Diagnosis Of Acute Post-streptococcal Glomerulonephritis Research Articles

Acute Post Streptococcal Glomerulonephritis among Children from Sokoto, North-Western Nigeria

Aims: To determine the clinical and laboratory profile of children with acute post streptococcal glomerulonephritis (APSGN) admitted into Usmanu Danfodiyo University Teaching Hospital (UDUTH) Sokoto, the outcome, and factors associated with in-hospital mortality.
 Study Design: A 5- year retrospective study.
 Place of Study: Emergency Paediatric Unit (EPU) and Paediatric Medical Ward (PMW) of the Department of Paediatrics, UDUTH Sokoto.
 Methodology: The records of children aged 4 to 14 years with the diagnosis of APSGN were reviewed. Relevant history, physical examination findings, laboratory and radiologic investigation findings were extracted from their case folders and recorded into a proforma sheet. Data was analyzed using SPSS version 23. (IBM SPSS Inc., USA). The level of statistical significance was set at 5%, which is p-value < 0.05.
 Results: Fifty-four (0.9%) of the 6128 children were managed for APSGN giving a prevalence of 10.8 APSGN cases per 1000 children. Forty-one folders were utilized for the study. There were 21(51.2%) females and 20(48.8%) males, with F:M ratio of 1.1:1. Mean age at presentation was 9.1± 3.1 years. Majority (92.6%) were ≥5 years and mainly 22(53.7%) of low socio-economic status. The main features were body swelling 40(97.6%), fever 25(61.0%), oliguria 24(58.5%), systemic hypertension 37(90.2%), proteinuria 41(100.0%), and haematuria 41(100.0%). Acute kidney injury was the commonest 25(61.0%) complication. Thirty (73.2%) cases were discharged, 5 (12.2%) died, 6(14.6%) left against medical advice. Low social status (0.03), requirement for dialysis (p=0.003), congestive cardiac failure (p=0.01), and pulmonary oedema (p=0.04) were significantly associated with in-hospital mortality. Requirement for dialysis (p=0.005) was the independent predictor of in-hospital mortality. At three months post discharge, 20(48.8%) of the 31 cases had achieved complete resolution of APSGN.
 Conclusion: APSGN is common in Sokoto and similar in pattern to other reports from Nigeria. The presence of complications at presentation increases the risk of in-hospital mortality.

Akut Post Streptokokal Glomerülonefrit Gelişiminde Mannoz-Bağlayıcı Lektinin Rolü Nedir?

Objective: This study aims to determine the effects of the mannose-binding lectin (MBL) gene polymorphism on the clinical and laboratory findings, response to treatment, and progress of patients with acute post-streptococcal glomerulonephritis (APSGN). Methods: Codon 54 polymorphism found in exon 1 of the MBL gene was investigated by polymerase chain reaction-restriction fragment length polymorphism method in 110 children followed up with the diagnosis of APSGN and compared with healthy control group. Results: The normal allele AA and, the variant alleles AB and BB gene frequencies were determined within the APSGN group as 74.5%, 20% and, 5.5%, respectively. No statistically significant difference was found with concerning to the gene polymorphism in the APSGN group when compared with the control group (p>0.05). No correlation was found in the patient group between gene polymorphism and the presence of hematuria, edema, central nervous system findings, and blood pressure (p>0.05). Concerning laboratory findings during the diagnosis, no correlation existed between the gene polymorphism and high levels of urea, creatine, total cholesterol, and triglycerides, low levels of albumin, and the presence of proteinuria (p>0.05). Within the first years following the diagnosis, no statistically significant difference was found in the glomerular filtration rates, blood creatine levels, proteinuria levels, duration of microscopic hematuria and proteinuria between the patients with the gene polymorphism and those without the gene polymorphism (p>0.05) Conclusion: Our study determined that the MBL gene polymorphism was not important in the development, the laboratory and clinical findings, or the progression of the patients with APSGN.

Pediatric post-streptococcal glomerulonephritis: Clinical and laboratory data.

Acute post-streptococcal glomerulonephritis (APSGN) is the most common post-infectious glomerulonephritis in childhood. The aim of this study was therefore to identify the possible risk factor(s) responsible for decreased glomerular filtration rate (GFR) in APSGN. The data of patients followed up with a diagnosis of APSGN in the Pediatric Nephrology Clinic of Gaziantep University Hospital between October 2014 and October 2016 were retrospectively evaluated. The total number of subjects was 75 (male/female, 42/33) with a mean age of 8.20 ± 3.25 years. The most common presentations were edema (86.7%), macroscopic hematuria (82.7%) and hypertension (73.3%, n = 55). On laboratory examination, 28 children (37.3%) had hypoalbuminemia, 58 (77.3%) had proteinuria, 20 (26.7%) had increased C-reactive protein (CRP), while 74 (98.7%) and 12 (16%) had decreased complement (C)3 and C4, respectively. The number of children with GFR <90 mL/min/1.73 m2 was 22 (29.3%). The risk of decreased GFR was significantly higher in patients with increased CRP (P = 0.001; OR, 3.58), hypoalbuminemia (P = 0.006; OR, 4.83), and decreased C4 (P = 0.010; OR, 11.53). Additionally, white blood cell (WBC) count, neutrophil count, and neutrophil/lymphocyte ratio (NLR) were significantly higher (P = 0.02, P = 0.006, P = 0.004, respectively) in patients with low GFR. Although the prognosis of APSGN in children is good, severe systemic complications and renal failure may develop during the follow-up period. Decreased C4, presence of hypoalbuminemia, and increased inflammatory markers (WBC, CRP, neutrophil count and NLR) might be possible risk factors for severity of renal involvement. Decreased C4, in particular, may be a risk factor for decreased GFR in those children.

A case of idiopathic membranoproliferative glomerulonephritis with a transient glomerular deposition of nephritis-associated plasmin receptor antigen

The differential diagnosis of acute poststreptococcal glomerulonephritis (APSGN) and idiopathic membranoproliferative glomerulonephritis (MPGN) is sometimes difficult, as they share several key features in their laboratory and histological findings, especially during the acute phase of the diseases. We herein report an idiopathic case of MPGN in which the glomerular deposition of nephritis-associated plasmin receptor (NAPlr), a recently identified nephritic antigen for APSGN, was demonstrated. A 24-year-old postpartum woman developed nephrotic syndrome and hypocomplementemia. Although she showed no apparent findings of a prior infection, her serum titer of antistreptolysin O antibody was elevated. Renal biopsies were performed twice at intervals of 6months, both of which showed findings fully consistent with those of MPGN. Of note, fluorescent immunostaining for NAPlr was positive in the glomeruli of the first biopsy but not in the second. Despite the use of a corticosteroid, hypocomplementemia persisted for more than 1year. It was therefore suggested that a streptococcal infection may have influenced the development of glomerular injury in this idiopathic case of MPGN.

Acute poststreptococcal glomerulonephritis superimposed on IgA nephropathy

Superimposition of poststreptococcal glomerulonephritis (PSGN) on the course of IgA nephropathy (IgAN) is uncommon. A case of PSGN during IgA nephropathy is presented. A 30-year-old man who had alternating gross and microscopic hematuria for 7 months underwent a renal biopsy. The first renal biopsy revealed IgAN with mesangial deposits of IgA and C3. Two months later, the patient suffered generalized edema, proteinuria, hematuria, an increased ASO titer and a decreased C3 level. A second renal biopsy revealed diffuse endocapillary proliferative glomerulonephritis with epimembranous hump-like electron-dense deposits of C3, but the original mesangial IgA deposits had disappeared. A diagnosis of acute PSGN was indicated. Two months after the onset of acute nephritic syndrome, the patient remained asymptomatic, except for microscopic hematuria and proteinuria. Some cases with persistent proteinuria or hematuria after PSGN are probably related to preexisting IgAN.

Changing epidemiology of acute post-streptococcal glomerulonephritis in Northeast Florida: a comparative study

The objective of this study was to review the epidemiological patterns of acute post-streptococcal glomerulonephritis (APSGN) in a pediatric population. We compared incidence, pathogenesis, clinical presentation and outcomes in two APSGN pediatric patient cohorts in northeastern Florida. Retrospective medical records were reviewed of children who were admitted to our institution with a diagnosis of APSGN. Patients admitted between 1999 and 2006 (recent cohort) were compared with a previously reported cohort of patients admitted between 1957 and 1973 (earlier cohort). The recent cohort comprised 45 children with APSGN of whom 87% were male and 13% were female; the median age was 7 years, and there was an average incidence of 6.4 patients per year. The earlier cohort comprised 153 children with APSGN of whom 62% were male and 38% were female; the median age 4.25 years, and there was an average incidence of 10.9 patients per year. The recent cohort was predominantly White-American (62%) and the earlier cohort predominately African American (87%). In the recent cohort, 64% of patients had antecedent pharyngitis, and in the earlier cohort, 66% of patients had antecedent pyoderma. In the recent cohort, 11% of APSGN cases occurred between August to October, and in the earlier cohort, 50% occurred during these months. In the recent cohort, symptoms of APSGN at presentation were milder and all cases recovered, but in the earlier cohort two deaths (1.3% mortality) were reported. In conclusion, there has been a decline in the incidence and severity of APSGN at our institute in recent decades. Pharyngitis has replaced impetigo as the predominant cause of APSGN. The etiological agent for impetigo has changed over the last decade, which has impacted the incidence, racial distribution, seasonal variation and severity of APSGN.

Posterior reversible encephalopathy syndrome revealing acute post-streptococcal glomerulonephritis.

A case of acute encephalopathy with posterior corticosubcortical vasogenic edema on magnetic resonance imaging is reported. Angiography showed cerebral arterial vasospasm. A diagnosis of acute post-streptococcal glomerulonephritis was made 2 days after admission. This report highlights the fact that acute post-streptococcal glomerulonephritis can be revealed by a posterior reversible encephalopathy syndrome and that cerebral vasospasm can concur with vasogenic edema in this condition.

M-associated protein antibodies in patients with rheumatic fever.

Sequential serum samples obtained from 50 rheumatic fever subjects and from control individuals matched for time, age and geographical location were tested for antibodies against the M-associated protein antigens, MAP I and MAP II. Antibody titres were determined by the complement fixation test with a partially-purified extract of Streptococcus pyogenes serotype M30 as the MAP I antigen and an acid extract of serotype M48 as the MAP II antigen. Titres of MAP I antibody exceeded those of MAP II antibody in all but six rheumatic fever subjects. Anti-MAP I titres in excess of 40 were significantly more common in rheumatic fever subjects than in matched controls (p less than 0.001) or matched subjects with a diagnosis of acute post-streptococcal glomerulonephritis (p less than 0.01). Peak MAP I titres were present at the time of admission to hospital in the sera of 40 of the 50 rheumatic fever subjects. In the remainder peak titres occurred within 10 days. Antibody titres were maintained for a mean of 10.3 weeks before declining. Changes in MAP antibody titres were independent of changes in antistreptolysin O and anti-DNAase B titres. Normal children aged between 6 and 15 had higher MAP antibody titres than 2-5-year-old children. Rheumatic fever subjects had significantly higher mean titres of MAP I antibody than matched controls in each age group.