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Glomerulonephritis block a trans

Glomerulonephritis block a trans

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Glomerulonephritis (GN)
OS 214: Renal
Dr. Agnes MejiaExam 1&2
March 6, 2009/Friday
Page 1 of 7Seth, Ian
OUTLINEI.IntroductionII.GlomerulonephritisIII.Pathogenesis of GlomerulonephritisIV.Approach to Patient withGlomerulonephritisV.Forms of GlomerulonephritisA.IgA NephropathyB.Poststreptococcal GlomerulonephritisC.Membranous GlomerulonephritisVI.SummaryVII.Socioeconomic impact oGlomerulonephritisVIII.Figures
Note: The lecturer did not provide a powerpoint. Thank you toIrving for sending pictures of the ppt for this trans. Please bereminded 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, presented with
:
o
high BP (160/100), HR 104, RR 30/min
o
pale, sallow (in between pallor and jaundice)
o
“peculiar fetor” – fruity smell
o
evidence of cardiac damage (Grade II Av block
hypertensive) but not yet in CHF due to absence of s3
o
no evidence of liver involvement
o
++ bipedal edema
o
Dry skin, good and equal pulses
o
Basal crepitant rales
B. Primary Impression: UREMIA
(symptom diagnosis)Symptoms seen in the ER
o
Vomiting
o
Tremors
o
Anorexia
o
Weakness
o
SOB
o
Pruritus
o
Easy fatigability
o
IrritabilityFull blown Uremia (not seen in ER)
o
Somnolence
o
Seizures
o
Disorientation
o
Coma*Azotemia
is a laboratory diagnosisUremia
a clinical diagnosis
C. Labs Requested
LabPurposeFinding in ERCBCCheck for anemia due topallor Low Hg (7)BUNTo asses kidney function,but creatinine is moreimportantElevated (60umol/L)*CreatinineSingle most importanttest for uremia (uremic if azotemic); if high, tellsyou that px likely haskidney diseaseIncreased (1800 umol/L)ElectrolytesCaTo check for acidosisDecreasedPhosphorusElevated
(6)
**KNeeded if urgent action isrequired (can easily killthe patient)Elevated
(5.9)
***ABGNeeded if urgent action isrequired
(pH7.2; pCO
2
35;pO
2
94; HCO
3
11;O
2
sat 92%)
SevereUncompensatedMetabolic acidosis (lowpH, low HCO3;causes tachypnea)CXRTo rule out pneumoniaHeart not enlarged butwith congestionShowed pulmonaryedemaEKGCheck for hyperkalemiaPeaked T waves(denotes hyperkalemia)
you have to givecalcium gluconate astreatmentUTZVisualize the kidney:If enlarged (e.g. 12cm)=acute GN, reversibleIf shrunken=ESRD,irreversible(Normal Filipino size:9.6cm in length; NormalCaucasia:11-12 cm)*Normal
globular, thickcortexSmall shrunken kidneyCortex should at least be4.5cm thickUrinalysiswindow to glomeruladisease”-early morning urineexpected to have a dark,intense color if kidney isable to concentrate urine- concentrated (Sp.gravity 1.020-1.030)-Acute GN – red cellcasts; RBCs degenerateto fine/coarse granular casts
reflects chronicity-Hyaline casts
can befound in a normal person-Most common cause of pus cells
non infectivepyuria-low sp. gravity-granular casts-Increase RBC andWBC-mucus threads rare
denotes that urine waswell collected-px has no fever but highWBC
may indicatesterile pyuria
*if creatinine is high, BUN is expected to be abnormal; if BUNis high, creatinine is not necessarily high*the presence of protein in the urine is not correlated with thespecific gravity of the urine since SG indicates the ability of the kidneys to concentrate. Even if this is intact, the kidneyscan still spill out urine.*those in asterisks are the cheaper tests, so they are the mosteconomical and efficient in terms of information.
D. Final Diagnosis
:
o
Uremia secondary to ESRD (CKD Stage V)secondary to Chronic Glomerulonephritis (CGN)Basis for diagnosis:CGN
o
young adult, hypertension at age 19 (hypertensivenephrosclerosis takes about 20 years to develop,and so it is an unlikely ddx)
o
hematuria, pyuria
o
small kidneys (denotes a chronic problem, not acute)ESRD
o
shrunken kidneys
o
uremia, anemia, low Ca
o
Inc phosphorus*Single most important determinant of chronicity
shrunkenkidneys*Severe renal failure
Ca low, Phosphorus high**ER is a UP student; inc BP at age 19 (140/90). ER waserroneously treated as UTI for 3 years in a male with nosymptoms and an abnormal urinalysis; ER passedengineering boards 3 days before he underwent hemodialysis!
 
Glomerulonephritis (GN)
OS 214: Renal
Dr. Agnes MejiaExam 1&2
March 6, 2009/Friday
Page 2 of 7Seth, Ian
My Goals (which I guess have to be our goals)
1.To be aware2.To be suspicious3.To Set the Alarm
II. Glomerulonephritis
 -inflammation of the glomerular capillariesa. Normal Kidneys:
o
smooth surface
o
pinkish cortex
o
reddish medulla
o
yellow calyces, pelvis
o
In GN: kidneys are pale*Kidney disease has 10 types but can manifest the same way.But if you look inside the kidneys, the pathology is actuallydifferent. They hit different parts of the kidney
thus histologyis important!b. Glomerulus
o
600 thousand 2 million (all in all) in a normalindividual*prematures have less glomeruli
higher tendencyfor hypertension
higher tendency for renal diseaseat age 50
o
is a ball of capillaries (“berries”) with afferent andefferent arterioles (histology: stalk – where efferentand afferent arterioles run)
o
glomerular capillaries filter 120-180 L/d of plasmawater 
o
filtration occurs through a physicochemical barrier governed by pore size and negative electrostaticcharge
o
glomerulus is an imperfect barrier *e.g. albumin-despite its negativity, readily passesthrough due to its small radius (3.6nm vs. 4nm radiusof glomerular basement mebrane (GBM) slit-pores);albumin is reabsorbed in the proximal tubules (urinenormally contains only 8-10 mg)*Glomerulonephritis can affect any part of the glomerulus(mesangium, parietal epithelium, basement membrane,podocytes) and will manifest differently.In GN: the glomeruli are full of scarsPathogenesis:
(1)(2)Circulating immune complexes In-situ immune complexesT-cells (CD 4/8) activationLoca activation of toll-like receptors on Glomerular CellsDeposition of Immune ComplexesComplement injuryGlomerular injuryMononuclear infiltrationCytokine releaseAttract more inflammatory cellsGlomerular damage
*In summary, GN may be caused by circulating or in situimmune complexes, but whichever the cause is, they bothfollow the path of inflammation via T-cell activation*Immunofluorescence can be used to determine whetheimmune complexes are in-situ or circulating*Overlapping etiologies may produce similar glomerulalesions display common patterns of injury (syndrome); this isevident in microscopy:IgA
paramesangial; can still see spaces in glomerulus; mostcommon in AsiansPoststrep GN (PSGN) – same pattern of injury can be seen inlupus; immune-complex GN; most common post infectiousMembranous GN (MGN) –same pattern can be seen inidiopathic, Hepatitis, and drug-induced; just hits the basementmembrane, causing it to thicken; most common in men
IV. Approach to Patient with Glomerulonephritis
A. History and PE (what to look at)
o
confined to the kidneys or systemic? acute or chronic?
o
signs and symptoms (what to ask the px)
dysuria – pain during urination?
nocturia – urination at night?
hematuria – blood in the urine
? (2 kinds grossand microscopic)
retention/incontinence incompletevoiding?
frequency – urinating more often?
Sediments- may “latak” sa ilalim ang ihi?
frothy urine – like beer?
edema
o
last known urinalysis/creatinine
o
pregnancy status (preeclampsia); birth control pills
o
last normal BP
o
Blood pressure
must give exact value, not just sayingnormal or high, because what is high for one person may be normal for another 
o
Urinalysis
window to glomerular disease
Quality of urine: clear, cloudy or bloody(gross hematuria)*if with gross hematuria and is painless
consider malignancy until proven otherwise; if painful,consider urethritis*Dilute urine
yellow concentrated*Cloudy
tea colored*Bloody
gross hematuriaTable 277-1. Urine assays for albumin/proteinuria
(HPIM 17
th
ed)
24Hr Albumin(mg/24h)Albumin/creatinineratio(mg/G)Dipstickproteinuria24HhUrineProtein(mg/24h)Normal8-10<30-<150Microalbuminuria30-30030-300-/trace/1+-Proteinuria>300>300Trace-3+>150
V. Forms of Glomerulonephritis (Patterns of Clinical GN)
FormPrototype DiseaseAcute NephriticIgA NephropathyInfectious DiseaseAssociated; NephriticPostStreptococcal GN(PSGN)NephroticMembranous GNBasement membraneAlports syndromeGlomerular Vascular Disease
ANCA small vessel vasculits
 
Glomerulonephritis (GN)
OS 214: Renal
Dr. Agnes MejiaExam 1&2
March 6, 2009/Friday
Page 3 of 7Seth, Ian
Pumonary-RenalGoodpastures disease*just focus on the first three as said by the lecturer, ayt?A.
IgA Nephropathy
CASE:
31 femaleRoutine annual Physical checkupUrinalysis
-
RBC –TNTC 
-
WBC – 0-3
-
Protein (-)
-
Casts (-)BP 
120/70 
o
immune complex mediated GN defined by thepresence of diffuse mesangial IgA deposits oftenassociated with mesangial hypercellularity
o
circulating immune complexes get deposited in themesangium or podocytes (not the basementmembrane [BM])
o
IgM, IgG, C3, or immunoglobulin light chains can becodistributed with IgA
o
Mild – do not undergo dialysis
o
RPGN (rapidly progessive)- end up in dialysis after 6mos
POSTstrep GN - tea colored urine happens 2weeks after infection
In IgA – happens with the infection
Pathogenesis: defective immune response
formation of immune complex
proinflammatory, proproliferative,proapoptotic, profibrotic + milieu in glomeruli
mesangial/podocyte injury, capillary hypertension, alteredperm selectivity, glomerulosclerosis, tubulo-interstitialfibrous
hematuria, proteinuria, decreased GFR
Epidemiology
o
most common form of GN worldwide
o
30% in Asia and Pacific RimEast > West
o
20% in southern Europe
o
low prevalence in N. Europe & N. America
o
Male > Female
o
peak incidence: 2
nd
-3
rd
decade of life
o
rare familial clustering
Presentation
o
most common presentations are:
recurrent episodic macroscopic hematuriafollowing a respiratory infection in children
asymptomatic microscopic hematuria seenin adults
o
between episodes, urinalysis is normal
o
in persistent hematuria, increasing proteinuria isfound
Differentials
o
Henoch-Schonlein Purpura- can bedistinguished for IgA Nephropathy by prominentsystemic sx, younger onset (<20yrs old),preceding infection and abdominal complaints
o
Crohn’s disease, chronic lover disease, GIadenocarcinoma, etc –also present with IgAdeposition in mesangium; can be differentiateddue to absence of significant glomerular inflammation.
Progression
o
generally a benign disease, but 25-30%progress to renal failure over 20-25 yrs.
o
5-30% go into complete remission
o
sometimes recur post transplant
o
risk factors for renal failure: HPN, proteinuria,absence of episodic macroscopic hematuria,male, older age of onset, sever renal biopsychanges
o
“Point of no return” – stage where treatment isinsufficient usually when creatinine is at least 2
o
the clinical prognostic index (CPI) of GN–madein Verona, Italy; a scoring system that predictsthe 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
o
Score of 0-2*: higher 10-year renal survival; 3-5:lower 10-year renal survival; most likely to endup in dialysis; hence, creatinine is the singlemost impt predictors of survival since itautomatically gives you 2pts if abnormal*Immunoflourescence
positive for IgA
Treatment
o
Evidence-based: ACEI-ARB, Steroids, fish oil(severe only), sequential, cyclophosphamide:azathioprine (progressive only)
o
Non-evidence Based: azathioprine/MMF, CNI(CsA Tacro), IVIg, Leflunomide,heparin/warfarin/dipyridamole, tonsillectomy*IgA GN
is common, progressive, but treatable
B. PostStreptococcal Glomerulonephritis (PSGN)
CASE:
22 male1 month impetigo in L leg Pus, crust, swelling, redness, fever 
tea colored urine, dec outpu, puffy eyelids, anorexi, easy fatigability, inc BP 
o
also known as Postinfectious GN
o
prototype for acute endocapillary proliferative GN
o
classically not a nephritic syndrome
Pathogenesis: putative streptococcal antigens circulating1-C, activation of complement with cell mediated injury
deposition in GBM
Epidemiology
o
typically sporadic
o
children between 2-14 yrs (10% in px>40yrs)
o
Males > Females
o
10% pts>40yrs
o
familial/cohabitant incidence is high-40%
o
M types of Streptococci (nephritogenic strains)
o
impetigo- M types 2, 47, 49, 55, 57, 60;PSGN develops 2-6 wks after a skin infection
o
Pharyngitis (nephritogenic strain)- M types1,2, 3, 4, 12, 25, 49; PSGN develops 1-3 wksafter strep upper respiratory infection(pharyngitis)
Labs
o
Decreased CH50, decreased C3
o
Inconsistently positive culture (10-70%)
o
Increased ASO titers (30%)
o
Anti-DNase (70%)
o
Antihyaluronidone Ab (40%)
Presentation

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