Endocapillary Proliferative Glomerulonephritis Research Articles

Association of hemophagocytic lymphohistiocytosis with kidney lesions in acute African swine fever virus infection

Glomerulonephritis due to African swine fever (ASF) is well documented. However, there is absence of good understanding of mechanisms involved in the development of pathology development. This study examines glomerulonephritis in association with acute infection induced by II genotype (Georgia 2007) of ASF virus. Taken together, the results of urinary analysis and the renal histological analysis led to the diagnosis of diffuse endocapillary proliferative glomerulonephritis with severe tubular injury associated with acute ASF (Georgia 2007). According to the pathogenesis, we have found that the diffuse endocapillary proliferative glomerulonephritis associated with the acute ASF develops with a delay of one to two days compared to development of hemophagocytic lymphohistiocytosis. The diagnosis of endocapillary proliferative glomerulonephritis confirms the characteristic of pathological changes in the composition of urine and urine sediment. The development of acute proliferative glomerulonephritis begins at 3 dpi, and finished at 4–6 dpi with the development of tubular necrosis. Our study demonstrates local macrophage proliferation. Local proliferation may be an important mechanism for amplifying macrophage-mediated renal injury. We have shown that the development of diffuse acute proliferative glomerulonephritis during ASF does not coincide with the presence of the virus in the blood or kidney tissues, but coincides with the developmental of ASFV derived hemophagocytic lymphohistiocytosis. The development of hemophagocytic lymphonocytosis also begins at least at 2–3 dpi and continues up to the terminal stage of the disease.

Clinical and pathological characteristics of children with C3 glomerulopathy

Objective To investigate the clinicopathological features and treatment of children with C3 glome-rulopathy(C3G). Methods Seven children diagnosed as C3G by clinical and pathological characteristics were enrolled in this study.The clinicopathological data and the prognosis were analyzed. Results Of the 7 cases, 4 cases were female and 3 cases were male, with the mean age of (7.7±3.1) years old (1.5-10.4 years old) at onset, the duration from onset to renal biopsy was (3.4±2.4) months(1-6 months) and 1 of them had a second renal biopsy 4.2 years later, and mean age was (8.4±3.6) years old (1.8-13.3 years old) on diagnosis.Clinical features: among the 7 patients, 6 cases had hematuria, among them 1 case had gross hematuria and 5 cases had microscopic hematuria; 6 cases had low level of serum complement C3, 5 cases had heavy proteinuria and low serum albumin, and anemia was observed in 2 cases respectively.Five cases had complement factor H and H factor antibody by examination, and 1 of them had low serum factor H, but none of them had serum antibody to factor H. Four cases had genetic evaluation, and only 1 case revealed risk variants in the C3 gene(R304R, T612T, V807V, A915A, P1632P)and CFH gene(p.H402Y, p.E936D). Clinically, 4 cases were diagnosed as nephrotic syndrome of nephritis type, 2 cases were diagnosed as nephritic syndrome, and 1 case was diagnosed as nephrotic syndrome of simple type.Immunofluorescence study showed that all the cases had intense deposition of C3, and 6 cases were accompanied by the deposition of immunoglobulin.Under light microscopy, 3 cases showed the feature of membrane proliferative glomemlonephritis, 2 cases with endocapillary prolifera-tive glomerulonephritis, 1 case with mesangial proliferative glomerulonephritis, and 1 case with endocapillary proliferative IgA nephropathy.Under electron microscopy, 3 cases who had typical ribbon-like dense deposits in glomerular basement membrane were of dense deposit disease, and the rest were C3 glomerulonephritis.All patients had steroid and immune inhibitor treatment, and during the follow-up stage of (2.6±1.8) years(1.1-5.6 years), 4 cases showed normal urinalysis, 2 cases had microproteinurine and microscopic hematuria, and 1 case had urinary protein ±to + + and microscopic hematuria. Conclusions C3G has variety of pathological -clinical manifestation.Interpretation of individual cases depends on integration of information from the biopsy together with clinical, serological, and genetic features.Patients with steroid and immune inhibitor treatment had some clinical improvement of their urinalysis. Key words: C3 glomerulopathy; Dense deposit disease; C3 glomerulonephritis; Child

Immunologically mediated endocapillary proliferative glomerulonephritis in children

Immunologically mediated endocapillary proliferative glomerulonephritis in children

The clinicopathologic characteristics and outcome of atypical anti-glomerular basement membrane nephritis

Classic anti-glomerular basement membrane (GBM) disease presents with rapidly progressive glomerulonephritis (GN) with or without pulmonary hemorrhage. On biopsy typical disease displays bright polytypic linear GBM staining for IgG by immunofluorescence and diffuse crescentic/necrotizing GN on light microscopy. Here, we studied 20 patients with atypical anti-GBM nephritis typified by bright linear GBM staining for immunoglobulins but without a diffuse crescentic phenotype. Patients had hematuria, proteinuria, and mild renal insufficiency, without pulmonary hemorrhage. Light microscopy showed endocapillary proliferative GN in 9 patients, mesangial proliferative GN in 6, membranoproliferative GN in 3, and focalsegmental glomerulosclerosis with mesangial hypercellularity in 2. Eight of the 20 showed features of microangiopathy. Crescents/necrosis were absent in 12 and were focal in 8 patients. Bright linear GBM staining for IgG was seen in 17 patients, IgM in 2, and IgA in 1 patient, which was polytypic in 10 patients and monotypic in 10 patients. No circulating α3NC1 antibodies were detected by commercial ELISA. The 1-year patient and renal survival rates were 93% and 85%, respectively. Thus, atypical anti-GBM nephritis is a rare variant of anti-GBM disease characterized clinically by an indolent course, no pulmonary involvement, and undetectable circulating α3NC1 antibodies. Further studies are needed to characterize the molecular architecture of GBM autoantigens in these patients and establish optimal therapy.

The clinical manifestations of children with endocapillary proliferative glomerulonephritis with isolated C3 deposition

Objective To study the patients' clinical characteristics and prognosis when only C3 deposition exists in endocapillary proliferative glomerulonephritis and try to understand deeply the role of C3 in kidney damage deeply. Methods The patients who were diagnosed with endocapillary proliferative glomerulonephritis but only had C3 deposited in immunofluorescence (to avoid false positive, C3≥2+ was included) were selected from Beijing Children's Hospital Affiliated to Capital Medical University during November 2010 to October 2014.Their clinical manifestations, laboratory examinations, treatments, prognosis, and pathological changes were analyzed, and literature review was performed.Their clinical characteristics and prognosis were summarized. Results There were 11 patients diagnosed with endocapillary proliferative glomerulonephritis which had only C3 deposition (≥2+ ). Nine of them had onset with acute nephritis syndrome (81.8%), and 2 cases presented recurrent paroxysmal gross hematuria(18.2%). Seven cases were diagnosed with acute post streptococcal glomerulonephritis (63.6%). Eleven cases' clinical manifestations were relatively severe, and the complement C3 was significantly lower than the normal (100.0%). Their light microscope showed capillary proli-ferative glomerulonephritis, and the electron microscope showed the immune complexes were deposited in the endothelium, the epithelium or the mesangial area.The patients received corresponding treatment respectively, and all the patients had good prognosis during following up of 7 months up to 39 months. Conclusions Streptococcus infection is a common cause in endocapillary proliferative glomerulonephritis with only C3 deposition.The clinical manifestations of some children are similar to post streptococcal glomerulonephritis but relatively severe.Only deposition of C3 without IgG may be involved in another complement activation mechanism. Key words: Complement 3; Endocapillary proliferative glomerulonephritis; Streptococcus infection

P-205: Nephrotic syndrome revealing Hodgkin’s disease

Objectifs The association between paraneoplasic nephrotic syndrome and Hodgkin’s disease is rare estimated to be about 0.5 to 1% (0.4% as minimal change disease and 0.1% as amyloid). Methodes We report the case of an Hodgkin’s disease revealed by an isolated nephrotic syndrome. Resultats A 34-year-old man presented with the clinical symptoms of nephrotic syndrome, Physical examination was notable for lower extremity edema. Though his hematologic evaluation was consistent with anemia (white blood cells = 11300/mm 3 ; hemoglobin, 7,9g/dL; platelets, 482000/mm 3 ), there was no evidence of hemolysis but a biologic inflammatory syndrome. Nephrotic range proteinuria (3,4g in 24 hours), acute renal failure (creatinine 160umol/L), and hypoalbuminemia (23g/L) were also present. Kidney biopsy revealed endocapillary proliferative glomerulone-phritis associated with vasculitis. A treatment with prednisone was started with favorable response. Two months after the diagnostic of nephrotic syndrome was made, the patient presented prolonged fever and weight loss. The physical examination showed cervical lymphadenopathy, which lymph node biopsy revealed Hodgkin lymphoma of the nodular sclerosing type. The patient was treated for Hodgkin disease stage IVB with ABVD regimen, and was in complete remission of both Hodgkin’s disease and nephrotic syndrome. Conclusion Causes of nephrotic syndrome in Hodgkin’s disease can include renal vein thrombosis, amyloidosis or paraneoplastic syndrome. This case attracts attention that a rare cause of nephrotic syndrome can be Hodgkin’s disease.

Update on endocarditis-associated glomerulonephritis

Glomerulonephritis (GN) due to infective endocarditis (IE) is well documented, but most available data are based on old autopsy series. To update information, we now present the largest biopsy-based clinicopathologic series on IE-associated GN. The study group included 49 patients (male-to-female ratio of 3.5:1) with a mean age of 48 years. The most common presenting feature was acute kidney injury. Over half of the patients had no known prior cardiac abnormality. However, the most common comorbidities were cardiac valve disease (30%), intravenous drug use (29%), hepatitis C (20%), and diabetes (18%). The cardiac valve infected was tricuspid in 43%, mitral in 33%, and aortic in 29% of patients. The two most common infective bacteria were Staphylococcus (53%) and Streptococcus (23%). Hypocomplementemia was found in 56% of patients tested and ANCA antibody in 28%. The most common biopsy finding was necrotizing and crescentic GN (53%), followed by endocapillary proliferative GN (37%). C3 deposition was prominent in all cases, whereas IgG deposition was seen in <30% of cases. Most patients had immune deposits detectable by electron microscopy. Thus, IE-associated GN most commonly presents with AKI and complicates staphylococcal tricuspid valve infection. Contrary to infection-associated glomerulonephritis in general, the most common pattern of glomerular injury in IE-associated glomerulonephritis was necrotizing and crescentic glomerulonephritis.

Acute kidney injury in patients with human immunodeficiency virus infection.

Acute kidney injury (AKI) is an important cause of hospitalization and morbidity in human immunodeficiency virus (HIV)-positive patients. However, the data on AKI in such patients is limited. The aim of the present study was to analyze the incidence, causes and outcome of AKI in HIV-positive patients from our antiretroviral therapy centre. All HIV-positive patients were evaluated for evidence of clinical AKI. AKI was noted in 138/3540 (3.9%) patients. Of 138 AKI patients, 96 (69.6%) had acquired immuno deficiency syndrome and 42 (30.4%) were HIV seropositive. Majority of AKI patients belonged to AKI network (AKIN) Stage II (42%) or III (48.5%) at presentation. Prerenal, intrinsic and postrenal AKI were noted in 53.6%, 44.2% and 2.2% of cases, respectively. Hypovolemia (44.2%) and sepsis (14.5%) contributed to AKI in vast majority of cases. AKI was multifactorial (volume depletion, sepsis and drugs) in 39% of patients. Acute tubular necrosis (ATN) was the most common intrinsic lesion. Acute interstitial nephritis and diffuse endocapillary proliferative glomerulonephritis were noted in five and two cases, respectively. In-hospital mortality was 24.64%. Lower CD4 count, decreased serum albumin level and Stage 4 WHO disease were associated with higher mortality. At 3 months or more follow-up complete recovery of renal function, chronic kidney disease Stage 3-5 and progression to end stage renal disease were noted in 58.69%, 14.5% and 2.2% of cases, respectively. Thus, prerenal factors and ischemic ATN were the most common cause of AKI in HIV-infected patients. Recovery of renal function was seen in 59% of cases, but AKI had high in-hospital mortality.

A case of post-pneumococcal acute glomerulonephritis with glomerular depositions of nephritis-associated plasmin receptor.

We report the case of a 12-year-old girl who was referred to our hospital with anuria associated with pneumonia. On admission, the patient's blood test results revealed severe renal failure, hypoproteinemia, and hypocomplementemia. Her urinalysis results revealed hematuria, proteinuria, and a positive titer for Streptococcus pneumoniae. S. pneumoniae was also detected in her sputum and blood cultures. The patient was diagnosed with post-pneumococcal acute glomerulonephritis (AGN) with acute renal failure. A renal biopsy demonstrated the infiltration of neutrophils and mononuclear cells into capillary loops. Immunofluorescence studies showed dominant-positive deposition of C3c along the capillary loops and nephritis-associated plasmin receptor (NAPlr) depositions in the mesangial area and capillary loops. Electron microscopy revealed dense deposits in the glomerular basement membrane without a hump in the subepithelial area. These findings were consistent with endocapillary proliferative glomerulonephritis. AGN associated with pneumococcal infection is very rare. This case suggests that NAPlr is the causative antigen not only of post-streptococcal AGN, but also of post-pneumococcal AGN. To our knowledge, this is the first report that shows a relationship between post-pneumococcal AGN and NAPlr depositions in the glomeruli.

Purpura rhumatoïde de l’adulte

Henoch-Schönlein purpura is a systemic vasculitis of the small vessels characterized by perivascular leucocyte infiltrates. It is an immunoglobulin A-related immune complex-mediated disease involving the skin, the joints and the gastrointestinal system. Renal disease may sometimes be associated to these clinical manifestations. Prevalence of the nephritis is highly variable, depending on the series. More rarely, other organs such as the lungs, the heart or the nervous system may be involved. The clinical diagnosis is confirmed by histopathology of the skin (leukocytoclastic vasculitis) and kidney (endo-capillary proliferative glomerulonephritis), showing IgA deposits in these tissues. Short-term prognosis depends on the severity of digestive involvement, but long-term prognosis depends on the renal disease. Recent publications of pediatric and adult series show that the chronic renal failure may progress, sometimes more than ten years after the initial flare. Treatment is usually supportive. The benefit of more specific treatments (corticosteroids or immunosuppressive drugs) in severe visceral forms (usually abdominal or kidney) has not yet been established.

Successful treatment of infectious endocarditis associated glomerulonephritis mimicking c3 glomerulonephritis in a case with no previous cardiac disease.

We report a 42-year-old man with subacute infectious endocarditis (IE) with septic pulmonary embolism, presenting rapidly progressive glomerulonephritis and positive proteinase 3-anti-neutrophil cytoplasmic antibody (PR3-ANCA). He had no previous history of heart disease. Renal histology revealed diffuse endocapillary proliferative glomerulonephritis with complement 3- (C3-) dominant staining and subendothelial electron dense deposit, mimicking C3 glomerulonephritis. Successful treatment of IE with valve plastic surgery gradually ameliorated hypocomplementemia and renal failure; thus C3 glomerulonephritis-like lesion in this case was classified as postinfectious glomerulonephritis. IE associated glomerulonephritis is relatively rare, especially in cases with no previous history of valvular disease of the heart like our case. This case also reemphasizes the broad differential diagnosis of renal involvement in IE.

FRI0276 Alpha-melanocyte stimulating hormone analogue: beneficial effect in murine lupus activity

BackgroundAlpha-Melanocyte stimulating hormone (α-MSH) is a neuropeptide that plays antiinflamatory activity through the modulation of key molecules involved in the immune response. There is no data about their role in...

Acute poststreptococcal glomerulonephritis with acute interstitial nephritis related to streptococcal pyrogenic exotoxin B.

A 20-year-old man presented with symptoms of edema. Three weeks prior to admission, he experienced an upper respiratory tract infection. On admission, blood pressure was 177/118 mmHg. Initial laboratory investigations revealed serum creatinine, 170 µmol/L; complement C3, 130 mg/L and antistreptolysin O titer, 538 IU/mL (reference, <239 IU/mL). Urinalysis showed nephrotic range proteinuria and hematuria. A percutaneous kidney biopsy was performed. Light microscopy contained 20 glomeruli, 4 of which were globally sclerotic and 1 of which showed cellular crescent formation. Diffuse endocapillary proliferative glomerulonephritis was identified (Figure 1A). Forty percent of the interstitium was infiltrated by inflammatory cells (Figure 1B). Immunofluorescent staining revealed complement C3, mainly on capillary walls. Fig. 1. (A and B) Findings of the kidney biopsy. Hematoxylin and eosin-stained section showing diffuse endocapillary proliferation with massive infiltration of neutrophils (A) and inflammatory cells infiltration in the cortical interstitium (B). (C–F ... Acute poststreptococcal glomerulonephritis (APSGN) with acute interstitial nephritis (AIN) was diagnosed. We administered methylprednisolone pulse therapy (1 g/day) for 3 days, followed by prednisolone at 80 mg/day. The serum creatinine level declined to 74 µmol/L and proteinuria decreased to <1 g/day. Transient type 4 renal tubular acidosis was observed during steroid treatment. AIN is found in the infectious diseases of children, particularly in streptococcal infection [1]. We investigated the localization of two streptococcal antigens, streptococcal pyrogenic exotoxin B (SPEB) and nephritis-associated plasmin receptor (NAPlr), using an anti-SPEB antibody (Abcam, Cambridge, MA) and a fluorescein isothiocyanate-conjugated anti-NAPlr antibody [1F10] (Abcam). Although NAPlr was not detected, SPEB was positive in the interstitium as well as glomeruli (Figure 1C–F). Chang et al. [2] reported a case of streptococcal infection-related AIN, in which SPEB was found in both tubular epithelial cells and interstitium. In the present case, negative results were obtained for SPEB in tubular epithelial cells. Similarly, SPEB and its precursors have been detected only in glomeruli and interstitium in the rat kidney [3]. SPEB has been reported in association with the pathogenesis of APSGN. The mechanisms of leukocyte infiltration could be mediated by chemotactic effects and the migration inhibitor factor-like activities of SPEB [3]. SPEB also induces proliferation of human mononuclear leukocytes [4]. SPEB may be one of the causes of streptococcal infection-related AIN.

Recurrent Proliferative Glomerulonephritis With Monoclonal IgG Deposits of IgG2λ Subtype in a Transplanted Kidney: A Case Report

Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a recently described disease entity. In the kidney transplantation literature, only 6 recurrent and 2 de novo PGNMID cases, including 7 of the IgG3 subclass (6 with κ light chain and 1 with λ light chain) and 1 of the IgG1 subclass (λ light chain), have been described to date. We describe a 52-year-old man with end-stage renal disease whose primary glomerular disease had been suggested to be membranoproliferative glomerulonephritis. The patient underwent living related donor kidney transplantation and presented with proteinuria, hematuria, and decreased kidney function at 4 months posttransplantation. Biopsy of the transplanted kidney showed diffuse endocapillary proliferative glomerulonephritis. Immunofluorescence microscopy showed prominent granular glomerular staining for IgG, C3, and λ light chain, with IgM, IgA, and κ light chain undetectable. Immunofluorescence staining for IgG subclass showed signal for IgG2 only. Retrospective analysis of the native kidney biopsy specimen also showed the same monoclonal glomerular staining for the IgG2λ subtype. These findings led us to the diagnosis of PGNMID of the IgG2λ subtype as both the primary glomerular disease and recurrent disease in the transplanted kidney. Recurrence was treated with high-dose prednisolone, which decreased proteinuria, hematuria, and serum creatinine level. The case demonstrates that PGNMID of the IgG2λ subtype also can recur in the transplanted kidney.

Henoch-Schönlein purpura nephritis in a patient with IgG4-related disease: A possible association

We report a case of Henoch- Schönlein purpura nephritis (HSPN) associated with tubulointerstitial nephritis (TIN) and chronic sclerosing sialoadenitis. The patient is a 75-year-old Japanese woman who had bilateral submandibular gland swelling, palpable purpura on the lower legs, and decreased renal function with hematoproteinuria and marked hypocomplementemia, but no skin lesion suggestive of systemic lupus erythematosus (SLE), and did not fulfill the classification criteria for SLE. Her serum IgG4 level was high and immunostaining of renal biopsies revealed marked infiltration by IgG4-positive plasma cells in the interstitium, confirming the diagnosis of IgG4- related disease. On the other hand, glomeruli showed endocapillary proliferative glomerulonephritis with mesangial IgA and C3 deposition demonstrated by immunofluorescence staining, which were typical glomerular lesions for HSPN. The glomerular and tubulointerstitial lesions responded to steroid therapy dramatically, and her renal function recovered to within the normal range within a month. This case suggests a possible new association between HSPN and IgG4-related disease.

Proliferative glomerulonephritis with monoclonal IgG2κ deposit successfully treated with steroids: a case report and review of the literature

A novel form of glomerular injury with monoclonal immunoglobulin (Ig) IgG deposition, termed "proliferative glomerulonephritis (GN) with monoclonal IgG deposits" (PGNMID), is a recently described entity. PGNMID presents with various histological patterns, such as membranoproliferative GN, endocapillary proliferative GN and membranous nephropathy (MN). The deposits are composed of monoclonal immunoglobulin, most commonly IgG3 and occasionally IgG2. At present, the clinical significance of each IgG subclass and the morphological patterns of glomerular injury have not been fully investigated due to the limited number of PGNMID cases reported. The patient was a 27-year-old woman presenting with a mild degree of proteinuria and no other physical or serological abnormalities. Monoclonal Ig could not be identified in her serum or urine. Renal biopsy found features of MN with deposition of monoclonal IgG2κ. Electron microscopy examination revealed non-organised electron-dense deposits predominantly in subepithelial locations. Based on a diagnosis of PGNMID, she was treated with prednisolone and proteinuria significantly decreased in less than 4weeks. Although the clinical outcomes of PGNMID remain to be defined, MN features may possibly be a sign of favourable prognosis-a hypothesis supported by recent reports. The absence of advanced chronic damage in the kidney, such as glomerulosclerosis or tubulointerstitial fibrosis, may also have contributed to the favourable outcome in the present case. Further studies on additional PGNMID cases that allow the correlation of morphological features and IgG subclasses with clinical outcomes are needed in order to confirm our findings and further solidify the clinical aspects of this new disease entity.

Transition from endocapillary proliferative glomerulonephritis to membranoproliferative glomerulonephritis in a patient with a prolonged human parvovirus B19 infection

We report a case in which renal biopsies were performed 4 years apart in a woman with a prolonged human parvovirus B19 (HPB19) infection. When she was 29 years old the first biopsy, performed because of microscopic hematuria and mild proteinuria, showed endocapillary and mesangial proliferative glomerulonephritis in light microscopy as well as deposits of immunoglobulins (Igs) and complement C3 on capillary walls. Mesangial, intramembranous, and subepithelial hump-like electron dense deposits were seen in electron microscopy. The principal differential diagnoses, acute poststreptococcal glomerulonephritis and lupus nephritis, were unlikely, and her serological positivity for IgM antibody for HPB19 made us diagnose acute glomerulonephritis associated with HPB19 infection. The second biopsy, performed 4 years later because of persistent proteinuria and prolonged positivity for IgM antibody for HPB19, showed membranoproliferative glomerulonephritis (MPGN) with mesangial interposition and with thickening and double contours of glomerular basement membrane. In tissues obtained in both biopsies, HPB19 DNA was detected by polymerase chain reaction. HPB19 infection has been widely known to cause various glomerular diseases. This case reveals that acute endocapillary proliferative glomerulonephritis can change into MPGN during prolonged HPB19 infection.

Angioimmunoblastic T cell lymphoma complicated with endocapillary proliferative glomerulonephritis

Angioimmunoblastic T cell lymphoma complicated with endocapillary proliferative glomerulonephritis

Acute Post-streptococcal Glomerulonephritis with Acute Kidney Injury in Nephrotic Syndrome with the Glomerular Deposition of Nephritis-associated Plasmin Receptor Antigen

We herein report the case of a 17-year-old man who developed an increased plasma creatinine level (11.1 mg/dL) and oliguria with massive proteinuria (27.3 g/day) four weeks after an abraded wound to his right knee. The histology of the renal biopsy specimens showed diffuse endocapillary proliferative glomerulonephritis with the deposition of nephritis-associated plasmin receptor in the glomerulus. A case of acute kidney injury due to nephrotic syndrome caused by acute post-streptococcal glomerulonephritis was diagnosed. His renal function and proteinuria were improved with supportive care, including hemodialysis, without the administration of immunosuppressive agents.

Human Parvovirus B19-Induced Acute Glomerulonephritis: A Case Report

Human parvovirus B19 (HPV B19) infection is well known as a cause of erythema infectiosum in children. Acute glomerulonephritis due to HPVB19 infection is rarely observed in adults. Here, we present the case of a 45-year-old female who showed acute glomerulonephritis induced by HPVB19 infection with various autoantibodies. She had proteinuria (175 mg/g creatinine) and hematuria (20–29 erythrocytes per high-power field) in a urinalysis, and various autoantibodies such as antinuclear antibodies, proteinase-3-antineutrophil cytoplasmic antibodies (PR3-ANCA), antiglomerular basement membrane (GBM) antibodies, and anticardiolipin antibodies in a blood examination. A renal biopsy showed that endocapillary proliferative glomerulonephritis comprised of mononuclear cell infiltration. By using immunofluorescence microscopy, IgG, IgA, IgM, C3, C4, and C1q deposits were detected mainly in glomerular capillaries. Electron-dense deposits were detected in the subendothelial area and mesangial area by using electron microscopy. All symptoms and abnormal laboratory data were self-improved. Our patient’s case may provide a clue to the etiology of ANCA-associated vasculitis or lupus nephritis.