{"id":8101,"date":"2021-11-15T22:59:47","date_gmt":"2021-11-15T20:59:47","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/nephrology\/renal-complication-in-systemic-immune-and-haematological-diseases-lupus-henoch-schonlein-nephropathy-haemolytic-uremic-syndrome-amyloidosis-myeloma\/"},"modified":"2022-01-05T17:32:39","modified_gmt":"2022-01-05T15:32:39","slug":"renal-complication-in-systemic-immune-and-haematological-diseases-lupus-henoch-schonlein-nephropathy-haemolytic-uremic-syndrome-amyloidosis-myeloma","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/nephrology\/renal-complication-in-systemic-immune-and-haematological-diseases-lupus-henoch-schonlein-nephropathy-haemolytic-uremic-syndrome-amyloidosis-myeloma\/","title":{"rendered":"Renal complication in systemic immune and haematological diseases (lupus, Henoch Sch\u00f6nlein nephropathy, haemolytic uremic syndrome, amyloidosis, myeloma)"},"content":{"rendered":"\n<p class=\"wp-block-paragraph\">The renal system is a major target in diseases that involve immune dysfunction such as vasculitis, production of autoantibodies, as well as abnormal protein load seen in amyloidosis and myeloma.<\/p>\n\n\n<span class=\"block-heading\" id=\"header_1\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Lupus nephritis<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">Renal involvement is common in SLE, leading to <strong>immune-complex glomerulonephritis<\/strong>.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Antibodies against nuclear elements circulate within the blood, form immune complexes, and deposite in the glomeruli.<\/li><li>Nearly all patients with SLE have some degree of renal damage.<\/li><li>Presents with SLE-related symptoms (rashes), along with symptoms seen in glomerulonephritis (hematuria, nephrotic-range proteinuria, edema and hypertension).<\/li><li>Can be classified based on the severity and involvement into 6 classes (I-VI):<ul><li>Class I minimum mesangial<\/li><li>Class II mesangial proliferative<\/li><li>Class III focal (&lt;50%) proliferative<\/li><\/ul><ul><li>Class IV diffuse (>50%) proliferative<\/li><li>Class V membranous<\/li><\/ul><ul><li>Class VI advanced sclerosing<\/li><\/ul><\/li><li><strong>Antiphospholipid syndrome<\/strong> may occur as a part of SLE (or by itself), where circulating lupus anticoagulants cause microthrombi, ischemia, and tissue damage.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<ul class=\"wp-block-list\"><li>Serology (ANAs)<\/li><li>Urinalysis and measurement of serum creatinine<\/li><li>Biopsy<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<ul class=\"wp-block-list\"><li>ACEi\/ARB<\/li><li>Prednisone and cyclophosphamide<\/li><li>Dialysis<\/li><li>Renal transplantation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Amyloidosis<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<p class=\"wp-block-paragraph\">Amyloids are misfolded fibrillar proteins that tend to aggregate in tissues.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Amyloidosis is a disease in which amyloid proteins are produced and deposited in tissues. Renal involvement is common.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Renal amyloid deposits<\/strong> typically occur in the glomerular membrane leading to proteinuria, but in some cases, the tubules are affected, leading to azotemia with minimal proteinuria.<\/li><li>Presents with <strong>nephrotic syndrome<\/strong> with marked hypoalbuminemia, edema or to end-stage renal disease.<\/li><li>The two main forms of amyloidosis are:<ul><li>Primary (AL amyloidosis; amyloid light-chain, most common form)<\/li><li>Secondary (AA amyloidosis; due to chronic inflammation and increase in SAA protein)<\/li><\/ul><\/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 title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<ul class=\"wp-block-list\"><li>Serum urine electrophoresis<\/li><li>Biopsy with congo-red staining with polarized light shows apple-green birefrengence<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<p class=\"wp-block-paragraph\">Prednisone and cyclophosphamide.<\/p>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Henoch-Sch\u00f6nlein purpura nephropathy<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<p class=\"wp-block-paragraph\">Henoch-Sch\u00f6nlein purpura (HSP, or <strong>IgA vasculitis<\/strong>) is a systemic small-vessel leukocytoclastic vasculitis associated with IgA1 deposition in vessels.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Typically appears with a tetrad of purpura, abdominal pain, arthritis, and glomerulonephritis.<\/li><li>Unknown etiology; associated with infections. <\/li><li>Typically appears in young patients and resolves by its own; in adults, the disease is typically chronic.<\/li><li>Presents with palpable purpura (typically in the legs), GI bleeding, joint pain, hematuria.<\/li><li>Make sure to not confuse IgA vasculitis with <strong>IgA nephropathy<\/strong>, which although related, is a different entity.<\/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 title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_8\">\n\n\n<ul class=\"wp-block-list\"><li>Diagnosis is generally based on the clinical signs and symptoms.<\/li><li>Can be confirmed with skin biopsy with immunofluorescence showing IgA and C3 deposits.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_9\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_9\">\n\n\n<ul class=\"wp-block-list\"><li>Supportive<\/li><li>In severe cases, prednisone and cyclophospamide.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_10\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Haemolytic uremic syndrome and thrombocytopenic purpura<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_10\">\n\n\n<p class=\"wp-block-paragraph\"><em>The following discusses HUS and TTP in short, focusing on the renal involvement of the diseases; click <a href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/hematology\/thrombocytopenia-and-platelet-disorders\/hemolytic-uremic-syndrome-hus-and-thrombotic-thrombocytopenia-purpura-ttp\/\">here<\/a> for the full article about HUS and TTP.<\/em> <\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Both HUS and TTP involve acute episodes of non-immunological destruction of platelets due to the deposition of loose strands of platelets and fibrin in small vessels and thrombosis, leading to RBC and platelet destruction, a condition known as thrombotic microangiopathy (TMA). <\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>They present with similar blood profile and histological changes, <strong>microangiopathic anemia<\/strong> with<strong> red blood cell fragmentation<\/strong>, <strong>thrombocytopenia,<\/strong> and <strong>acute kidney injury<\/strong>.<\/li><li>Although there&#8217;s much overlap between the two, they are treated as distinct entities.<\/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 title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_11\">\n\n\n<ul class=\"wp-block-list\"><li>Blood panels<\/li><li>Urinalysis<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_12\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_12\">\n\n\n<ul class=\"wp-block-list\"><li>HUS<ul><li>For typical cases, supportive care including fluid replacement, hemodialysis<\/li><li>For atypical HUS, anti-C5 mAb (eculizumab or ravulizumab)<\/li><\/ul><\/li><li>TTP<ul><li>Plasma exchange with fresh frozen plasma\u00a0and cryosupernatant plasma<\/li><\/ul><ul><li>Anti-vWF mAb (caplacizumab) is given in some cases<\/li><li>Immunosuppression in acquired TTP<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_13\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Multiple myeloma<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_13\">\n\n\n<p class=\"wp-block-paragraph\"><em><em>The following discusses MM in short, focusing on the renal involvement of the disease; click <a href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/hematology\/oncological-disorders\/plasma-cell-disorders-dyscrasias\/multiple-myeloma\/\">here<\/a> for the full article about MM.<\/em>  <\/em><\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Multiple myeloma (MM) is a clonic proliferation of plasma cells in the bone marrow. The cells are producing <strong>monoclonal antibodies<\/strong>, typically of IgG type. Renal involvement is common.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Bence-Jones protein<\/strong> is pathognemonic for MM; it is the aggregation of the immunoglobulin light chains.<ul><li>Cause direct renal toxicity, leading to renal failure.<\/li><\/ul><ul><li>Seen as an &#8220;M-spike&#8221; in urine and serum electrophoresis.<\/li><\/ul><\/li><li>Presents with CRAB:<ul><li>Hyper<strong>c<\/strong>alcemia<\/li><li><strong>R<\/strong>enal insufficiency (initially, may present with <strong>Fanconi syndrome<\/strong>)<\/li><li><strong>A<\/strong>nemia<\/li><li><strong>B<\/strong>one lesions<\/li><\/ul><\/li><li>Patients may develop amyloidosis.<\/li><li>Most common primary bone tumor.<\/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 title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_14\">\n\n\n<ul class=\"wp-block-list\"><li>Blood panels (ESR is >100mm\/hr; patients presenting with such ESR + bone pain are classical cases of MM)<\/li><li>X-ray displaying punched-out bony lesions<\/li><li>Serum and urine electrophoresis<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_15\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_15\">\n\n\n<p class=\"wp-block-paragraph\">Can be intensive or non-intensive depending on the age of the patient (see <a href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/hematology\/oncological-disorders\/plasma-cell-disorders-dyscrasias\/multiple-myeloma\/\">Multiple myeloma<\/a>).<\/p>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Lupus nephritis<\/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\">Amyloidosis<\/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\">Henoch-Sch\u00f6nlein purpura 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\">Haemolytic uremic syndrome and thrombocytopenic purpura<\/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\">Multiple myeloma<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><\/div>","protected":false},"excerpt":{"rendered":"<p>The renal system is a major target in diseases that involve immune dysfunction such as vasculitis, production of autoantibodies, as well as abnormal protein load seen in amyloidosis and myeloma. Lupus nephritis Renal involvement is common in SLE, leading to immune-complex glomerulonephritis. Antibodies against nuclear elements circulate within the blood, form immune complexes, and deposite [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":685,"menu_order":7,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-8101","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>Renal complication in systemic immune and haematological diseases (lupus, Henoch Sch\u00f6nlein nephropathy, haemolytic uremic syndrome, amyloidosis, myeloma) &#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\/renal-complication-in-systemic-immune-and-haematological-diseases-lupus-henoch-schonlein-nephropathy-haemolytic-uremic-syndrome-amyloidosis-myeloma\/\" \/>\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\\\/renal-complication-in-systemic-immune-and-haematological-diseases-lupus-henoch-schonlein-nephropathy-haemolytic-uremic-syndrome-amyloidosis-myeloma\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/nephrology\\\/renal-complication-in-systemic-immune-and-haematological-diseases-lupus-henoch-schonlein-nephropathy-haemolytic-uremic-syndrome-amyloidosis-myeloma\\\/\",\"name\":\"Renal complication in systemic immune and haematological diseases (lupus, Henoch Sch\u00f6nlein nephropathy, haemolytic uremic syndrome, amyloidosis, myeloma) &#8211; 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