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Noninfectious Pulmonary Manifestations of Renal Disease In Children
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Stephen T. Lawless, H. Jorge Baluarte
Two additional histologic lesions often discussed are mesangial proliferation and focal glomerulosclerosis, which account for 9 to 15% of the total children with nephrotic syndrome. Children with these glomerular lesions are clinically indistinguishable at presentation from those with minimal change nephrotic syndrome but show a relative lack of response to the usual regimen of prednisone therapy. Other histologic lesions in patients with nephrotic syndrome are membranous nephropathy and membranoproliferative glomerulonephritis. The latter type is rarely confused with minimal change nephrotic syndrome either at clinical presentation or after initial diagnostic studies.
Streptococcus pyogenes
Published in Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward, Case Studies in Infectious Disease, 2010
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward
Systemic causes of glomerular nephritis: Wegener granulomatosis.Hypersensitivity vasculitis.Cryoglobulinemia.Systemic lupus erythematosus.Polyarteritis nodosa.Henoch-Schönlein purpura.Goodpasture syndrome.Renal diseases.Membranoproliferative glomerulonephritis.
Urinary System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Kendall S. Frazier, John Curtis Seely
Biopharmaceutical macromolecules and some classical small molecules such as D-penecillamine have been associated with drug-induced glomerulonephritis in preclinical toxicity studies (Donker et al. 1984). In all of its manifestations, glomerulonephritis is characterized by cellular proliferation. Glomerulonephritis can be divided into membranoproliferative and crescentic forms in rodents, dogs, and monkeys. Both forms are associated with inflammatory cytokine involvement and potential complement activation within the glomerular capillaries. While some authors have further separated a subset of membranoproliferative glomerulonephritis in laboratory animals into a membranous form based on human classifications, this is probably an unnecessary division as the two are quite similar and there is significant overlap in etiopathogenesis. In humans, membranous glomerulonephritis refers to a condition with primarily basement membrane thickening, while the syndrome of membranoproliferative glomerulonephritis involves thickened capillary walls with cellular proliferation. In laboratory animal species, all three lesions are usually noted simultaneously. A third variety of glomerular change is noted in both preclinical species and humans that we label mesangioproliferative glomerulopathy. It is described separately in this text as “glomerulopathy” rather than “glomerulonephritis,” as this latter form lacks significant capillary involvement or inflammation, and primarily involves damage to the mesangium. The presence of fibrin in Bowman’s space or inflammatory cells within tufts should connote the use of the term glomerulonephritis rather than glomerulopathy. Glomerulonephritis may not only arise secondary to antibody deposition (such as in the Heymann nephritis model in rats or in dogs with Lyme disease), but also as sequela to nephrotoxin-mediated injury to podocytes, glomerular endothelium, and/or the basal lamina. Antibodies can bind to a glomerular structural antigen or may be deposited in the glomerulus from circulating antibody complexes formed distantly. In some cases, drugs such as procainamide act as haptens (Adams et al. 1993). Cell-mediated immunity may also be stimulated by some agents and downstream effects may directly or indirectly injure glomerular components. This has been reported with cyclosporine (Remuzzi and Perico 1995).
Retinal findings in glomerulonephritis
Published in Clinical and Experimental Optometry, 2022
Heather G Mack, Deborah J Colville, Phillip Harraka, Judith Anne Savige, Alessandro Invernizzi, Samantha Fraser-Bell
Membranoproliferative glomerulonephritis was previously classified into three patterns based on immunopathology and ultrastructural location of electron dense deposits in the glomerular basement membrane. Membranoproliferative glomerulonephropathy is now classified as C3 complement-mediated disease recognising the key role of Complement 3 in its pathogenesis. When the alternative complement pathway is activated two subtypes are recognised 1) with renal dense deposits, the previous type II membranoproliferative glomerulonephritis, and 2) without dense deposits, known as C3 glomerulonephritis. C3 complement mediated glomerulonephritis may also involve the classical complement pathway (membranoproliferative glomerulonephritis type I) and both alternative and classical pathways (membranoproliferative glomerulonephritis type III).27 C3 glomerulonephropathy is associated with mutations in Complement 3, Complement factor H, complement factor B, and complement factor H-related 1, 2 and 5, as well as a circulating auto-antibody C3 nephritic factor in many individuals, and autoantibodies to factor H, C3 and factor B in some individuals.
Acquired partial lipodystrophy treated with poly-L-lactic acid and hyaluronic acid fillers: a case report
Published in Journal of Cosmetic and Laser Therapy, 2019
Amy J. Zhang, Eleni Moraites, Noah Goldfarb, Walter Liszewski, Ronda S. Farah
APL is a rare disorder characterized by subcutaneous fat loss in the face, trunk, and arms with cephalocaudal spread that classically spares the legs (1). It typically occurs in childhood or adolescence, with a four-time greater female preponderance. The etiology is thought to be due to an autoimmune complement mediated lysis of adipocytes, due to an elevated C3 nephritic factor (1). Mutation in the LMNB2 gene, which encodes the nuclear lamina protein lamin B2, has also been implicated in approximately half of patients (2). Patients with APL may develop metabolic abnormalities, including insulin-resistant diabetes mellitus and dyslipidemia (1). One-fifth of patients develop membranoproliferative glomerulonephritis through a complement-mediated mechanism (1).
Focal Segmental Membranoproliferative Glomerulonephritis: A Histological Variant of Denys-Drash Syndrome.
Published in Fetal and Pediatric Pathology, 2021
A. B. Karmila, Y. C. Yap, M. Appadurai, L. Oh, M. Fazarina, F. Abd Ghani, H. Ariffin
Individuals with DDS often present with nephrotic syndrome and develop progressive renal failure with the majority of affected individuals succumbing in early childhood. Nephropathy in DDS is predominantly due to diffuse mesangial sclerosis (DMS) [1,2]. Other histological subtypes are not well-described although cases of membranoproliferative glomerulonephritis (MPGN) have been occasionally reported. Here, we discuss the clinico-pathological findings of two male patients with DDS and MPGN. We also review the literature of this uncommon histological subtype of DDS to identify phenotypic similarities amongst the cases.