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Anjali A. Satoskar - One of the best experts on this subject based on the ideXlab platform.

  • Acute Glomerulonephritis with large confluent IgA-dominant deposits associated with liver cirrhosis - Fig 1
    2018
    Co-Authors: Jessica Hemminger, Vidya Arole, Isabelle Ayoub, Sergey V. Brodsky, Tibor Nadasdy, Anjali A. Satoskar
    Abstract:

    Light microscopy, immunofluorescence, and electron microscopy findings: A-F, Patient 1 and G-I, Patient 6. A) Mild staining for IgG (400x). B) Strong staining for IgA (400x). C) Strong staining for C3 (400x). D) Thickened capillary loops with "wire-loop lesions” (arrow) (Periodic Acid Schiff; 630x). E) and F) Large subendothelial electron dense immune-type deposits on ultrastructural examination (lead citrate and uranyl acetate fixation; 4,000x and 12,000x, respectively). G) Thickened capillary loops (Periodic Acid Schiff; 400x); H) and I). Large subepithelial electron dense immune-type deposits (lead citrate and uranyl acetate fixation; 6000x and 12,000x, respectively).

  • Acute Glomerulonephritis with large confluent IgA-dominant deposits associated with liver cirrhosis
    2018
    Co-Authors: Jessica Hemminger, Vidya Arole, Isabelle Ayoub, Sergey V. Brodsky, Tibor Nadasdy, Anjali A. Satoskar
    Abstract:

    BackgroundSmall glomerular IgA deposits have been reported in patients with liver cirrhosis, mainly as an incidental finding in autopsy studies. We recently encountered nine cirrhotic patients who presented with Acute proliferative Glomerulonephritis with unusually large, exuberant glomerular immune complex deposits, in the absence of systemic lupus erythematosus (SLE) or monoclonal gammopathy-related kidney disease. Deposits were typically IgA dominant/codominant. Our aim was to further elucidate the etiology, diagnostic pitfalls, and clinical outcomes.MethodsWe present clinical features and kidney biopsy findings of nine cirrhotic patients with an unusual Acute immune complex Glomerulonephritis. We also identified native kidney biopsies from all patients with liver cirrhosis at our institution over a 13-year period (January 2004 to December 2016) to evaluate presence of glomerular IgA deposits in them (n = 118).ResultsSix of nine cirrhotic patients with the large immune deposits had a recent/concurrent Acute bacterial infection, prompting a diagnosis of infection-associated Glomerulonephritis and treatment with antibiotics. In the remaining three patients, no infection was identified and corticosteroids were initiated. Three of nine patients recovered kidney function (one recovered kidney function after liver transplant); three patients developed chronic kidney disease but remained off dialysis; two patients became dialysis-dependent and one patient developed sepsis and expired shortly after biopsy. Within the total cohort of 118 patients with cirrhosis, 67 others also showed IgA deposits, albeit small; and 42 patients had no IgA deposits.ConclusionsThese cases provide support to the theory that liver dysfunction may compromise clearance of circulating immune complexes, enabling deposition in the kidney. At least in a subset of cirrhotic patients, a superimposed bacterial infection may serve as a “second-hit” and lead to Acute Glomerulonephritis with exuberant immune complex deposits. Therefore, a trial of antibiotics is recommended and caution is advised before immunosuppressive treatment is offered. Unfortunately, most of these patients have advanced liver failure; therefore both diagnosis and management remain a challenge.

Masami Imakita - One of the best experts on this subject based on the ideXlab platform.

  • a patient with membranoproliferative Glomerulonephritis diagnosed by the third biopsy via endocapillary proliferative Glomerulonephritis and focal membranoproliferative Glomerulonephritis
    Clinical and Experimental Nephrology, 2003
    Co-Authors: Kenichi Kano, Kiyoshi Nishikura, M Kojima, Yumi Yamada, Osamu Arisaka, Shigeki Tomita, Tsunesuke Shimotsuji, Yasuhiro Fujikawa, Sadamitsu Inafuku, Masami Imakita
    Abstract:

    We present a girl with type I membranoproliferative Glomerulonephritis (MPGN) diagnosed by the third renal biopsy. The first renal biopsy was performed at age 11.2 years after microscopic hematuria (which was revealed by school urinary screening) had persisted for 3 months, along with a low level of serum C3. Pathological examination of the biopsied specimen revealed endocapillary proliferative Glomerulonephritis with multiple humps. The serum C3 level increased to within the normal range 2 months after the first renal biopsy, and the microscopic hematuria disappeared at age 12.3. However, microscopic hematuria, proteinuria, and the low serum complement level reappeared at age 12.8. Pathological examination of a further renal biopsy that was performed at age 13.2 revealed focal MPGN with humps. Prednisolone therapy was subsequently initiated. Fluvastatin was added to her treatment regime when she developed hypercholesterolemia at age 13.6 and was continued even after normal cholesterol levels were reestablished. Pathological examination of the third renal biopsy, which was performed at age 15.2, revealed type I MPGN with humps. Serum C3 normalized 6 months after the cessation of prednisolone at age 15.9. It is clinically important that patients with nontypical Acute Glomerulonephritis should be observed over a long period and repeated renal biopsies should be performed.

Takashi Oda - One of the best experts on this subject based on the ideXlab platform.

  • crescentic poststreptococcal Acute Glomerulonephritis accompanied by small vessel vasculitis case report of an elderly male
    BMC Nephrology, 2019
    Co-Authors: Keiko Yano, Hiroyuki Suzuki, Takashi Oda, Yoshihiko Ueda, Tatsuo Tsukamoto, Eri Muso
    Abstract:

    Poststreptococcal Acute Glomerulonephritis (PSAGN) in the elderly tends to have a severe clinical course and often presents with crescentic necrotizing Glomerulonephritis in the renal biopsy. However, vasculitis lesions are unusual. We present a 71-year-old man who was admitted to our hospital for a recurrent gout attack with a rapid decline of renal function. Low C3 levels and a high anti-streptolysin O titer were observed, while myeloperoxidase- and proteinase 3- antineutrophil cytoplasmic antibody (ANCA) were negative. In addition to cellular crescent and necrosis lesions, diffuse peritubular capillaritis and venulitis as well as small arteriole vasculitis in the glomerular hilus were also apparent. Although granular C3c deposits in the capillary wall and hump lesions were not found, immunofluorescent staining for nephritis-associated plasmin receptor (NAPlr) and in situ zymography for plasmin activity were both positive. We thus diagnosed PSAGN accompanied by small vessel vasculitis. Steroid therapy gradually improved the patient’s renal function, and hemodialysis was discontinued after 1 month. In our case, streptococcus infection might have concurrently provoked vasculitis, and NAPlr staining was useful for confirming diagnosis.

  • transition from endocapillary proliferative Glomerulonephritis to membranoproliferative Glomerulonephritis in a patient with a prolonged human parvovirus b19 infection
    Clinical Nephrology, 2013
    Co-Authors: Takahiro Uchida, Takashi Oda, Atsushi Watanabe, Kojiro Yamamoto, Yuka Katsurada, Hideyuki Shimazaki, Seiichi Tamai, Hiroo Kumagai
    Abstract:

    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.

  • A case of dense deposit disease associated with a group A streptococcal infection without the involvement of C3NeF or complement factor H deficiency
    Pediatric Nephrology, 2010
    Co-Authors: Kenichi Suga, Takashi Oda, H Kitamura, Shuji Kondo, Sato Matsuura, Yukiko Kinoshita, Etsuko Kitano, Michiyo Hatanaka, Yoshihiko Hidaka, Shoji Kagami
    Abstract:

    A 14-year-old girl presented with Acute Glomerulonephritis. Tests revealed hypocomplementemia and elevated Antistreptolysin-O titers, and renal biopsy revealed endocapillary and mesangial proliferative Glomerulonephritis with double contours of the glomerular basement membrane (GBM). Despite methylprednisolone pulse therapy and the administration of oral prednisolone, overt proteinuria and hypocomplementemia persisted. A second renal biopsy 6 months later confirmed the initial diagnosis of dense deposit disease (DDD) based on electron-dense deposits in the GBM. C3 nephritic factor (C3NeF) and a deficiency of complement factor H (CFH) were not evident. A nephritis-associated plasmin receptor (NAPlr), nephritogenic group A streptococcal antigen, and the plasmin activity by in situ zymography were been in both the first and second biopsy specimens. The patient received combined immunomodulatory therapy with prednisolone and mizoribine, and the urinary protein decreased to a mild level at 27 months after disease onset. These findings suggest that persistent glomerular NAPlr deposition may be associated with the pathogenesis of DDD in some patients without the involvement of C3NeF or CFH mutation and that DDD patients of this type may respond to immunomodulatory treatment.

David P Witte - One of the best experts on this subject based on the ideXlab platform.

  • Acute non proliferative glomerulitis a cause of renal failure unique to children
    Pediatric Nephrology, 2000
    Co-Authors: Clark D West, A J Mcadams, David P Witte
    Abstract:

    Over a 31-year period, we have encountered 13 children with a disease entity not reported by other clinics that leads to rapidly progressive crescentic Glomerulonephritis. Gross hematuria, rapidly declining renal function, and a serum C3 level at the lower limit of normal or slightly depressed usually characterized the disease onset; hypertension and nephrotic syndrome were absent. Glomerular IgG was absent, but large C3-containing subepithelial deposits on the paramesangial basement membrane (GBM) were always present. Because of these deposits and because dense alteration of the GBM was found in 3 patients, the disease may resemble membranoproliferative Glomerulonephritis type II, but is distinguishable on other morphological and clinical grounds. The absence of anti-neutrophil cytoplasmic antibody, tested for in 5 of 13 patients, is one of several ways the disease differs from the pauci-immune Glomerulonephritis of adults. Clinically and by glomerular morphology, it also differs from severe poststreptococcal Acute Glomerulonephritis. Treatment with high-dose corticosteroids has been highly successful. Because in this series the disease occurred only in children under age 12 years and the amount of silver-positive mesangial matrix was normal, indicating absence of mesangial proliferation, it has been designated juvenile Acute non-proliferative glomerulitis.

Alexander N Suvorov - One of the best experts on this subject based on the ideXlab platform.

  • complete genome sequence of an m1 strain of streptococcus pyogenes
    Proceedings of the National Academy of Sciences of the United States of America, 2001
    Co-Authors: Joseph J Ferretti, William M Mcshan, Dragana Ajdic, Dragutin J Savic, Gorana Savic, Kevin Lyon, Charles Primeaux, S Sezate, Alexander N Suvorov
    Abstract:

    Abstract The 1,852,442-bp sequence of an M1 strain of Streptococcus pyogenes, a Gram-positive pathogen, has been determined and contains 1,752 predicted protein-encoding genes. Approximately one-third of these genes have no identifiable function, with the remainder falling into previously characterized categories of known microbial function. Consistent with the observation that S. pyogenes is responsible for a wider variety of human disease than any other bacterial species, more than 40 putative virulence-associated genes have been identified. Additional genes have been identified that encode proteins likely associated with microbial “molecular mimicry” of host characteristics and involved in rheumatic fever or Acute Glomerulonephritis. The complete or partial sequence of four different bacteriophage genomes is also present, with each containing genes for one or more previously undiscovered superantigen-like proteins. These prophage-associated genes encode at least six potential virulence factors, emphasizing the importance of bacteriophages in horizontal gene transfer and a possible mechanism for generating new strains with increased pathogenic potential.