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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2014  |  Volume : 25  |  Issue : 3  |  Page : 567-571
Acute post-infectious glomerulonephritis in adults: A single center report

Department of Nephrology, Fattouma Bourguiba Hospital; University Faculty of Medicine, Monastir, Turkey

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Date of Web Publication9-May-2014


Acute post-infectious glomerulonephritis (APIGN) is uncommonly seen in adults; its incidence is progressively declining, particularly in developed countries. The aim of this study was to evaluate the epidemiological, clinical and biologic features of APIGN in a Tunisian center. A retrospective descriptive analytic study was carried out on 50 patients aged more than 15 years who were admitted to the Monastir Hospital between 1991 and 2007, with a diagnosis of APIGN. There were more males than females (66% vs. 34%), and the mean age of the patients was 36.8 ± 10 years. Only 10% had an immunocompromised background, including diabetes. The most common site of infection was upper respiratory tract, followed by skin and pneumonia. The most common causative agent was Streptococcus (66%), followed by Staphylococcus (12%). 73.8% of the patients had low C3 complement levels. The mean peak serum creatinine was 190 μmol, and 4% of patients required acute dialysis. The patients were followed-up for a mean period of 18 months (range, 0.16-97 months). During follow-up, of the 46 patients reviewed in the consultation, the majority showed complete remission, 12 patients had persisting abnormalities such as hypertension in 17%, chronic renal failure in 8% and proteinuria in 6.5%, and one patient had concomitant hypertension and chronic renal failure. Our study suggests that APIGN is still endemic in some parts of the world such as Tunisia, and our data showed a favorable prognosis in adults.

How to cite this article:
Hamouda M, Mrabet I, Dhia N B, Aloui S, Letaif A, Frih M A, Skhiri H, Elmay M. Acute post-infectious glomerulonephritis in adults: A single center report. Saudi J Kidney Dis Transpl 2014;25:567-71

How to cite this URL:
Hamouda M, Mrabet I, Dhia N B, Aloui S, Letaif A, Frih M A, Skhiri H, Elmay M. Acute post-infectious glomerulonephritis in adults: A single center report. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2021 Oct 21];25:567-71. Available from: https://www.sjkdt.org/text.asp?2014/25/3/567/132185

   Introduction Top

Acute post-infectious glomerulonephritis (APIGN) is an immunologically mediated disease. In the recent decades, the prevalence of APIGN has tended to decline in most industrialized countries, but high rates persist in some developing communities. [1],[2],[3] The aim of this study was to evaluate the epidemiological, clinical and biologic features of APIGN in a Tunisian center.

   Patients and Methods Top

A retrospective descriptive analytic study was carried out on 50 patients aged more than 15 years with the diagnosis of APIGN, who were admitted to the Monastir Hospital between 1991 and 2007. The medical records of all patients were reviewed.

The diagnosis of APIGN was based on clinical manifestations, including hematuria, edema, hypertension and oliguria with a history of recent infection. Laboratory findings such as proteinuria, complement deficiency and increased serum creatinine were also reviewed.

The diagnosis of APIGN required positive testing of recent group A-beta hemolytic Streptococcal infection by either anti-streptolysin O antibody (ASO) or positive culture; ASO was considered to be elevated at levels >200 IU/mL.

The diagnosis of post non-streptococcal glomerulonephritis (GN) was made when organisms other than group A-beta hemolytic Streptococcus were grown on culture, either bacteria or non-bacterial organisms.

The clinical indications for renal biopsy were rapidly progressive GN or familial nephritis, and persisting azotemia. Data were collected using hospital records on admission, hospital progress notes and outpatient follow-up. Oliguria was defined as urine output <500 mL over 24 h and anuria as urine output <100 mL over 24 h.

   Results Top

During the 17-year study period, 50 patients presented with APIGN in accordance with the inclusion criteria: 11 cases between 1991 and 1996, 21 cases between 1997 and 2003 and 12 cases between 2003 and 2007. The demographic and clinical data on this patient cohort are presented in [Table 1]. There were more males than females (66% vs. 34%), and the mean age of patients was 36.8 ± 10 years. Most patients were aged between 16 and 35 years (56%). Only 8% of patients were older than 65 years.
Table 1: Demographic data and clinical features of the study patients.

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Five patients (10%) had a history of diabetes mellitus type-2. The site of infection was identified in 90% of the patients, the most common site being the upper respiratory tract (44%), followed by skin (30%), lung (pneumonia) (12%) and associations of the upper respiretory tract and skin concurrently (4%) [Table 1].

The mean duration from clinical onset of infection to renal disease was 13.5 ± 8 days. This delay was less than two weeks in 95.4% of patients with upper respiratory tract infection, and more than three weeks in majority (60%) of the patients with skin lesions. The reasons for consultation were fever in 22%, abdominal symptoms in 6% and headache in 6%. The majority of patients (66%) showed direct signs of APIGN such as macroscopic hematuria, edema, hypertension and oliguria. At presentation, 68% of the patients had hypertension, including severe hypertension in 16% of the patients (systolic arterial pressure >180 mm Hg and/or diastolic pressure >110 mm Hg). Peripheral edema was present in 94% of the patients. Sixteen percent of the patients had oliguria and 4% had anuria.

The mean peak serum creatinine was 190 μmol, the mean glomerular filtration rate (GFR) at presentation was 37 mL/min and 4% of the patients required acute dialysis. Twenty-four patients (48%) had creatinine values >120 μmol/L. Proteinuria was in the nephritic range in 10% of the patients. The most common causative agent was Streptococcus (66%), followed by Staphylococcus (12%). Testing for serum complement (C) was performed in 42 patients, of whom 73.8% had lowered C3 and 19% had lowered C4.

Test for anti-neutrophil cytoplasmic auto-antibody was performed in two patients having rapidly progressive acute renal failure. The test was negative in both cases. Test for serum cryoglobulin was performed in three patients; all had negative titers. The anti-nuclear factor was looked for in seven patients, and was negative in all.

Renal biopsy was performed in 16 patients. In 12 patients (75%), histology showed endocapillary proliferation without any crescents and with immunoglobulin G (IgG) and C3 fraction deposits. In two patients who presented with rapidly progressive renal failure, renal histology showed features of extensive extra-capillary proliferation (crescentic glomerulonephritis). In two other patients who presented with persistent macroscopic hematuria, histology showed mesangial proliferation without IgA deposits.

The initial evolution was assessed using data collected during the period of hospitalization and at the end of the patient's stay in the hospital (mean of 10 days). Edema had resolved in 96% and hypertension in 90% of the cases. Diuretic therapy (furosemide) had been used in 74% of the patients for a mean of seven days, and a second anti-hypertensive drug had been administered to 66% of the patients for a mean of five days.

Patients with known active infection were treated with antibiotics. Penicillin G was given to patients with Streptococcal infection (20%); in patients allergic to penicillin, macrolides were used. All patients with Staphylococcal infection were treated with Oxacilin. The mean GFR at discharge was 59 mL/min.

Patients were followed-up for a mean period of 18 months (range, 2-97 months), until macroscopic hematuria, proteinuria, hypo-complementemia and renal impairment resolved. Four patients were lost to follow-up and their data could not be assessed. Hematuria resolved in six months in 93% (43/46) and proteinuria resolved before six months in 91% (40/46) of the patients. The mean GFR at six months was 62 mL/min.

During follow-up, of the 46 patients reviewed, the majority showed complete remission, while 12 patients had some residual abnormalities: eight (17%) had hypertension, four patients (8%) had chronic renal failure, three patients (6.5%) had proteinuria and one patient had concomitant hypertension and chronic renal failure.

   Discussion Top

Post-infectious GN is an immunologic response of the kidney to infection, commonly triggered by Streptococci, although many other organisms can cause the condition. GN occurs primarily in children (aged 6-10 years) and young adults, with a male predominance of 2-3:1. [1],[2],[4] In recent years, affected patients in the developed world, especially Europe and the United States (US), tend to be adults. Individuals with comorbidities such as diabetes and alcoholism are at an increased risk of developing the disease; one-third of individuals with APIGN have one or two of these comorbidities. [3],[5] This finding is in contrast to reports published between 1960 and 1980, in which most of the affected patients had no notable medical history. [6],[7] The changes in the pattern of APIGN have not been clearly delineated; improvement in socio-economic status and living standards of many communities and the widespread and early use of antibiotics may be responsible, at least in part. [3] In our study, there were more males than females and 10% had an immunocompromised background, including diabetes.

APIGN is a typical form of acute nephritic syndrome and is characterized by hematuria, proteinuria, edema and, often, by hypertension and a mild degree of acute kidney injury. The typical patient with APIGN is a child who abruptly develops puffiness of the eyelids and edema after infection, followed by smoky and scanty urine and increasing blood pressure. Anuria and nephrotic-range proteinuria are sometimes observed. [1],[3],[4] In our study, we observed anuria in 4% and nephrotic-range proteinuria in 10% of patients.

Urine volume usually increases four to seven days after hospital admission, and this increase is rapidly followed by resolution of edema and normalization of blood pressure. Microscopic hematuria takes several months to resolve, and can persist for up to one year after the acute attack. [5],[6]

APIGN usually presents after Streptococcal pharyngeal or skin infections, although other suppurative infections (including acute bacterial endocarditis and pneumococcal pneumonia), protozoa and viruses have also been linked to the disease. [7],[8],[9] About 90% of the patients in our study had a known recent history of previous infection involving the upper respiratory tract or skin.

On rare occasions (4.6% of biopsy specimens), APIGN, especially the post-streptococcal form, is complicated by rapidly rising azotemia. Such cases are diagnosed as rapidly progressive nephritic syndrome. [10]

A variety of infections have clinic-pathologic presentations that are similar to those of post-streptococcal GN. This suggests that a marked overlap exists among the molecular and cellular responses to these pathogens. [11] This also indicates that no single antigen is the sole cause of post-streptococcal GN in all patients. Individual susceptibility, possibly determined by the host's genetic factors, might have a huge influence on the pathogenicity of the precipitating organism. [12]

Treatment of APIGN is mainly supportive unless recovery of renal function fails to occur despite eradication of the causative organism. [5],[6] The prognosis of patients with APIGN is largely influenced by the specific presentation and histopathology. Crescentic glomerulonephritis and the "garland" immunofluorescence pattern carry a poorer outcome than other pathologic patterns. However, other factors such as age, type of pathogen and co-existing diseases, including diabetes and cardiovascular, influence the prognosis. [13],[14]

In general, chronic renal failure resulting from APIGN is exceptional. The group of patients with especially poor long-term prognosis is elderly patients who develop persistent proteinuria in the nephrotic range; 77% of these patients develop chronic renal failure. [15],[16],[17],[18],[19],[20]

   Conclusion Top

APIGN is still endemic in some parts of the world such as Tunisia. Our data showed a favorable prognosis in the study patients, but severe systemic complications are possible because of sodium and water retention in the acute phase. APIGN can be potentially prevented with early antibiotic treatment.

   References Top

1.Rodriguez-Iturbe B, Musser JM. The current state of poststreptococcal glomerulonephritis. J Am Soc Nephrol 2008;19:1855-64.  Back to cited text no. 1
2.Tejani A, Ingulli E. Poststreptococcal glomerulonephritis. Current clinical and pathologic concepts. Nephron 1990;55:1-5.  Back to cited text no. 2
3.Kanjanabuch T, Kittikowit W, Eiam-Ong S. An update on acute postinfectious glomerulonephritis worldwide. Nat Rev Nephrol 2009; 5:259-69.  Back to cited text no. 3
4.Sarkissian A, Papazian M, Azatian G, Arikiants N, Babloyan A, Leumann E. An epidemic of acute postinfectious glomerulonephritis in Armenia. Arch Dis Child 1997;77:342-4.  Back to cited text no. 4
5.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;87:21-32.  Back to cited text no. 5
6.Baldwin DS, Gluck MC, Schacht RG, Gallo G. The long-term course of poststreptococcal glomerulonephritis. Ann Intern Med 1974;80: 342-58.  Back to cited text no. 6
7.Lien JW, Mathew TH, Meadows R. Acute post-streptococcal glomerulonephritis in adults: A long-term study. Q J Med 1979;48:99-111.  Back to cited text no. 7
8.Barsoum RS. Malarial nephropathies. Nephrol Dial Transplant 1998;13:1588-97.  Back to cited text no. 8
9.Komatsuda A, Ohtani H, Nimura T, et al. Endocapillary proliferative glomerulonephritis in a patient with parvovirus B19 infection. Am J Kidney Dis 2000;36:851-4.  Back to cited text no. 9
10.El-Husseini AA, Sheashaa HA, Sabry AA, Moustafa FE, Sobh MA. Acute postinfectious crescentic glomerulonephritis: Clinicopathologic presentation and risk factors. Int Urol Nephrol 2005;37:603-9.  Back to cited text no. 10
11.Rodríguez-Iturbe B, Batsford S. Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. Kidney Int 2007; 71:1094-104.  Back to cited text no. 11
12.Nordstrand A, Norgren M, Holm SE. Pathogenic mechanism of acute post-streptococcal glomerulonephritis. Scand J Infect Dis 1999; 31:523-37.  Back to cited text no. 12
13.Moroni G, Pozzi C, Quaglini S, et al. Long-term prognosis of diffuse proliferative glomerulonephritis associated with infection in adults. Nephrol Dial Transplant 2002;17:1204-11.  Back to cited text no. 13
14.Srisawat N, Aroonpoonsub L, Lewsuwan S, et al. The clinicopathology and outcome of post-infectious glomerulonephritis: Experience in 36 adults. J Med Assoc Thai 2006;89 Suppl 2:S157-62.  Back to cited text no. 14
15.Vogl W, Renke M, Mayer-Eichberger D, Schmitt H, Bohle A. Long-term prognosis for endocapillary glomerulonephritis of poststreptococcal type in children and adults. Nephron 1986;44:58-65.  Back to cited text no. 15
16.Cass A, Cunningham J, Wang Z, Hoy W. Social disadvantage and variation in the incidence of end-stage renal disease in Australian capital cities. Aust N Z J Public Health 2001; 25:322-6.  Back to cited text no. 16
17.Sesso R, Pinto SW. Five-year follow-up of patients with epidemic glomerulonephritis due to Streptococcus zooepidemicus. Nephrol Dial Transplant 2005;20:1808-12.  Back to cited text no. 17
18.Kasahara T, Hayakawa H, Okubo S, et al. Prognosis of acute poststreptococcal glomerulonephritis (APSGN) is excellent in children, when adequately diagnosed. Pediatr Int 2001; 43:364-7.  Back to cited text no. 18
19.Nenov V, Maarten WT, Sakharova OV, Brener BM. Multi-hit nature of chronic renal disease. Curr Opin Nephrol Hypertens 2000;9:85-97.  Back to cited text no. 19
20.Yoshizawa N. Acute glomerulonephritis. Intern Med 2000;39:687-94.  Back to cited text no. 20

Correspondence Address:
Dr. Mouna Hamouda
Department of Nephrology, Fattouma Bourguiba Hospital, Monastir 5000
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DOI: 10.4103/1319-2442.132185

PMID: 24821153

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