{"id":7881,"date":"2021-10-29T19:58:32","date_gmt":"2021-10-29T17:58:32","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/nephrology\/primary-glomerulonephritis-pathogenesis-clinical-syndromes-pathological-appearance\/"},"modified":"2022-01-12T00:25:25","modified_gmt":"2022-01-11T22:25:25","slug":"primary-glomerulonephritis-pathogenesis-clinical-syndromes-pathological-appearance","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/nephrology\/primary-glomerulonephritis-pathogenesis-clinical-syndromes-pathological-appearance\/","title":{"rendered":"Primary glomerulonephritis; pathogenesis, clinical syndromes, pathological appearance"},"content":{"rendered":"<span class=\"block-heading\" id=\"header_1\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Introduction<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">Glomerular diseases exist on two opposing spectrums based on <strong>proteinuria<\/strong> (<strong>nephrotic spectrum<\/strong>) and <strong>hematuria<\/strong> (<strong>nephritic spectrum<\/strong>). <\/p>\n\n\n\n<p class=\"wp-block-paragraph\">When strictly referring to glomerular diseases:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Proteinuria <\/strong>is present in most glomerular diseases.<\/li><li><strong>Hematuria<\/strong> is only present in inflammatory glomerular diseases (<strong>glomerulonephritis<\/strong>). <\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">The two extremes of these spectrums describe two clinical syndromes:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Nephrotic syndrome<\/strong> which encompasses <strong>severe proteinuria (&gt;3.5g\/day)<\/strong> along with <strong>edema<\/strong>, <strong>hypoalbuminemia<\/strong>, <strong>hyperlipidemia<\/strong>, and <strong>oval fat bodies in the urine<\/strong>, seen in <strong>degenerative glomerular diseases<\/strong> (conditions without inflammation).<\/li><li><strong>Nephritic syndrome<\/strong> which encompasses <strong>hematuria <\/strong>along with with hypertension, azotemia, oliguria, and mild proteinuria (rarely absent).<\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">Some glomerular diseases, however, may manifest with symptoms that overlap both nephrotic and nephritic syndrome, for example:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Lupus nephritis<\/li><li>Membranoproliferative glomerulonephritis (MGN)<\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">Glomerular diseases can be classified into <strong>primary<\/strong> (idiopathic) and <strong>secondary <\/strong>(diabetes, HTN, SLE, PSGN)<strong> glomerular diseases<\/strong>.<\/p>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Primary glomerulonephritis<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<p class=\"wp-block-paragraph\">Primary GN is caused due to an intrinsic condition of the kidney, typically through an immune-mediated process.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">The entities belonging to this group include:<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>IgA nephropathy<\/li><li>Membranous nephropathy<\/li><li>Membranoproliferative glomerulonephritis<\/li><li>Fibrillary and immunotactoid GN<\/li><li>Idiopathic crescentic GN<\/li><\/ul>\n\n\n\n<p class=\"wp-block-paragraph\">These entities can be primary (idiopathic) or secondary to another disease.<\/p>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">IgA nephropathy<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<p class=\"wp-block-paragraph\">IgA nephropathy (IgAN, also known as <strong>Berger disease<\/strong>) is GN caused by the deposition of IgA1-containing immune complexes in the glomeruli. <\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>The most common cause of glomerular hematuria, typically presenting as <strong>macrohematuria<\/strong> appearing 2-3 days after an URI<\/li><li>Associated with increased IgA1 production, deficient galactosylation, decreased clearance, and other immunological defects.<\/li><li>Mesangial deposition of IgA and C3 over years, leading to HTN, renal failure and ESRD.<\/li><li>Make sure to not confuse IgAN with <strong>Henoch-Sch\u00f6nlein Purpura<\/strong>, which although related, is a different entity.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<ul class=\"wp-block-list\"><li>Urinalysis<\/li><li>Renal biopsy with immunoflurecense displaying IgA and C3 deposition<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<ul class=\"wp-block-list\"><li>ACEi\/ARBs<\/li><li>Steroids<\/li><li>Cyclophosphamide<\/li><li>Tonsillectomy<\/li><li>Omega-3 supplementation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Membranous nephropathy<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<p class=\"wp-block-paragraph\">Membranous nephropathy (MN, also known as <strong>membranous GN<\/strong>) is GN caused by the deposition of immune complexes in the GBM.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Presents with mixed nephrotic and nephritic syndrome characteristics.<\/li><li>Typically idiopathic, but may be associated with certain drugs, infections, autoimmune diseases, and underlying tumors<\/li><li>More common in adults<span style=\"color: initial;\">.<\/span><\/li><li>The antibodies of the immune complexes are formed either as autoantibody targeting the GBM, or against proteins attached to the GBM.<ul><li>The <strong>M-type phospholipase A2 receptor<\/strong> is a major target for the autoantibodies.<\/li><\/ul><ul><li><strong>Cationic bovine serum albumin<\/strong> (from milk and beef, due to defective intestinal barrier) has been identified as a possible exogenous antigen attaching to the anionic glomerulus, leading to immune complex formation.<\/li><li>Subepithelial deposition, with later thickening of the GBM, without cellular proliferation or necrosis, and <strong>without the involvement of the mesangium<\/strong><\/li><\/ul><\/li><li>Renal vein thrombosis is a possible complication (although typically asymptomatic).<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<ul class=\"wp-block-list\"><li>Clinical presentation<\/li><li>Biopsy (gold standard)<\/li><li>Screening for secondary causes (hepatitis, autoimmune, tumors)<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_8\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_8\">\n\n\n<ul class=\"wp-block-list\"><li>Treatment of underlying diseases (hepatitis, tumors, autoimmune diseases) and nephrotic syndrome (ACEi\/ARBs, diuretics)<\/li><li>Corticostertoids<\/li><li>Renal  transplantation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_9\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Membranoproliferative glomerulonephritis <\/h3>\n<\/span><span class=\"block-content\" id=\"contents_9\">\n\n\n<p class=\"wp-block-paragraph\">Membranoproliferative GN (MPGN, also known as <strong>mesangiocapillary glomerulonephritis<\/strong>, MCGN) is a group of disorders caused by the deposition of immune complexes in the GBM and mesangium.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">It is divided into three types (MPGN type I, II, and III). All three types may be primary (idiopathic) or secondary to another condition, although the secondary form is more common in type I.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">MPGN should not be confused with membranous nephropathy as they are separate entities; <strong>MPGN involves the GBM and the mesangium<\/strong> (as its synonym MCGN suggests), while <strong>membranous nephropathy only involves the GBM<\/strong> (without the mesangium, see above).<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Presents with mixed nephrotic and nephritic syndrome characteristics.<\/li><li>Mostly affects children.<\/li><li>The immune complexes are deposited based on the type (subendothelial and mesangial for type I, intramembranous for type II, subepithelial for type III).<\/li><li>Poor prognosis; half of the patients undergo ESRD.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_10\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_10\">\n\n\n<ul class=\"wp-block-list\"><li>Serum complement test (demonstrating low C3 levels)<\/li><li>Biopsy<\/li><li>Screening for secondary causes (hepatitis, autoimmune, tumors)<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_11\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_11\">\n\n\n<ul class=\"wp-block-list\"><li>Treatment of underlying diseases (hepatitis, tumors, autoimmune diseases) and nephrotic syndrome (ACEi\/ARBs, diuretics)<\/li><li>Corticosteroids in children<\/li><li>Aspirin and dipiridamole (anti-platelet medication) in adults<\/li><li>Renal transplantation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_12\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Fibrillary and immunotactoid GN<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_12\">\n\n\n<p class=\"wp-block-paragraph\">Fibrillary and immunotactoid GN are rare conditions caused by the deposition of non-amyloid fibrillar substances within the GBM and mesangium.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Presents with mixed nephrotic and nephritic syndrome characteristics.<\/li><li>May be primary, or associated with certain drugs, infections, autoimmune diseases, and underlying tumors (leukemias\/lymphomas).<\/li><li>Poor prognosis; half of the patients undergo ESRD.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_13\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_13\">\n\n\n<ul class=\"wp-block-list\"><li>Biopsy<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_14\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_14\">\n\n\n<ul class=\"wp-block-list\"><li>Treatment of underlying diseases (hepatitis, tumors, autoimmune diseases) and nephrotic syndrome (ACEi\/ARBs, diuretics)<\/li><li>Corticosteroids<\/li><li>Renal transplantation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_15\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Idiopathic crescentic GN<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_15\">\n\n\n<p class=\"wp-block-paragraph\">Crescentic GN (rapidly progressive GN) is characterized by the formation of crescents due to cellular proliferation, leading to rapidly progressive renal failure.<\/p>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">Introduction<\/h2><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">Primary glomerulonephritis<\/h2><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">IgA nephropathy<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Membranous nephropathy<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Membranoproliferative glomerulonephritis <\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Fibrillary and immunotactoid GN<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Idiopathic crescentic GN<\/h3><\/div>","protected":false},"excerpt":{"rendered":"<p>Introduction Glomerular diseases exist on two opposing spectrums based on proteinuria (nephrotic spectrum) and hematuria (nephritic spectrum). When strictly referring to glomerular diseases: Proteinuria is present in most glomerular diseases. Hematuria is only present in inflammatory glomerular diseases (glomerulonephritis). The two extremes of these spectrums describe two clinical syndromes: Nephrotic syndrome which encompasses severe proteinuria [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":685,"menu_order":5,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-7881","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.9 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Primary glomerulonephritis; pathogenesis, clinical syndromes, pathological appearance &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/nephrology\/primary-glomerulonephritis-pathogenesis-clinical-syndromes-pathological-appearance\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"4 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/nephrology\\\/primary-glomerulonephritis-pathogenesis-clinical-syndromes-pathological-appearance\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/nephrology\\\/primary-glomerulonephritis-pathogenesis-clinical-syndromes-pathological-appearance\\\/\",\"name\":\"Primary glomerulonephritis; 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