A 61 YEAR DIABETIC MAN WITH METHICILLIN‐SENSITIVE <i>STAPHYLOCOCCUS AUREUS</i> SEPTIC ARTHRITIS AND ACUTE RENAL FAILURE: A CASE OF IGA‐DOMINANT POSTINFECTIOUS GLOMERULONEPHRITIS

Erqou, Sebhat; Kamat, Nitin; Moschos, Stergios; Im, Annie; Bastacky, Sheldon

doi:10.1111/j.1440-1797.2012.01602.x

Cited by 6 publications

(5 citation statements)

References 8 publications

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“…High-dose steroid therapy is often recommended for severe, rapidly advancing IgAN; however, this therapy is often not recommended for IgA-dominant IAGN. There have been some reports of successful treatment of IgA-dominant IAGN with antibiotics only [5,6,20,23]. Steroids therapy may play a role in the treatment of resistant cases who do not respond to antibiotics alone and several case reports of successful treatment of resistant cases with steroids [25,30,32].…”

Section: Discussionmentioning

confidence: 99%

“…One study was excluded due to the presence of idiotypic IgAN combined with infecion [11]; 3 references were excluded because of publication type (i.e., review) [2,12,13]; and 3 studies were excluded due to unavailable relevant original data [14,15,16]. Finally, 28 eligible reports concerning IgA-dominant IAGN were obtained and reviewed again based on the exclusion criteria [4,5,6,7,8,9,10,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37]. …”

Section: Methodsmentioning

confidence: 99%

“…It is an immune complex-mediated form of GN that mimics classic APIGN. In contrast to typical APIGN, which is characterized by glomerular deposition of C3 and IgG or C3 only, IgA is the dominant or co-dominant immunoglobulin (Ig) detected using immunofluorescence (IF) in IgA-dominant IAGN [4,5,6]. This disease is often caused by various infections, such as visceral abscesses, skin infections, or joint infections [7].…”

Section: Introductionmentioning

confidence: 99%

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Clinicopathologic Features of IgA-Dominant Infection-Associated Glomerulonephritis: A Pooled Analysis of 78 Cases

Bu¹,

Li²,

Duan³

et al. 2015

Am J Nephrol

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Backgrounds: IgA-dominant infection-associated glomerulonephritis (IgA-dominant IAGN) is a unique form of glomerulonephritis. There are numerous case reports in the literature. However, the risk factors, treatment approach, and outcomes of the disease are not clearly characterized. Methods: We completed a pooled analysis based on published literature. Clinical features, laboratory findings, and histopathological changes were analyzed. A logistic regression model was employed to identify the determinants of disease outcome, for example, end-stage renal disease (ESRD) or death. Results: Seventy-eight patients with IgA-dominant IAGN from 28 reports were analyzed. All of these patients showed granular IgA deposits predominantly along the glomerular peripheral capillary walls using immunofluorescence and majority showed subepithelial ‘hump-shaped' electron-dense deposits using electron microscopy. The majority of patients had hematuria (76/78), proteinuria (75/78), acute kidney injury (AKI) (66/78) and hypocomplementemia (43/75) without a previous history of renal disease. All of the patients had clinical infections at the time of presentation. Skin infections (19/78) and visceral abscesses (15/78) were frequently encountered, and staphylococcus was the most common pathogen. After treatment with antibiotics and/or supportive therapy, the renal function of 42 patients (54.5%) improved, 9 patients (11.7%) had persistent renal dysfunction, 15 patients (19.5%) progressed to ESRD, and 11 patients (14.3%) died. A multivariate regression analysis revealed that age (odds ratio [OR], 30.71; 95% confidence interval [CI], 2.53-373.07; p = 0.007) and diabetes mellitus (DM) (OR, 16.65; 95% CI, 1.18-235.84; p = 0.038) were independent risk factors for ESRD or death. Conclusions: IgA-dominant IAGN has unique clinicopathological manifestations and treatment responses. Age and DM are independent risk factors associated with an unfavorable prognosis for IgA-dominant IAGN.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Clinicopathologic Features of IgA-Dominant Infection-Associated Glomerulonephritis: A Pooled Analysis of 78 Cases

Bu¹,

Li²,

Duan³

et al. 2015

Am J Nephrol

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“…Fifty-one percentage of the cases (in which an infection site was identified) were due to cellulitis, and Staphylococcus is the most commonly associated pathogen, but there are also reports indicating occurrence in patients with urinary tract infections. [1][2][3][4][5][6]8,9 The clinical manifestations include acute nephritic syndrome with severe renal failure (acute or rapidly progressive), new onset of gross hematuria with or without RBC casts (25% of the cases), nephrotic and non-nephrotic range proteinuria, edema, and hypertension (∼75% at presentation). Extrarenal manifestations rarely occur in adults with IRGN.…”

Section: Discussionmentioning

confidence: 99%

“…The IgA-rich environment in diabetics coupled with IgA-specific responses to the proposed staphylococcal superantigen may precipitate a unique variant of PIGN with glomerular IgA deposition and explain the predilection for more severe IgA dominant IRGN in diabetic patients. 3,5,8,9…”

Section: Discussionmentioning

confidence: 99%

IgA-dominant post-infectious glomerulonephritis presenting as a fatal pulmonary-renal syndrome

Saad

Daoud

Nasr

et al. 2015

IJNRD

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Over the last decades, post-infectious glomerulonephritis underwent major changes in its epidemiology, pathophysiology, and outcomes. We are reporting a case of IgA-dominant post-infectious glomerulonephritis (IgA-PIGN) presenting as a fatal pulmonary-renal syndrome. An 86-year-old Filipino man presented with worsening dyspnea, hemoptysis, and decreased urine output over 2 weeks. Past medical history is significant for hypertension, chronic kidney disease stage III, and pneumonia 3 weeks prior treated with intravenous cefazolin for methicillin-sensitive Staphylococcus aureus bacteremia. Physical examination was remarkable for heart rate of 109/min and respiratory rate of 25/min saturating 99% on 3 liters via nasal cannula. There were bibasilar rales in the lungs and bilateral ankle edema. A chest radiograph showed bibasilar opacifications. Blood work was significant for hemoglobin of 8.3 g/dL and creatinine of 9.2 mg/dL (baseline of 1.67). TTE showed EF 55%. Urinalysis revealed large blood and red blood cell casts. Kidney ultrasound showed bilateral echogenicity compatible with renal disease. Pulse methylprednisolone therapy and hemodialysis were initiated with patient’s condition precluding kidney biopsy. Serology workup for rapidly progressive glomerulonephritis was negative. On day 7, the patient required mechanical ventilation; bronchoscopy showed alveolar hemorrhage and plasmapheresis was initiated. Renal biopsy revealed IgA-PIGN with endocapillary and focal extracapillary proliferative and exudative features. IgA-PIGN occurs in diabetic elderly (mean age of 60 years), 0–16 weeks after an infection mainly by Staphylococcus. However, this nondiabetic patient had normal complement IgA-PIGN with fatal pulmonary-renal syndrome. Understanding the pathogenesis and identifying the nephrotoxic bacteria species and the aberrant IgA molecule will open new insights toward prevention and treatment.

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Defining the spectrum of immunoglobulin A–dominant/codominant glomerular deposition in diabetic nephropathy

Cossey

Messias

et al. 2014

Human Pathology

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A 61 YEAR DIABETIC MAN WITH METHICILLIN‐SENSITIVE STAPHYLOCOCCUS AUREUS SEPTIC ARTHRITIS AND ACUTE RENAL FAILURE: A CASE OF IGA‐DOMINANT POSTINFECTIOUS GLOMERULONEPHRITIS

Cited by 6 publications

References 8 publications

Clinicopathologic Features of IgA-Dominant Infection-Associated Glomerulonephritis: A Pooled Analysis of 78 Cases

Clinicopathologic Features of IgA-Dominant Infection-Associated Glomerulonephritis: A Pooled Analysis of 78 Cases

IgA-dominant post-infectious glomerulonephritis presenting as a fatal pulmonary-renal syndrome

Defining the spectrum of immunoglobulin A–dominant/codominant glomerular deposition in diabetic nephropathy

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