Diffuse Endocapillary Proliferative Glomerulonephritis Research Articles

POS-058 CLINICAL OUTCOMES IN IRGN - A SINGLE CENTRE EXPERIENCE IN 21 PATIENTS FROM SOUTH INDIA

IRGN is one of the common causes of glomerulonephritis in India with a changing spectrum of clinical presentation and variable course. The most classical description of Light microscopy is diffuse endocapillary proliferative exudative Glomerulonephritis, but other findings of Light microscopy can also be found.

Recurrent Crescentic Infection Related Glomerulonephritis: a rare presentation

Infection Related Glomerulonephritis (IRGN) is an immune-mediated disease caused by non-renal infections. The most common histopathology is diffuse endocapillary proliferative glomerulonephritis with neutrophilic infiltrate. IRGN presenting as crescentic glomerulonephritis is exceptionally uncommon. We describe a 17-year-old girl, with no prior comorbidities who presented with recurrent crescentic IRGN. The first episode was in 2014; she made a complete recovery with immunosuppression. She developed a repeat episode of crescentic Infection-Related Glomerulonephritis in 2019, which was also treated with immunosuppression. This case report presents an extremely rare presentation of recurrent IRGN with crescents.

A case of aggressive atypical anti-GBM disease complicated by CMV pneumonitis

BackgroundAnti-glomerular basement membrane (anti-GBM) disease is characterized by circulating IgG glomerular basement membrane antibodies and is clinically expressed as a rapidly progressive crescentic glomerulonephritis (GN), with 30–60% of patients also developing pulmonary hemorrhage. Classically, the renal biopsy shows glomerular crescent formation, bright linear staining of glomerular basement membranes (GBM) for IgG on direct immunofluorescence (IF), and the serologic presence of circulating anti-GBM antibodies. Recently, patients with linear IgG IF staining, undetectable circulating anti-GBM antibodies and glomerular changes atypical for anti-GBM disease have been described as “atypical anti-GBM disease”, with a distinctly more benign clinical course than typical anti-GBM disease. We present a case report of a patient with negative anti-GBM serology but positive linear IgG staining by IF, severe diffuse crescentic and endocapillary proliferative glomerulonephritis, and renal failure, complicated by severe pulmonary hemorrhage after immunosuppression, likely due to cytomegalovirus (CMV) pneumonitis.Case presentationA 24-year-old man was admitted to hospital with hemoptysis and renal failure. Investigations for anti-GBM serology by addressable laser bead immunoassay (ALBIA) was negative for anti-GBM antibodies. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis with membranoproliferative features and diffuse circumferential crescents. Direct IF showed strong linear staining for IgG along GBMs. The patient’s hemoptysis improved with immunosuppression, but 1 month later he was readmitted with gross hemoptysis, which was refractory to further cyclophosphamide, plasma exchange and rituximab. Bronchoalveolar lavage (BAL) and blood work confirmed CMV pneumonitis, and the patient’s hemoptysis resolved with ganciclovir, though he became dialysis dependent.ConclusionsThis case demonstrates an atypical presentation of anti-GBM disease with both crescents and endocapillary hypercellularity and negative serology. The patient is dialysis dependent, unlike most previously described patients with atypical anti-GBM disease. The course was complicated by CMV pneumonitis, which contributed to the severity of the pulmonary manifestations and added diagnostic difficulty.

TAFRO syndrome with refractory thrombocytopenia responding to tocilizumab and romiplostim: a case report.

Thrombocytopenia, anasarca, fever, reticulin fibrosis, organomegaly (TAFRO) syndrome is a unique clinicopathologic subtype of multicentric Castleman's disease that has recently been identified in Japan. However, little is known about its renal histological changes and the optimal treatment for TAFRO syndrome. An 80-year-old Japanese woman was admitted to our hospital for evaluation of severe anasarca and weight gain (10kg in a month). She had polyneuropathy, monoclonal plasma cell proliferative disorder with positive kappa M-protein, a sclerotic bone lesion, elevation of vascular endothelial growth factor (VEGF), skin changes, and extravascular volume overload, which fulfilled the diagnostic criteria for POEMS (polyneuropathy, organomegaly, endocrinopathy, and monoclonal protein, skin changes) syndrome. However, kappa-type M-protein and thrombocytopenia with positivity of platelet-associated immunoglobulin G antibody were unusual, and fitted the diagnostic criteria for TAFRO syndrome. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis with endothelial swelling and the infiltration of monocytes and neutrophils without specific immunoglobulin deposits. Her systemic symptoms were refractory to initial treatment with high-dose melphalan and glucocorticoids. Alternative therapy with an anti-interleukin-6 (IL-6) receptor antibody (tocilizumab) effectively controlled the symptoms, while a thrombopoietin receptor agonist (romiplostim) was effective for her thrombocytopenia. Results suggest that IL-6-VEGF axis and an autoimmune mechanism may be responsible for TAFRO syndrome with clinical features of POEMS and refractory thrombocytopenia, which can be successfully treated with combination of tocilizumab and romiplostim.

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.

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.

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.

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.

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.

C3 glomerulonephritis: clinicopathological findings, complement abnormalities, glomerular proteomic profile, treatment, and follow-up

C3 Glomerulonephritis (C3GN) is a recently described disorder that typically results from abnormalities in the alternative pathway of complement. Here, we describe the clinical features, kidney biopsy findings, alternative pathway abnormalities, glomerular proteomic profile, and follow-up in 12 cases of C3GN. This disorder equally affected all ages, both genders, and typically presented with hematuria and proteinuria. In both the short and long term, renal function remained stable in the majority of patients with native kidney disease. In two patients, C3GN recurred within one year of transplantation and resulted in a decline in allograft function. Kidney biopsy mainly showed a membranoproliferative pattern; although both mesangial proliferative and diffuse endocapillary proliferative glomerulonephritis were noted. Alternative pathway abnormalities were heterogeneous; both acquired and genetic. The most common acquired abnormality was the presence of C3 nephritic factors, while the most common genetic finding was the presence of H402 and V62 alleles of Factor H. In addition to these risk factors, other abnormalities included Factor H auto-antibodies and mutations in CFH, CFI and CFHR genes. Laser dissection and mass spectrometry of glomeruli from patients with C3GN showed accumulation of alternative pathway and terminal complement complex proteins. Thus, C3GN results from diverse abnormalities of the alternative complement pathway leading to subsequent glomerular injury.

Proliferative glomerulonephritis with monoclonal immunoglobulin G3κ deposits in association with parvovirus B19 infection

Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits is a recently described disease entity, characterized by nonorganized electron-dense deposits in glomeruli and immunofluorescence findings indicating monoclonal immunoglobulin G deposits. The pathogenesis of many cases of proliferative glomerulonephritis with monoclonal immunoglobulin G deposits remains unknown. We herein report 2 patients with parvovirus B19 infection who developed acute nephritic syndrome with hypocomplementemia (patient 1) or persistent proteinuria and congestive heart failure (patient 2); however, neither patient had detectable levels of serum monoclonal immunoglobulin G. Renal biopsy in both patients showed diffuse endocapillary proliferative glomerulonephritis with monoclonal immunoglobulin G3κ deposits, and electron microscopy showed nonorganized electron-dense deposits mainly in the subendothelial and mesangial areas. Clinical symptoms, abnormal laboratory findings, and urinary abnormalities recovered spontaneously in both cases within 4 weeks. Our 2 cases may be the first reported patients with proliferative glomerulonephritis with monoclonal immunoglobulin G deposits possibly associated with parvovirus B19 infection. Virus infection-associated immune disorders could be implicated in the pathogenesis of proliferative glomerulonephritis with monoclonal immunoglobulin G deposits.

Clinicopathologic Features of IgA-Dominant Postinfectious Glomerulonephritis

BackgroundIgA-dominant acute postinfectious glomerulonephritis (APIGN) is a recently recognized morphologic variant of APIGN, but its clinicopathologic features were not clearly characterized. We will present demographic, clinical and renal biopsy findings from seven patients with IgA-dominant APIGN with a literature review.MethodsAll renal biopsy specimens (n=1,119) processed by the Department of Pathology in Hanyang University Hospital from 2005 to 2009 were reviewed. Seven patients with IgA-dominant APIGN were identified, and their clinical data analyzed.ResultsAll patients had renal failure, hematuria and proteinuria. One was diabetic, and none of the patients had previous renal diseases. Three had clinical infections at the time of presentation: 2 with methicillin-resistant Staphylococcus aureus and one with rickettsial infection. Light microscopically diffuse endocapillary proliferative and exudative glomerulonephritis was found in all cases. Immunofluorescence microscopy showed granular IgA deposits along peripheral capillary walls and in mesangium. Ultrastructurally, subepithelial 'humps' with mesangial deposits were noted. End-stage renal disease developed in two patients, chronic renal failure was stationary in two, and azotemia improved in three.ConclusionsVarious infections including rickettsiosis preceded IgA-dominant APIGN in both diabetics and nondiabetics. Because the prognosis of IgA-dominant APIGN is poor, early diagnosis based on renal biopsy is required.

Acute Glomerulonephritis in an Immunocompetent Elderly Woman after Contact with a Child who Had Been Diagnosed as Erythema Infectiosum

The prevalence of postinfectious glomerulonephritis has decreased in most developed countries. We report the case of a previously healthy, immunocompetent 65-year-old woman who developed acute glomerulonephritis associated with human parvovirus B19 infection. She was referred by her primary care physician for suspected congestive heart failure but she had an elevated creatinine level and an abnormal urinalysis. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. After biopsy, we learned that she had been in frequent contact with her grandson who had been diagnosed with erythema infectiosum. Her human parvovirus B19 serum IgM titer was elevated at 3.50, indicating current infection.

IgA-Dominant Postinfectious Glomerulonephritis: Not Peculiar to Staphylococcal Infection and Diabetic Patients

Background: IgA-dominant postinfectious glomerulonephritis (PIGN) is a unique form of PIGN. It has been linked to staphylococcal infection and underlying diabetic glomerulosclerosis. However, the significance of glomerular IgA-dominant deposition in PIGN remains unclear. Methods: We reported 10 patients with IgA-dominant PIGN encountered at a single center, each characterized by subepithelial humps. Their demographic, clinical, and renal biopsy findings were summarized and compared with the data of 32 patients with non-IgA-dominant PIGN. Results: The mean age was 57 years. An immunocompromised background was present in 70% of patients; only one patient had diabetes mellitus. The causative infectious agents included Staphylococcus (30%), Streptococcus (20%), and gram-negative organisms (50%). Decreased serum complement was present in 60%. Increased serum IgA was noted in 75%. The mean peak serum creatinine was 5.1 mg/dL, and 20% required acute dialysis. Diffuse endocapillary-proliferative glomerulonephritis was found in all cases, and three patients also had crescentic glomerulonephritis. Electron microscopy revealed large subepithelial hump-shaped deposits in all cases. At the last follow-up, one patient had died, five had achieved complete recovery, three had persistent renal insufficiency, and one was on chronic dialysis. Compared to patients with non-IgA-dominant PIGN, increased serum IgA was more commonly present in IgA-dominant group (p = 0.007). There were no significant differences in other clinical parameters and outcome between the two groups. Conclusions: IgA-dominant PIGN resembles poststreptococcal glomerulonephritis in its histological spectrum and ultrastructural appearance. Increasing serum IgA may be involved in the pathogenesis of this form of PIGN. Our data suggested that IgA-dominant PIGN was not peculiar to staphylococcal infection and diabetic patients.

The Spectrum of Adult Postinfectious Glomerulonephritis in the New Millennium

Background. Postinfectious glomerulonephritis is rare in adults. The characteristics of the disease now differ from what were described decades ago. The goal of this study is to illustrate the clinicopathological spectrum of the disease in the modern era. Methods. Between July 2000 and June 2008, 20 adult cases of postinfectious glomerulonephritis were identified at a medical center in Taiwan. The patients' records were retrospectively reviewed with respect to clinical presentation, microbiology, serology, morphology of renal biopsy, and clinical course. Results. There were 14 males and 6 females. The mean age was 61 years. All patients developed acute renal failure, and the majority (65%) required dialysis support during the disease course. Hypocomplementemia was present in 60% of patients. The most frequently identified infectious agent was Staphylococcus (60%). Histological characteristics showed two distinct patterns of glomerulonephritis: diffuse endocapillary proliferative glomerulonephritis (65%) and focal mesangial proliferative glomerulonephritis (35%). There were no significant differences in the clinical presentation and outcome between the two groups. However, glomerular neutrophil infiltration was more commonly present in diffuse endocapillary proliferative pattern (p = 0.017). The percentage of patients with focal mesangial proliferative pattern significantly increased over time (p < 0.001). At the last follow-up, 6 patients (30%) had died, 6 (30%) were in complete remission, 4 (20%) had partial remission with renal insufficiency, and 4 (20%) were on chronic dialysis. Conclusions. Our data suggested that Staphylococcus had become the leading pathogen in adult postinfectious glomerulonephritis over the past 10 years. Furthermore, atypical histological feature with focal mesangial proliferative pattern was increasingly identified over time. The prognosis was still guarded, carrying a considerable mortality rate and risk for developing chronic renal failure.

Clinicopathological study of infection-associated glomerulonephritis in adults

Infection-associated glomerulonephritis is uncommon in adults. In the present study, we have tried to determine the mode of presentation, the spectrum of morphology, and the prognostic factors for renal outcome in adult patients with infection-associated glomerulonephritis. Between July 2000 and June 2008, 20 adults (14 males, 6 females) with infection-associated glomerulonephritis were managed at a medical center in Taiwan. The patients' records were retrospectively reviewed with respect to clinical presentation, microbiology, serology, morphology of renal biopsy, and clinical course. All patients developed acute renal failure and the majority required dialysis support. The most frequently identified infectious agent was Staphylococcus (60%). Histological characteristics showed two distinct patterns of glomerulonephritis. One was diffuse endocapillary proliferative glomerulonephritis (65%) and the other was focal mesangial proliferative glomerulonephritis (35%). There were no significant differences in the clinical presentation and outcome between the two groups. However, glomerular neutrophil infiltration and subepithelial hump-shaped deposits were more commonly present in diffuse endocapillary proliferative pattern (P = 0.017, 0.004, respectively). Moreover, the percentage of patients with focal mesangial proliferative pattern significantly increased over time (P < 0.001). At the end of follow-up, 6 patients (30%) had died, 6 (30%) were in remission, 4 (20%) had renal insufficiency, and 4 (20%) were on chronic dialysis. The prognostic factors for renal outcome were peak serum creatinine, percentage of glomeruli affected by crescents, and interstitial infiltration (P = 0.02, 0.05, 0.01, respectively). Our data suggested that Staphylococcus had become the leading pathogen in adult infection-associated glomerulonephritis over the past 10 years. Furthermore, atypical histological feature with focal mesangial proliferative pattern was increasingly identified over time. The prognosis was still guarded, with a considerable mortality rate and risk for developing chronic renal failure.

Diabetic glomerular disease: pitfalls in diagnosis.

Sir, Diabetic nephropathy is a common but not an invariable complication of type 1 and 2 diabetes mellitus. However, diabetes mellitus itself is very common, and therefore, other causes of renal impairment co-exist in this population. Even with a renal biopsy, the correct diagnosis may not always be immediately evident as other pathologies can also mimic diabetic nephropathy. We present a case where diabetes mellitus was incorrectly assumed to be the cause of the patient's renal impairment. The case is of a 54-year-old man diagnosed with type 1 diabetes mellitus 20 years earlier. He had proliferative retinopathy and autonomic neuropathy but no proteinuria and no hypertension. He developed sudden onset nephrotic syndrome with eGFR >60 ml/min/1.73 m2. On renal biopsy, the light microscopic appearance was of a diffuse and nodular diabetic glomerulosclerosis with arteriolar hyalinosis. However, the degree of mesangial and endocapillary proliferation was atypical. EM examination disclosed large mesangial, para-mesangial and small extra-mesangial sub-endothelial electron-dense deposit but no specific features of light chain deposition disease. Over the next 6 months, his eGFR deteriorated to 9 ml/min/ 1.73 m2. The repeat biopsy revealed a new focal necrotising and crescentic glomerulonephritis. On immunohistochemistry, there were IgA and C3 deposits in the glomerular mesangium and extra-mesangial capillary walls (Figure ​(Figure1).1). The final histological diagnosis was that of diffuse (endocapillary) proliferative glomerulonephritis–IgA nephropathy superimposed on diffuse and nodular diabetic glomerulosclerosis that later evolved into a focal and necrotising crescentic glomerulonephritis. The patient's renal function deteriorated further and he started dialysis. Fig. 1 Mesangial deposits of IgA × 400. The sudden onset of nephrotic syndrome in our case should suggest an alternative diagnosis to diabetic nephro- pathy, as this alone would usually be preceded by lesser degrees of proteinuria. Despite diabetic nephropathy being the leading cause of end-stage renal failure in the Western world, we must remain suspicious for alternative non-diabetic causes of renal impairment that may co-exist with diabetic nephropathy. Furthermore, other diseases, in particular light chain deposition disease, can mimic the typical nodular lesions of diabetic glomerulosclerosis. Our case emphasizes the importance of immunochemical and ultrastructural evaluation of biopsy tissue submitted from all such patients [1]. Conflict of interest statement. None declared.

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.

Acute poststaphylococcal glomerulonephritis superimposed on diabetic glomerulosclerosis

Acute poststaphylococcal glomerulonephritis superimposed on diabetic glomerulosclerosis