Mesangiocapillary glomerulonephritis associated with hydatid disease

Rincón, Bladimiro; Bernis, Carmen; Arcia, Adriana; Traver, J. A.

doi:10.1093/ndt/8.8.783

Cited by 13 publications

(7 citation statements)

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“…8,[10][11][12][13] In addition to viral infections, chronic bacterial infections (e.g., endocarditis, shunt nephritis, and abscesses), fungal infections, and parasitic infections are associated with MPGN, particularly in the developing world. [14][15][16][17][18] Bacteria associated with MPGN include staphylococcus, Mycobacterium tuberculosis, streptococci, Pro-pionibacterium acnes, Mycoplasma pneumoniae, brucella, Coxiella burnetii, nocardia, and meningococcus. [19][20][21][22][23][24][25][26][27][28][29][30]…”

Section: Hepatitis C and Other Infectionsmentioning

confidence: 99%

Membranoproliferative Glomerulonephritis — A New Look at an Old Entity

2012

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M embranoproliferative glomerulonephritis (MPGN), also termed mesangiocapillary glomerulonephritis, is diagnosed on the basis of a glomerular-injury pattern that is common to a heterogeneous group of diseases. MPGN accounts for approximately 7 to 10% of all cases of biopsy-confirmed glomerulonephritis 1-4 and ranks as the third or fourth leading cause of end-stage renal disease among the primary glomerulonephritides. 2,5 Although some diseases associated with MPGN are well known, recent advances have identified additional MPGN-associated conditions. Cl inic a l Pr e sen tat ion MPGN most commonly presents in childhood but can occur at any age. The clinical presentation and course are extremely variable-from benign and slowly progressive to rapidly progressive. Thus, patients can present with asymptomatic hematuria and proteinuria, the acute nephritic syndrome, the nephrotic syndrome, chronic kidney disease, or even a rapidly progressive glomerulonephritis. The varied clinical presentation is caused by differences in the pathogenesis of the disorder and in the timing of the diagnostic biopsy relative to the clinical course. The degree of kidney impairment also varies, and hypertension may or may not be present. Patients who present early in the disease process, when the kidney biopsy shows proliferative lesions, are more likely to have a nephritic phenotype, and those with crescentic MPGN may present with a rapidly progressive glomerulonephritis. In contrast, patients with biopsies showing advanced changes that include both repair and sclerosis are more likely to have a nephrotic phenotype. Patients with classic MPGN often have features of both the acute nephritic syndrome and the nephrotic syndrome-termed the nephritic-nephrotic phenotype. Cl a ssific at ion a nd Pathoph ysiol o gy The typical features of MPGN on light microscopy include mesangial hypercellularity, endocapillary proliferation, and capillary-wall remodeling (with the formation of double contours)-all of which result in lobular accentuation of the glomerular tufts. These changes result from the deposition of immunoglobulins, complement factors, or both in the glomerular mesangium and along the glomerular capillary walls. On the basis of the electron-microscopical findings, MPGN is traditionally classified as primary (idiopathic) MPGN type I (MPGN I), type II (MPGN II), or type III (MPGN III) or secondary MPGN. MPGN I, the most common form, is characterized by subendothelial deposits, and MPGN III has both subepithelial and subendothelial deposits. 6,7 MPGN II is characterized by dense deposits in the glomerular basement membrane

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Section: Hepatitis C and Other Infectionsmentioning

confidence: 99%

Membranoproliferative Glomerulonephritis — A New Look at an Old Entity

2012

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“…Infections, which have been identified as the primary cause of MPGN include, hepatistis C virus ( Fig. 2), hepatitis B virus, bacterial, fungal, and parasitic infections (4,(11)(12)(13)(14)(15)(16)(17)(18). Autoimmune disorders, which may be involved in the pathogenesis of MPGN include, Sjogren syndrome, systemic lupus erythematosus, and rheumatoid arthritis (19)(20)(21).…”

Section: A/immune-complex-mediated Mpgnmentioning

confidence: 99%

Understanding the complement‐mediated glomerular diseases: focus on membranoproliferative glomerulonephritis and C3 glomerulopathies

Lionaki

Gakiopoulou

Boletis

2016

APMIS

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An enhanced understanding of the role of complement in the pathogenesis of membranoproliferative glomerulonephritis has led to reclassification of the latter into immunoglobulin-mediated and non-immunoglobulin-mediated disease. The new classification schema resulted in improved diagnostic clinical algorithms, while it brought into light again the diseases, which are characterized by the presence of glomerular deposits, composed predominantly by C3, in the absence of significant amounts of immunoglobulins in renal biopsy, namely, C3 glomerulopathies (dense deposit disease and C3 glomerulonephritis). Despite the lack of randomized controlled trials following the advances in the understanding of the pathogenetic pathways involved in membranoproliferative glomerulonephritis, it is important that the new mechanistic approach has opened new roads for the exploration and discovery of targeted therapies.

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“…[5][6][7][8][9][10][11][12][13][14] Indeed, infections are an important cause of immune-complex GN in both developing and developed countries. [15][16][17][18][19][20] The pattern of glomerular injury is variable, and depending, in part, on the etiology, there may be no lesion by LM, mesangial proliferative, endocapillary proliferative, exudative, membranoproliferative, necrotizing and crescentic, sclerosing, or a combination of these patterns.…”

mentioning

confidence: 99%

Mayo Clinic/Renal Pathology Society Consensus Report on Pathologic Classification, Diagnosis, and Reporting of GN

Sethi

Haas

Markowitz

et al. 2015

JASN

227

153

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Renal pathologists and nephrologists met on February 20, 2015 to establish an etiology/pathogenesis-based system for classification and diagnosis of GN, with a major aim of standardizing the kidney biopsy report of GN. On the basis of etiology/pathogenesis, GN is classified into the following five pathogenic types, each with specific disease entities: immune-complex GN, pauci-immune GN, antiglomerular basement membrane GN, monoclonal Ig GN, and C3 glomerulopathy. The pathogenesis-based classification forms the basis of the kidney biopsy report. To standardize the report, the diagnosis consists of a primary diagnosis and a secondary diagnosis. The primary diagnosis should include the disease entity/pathogenic type (if disease entity is not known) followed in order by pattern of injury (mixed patterns may be present); score/grade/class for disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and additional features as detailed herein. A pattern diagnosis as the sole primary diagnosis is not recommended. Secondary diagnoses should be reported separately and include coexisting lesions that do not form the primary diagnosis. Guidelines for the report format, light microscopy, immunofluorescence microscopy, electron microscopy, and ancillary studies are also provided. In summary, this consensus report emphasizes a pathogenesis-based classification of GN and provides guidelines for the standardized reporting of GN.

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Mesangiocapillary glomerulonephritis associated with hydatid disease

Cited by 13 publications

References 0 publications

Membranoproliferative Glomerulonephritis — A New Look at an Old Entity

Membranoproliferative Glomerulonephritis — A New Look at an Old Entity

Understanding the complement‐mediated glomerular diseases: focus on membranoproliferative glomerulonephritis and C3 glomerulopathies

Mayo Clinic/Renal Pathology Society Consensus Report on Pathologic Classification, Diagnosis, and Reporting of GN

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