NOTES Leute NEPHRITIC SYNDROME GENERALLY, WHAT IS 1T? ———— PATHOLOGY & CAUSES + Diseases caused by inflammation, darrage to glomerulof kidney; become more permeable, alow red blood cells (RBCs) into urine -» hematuria CAUSES + Children/adolescents: IgA nephropathy, post-streptococcal glomerulonephrits, hemolytic uremic syndrome + Aduits: systemic lupus erythematosus, Goodpasture's syndrome, rapidly progressive glomerulonephriis COMPLICATIONS. + Acute kidney failure SIGNS & SYMPTOMS: = Damaged, permeable glomeruli + hematuria, proteinuria + Decreased glomerular filtration rate ‘edema, hypertension + Less waste product excreted + uremia LAB RESULTS + Proteinfblood, RBC casts in urine + Decreased glomerular fitration kidney biopsy * Changes under lightelectron microscope, immunefluorescence TREATMENT MEDICATIONS + Edema + Diuretics furosemide}, medical nutrition therapy + Blood pressure control » Angiotensin converting enzyme Inhibiters (ACE) inhibitors OTHER INTERVENTIONS. + Reduce salt, potassium intake (OsMosis.org OSMOSIS.ORG 825ACUTE PROLIFERATIVE GLOMERULONEPHRITIS 3 PATHOLOGY & CAUSES + Inflammation of glomeruli, complication of bacterial infection + AKA poststreptococeal glomerulonephtitis, * Commonly arises several weeks after group A beta-hemolytic streptococcus infection + Type lll hypersensitivity reaction + IgGiigM antibodies bind to bacterial antigens, form immune complexes —> ‘complexes travel through bloodstream to glomerulus, deposit in glomerular basement membrane + Immune complexicomplement deposits ‘wigger immune reactions Activate complement system —» fenzyme cascade —+ formation of membrane attack complex + damage to podocytes, mesangial cells * Recruit inflammatory cells > proteases, ‘oxidants release —+ basement membrane damage -» hematuria proteinuria —+ nephritic syndrome CAUSES + Group A beta-hemolytic streptococcus infection RISK FACTORS + Most commonly in children (who are biologically male) + Six weeks after impetigo, 1-2 weeks after throat infection COMPLICATIONS. + Rapidly progressive glomerulonephvits, renal failure 826 OSMOSISORG / proliferative-glomerulonephritis SIGNS & SYMPTOMS + Nephritic syndrome: hematuria, oliguta, fedema, hypertension + Fever, headache, malaise, snorexia, nausea DIAGNOSIS LAB RESULTS + Protein/blood in urine + Antibodies against group A streptococcus (eg. anti-DNase B antibodies, anti- ‘Streptelysin O antibody} += Decreased complement levels Renal biopsy + Light microscopy = Mesangial proliferation -+ hypercellular glomerulus Electron ericroscopy » Subepithelal deposits of immune complexes, “humps” + Immunofluerescence "Starry sky.” granular deposition of l9G, complement in basement membrane, ‘mesangium TREATMENT + Usually supportiveChapter 117 Nephritic Syndrome (Popov veeusessve)y CresceWtic aaa GLOMEPULONEPHEITIS. ‘ NEPHRITIC: SYNDROME « Crescenr-suarer Cet PROLIFERATION 7 Revni Faure CLUFLAMMATION: a) Figure 1174 The effect of crescentic glomerulonephrits on the nephron, HEMATURIA, Feo Bug0d ce > UPINC CRESCENT MONOCYTES MacROPHAGES. Punsaan PRTaNS (C32) FIBRIN PARIETAL EPITHELIAL, ceus Ufeourcenre Figure 117.3 Histological appearance of the glomerulus in post-infective crescent-shaped proliferation of cells in Bowman's capsule -» renal failure within ‘weeksimonths + Inflammation damages glomerular basement membrane — inflammatory mediators, complement proteins. fibrin, monocytes macrophages pass into Bowman's space ~» expansion of parietal layer of cals into thick, crescent-moon shape > may undergo sclerosisscarting TYPES Primary + Idiopathic Secondary + Type k:anti-GBM antibodies * Goodpasture syndrome + Type i: immune complexes » Poststreptococcal glomerulonephits, systemic lupus erythematosus. IgA, nephropathy, Henoch-Schonlein purpura + Type i: anti-neutrophilc cytoplasrnic antibodies (ANCA) + Cytoplasmic ANCA (C-ANCA Wegener's granulomatosis, * Perinuclear ANCA (P-ANCA microscopic polyangitis, Churg-Strauss syndrome COMPLICATIONS. + if untreated: rapid progression to acute renal falure 832 OSMOSISORG ISU SIGNS & SYMPTOMS + Nephritie syndrome * Hematura, oliguria, edema, hypertension LAB RESULTS kidney biopsy + Light microscopy: crescent-shaped glomeruli Immunofluorescence + Type I: linear, antibadies bind to collagen of glomerular basement membrane + Type I granular, immune complex deposition in subendothelum += Type ill: negative (pauci-immune) Type Il associated with ANCAS in blood TREATMENT MEDICATIONS + Pulse methylprednisolone, then prednisonelcyciophosphamidekituximab/ plasmapheresis OTHER INTERVENTIONS. + if renal failure reversible + Dialysis/kidney transplantChapter 117 Nephritic Syndrome maids mea ad Erecerrsrty Seed pois ecard Pi PART 1 ieee! cart) Mostyn symetons Pieri Lion nce UUprtmicescopy fork ‘Sromeal sees, stacement of posnerte memunoorscene: Tart mioseapy aes shapes lamer econ meroscony song som Neste syrome ane mrosepy mesa depots iets ACEnnotors| esmeahess| pia est nang cause ycephospraride OSMOSISORG 833834 OSMOSISORG matt S Ml wel wR) a hy PROLIFERATIVE. a Presnety DISEASE Patra mrt piotirrr) Eos PRESENTATION Lae) Prot. Type subendotata Jssement membrane fram Se Preise Tamatura | Typetaeposts tna | vaning eecveness ticeening of GM ‘ranula epost seit deposits Jeecron microscopy “spk ocament of pods Hg kot predisonatusina Neste [econ mroseopy prima | etoeemercot toot negate ont meres (ames) mesangium tay so) Lah mcsepy norma Pd Canemcosceny cescene | ‘ypel. gran etprodrisloe. ‘yopnarohamide. poemapherese