu GA, Mezzano S, Bannan JD, Zabriskie JB. Immunohistochemical and serological evidence for the role of streptococcal proteinase in acute post-streptococcal glomerulonephritis. Kidney Int. 1998 Sep. 54(3):819-26. [Medline].

  13. García R, Rubio L, Rodríguez-Iturbe B. Long-term prognosis of epidemic poststreptococcal glomerulonephritis in Maracaibo: follow-up studies 11-12 years after the acute episode. Clin Nephrol. 1981 Jun. 15(6):291-8. [Medline].

  14. Perlman LV, Herdman RC, Kleinman H, Vernier RL. Poststreptococcal glomerulonephritis. A ten-year follow-up of an epidemic. JAMA. 1965 Oct 4. 194(1):63-70. [Medline].

  15. Kandoth PW, Agarwal GJ, Dharnidharka VR. Acute renal failure in children requiring dialysis therapy. Indian Pediatr. 1994 Mar. 31(3):305-9. [Medline].

  16. Baldwin DS, Gluck MC, Schacht RG, Gallo G. The long-term course of poststreptococcal glomerulonephritis. Ann Intern Med. 1974 Mar. 80(3):342-58. [Medline].

  17. World Health Organization. Countries. Available at http://www.who.int/countries/en/. Accessed: January 10, 2008.

  18. Treser G, Semar M, McVicar M, Franklin M, Ty A, Sagel I, et al. Antigenic streptococcal components in acute glomerulonephritis. Science. 1969 Feb 14. 163(868):676-7. [Medline].

  19. Balter S, Benin A, Pinto SW, et al. Epidemic nephritis in Nova Serrana, Brazil. Lancet. 2000 May 20. 355(9217):1776-80. [Medline].

  20. Francis AJ, Nimmo GR, Efstratiou A, Galanis V, Nuttall N. Investigation of milk-borne Streptococcus zooepidemicus infection associated with glomerulonephritis in Australia. J Infect. 1993 Nov. 27(3):317-23. [Medline].

  21. McIntosh RM, Kulvinskas C, Kaufman DB. Alteration of the chemical composition of human immunoglobulin G by Streptococcus pyogenes. J Med Microbiol. 1971 Nov. 4(4):535-8. [Medline].

  22. Gewurz H, Pickering RJ, Naff G, Snyderman R, Mergenhagen SE, Good RA. Decreased properdin activity in acute glomerulonephritis. Int Arch Allergy Appl Immunol. 1969. 36(6):592-8. [Medline].

  23. Wyatt RJ, Forristal J, West CD, Sugimoto S, Curd JG. Complement profiles in acute post-streptococcal glomerulonephritis. Pediatr Nephrol. 1988 Apr. 2(2):219-23. [Medline].

  24. Wyatt RJ, McAdams AJ, Forristal J, Snyder J, West CD. Glomerular deposition of complement-control proteins in acute and chronic glomerulonephritis. Kidney Int. 1979 Oct. 16(4):505-12. [Medline].

  25. Hisano S, Matsushita M, Fujita T, Takeshita M, Iwasaki H. Activation of the lectin complement pathway in post-streptococcal acute glomerulonephritis. Pathol Int. 2007 Jun. 57(6):351-7. [Medline].

  26. Derrick CW, Reeves MS, Dillon HC Jr. Complement in overt and asymptomatic nephritis after skin infection. J Clin Invest. 1970 Jun. 49(6):1178-87. [Medline]. [Full Text].

  27. Levy M, Sich M, Pirotzky E, Habib R. Complement activation in acute glomerulonephritis in children. Int J Pediatr Nephrol. 1985 Jan-Mar. 6(1):17-24. [Medline].

  28. Sjöholm AG. Complement components and complement activation in acute poststreptococcal glomerulonephritis. Int Arch Allergy Appl Immunol. 1979. 58(3):274-84. [Medline].

  29. Strife CF, McAdams AJ, McEnery PT, Bove KE, West CD. Hypocomplementemic and normocomplementemic acute nephritis in children: a comparison with respect to etiology, clinical manifestations, and glomerular morphology. J Pediatr. 1974 Jan. 84(1):29-38. [Medline].

  30. Tina LU, D'Albora JB, Antonovych TT, Bellanti JA, Calcagno PL. Acute glomerulonephritis associated with normal serum B1C-globulin. Am J Dis Child. 1968 Jan. 115(1):29-36. [Medline].

  31. West CD, McAdams AJ. Serum and glomerular IgG in poststreptococcal glomerulonephritis are correlated. Pediatr Nephrol. 1998 Jun. 12(5):392-6. [Medline].

  32. Eison TM, Ault BH, Jones DP, Chesney RW, Wyatt RJ. Post-streptococcal acute glomerulonephritis in children: clinical features and pathogenesis. Pediatr Nephrol. 2011 Feb. 26(2):165-80. [Medline].

  33. Ilyas M, Tolaymat A. Changing epidemiology of acute post-streptococcal glomerulonephritis in Northeast Florida: a comparative study. Pediatr Nephrol. 2008 Jul. 23(7):1101-6. [Medline].

  34. Longcope WT, O'Brien DP, McGuire J, Hansen OC, Denny ER. Relationship of acute infections to glomerular nephritis. J Clin Invest. 1927 Dec. 5(1):7-30. [Medline]. [Full Text].

  35. Dixon FJ, Feldman JD, Vazquez JJ. Experimental glomerulonephritis. The pathogenesis of a laboratory model resembling the spectrum of human glomerulonephritis. J Exp Med. 1961 May 1. 113:899-920. [Medline]. [Full Text].

  36. Wong W, Lennon DR, Crone S, Neutze JM, Reed PW. Prospective population-based study on the burden of disease from post-streptococcal glomerulonephritis of hospitalised children in New Zealand: epidemiology, clinical features and complications. J Paediatr Child Health. 2013 Oct. 49(10):850-5. [Medline].

  37. Wu SH, Liao PY, Yin PL, Zhang YM, Dong L. Elevated expressions of 15-lipoxygenase and lipoxin A4 in children with acute poststreptococcal glomerulonephritis. Am J Pathol. 2009 Jan. 174(1):115-22. [Medline]. [Full Text].

  38. Lange K, Azadegan AA, Seligson G, Bovie RC, Majeed H. Asymptomatic poststreptococcal glomerulonephritis in relatives of patients with symptomatic glomerulonephritis. Diagnostic value of endostreptosin antibodies. Child Nephrol Urol. 1988-1989. 9(1-2):11-5. [Medline].

  39. Seligson G, Lange K, Majeed HA, Deol H, Cronin W, Bovie R. Significance of endostreptosin antibody titers in poststreptococcal glomerulonephritis. Clin Nephrol. 1985 Aug. 24(2):69-75. [Medline].

  40. Rodriguez-Iturbe B, Musser JM. The current state of poststreptococcal glomerulonephritis. J Am Soc Nephrol. 2008 Oct. 19(10):1855-64. [Medline].

  41. Greenbaum LA, Kerlin BA, Van Why S, Punzalan RC, Trost BA, Pan CG, et al. Concurrent poststreptococcal glomerulonephritis and autoimmune hemolytic anemia. Pediatr Nephrol. 2003 Dec. 18(12):1301-3. [Medline].

  42. Lau KK, Hastings MC, Delos Santos NM, Gaber LW, Ault BH. A child with post-streptococcal glomerulonephritis complicated by Coombs positive autoimmune haemolytic anemia. Internet J Nephro. 2007.

  43. Haas M, Racusen LC, Bagnasco SM. IgA-dominant postinfectious glomerulonephritis: a report of 13 cases with common ultrastructural features. Hum Pathol. 2008 Sep. 39(9):1309-16. [Medline].

  44. Pais PJ, Kump T, Greenbaum LA. Delay in diagnosis in poststreptococcal glomerulonephritis. J Pediatr. 2008 Oct. 153(4):560-4. [Medline].

  45. Tokura T, Morita Y, Yorimitsu D, Horike H, Sasaki T, Kashihara N. Co-occurrence of poststreptococcal reactive arthritis and acute glomerulonephritis. Mod Rheumatol. 2008. 18(5):526-8. [Medline].

  46. Lewy JE, Salinas-Madrigal L, Herdson PB, Pirani CL, Metcoff J. Clinico-pathologic correlations in acute poststreptococcal glomerulonephritis. A correlation between renal functions, morphologic damage and clinical course of 46 children with acute poststreptococcal glomerulonephritis. Medicine (Baltimore). 1971 Nov. 50(6):453-501. [Medline].

  47. Dodge WF, Spargo BH, Travis LB, et al. Poststreptococcal glomerulonephritis. A prospective study in children. N Engl J Med. 1972 Feb 10. 286(6):273-8. [Medline].

  48. Sarkissian A, Papazian M, Azatian G, Arikiants N, Babloyan A, Leumann E. An epidemic of acute postinfectious glomerulonephritis in Armenia. Arch Dis Child. 1997 Oct. 77(4):342-4. [Medline]. [Full Text].

  49. Bingler MA, Ellis D, Moritz ML. Acute post-streptococcal glomerulonephritis in a 14-month-old boy: why is this uncommon?. Pediatr Nephrol. 2007 Mar. 22(3):448-50. [Medline].

  50. Li Volti S, Furnari ML, Garozzo R, Santangelo G, Mollica F. Acute post-streptococcal glomerulonephritis in an 8-month-old girl. Pediatr Nephrol. 1993 Dec. 7(6):737-8. [Medline].

  51. Burke EC, Titus JL. Poststreptococcal acute glomerulonephritis in children. Med Clin North Am. 1966 Jul. 50(4):1141-58. [Medline].

  52. Travis LB, Dodge WF, Beathard GA, Spargo BH, Lorentz WB, Carvajal HF, et al. Acute glomerulonephritis in children. A review of the natural history with emphasis on prognosis. Clin Nephrol. 1973 May-Jun. 1(3):169-81. [Medline].

  53. Rodríguez-Iturbe B. Epidemic poststreptococcal glomerulonephritis. Kidney Int. 1984 Jan. 25(1):129-36. [Medline].

  54. Bouhard BH, Travis LB. Acute postinfectious glomerulonephritis. Eldeman CM, Ed. Pediatric Kidney Disease. 2nd ed. Boston, Mass: Little, Brown and Company; 1992. 1199-1221.

  55. Choyke PL, Bluth EI, Bush WH Jr, et al, and the Expert Panel on Urologic Imaging. ACR Appropriateness Criteria: hematuria. [online publication]. Reston,Va: American College of Radiology (ACR); 2005.

  56. Jennings RB, Earle DP. Post-streptococcal glomerulo-nephritis: histopathologic and clinical studies of the acute, subsiding acute and early chronic latent phases. J Clin Invest. 1961 Aug. 40:1525-95. [Medline]. [Full Text].

  57. Anand SK, Trygstad CW, Sharma HM, Northway JD. Extracapillary proliferative glomerulonephritis in children. Pediatrics. 1975 Sep. 56(3):434-42. [Medline].

  58. Roy S 3rd, Murphy WM, Arant BS Jr. Poststreptococcal crescenteric glomerulonephritis in children: comparison of quintuple therapy versus supportive care. J Pediatr. 1981 Mar. 98(3):403-10. [Medline].

  59. 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].

  60. Fish AJ, Herdman RC, Michael AF, Pickering RJ, Good RA. Epidemic acute glomerulonephritis associated with type 49 streptococcal pyoderma. II. Correlative study of light, immunofluorescent and electron microscopic findings. Am J Med. 1970 Jan. 48(1):28-39. [Medline].

  61. McCluskey RT, Vassalli P, Gallo G, Baldwin DS. An immunofluorescent study of pathogenic mechanisms in glomerular diseases. N Engl J Med. 1966 Mar 31. 274(13):695-701. [Medline].

  62. Yoshizawa N. Acute glomerulonephritis. Intern Med. 2000 Sep. 39(9):687-94. [Medline].

  63. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005 Nov. 5(11):685-94. [Medline].

  64. Shank JC, Powell TA. A five-year experience with throat cultures. J Fam Pract. 1984 Jun. 18(6):857-63. [Medline].

  65. Centor RM, Witherspoon JM, Dalton HP, Brody CE, Link K. The diagnosis of strep throat in adults in the emergency room. Med Decis Making. 1981. 1(3):239-46. [Medline].

  66. McIsaac WJ, White D, Tannenbaum D, Low DE. A clinical score to reduce unnecessary antibiotic use in patients with sore throat. CMAJ. 1998 Jan 13. 158(1):75-83. [Medline]. [Full Text].

  67. Edmonson MB, Farwell KR. Relationship between the clinical likelihood of group a streptococcal pharyngitis and the sensitivity of a rapid antigen-detection test in a pediatric practice. Pediatrics. 2005 Feb. 115(2):280-5. [Medline].

  68. American Academy of Pediatrics, Committee in Infectious Diseases. Group A streptococcal infections. The Red Book. Elk Grove Village, Ill: American Academy of Pediatrics; 2000. 526-92.

  69. Dale JB, Penfound T, Chiang EY, Long V, Shulman ST, Beall B. Multivalent group A streptococcal vaccine elicits bactericidal antibodies against variant M subtypes. Clin Diagn Lab Immunol. 2005 Jul. 12(7):833-6. [Medline]. [Full Text].

  70. Ahn SY, Ingulli E. Acute poststreptococcal glomerulonephritis: an update. Curr Opin Pediatr. 2008 Apr. 20(2):157-62. [Medline].

  71. Batsford SR, Mezzano S, Mihatsch M, Schiltz E, Rodríguez-Iturbe B. Is the nephritogenic antigen in post-streptococcal glomerulonephritis pyrogenic exotoxin B (SPE B) or GAPDH?. Kidney Int. 2005 Sep. 68(3):1120-9. [Medline].

  72. Cole BR, Salinas-Madrigal L. Acute Proliferative glomerulonephritis and crescentic glomerulonephritis. Barratt TM, Avner ED, Harmon WE, eds. Pediatric Nephrology. 4th ed. Philadelphia, Pa: Lippincott; 1999. 669-89.

  73. Cu GA, Mezzano S, Bannan JD, Zabriskie JB. Immunohistochemical and serological evidence for the role of streptococcal proteinase in acute post-streptococcal glomerulonephritis. Kidney Int. 1998 Sep. 54(3):819-26. [Medline].

  74. [Guideline] Finnish Medical Society Duodecim. Nephropathia epidemica (NE). EBM Guidelines. Evidence-Based Medicine [Internet]. Apr 4 2007. [Full Text].

  75. Kambham N. Postinfectious glomerulonephritis. Adv Anat Pathol. 2012 Sep. 19(5):338-47. [Medline].

  76. Moroni G, Pozzi C, Quaglini S, Segagni S, Banfi G, Baroli A. Long-term prognosis of diffuse proliferative glomerulonephritis associated with infection in adults. Nephrol Dial Transplant. 2002 Jul. 17(7):1204-11. [Medline].

  77. Nasr SH, Markowitz GS, Stokes MB, Said SM, Valeri AM, D'Agati VD. 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].

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

  79. Poon-King R, Bannan J, Viteri A, Cu G, Zabriskie JB. Identification of an extracellular plasmin binding protein from nephritogenic streptococci. J Exp Med. 1993 Aug 1. 178(2):759-63. [Medline].

  80. Ramchandani P, Kisler T, Francis IR, et al, and The Expert Panel on Urologic Imaging. ACR Appropriateness Criteria: hematuria. [online publication]. Reston, Va: American College of Radiology (ACR); 2008.

  81. Rodríguez-Iturbe B. Nephritis-associated streptococcal antigens: where are we now?. J Am Soc Nephrol. 2004 Jul. 15(7):1961-2. [Medline].

  82. Yamakami K, Yoshizawa N, Wakabayashi K, Takeuchi A, Tadakuma T, Boyle MD. The potential role for nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis. Methods. 2000 Jun. 21(2):185-97. [Medline].

  83. Yoshizawa N, Yamakami K, Oda T. Nephritogenic antigen for acute poststreptococcal glomerulonephritis. Kidney Int. 2006 Mar. 69(5):942-3; author reply 942. [Medline].

 
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Schematic representation of proposed mechanisms involved in the development of acute poststreptococcal glomerulonephritis (APSGN).MES: mesangial cell; END: endothelial cell; PMN: polymorphonuclear cell; MΦ: macrophage; T: T lymphocyte; GMB: glomerular basement membrane; C: complement; Anti-NAPlr-Ab: Anti-NAPlr-antibody.Courtesy of open access article, "The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection." Oda T, Yoshizawa N, Yamakami K, et al. Journal of Biomedicine and Biotechnology, 2012; doi: 10.1155/417675.
 
 
 
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