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Year : 2021  |  Volume : 4  |  Issue : 2  |  Page : 85-88

Concurrent acute poststreptococcal glomerulonephritis and acute rheumatic carditis in a patient

1 Department of Nephrology, Aster Medcity, Kochi, India
2 Department of Cardiology, Aster Medcity, Kochi, India

Date of Submission09-Jul-2021
Date of Decision10-Oct-2021
Date of Acceptance12-Nov-2021
Date of Web Publication28-Dec-2021

Correspondence Address:
Narayanan V Unni
Lead Senior Consultant, Department of Nephrology, Aster Medcity, Cheranalloor, Kochi - 682 027, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajpn.ajpn_28_21

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A 15-year-old child presented to our center with acute glomerulonephritis (GN) preceded by history of sore throat and fever. He had features of rheumatic carditis and echocardiographic evidence of severe eccentric mitral regurgitation and aortic regurgitation. Renal biopsy showed features consistent with diffuse proliferative GN. Simultaneous occurrence of acute GN and rheumatic fever in the same patient is very rare. He responded to treatment with steroids and renal function recovered over 3 months.

Keywords: Acute poststreptococcal glomerulonephritis, acute rheumatic fever, diffuse proliferative glomerulonephritis

How to cite this article:
Abdulkader HB, Unni NV, Kumar K V, Sreekumar P. Concurrent acute poststreptococcal glomerulonephritis and acute rheumatic carditis in a patient. Asian J Pediatr Nephrol 2021;4:85-8

How to cite this URL:
Abdulkader HB, Unni NV, Kumar K V, Sreekumar P. Concurrent acute poststreptococcal glomerulonephritis and acute rheumatic carditis in a patient. Asian J Pediatr Nephrol [serial online] 2021 [cited 2022 Jul 5];4:85-8. Available from: https://www.ajpn-online.org/text.asp?2021/4/2/85/334033

  Introduction Top

Acute poststreptococcal glomerulonephritis (APSGN) and acute rheumatic fever (ARF) are both well-recognized nonsuppurative sequelae of group A beta-hemolytic streptococcus infections.[1] The serotypes of group A streptococci can be divided into those with rheumatogenic and nephritogenic potential.[2] Poststreptococcal glomerulonephritis (GN) and rheumatic fever (RF) have different epidemiology and immunological features; their concurrent development in the same patient is very rare,[3] because of different pathophysiologic mechanisms.[1],[4]

  Case Report Top

A 15-year-old boy presented with a history of fever 3 weeks ago associated with sore throat. Twenty days after the onset of fever, he noticed puffiness of the face followed by progressive worsening of edema involving the rest of the body. He had bilateral pedal edema and abdominal distension, associated with reduced urine output. He had arthralgia involving both knee joints and noticed cola-colored urine. He had gradual worsening of dyspnea and tachypnea. Before presenting to our hospital, he was evaluated at another center, where urine examination showed numerous red blood cells (RBCs) and proteinuria. Serum creatinine was 1.8 mg/dL. There was a weight gain of 8 kg.

On admission to our center, he was febrile and blood pressure was 106/68 mm Hg (corresponding to 90th centile). His height was 162 cm and weight was 42 kg with a body mass index of 15.4 and body surface area of 1.43. He had pallor and facial and pedal edema, He had a grade 3/6 pansystolic murmur in the mitral area radiating to the axilla. No other murmurs could be appreciated. There were no clinical signs of infective endocarditis or congestive cardiac failure. There was no evidence of subcutaneous nodules, erythema marginatum, or features of arthritis.

Investigations revealed hemoglobin 9.9 g/dL white blood cell count 8100/mm3, platelet count 242,000/mm3, erythrocyte sedimentation rate (ESR) 44 mm/h, C-reactive protein 103.5 mg/dL, serum creatinine 1.77 mg/dL, and serum albumin 2.8 g/dL. Urinalysis showed microscopic hematuria and proteinuria (6.1 g/day). He had elevated antistreptolysin O (ASO) titers (>800 IU/mL) and hypocomplementemia (serum C3 45 mg/dL and C4 20 mg/dL). X-ray chest showed bilateral blunting of costophrenic angles. An electrocardiogram showed prolonged PR interval (0.32 s). Ultrasonogram of the abdomen showed bulky kidneys (right kidney of 11.6 cm and left kidney of 11 cm) with diffusely increased echotexture without evidence of hydroureteronephrosis. Serum creatinine increased to 6.9 mg/dL over 10 days. Blood and urine cultures were sterile. The throat swab showed no growth.

Renal biopsy was done after initiation of dialysis and showed features of diffuse exudative proliferative GN with neutrophilic exudate [Figure 1]a, [Figure 1]b, [Figure 1]c. Immunofluorescence revealed granular capillary wall staining for immunoglobulin G (3+) and C3 (2+). The picture was consistent with infection-related GN.
Figure 1: Kidney biopsy showing (a) enlarged glomeruli, interstitial edema, interstitial inflammation, and red blood cell casts in the tubular lumina (H and E, ×20); (b) diffuse endocapillary proliferation (yellow arrow, (H and E, ×40); and (c) mononuclear and neutrophilic exudate (Green arrow, H and E, ×40)

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Echocardiogram (two-dimensional) showed dilated left atrium and left ventricle, right coronary cusp prolapse, and severe aortic regurgitation (AR). The aortic valve showed multiple jets suggestive of perforation [Figure 2]b. The anterior mitral leaflet was thickened [Figure 2]a, and there was severe eccentric mitral regurgitation with chordal rupture) [Figure 2]c. Left ventricular function was good (ejection fraction of 65%) without evidence of vegetation. Transesophageal echocardiogram confirmed the findings.
Figure 2: Two-dimensional Echocardiology: Parasternal long axis view showing (a) valvular thickening of mitral and aortic leaflets (arrows); (b) aortic regurgitation with multiple jets in perforation (arrow) and (c) mitral valve regurgitation (arrow)

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As he had one major and two minor criteria of modified Jones criteria, he was diagnosed to have ARF. Infective endocarditis was ruled out as repeated blood cultures were sterile, and there was no evidence of vegetation on the echocardiogram.

As he had a diffuse proliferative GN with massive proteinuria and renal failure, he was started on prednisolone 60 mg/day (1.5 mg/kg/day). Renal functions improved gradually after initiation of steroids. He was continued on oral furosemide and enalapril. Injection benzathine penicillin 12 lakhs IU intramuscularly was advised every 3 weeks. He improved remarkably on treatment with steroids.

The AR improved from severe AR to mild AR over 10 days but moderate mitral regurgitation persisted. At the time of discharge, his serum creatinine was 2.9 mg/dL. Steroids were tapered and stopped after 3 months. On follow-up at the end of 6 months, serum creatinine was 0.7 mg/dL (estimated glomerular filtration rate of 96 ml/min/1.73 m2 based on modified Schwartz equation), ESR 15 mm at the end of 1 h, and urine analysis showed 5 RBCs/hpf without albuminuria.

  Discussion Top

Our patient presented with features suggestive of acute GN and features of acute rheumatic carditis preceded by an upper respiratory tract infection. The child had a dramatic response to steroids with good resolution of renal and cardiac function.

APSGN occurs usually between the age group of 5 and 15 years;[5] boys are affected twice as often as girls. Postinfectious GN is associated with a previous skin or throat infection by Group A streptococcus (Streptococcus pyogenes), or occasionally Group C or G streptococcus. Pyoderma-associated APSGN occurs more often in summer. A review estimated that over 470,000 cases of APSGN occur annually worldwide and 97% of these cases were in less developed countries with an annual incidence that ranges from 9.5–28.5 per 100,000 individuals.[6] Studies from India have reported that APSGN constitutes about 6%–8% of all renal biopsy specimens. RF can occurs at any age, although most cases occur in children 5–15 years of age.[6] There are about 233,000 deaths worldwide attributable to RF or rheumatic heart disease (RHD) each year.[6] The mean incidence of RF is 19 per 100,000 school-aged children worldwide.[7] RF occurs more often in winter months. Two antigens have been implicated: The glycolytic enzyme, identified as glyceraldehyde-3-phosphate dehydrogenase, and streptococcal proteinase exotoxin B (zymogen), both activating the alternate pathway of the complement system.[8] APSGN is due to the antibody-mediated response to bacterial infection with nephritogenic strain of S. pyogenes. The immune complexes may also get deposited in glomeruli, and in situ formation of immune complexes can occur; followed by a glomerular inflammatory response with leukocyte infiltration and complement activation.[9] Nephritogenic strains associated with the development of APSGN include M types 1, 4, 12, 15 (cause throat infection and APSGN), and 2, 42, 49, 55, 57, and 60 (cause pyoderma and APSGN).[10] A streptococcal strain capable of causing a well-documented pharyngitis almost always is potentially capable of causing RF.[11] However, M types associated with RF are 1, 3, 5, 6, 11, 12, 14, 17, 18, 19, 24, 27, 29, 30, 32, and 41.[12] The lack of specific rheumatogenic strains can also explain the relatively high risk for recurrent disease with new streptococcal infections, in contrast to poststreptococcal GN, in which only a few nephritogenic strains appear to be capable of inducing the disease, and hence, recurrent disease is uncommon.

ARF is caused by the mechanism of molecular mimicry. M protein and hyaluronate capsule causes inflammation by inducing cross-reacting autoantibodies against human tissue proteins stimulated by cell-mediated immunity in genetically predisposed patients.[10] Early recognition of ARF is very important because of the possibility of developing RHD, if not treated.

Coexistent ARF and poststreptococcal GN were seen in our patient. The coexistence of APSGN and ARF rarely occurs, as has been previously described.[1],[3] Simultaneous occurrence of APSGN and acute RF was first reported in 1981. After that, 17 cases have been reported. Most of the cases had acute RF preceding or after the event of APSGN. Only six of 17 patients had simultaneous occurrence of acute RF and APSGN, as seen in our case.[13] The explanation for the co-occurrence might be that, certain strains have both nephritogenic and rheumatogenic potential (M type 1, 12), which can result in the occurrence of both conditions.[3] Although some serotypes are both rheumatogenic and nephritogenic, it cannot be said with certainty whether a single pharyngeal infection resulted in both APSGN and acute RF in this case; however, the possibility of a single infection causing both PSGN and RF cannot be ruled out. We could not isolate the organism on throat swab culture.

Mitral insufficiency is frequently seen in patients with concurrent acute RF and APSGN; however, only two cases of aortic insufficiency have been reported so far in this condition. Our patient had both mitral and aortic insufficiency.[1]

In patients associated with acute RF, focal and mesangial proliferative GN has been reported; diffuse exudative proliferative GN which is typical of APSGN is rare; our patient had diffuse proliferative GN.[3]

  Conclusion Top

Coexistence of RF and APSGN in the same patient, although rare, can occur in some patients. Awareness of infection risk and prevention strategies at the grassroots level is essential to lessen the burden of postinfectious GN in our country.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kula S, Saygili A, Tunaoğlu FS, Olguntürk R. Acute poststreptococcal glomerulonephritis and acute rheumatic fever in the same patient: A case report and review of the literature. Anadolu Kardiyol Derg 2003;3:272-4.  Back to cited text no. 1
Bisno AL. Group A streptococcal infections and acute rheumatic fever. N Engl J Med 1991;325:783-93.  Back to cited text no. 2
Bisno AL. The coexistence of acute rheumatic fever and acute glomerulonephritis. Arthritis Rheum 1989;32:230-2.  Back to cited text no. 3
Vilija C, Paulius K, Karolis A, Augustina J. Acute poststreptococcal glomerulonephritis and acute rheumatic fever: An uncommon coincidence. Ann Pediatr Cardiol 2016;9:268-9.  Back to cited text no. 4
Nasr SH, Fidler ME, Valeri AM, Cornell LD, Sethi S, Zoller A, et al. Postinfectious glomerulonephritis in the elderly. J Am Soc Nephrol 2011;22:187-95.  Back to cited text no. 5
Rodriguez-Iturbe B, Musser JM. The current state of poststreptococcal glomerulonephritis. J Am Soc Nephrol 2008;19:1855-64.  Back to cited text no. 6
Whitnack E, Bisno L. Rheumatic fever and other immunologically-mediated cardiac diseases. In: Parker C, editor. Clinical Immunology. Vol. 2. Philadelphia: WB Saunders; 1980. p. 894-929.  Back to cited text no. 7
Cunningham MW. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev 2000;13:470-511.  Back to cited text no. 8
Rodriguez-Iturbe B, Haas M. Post-streptococcal glomerulonephritis. In: Ferretti JJ, Stevens DL, Fischetti VA, editors. Streptococcus pyogenes: basic biology to clinical manifestations. Oklahoma City:The University of Oklahoma Health Sciences Center; 2016. p. 869-92.  Back to cited text no. 9
De Dassel JL, Ralph AP, Carapetis JR. Controlling acute rheumatic fever and rheumatic heart disease in developing countries: Are we getting closer? Curr Opin Pediatr 2015;27:116-23.  Back to cited text no. 10
Metzgar D, Zampolli A. The M protein of group A Streptococcus is a key virulence factor and a clinically relevant strain identification marker. Virulence 2011;2:402-12.  Back to cited text no. 11
Martin WJ, Steer AC, Smeesters PR, Keeble J, Inouye M, Carapetis J, et al. Post-infectious group A streptococcal autoimmune syndromes and the heart. Autoimmun Rev 2015;14:710-25.  Back to cited text no. 12
Watanabe T. Atypical clinical manifestations of acute poststreptococcal glomerulonephritis. In: Sharma P, editor. An Update on Glomerulopathies – Clinical and treatment aspects. Croatia: In Tech Publishing; 2011. p. 151-68.  Back to cited text no. 13


  [Figure 1], [Figure 2]


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