Transcript
OS 214: Renal
Dr. Dr. Agnes Mejia Exam 1&2
Glomerulonephritis Glomeruloneph ritis (GN)
OUTLINE I. II. III III. IV.
Introduction Glomerulonephritis Path athogen ogenes esis is of Glom lomeru erulon loneph ephriti ritis s Approach to to Patient with Glomerulonephritis V. Forms of Glomerulonephritis A. IgA IgA Neph Nephro ropa path thy y B. Posts Poststre trepto ptococ coccal cal Glome Glomerul rulone onephr phriti itis s C. Membra Membranou nous s Glomeru Glomerulon loneph ephrit ritis is VI. Summary VII. Socioeconomic impact of Glomerulonephritis VIII. Figures
CXR
To rule out pneumonia
EKG
Check for hyperkalemia
UTZ
Visualize the kidney: If enlarged (e.g. 12 cm)=acute GN, reversible If shrunken=ESRD,irreversi ble (Normal Filipino size:9.6 cm in length; Normal Caucasia:11-12 cm) *Normal globular, thick cortex “window to to gl glomerular disease” -early morning urine expected to have a dark, intense color if kidney is able to concentrate urine - concentrated (Sp. gravity 1.020-1.030) -Acute GN – red cell casts; RBCs degenerate to fine/coarse granular casts reflects chronicity -Hyaline casts can be found in a normal person -Most common cause of pus cells non infective pyuria
Note: Note: The lecturer lecturer did not provide provide a powerpoint powerpoint.. Thank you to Irving for sending pictures of the ppt for this trans. Please be reminded that the exam questions will come mainly from HPIM 17 th ed.; topics included are general information on glomerular disease, GN, IgA nephropathy, PSGN and MGN.
I. INTRODUCTION A. Case of ER, ER, presented with: with: high BP (160/100), HR 104, RR 30/min o pale, sallow (in between pallor and jaundice) o “peculiar fetor” – fruity smell o o evidence evidence of cardiac cardiac damage damage (Grade (Grade II Av block hypertensive) but not yet in CHF due to absence of s3 no evidence of liver involvement o ++ bipedal edema o Dry skin, good and equal pulses o Basal crepitant rales o B. Primary Impression: UREMIA (symptom diagnosis) Symptoms seen in the ER Vomiting o Tremors o Anorexia o Weakness o SOB o Pruritus o Easy fatigability o Irritability o Full blown Uremia (not seen in ER) Somnolence o Seizures o Disorientation o Coma o
BUN
*Creatini ne ne
Electrolytes Ca Phosphorus **K
***ABG
Needed if urgent action is required required (can easily kill the patient) Needed if urgent action is required
March 6, 2009/Friday
*if creatinine is high, BUN is expected to be abnormal; if BUN is high, creatinine is not necessarily high *the presence of protein in the urine is not correlated with the specific gravity of the urine since SG indicates the ability of the kidneys to concentrate. Even if this is intact, the kidneys can still spill out urine. *those in asterisks are the cheaper tests, so they are the most economical and efficient in terms of information.
V)
Finding in ER Low Hg (7)
Basis for diagnosis: CGN young adult, hypertension at age 19 (hypertensive o nephroscler nephrosclerosis osis takes about 20 years to develop, develop, and so it is an unlikely ddx) hematuria, pyuria o small kidneys (denotes a chronic problem, not acute) o
Elevated (60umol/L)
ESRD
C. Labs Requested Purpose Check for anemia due to pallor To asses kidney function, but but crea creati tinin nine e is more more important Single most important test for uremia (uremic if azotem azotemic) ic);; if high, high, tells tells you you that that px like likely ly has has kidney disease To check for acidosis
-low sp. gravity -granular casts -Increase RBC and WBC -mucus threads rare denotes that urine was well collected -px has no fever but high WBC may indicate sterile pyuria
D. Final Diagnosis: Diagnosis : Urem Uremia ia seco second ndar ary y to ESRD ESRD (CKD (CKD Stag Stage e o secondary to Chronic Glomerulonephritis (CGN)
*Azotemia is a laboratory diagnosis Uremia a clinical diagnosis
Lab CBC
Urinalysis
O2sat 92%) Severe Uncompensated Metabolic acidosis (low pH, low HCO3; causes tachypnea) Heart not enlarged but with congestion Showed pulmonary edema Peaked T waves (denotes (denotes hyperkale hyperkalemia) mia) you have have to give give you calc calciu ium m gluc glucon onat ate e as treatment Small shrunken kidney Cortex should at least be 4.5cm thick
o
Increased (1800 umol/L)
o o
Decreased Elevated (6) Elevated (5.9)
(pH7.2; pCO235; pO294; HCO311;
shrunken kidneys uremia, anemia, low Ca Inc phosphorus
*Single most important determinant of chronicity shrunken kidneys *Severe renal failure Ca low, Phosphorus high **ER is a UP student; inc BP at age 19 (140/90). ER was erroneously treated as UTI for 3 years in a male with no symp sympto toms ms and and an abno abnorm rmal al urin urinal alys ysis is;; ER pass passed ed engineering boards 3 days before he underwent hemodialysis!
Page 1 of 7 Seth, Ian
OS 214: Renal
Dr. Dr. Agnes Mejia Exam 1&2
Glomerulonephritis Glomeruloneph ritis (GN)
*Immun *Immunofl ofluor uoresc escenc ence e can be used used to determ determine ine whethe whether r immune complexes are in-situ or circulating My Goals (which I guess have to be our goals) 1. To be aware 2. To be be su suspic spicio ious us 3. To Set Set the Alar larm II. Glomerulonephritis Glomerulonephritis -inflammation of the glomerular capillaries a. Normal Kidneys: smooth surface o pinkish cortex o reddish medulla o yellow calyces, pelvis o In GN: kidneys are pale o
*Overlapp *Overl apping ing etiolo etiologie gies s may produc produce e simila similarr glomer glomerula ular r lesions display common patterns of injury (syndrome); this is evident in microscopy: IgA paramesangial; can still see spaces in glomerulus; most common in Asians Poststrep GN (PSGN) – same pattern of injury can be seen in lupus; immune-complex GN; most common post infectious Membra Membranou nous s GN (MGN) (MGN) –same –same patter pattern n can be seen seen in idiopathic, Hepatitis, and drug-induced; just hits the basement membrane, causing it to thicken; most common in men IV. Approach to Patient with Glomerulonephritis
*Kidney disease has 10 types but can manifest the same way. But if you look inside the kidneys, the pathology is actually different. They hit different parts of the kidney thus histology is important!
A. History and PE (what to look at) conf confin ined ed to the the kidn kidney eys s or syst system emic ic? ? acut acute e or o chronic? signs and symptoms (what to ask the px) o dysuria – pain during urination? nocturia – urination at night? •
b. Glomerulus 600 600 thou thousa sand nd – 2 mill millio ion n (all (all in all) all) in a norm normal al o individual *prematures have less glomeruli higher tendency for hypertension higher tendency for renal disease at age 50 is a ball of capillaries (“berries”) with afferent and o efferent arterioles (histology: stalk – where efferent and afferent arterioles run) glomerular glomerular capillaries capillaries filter filter 120-180 120-180 L/d of plasma plasma o water filtratio filtration n occurs through a physicochem physicochemical ical barrier barrier o govern governed ed by pore pore size size and negati negative ve electr electrost ostati atic c charge glomerulus is an imperfect barrier o *e.g. albumin-de albumin-despite spite its negativit negativity y, readily readily passes through due to its small radius (3.6nm vs. 4nm radius of glomerular basement mebrane (GBM) slit-pores); albumin is reabsorbed in the proximal tubules (urine normally contains only 8-10 mg) *Glomerulo *Glomerulonephri nephritis tis can affect any part of the glomerulu glomerulus s (mesan (mesangiu gium, m, pariet parietal al epithe epitheliu lium, m, basem basement ent membr membrane ane,, podocytes) and will manifest differently. differently. In GN: the glomeruli are full of scars Pathogenesis: (1) Circulating immune complexes
(2) In-situ immune complexes
T-cells (CD 4/8) activation Loca activation of toll-like receptors on Glomerular Cells Deposition of Immune Complexes Complement injury Glomerular injury
•
•
hematuria – blood in the urine? (2 kinds gross and microscopic)
rete retent ntio ion/ n/in inco cont ntin inen ence ce – inco incomp mple lete te voiding? frequency – urinating more often? Sediments- may “latak” sa ilalim ang ihi? frothy urine – like beer? edema last known urinalysis/creatinine pregnancy status (preeclampsia); birth control pills last normal BP Blood pressure must must give give exac exactt valu value, e, not not just just sayin saying g normal or high, because what is high for one person may be normal for another Urinalysis window to glomerular disease Qualit Quality y of urine: urine: clear clear,, cloudy cloudy or bloody bloody (gross hematuria) *if with gross hematuria and is painless consider mali malign gnan ancy cy unti untill prov proven en othe otherw rwis ise; e; if pain painfu ful, l, consider urethritis •
• • • •
o o o o
•
o
• •
*Dilute urine yellow concentrated *Cloudy tea colored *Bloody gross hematuria Table 277-1. Urine assays for albumin/proteinuria (HPIM 17th ed) 24Hr Albumin/ Dipstick 24Hh Albumin creatinine proteinuri Urine (mg/24h) ratio a Protein (mg/G) (mg/24h) Normal 8-10 <30 <150 Microalbu 30-300 30-300 -/trace/1+ minuria Proteinuria >300 >300 Trace-3+ >150
Mononuclear infiltration Cytokine release Attract more inflammatory cells Glomerular damage
*In summary, GN may be caused by circulating or in situ immune complexes, but whichever the cause is, they both follow the path of inflammation via T-cell activation
March 6, 2009/Friday
V. Forms of Glomerulonephritis Glomerulonephritis (Patterns of Clinical GN) Form Acute Nephritic Infectious Disease Associated; Nephritic Nephrotic Basement membrane Glomerular Vascular Disease
Prototype Disease IgA Nephropathy PostS ostSttrept reptoc ococ occa call (PSGN) Membranous GN
GN
Alport’s syndrome ANCA small vessel vasculits
Page 2 of 7 Seth, Ian
OS 214: Renal
Dr. Dr. Agnes Mejia Exam 1&2
Glomerulonephritis Glomeruloneph ritis (GN)
Pumonar y-Renal
Goodpasture’s di disease
o o
*just focus on the first three as said by the lecturer, ayt?
A. IgA Nephropathy
o
CASE:
31 female Routine annual Physical checkup Urinalysis RBC –TNTC WBC – 0-3 Protein (-) Casts (-) BP 120/70 o
o
o
o o
immu immune ne comp comple lex x medi mediat ated ed GN defi define ned d by the the presence presence of diffuse diffuse mesangial mesangial IgA deposits deposits often often associated with mesangial hypercellularity circulating immune complexes get deposited in the mesa mesang ngiu ium m or podo podocy cyte tes s (not (not the the base baseme ment nt membrane [BM]) IgM, IgG, C3, or immunoglobulin light chains can be codistributed with IgA Mild – do not undergo dialysis RPGN (rapidly progessive)- end up in dialysis after 6 mos POSTstrep GN - tea colored urine happens 2 weeks after infection In IgA – happens with the infection
o
sometimes recur post transplant risk factors factors for renal failure: failure: HPN, proteinuri proteinuria, a, absenc absence e of episod episodic ic macros macroscop copic ic hematu hematuria ria,, male, male, older older age of onset, onset, sever sever renal renal biopsy biopsy changes “Point of no return” – stage where treatment is insufficient usually when creatinine is at least 2 the clinical prognostic index (CPI) of GN–made in Verona, Italy; a scoring system that predicts the prognosis of GN 2pts for Serum Creatinine> 1.4mg/dl 1pt for Proteinuria> 1g/24 hrs 1pt for presence of HPN 1pt patient > 30 years old Score of 0-2*: higher 10-year renal survival; 3-5: lower 10-year renal survival; most likely to end up in dialysi dialysis; s; hence, hence, creati creatinin nine e is the single single most most impt impt pred predic icto tors rs of surv surviv ival al sinc since e it automatically gives you 2pts if abnormal • • • •
o
*Immunoflourescence positive for IgA •
Treatment o
o
•
•
Evidence-based: ACEI-ARB, ACEI-ARB, Steroids, fish oil (severe only), sequential, cyclophosphamide: azathioprine (progressive only) Non-evidence Based: azathioprine/MMF, azathioprine/MMF, CNI (CsA Tacro), IVIg, Leflunomide, heparin/warfarin/dipyridamole, tonsillectomy
*IgA GN is common, progressive, but treatable •
Pathogenesis: defective immune response formation of immune immune comple complex x proinflammatory, proinflammatory, proproliferative, proa proapo popt ptot otic ic,, prof profib ibro roti tic c + mili milieu eu in glom glomer erul ulii mesangial/podocyte injury, capillary hypertension, altered perm selectivity selectivity,, glomerulosc glomerulosclerosi lerosis, s, tubulo-int tubulo-intersti erstitial tial fibrous hematuria, proteinuria, decreased GFR
•
•
Epidemiology most common form of GN worldwide o 30% in Asia and Pacific RimEast > W est o 20% in southern Europe o low prevalence in N. Europe & N. America o Male > Female o o peak incidence: 2nd-3rd decade of life rare familial clustering o Presentation most common presentations are: o recurrent recurrent episodic episodic macroscopic macroscopic hematuria hematuria following a respiratory infection in children asymptomat asymptomatic ic microscopic microscopic hematuria hematuria seen in adults between episodes, urinalysis is normal o in persistent hematuria, increasing proteinuria is o found
B. PostStreptococcal Glomerulonephritis Glomerulonephritis (PSGN) CASE:
22 male 1 month impetigo in L leg Pus, crust, swelling, redness, fever tea colored urine, dec outpu, puffy eyelids, anorexi, easy fatigability, fatigability, inc BP o o o
•
•
Epidemiology typically sporadic o children between 2-14 yrs (10% in px>40 yrs) o Males > Females o 10% pts>40yrs o familial/cohabitant incidence is high-40% o M types of Streptococci (nephritogenic strains) o impe impeti tigo go-- M types types 2, 47, 47, 49, 49, 55, 55, 57, 57, 60; 60; o PSGN develops 2-6 wks after a skin infection o Pharyngiti Pharyngitis s (nephritog (nephritogenic enic strain)strain)- M types 1,2, 3, 4, 12, 25, 49; PSGN develops 1-3 wks afte afterr stre strep p uppe upperr resp respir irat ator ory y infe infect ctio ion n (pharyngitis)
•
Labs Decreased CH50, decreased C3 o Inconsistently positive culture (10-70%) o Increased ASO titers (30%) o Anti-DNase (70%) o Antihyaluronidone Ab (40%) o
•
Presentation
•
•
Differentials Henoch-Schonlein Purpuracan be o distinguished for IgA Nephropathy by prominent syst system emic ic sx, sx, youn younge gerr onse onsett (<20 (<20yr yrs s old) old),, preceding infection and abdominal complaints Croh Crohn’ n’s s dise diseas ase, e, chro chroni nic c love loverr dise diseas ase, e, GI o adenoc adenocarc arcino inoma, ma, etc –also –also presen presentt with with IgA deposition deposition in mesangium; mesangium; can be different differentiated iated due due to abse absenc nce e of sign signif ific ican antt glom glomer erul ular ar inflammation. Progression gene genera rall lly y a beni benign gn dise diseas ase, e, but but 25-3 25-30% 0% o progress to renal failure over 20-25 yrs. 5-30% go into complete remission o
March 6, 2009/Friday
Pathogenesis: putative streptococcal antigens circulating 1-C, activation of complement with cell mediated injury deposition in GBM
•
•
also known as Postinfectious GN prototype for acute endocapillary proliferative GN classically not a nephritic syndrome
Page 3 of 7 Seth, Ian
OS 214: Renal
Dr. Dr. Agnes Mejia Exam 1&2
Glomerulonephritis Glomeruloneph ritis (GN)
o
o o o
o
o
classi classic c presen presentat tation ion of acute acute nephri nephritic tic px: HPN, HPN, hematu hematuria ria,, RBC casts, casts, pyuria pyuria,, mild mild to modera moderate te proteinuria oliguric renal failure systemic symptoms include headache, malaise, anorexia, flank pain (swollen renal capsule) in 50% of cases in the 1st week of symptoms: 90% have depressed CH50, decreased C3 (because they are circulating and get deposited in the GBM) positive strep cultures are inconsistent
•
•
Edema There are 2 theories for the c ause of edema due to NS:
1.
Underfill protein protein spillage spillage low albumin albumin (albumin acts as the magnet that attracts fluid) pressure low intravascu intravascular lar low oncotic pressure volume second secondary ary sodium sodium retent retention ion EDEMA 2. Overfill low GFR low RPF and low FF primary Na retention Expanded ECF volume EDEMA Nephrotic syndrome (NS) is described as: 24hr total Pr>3gm, hypertension, hypercholesterolemia, hypoalbuminemia, edema/anasarca
Renal Biopsy diffuse proliferative: little bowman’s space seen o hypercellularity of mesangial and endothelial cells o glomerular infiltrates of PMN leukocytes o granular granular subendothel subendothelial ial immune immune deposits deposits of IgG, o IgM, C3, C4, C5-9 subepithelial deposits-“humps” o RPGN – with crescents o •
Diagnosis renal biopsy is not necessary o subc subcli lini nica call case cases s are are repo report rted ed to be more more o common than clinical nephritis and charact characteri erized zed by asympt asymptom omati atic c micros microscop copic ic hematuria and low serum complement levels
•
Treatment supportive o •
for HTN
for Edema Dialysis if indicated (oliguric) anti antibi biot otic ic tx for for stre strep p infe infect ctio ion n for for px and and cohabitants no role role for for immu immuno nosu supp ppre ress ssiv ive e tx even even if crescents are present good good progno prognosis sis,, rare rare recurr recurrenc ence, e, perman permanent ent renal failure is very uncommon (1-3%) complete resolution of hematuria and proteinuria in childr children en occu occurr in 3- 6 week weeks s of onset onset of nephritis •
*therapy of edema in NS: low Na diet, oral loop diuretic, goal of 1-2lbs edema loss/day Renal Biopsy LM: uniform thickening of the BM along the o peripheral capillary loops Immunoflorescence: diffuse granular deposits of o IgG and C3 EM: electron dense subepithelial deposits o •
Progression some some report reports s sugges suggestt that that degree degree of tubula tubular r o atro atroph phy y or inte inters rsti titi tial al fibr fibros osis is are are bett better er predictors than the stage of glomerular disease high recurrence rates o Abrupt onset of edema o spon sponta tane neou ous s remi remissi ssion on occu occurr in 20-3 20-30% 0% of o patients and occur late in the course after year of NS 1/3 have relapsing NS but maintain normal renal o functions 1/3 develop Renal failure of die of complications o of NS risk factors for worse prognosis: male, older age, o HPN, persistent proteinuria MGN has highes highestt report reported ed incide incidence nce of renal renal o vein thrombosis, pulmonary embolism and DVT complications among NS
•
Treatment sympt symptom omat atic ic trea treatm tmen ent: t: edem edema a (ora (orall loop loop o diuretics, low Na diet, target is loss of 1-2lbs or fluid per day), HPN, dyslipidemia, hypercholesterolinemia (lipid lowering agents to decrea decrease se risk risk for CVS diseas disease), e), protei proteinur nuria ia (inhibition of RAS) immu immuno nosu supp ppre resi siv ve drug drugs s (st (steroi eroids ds and and o cyclophospha cyclophosphamide, mide, chlorambuci chlorambucil, l, cyclosporine, cyclosporine, tacrol tacrolimu imus, s, rituxi rituximab mab)) for primar primary y MGN and persistent proteinuria (>3.0g/24hrs) experience with mycophenolate mofetil or antio CD20 antibody is limited prophylacti prophylactic c anticoagul anticoagulation ation (controvers (controversial ial but o recommended) in px with sever proteinuria
•
o
o
o
o
C. Membranous Glomerulonephritis Glomerulonephritis (MPGN/MGN) also called Mebranous Nephropathy (MGN) o in situ formation of immune complexes with megalino receptor associated protein as the putative agent •
Epidemiology 30% of nephrotic syndrome (NS) in adults o rare in children but most common NS in the elderly o peak incidence between 30-50 years o Males > Females (2:1) o 25-30% 25-30% secondary secondary to malignancy malignancy (tumors (tumors of lung, o brea breast st,, col colon), on), infect fectio ion n (He (Hep B, mala malari ria, a, schistosomiasis), rheumatologic disorders (lupus) other etiologies are Drug-induced MGN o Unknown/Idiopathic is still the most common MGN o Causes: •
•
•
Idiopathic Seco Second ndar ary: y: mali malign gnan ancy cy,i ,inf nfec ecti tive ve Hep Hep B, Rheumatology (SLE), Drugs (Gold) 25-30% is secondary
Presentation 80% with nephrotic syndrome (NS)* and o nonselective proteinuria 50% with microscopic hematuria o Nephrotic Syndrome
March 6, 2009/Friday
heavy proteinuria (24h urine total protein > 3g), minimal hematuria, hypoalbuminemia, hypercholesterolemia, HPN if untreated leads to progressive glomerular injury, decline in GFR and renal failure
Low risk Normal renal function Protein <4 Medium Normal fxn
Page 4 of 7 Seth, Ian
OS 214: Renal Glomerulonephritis Glomeruloneph ritis (GN)
Dr. Dr. Agnes Mejia Exam 1&2
Protein >=4 <8 High Abnormal fxn Protein >= 8
VI. SUMMARY
Be aware Family Family Histor History: y: HTN, HTN, DM, CVD, CVD, Gout, Gout, Dialysi Dialysis, s, o ESRD Be suspicious BP > 140/90 o Frothy/cloudy urine o Crea > 1.5 mg/dL or 132 umol/L o GFR < 60 o Nocturia o Dysuria o Set the Alarm Urinalysis o BP >130/80 o Crea 1.5mg/dl, 132 mmol/L o 3 Syndromes and their signs Form Prototype Disease Acute IgA Nephropathy Nephritic Infectious PSGN Disease Associated; Nephritic Nephrotic MGN
Proteinuria +/++
Albuminuria +++
+/++
+++
++++
+
*the *the GFR should should be greatl greatly y decrea decreased sed before before creati creatinin nine e manifests with an abnormality. Hence, be suspicious agad! *A normal normal creati creatinin nine e doesn’ doesn’tt mean mean there’ there’s s normal normal kidney kidney function, so always compute! Therapeutic Intervention AntiInfla AntiInflammat mmatory: ory: Prednisone, Prednisone, tacrolimus tacrolimus,, MMF, MMF, o ritazimab Reduce Proteinuria: ACEI, ARB o e.g. e.g. FSGS FSGS-p -pro rogr gres essi sion on,, remi remissi ssion on,, rela relaps pse e if mainatained on prednisone, but if given combination therapy therapy of prednisone prednisone and mycophenola mycophenolate, te, disease disease is kept in remission
Postinfectious (poststreptococcal) glomerulonephritis.The glomerulonephritis.The glomerular tuft shows proliferative changes with numerous PMNs, with a crescentic reaction in severe cases (A1 ( A1). ). These deposits localize in the mesangium and along the capillary wall in a subepithelial pattern and stain dominantly for C3 and to a lesser extent for IgG (A2 ( A2). ). Subepithelial hump-shaped deposits are seen by electron microscopy (A3 ( A3). ).
VII. Socioeconomic impact of Glomerulonephritis Dialysis: Php40,000 per month o Kidney transplant: Php1.2 M o Maintenance medications: Php60,000 per month o *Hen *Hence ce:: set set the the alar alarm! m! Beca Becaus use e GN is a TREA TREAT TABLE ABLE disease; if treated early, there’s no need for these expensive interventions. VIII. Figures
March 6, 2009/Friday
Page 5 of 7 Seth, Ian
OS 214: Renal
Dr. Dr. Agnes Mejia Exam 1&2
Glomerulonephritis Glomeruloneph ritis (GN)
IgA nephropathy There is variable mesangial expansion due to mesangial deposits, with some cases also showing endocapillary proliferation or segmental sclerosis ((C1 C1). ). By immunofluorescence, deposits are evident (C2 (C2). ).
Membranous glomerulopathy. glomerulopathy. Membranous glomerulopathy is due to subepithelial deposits, with resulting basement membrane reaction, resulting in the appearance of spike-like projections on silver stain (B1). B1). The deposits are directly visualized by fluorescent anti IgG, revealing diffuse granular capillary loop staining (B2 ( B2). ). By electron microscopy, microscopy, the subepithelial location of the deposits and early surrounding basement membrane reaction is evident, with overlying foot process effacement (B3 ( B3))
Hyaline Cast
Berry-like configuration of the glomeruli.
March 6, 2009/Friday
Page 6 of 7 Seth, Ian
OS 214: Renal
Dr. Dr. Agnes Mejia Exam 1&2
Glomerulonephritis Glomeruloneph ritis (GN)
Immunofluorescent Immunofluorescent staining of glomeruli with labeled antiIgG demonstrating linear staining (D1 (D1)) from a patient with antiGBM disease or immune deposits from a patient with membranous glomerulonephritis compared to IgG lumpybumpy staining (D2 (D2). ). Preformed immune deposits can preciptate from the circulation and collect along the glomerular basement membrane (GBM) in the subendothelial space or can form in situ along the subepithelial space.
March 6, 2009/Friday
The mechanisms of glomerular injury have a complicated pathogenesis. Immune deposits and complement deposition classically draw macrophages and neutrophils into the glomerulus. T lymphocytes may follow to participate in the injury pattern as well. *Amplification
mediators such as locally derived oxidants and proteases expand this inflammation, inflammation, and depending on the location of the target antigen and the genetic polymorphisms polymorphisms of the host, basement membranes are damaged with either endocapillary or extracapillary extracapillary proliferation proliferation
Page 7 of 7 Seth, Ian
