Glomerulo nephritis
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Transcript of Glomerulo nephritis
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Glomerulonephritis is an infamation of the glomerular capilaries
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Causes of nephritic syndrome
Primary glomerulonephritis– Acute GN
• Post streptoccocal• Non streptococal
Rappidly progressive GNMembranoproliferative GNFocal GNIgA nephropathy GN
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Systemic disease:SLEPolyarteritis nodosaWegener’s granulomatosisHenoch schonlein purpuracryoglobulinaemia
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Classification of glomerular disease
Primary glomerulonephritis– Acute GN
• Post streptoccocal• Non streptococal
Rappidly progressive GNMinimal change GNMembranous GNMembranoproliferative GNFocal GNIgA nephropathy GNChronic GN
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SECONDARY SYSTEMIC GLOMERULAR DISEASE
Lupus nephritisDiabetic nephropathyAmyloidosisPolyarteritis nodosaWegener’s granulomatosisHenoch schonlein purpuraGoodspasture’s syndromeSystemic infectious diseases
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Hereditary nephritis
Alport’s syndromeFabry’s diseaseNail patella syndrome
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Nephritis Caused by Circulating immune Complexes
With circulating immune complex-mediated disease, the gromerulus is considered “innocent bystander” because it does not incite the reaction. The antigen is not of glomerular origin. It may be endogenous, as in the GN associated with SLE, or it may be exogenous, as is probable in the GN that follows certain bacterial, viral, parasitic and spirochetal infections.Often the inciting antigen is unknown, as in most cases of membranous nephropathy.
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Whatever the antigen may be, antigen-antibody complexes are formed in situ or in the circulation and are then trapped in the glomeruli,
where they produce injury, in large part through the activation of complement and the recruitment of leukocytes.
Regardless of the mechanism, the glomerular lesions usually consist of leukocytic infiltration into glomeruli and variable proliferation of endothelial, mesangial, and parietal epithelial cells.
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Electron microscopy reveals the immune complexes as electron-dense deposits or clumps that lie at one of three sites:
in the mesangium,
between the endothelial cells and the GBM, or
between the outer surface of the GBM and the podocytes.
Seen in most cases of poststreptococcal or acute infection-related GN.
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Nephritis Caused by in Situ Immune Complexes
Anti-Glomerular Basement Membrance (GBM) Antibody
Glomerulonephritis.
In this type of injury,
antibodies are directed against fixed antigens in the GBM.
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Cell-Mediated Immune Glomerulonephritis
It has often been suggested that sensitized T cells, formed during the course of a cell-mediated immune reaction, can cause glomerular injury.
In some forms of experimental GN in rodents, the disease can be induced by transfer of sensitized T cells.
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T cell-mediated injury may account for the instances of GN in which either there are no deposits of antibodies or immune complexes or the deposits do not correlate with the severity of damage.
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Mediators of Immune Injury
Glomerular damage, reflected by loss of glomerular barrier function, is manifested by proteinuria and, in some instances, by reduction in GFR.
A major pathway of antibody –initiated injury is complement-leukocyte-mediated
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Activation of complemnt leads to the generation of chemo tactic agents and the recruitment of neutrophils and monocytes.
Neutrophils release proteases, which cause GBM degradation; oxygen-derived free radicals, which cause cell damage; and arachidonic acid metabolites, which contribute to reduction in GFR.
This mechanism applies only to some types of GN.
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Some models suggest complement-dependent but not neutrophil-dependent injury, due to an effect of the C5 lytic component of complement,
which causes epithelial cell detachment and stimulates mesangial and epithelial cells to secrete various mediators of cell injury.
Thus giving rise to altered GBM composition and thickening.
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Other mediators of glomerular damage include (1)monocytes and macrophages, which infiltrate the glomerulus in antibody- and cell-mediated reactions and, when activated, release a vast number of biologically active molecules;
(2) platelets, which aggregate in the glomerulus during immune-mediated injury and release prostaglandins and growth factors;
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(3) Resident glomerular cells, which can be stimulated to secrete mediators such as cytokines arachidonic acid metabolites, growth factors, nitric oxide, and endothelin; and
(4) fibrin-related products, which cause leukocyte infiltration and glomerular cell proliferation as a consequence of intraglomerular thrombosis.
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Other Mechanisms of Glomerular Injury
Two that deserve special mention are podocyte injury and injury secondary to nephron loss.
Podocyte Injury:
This can be induced by antibodies to visceral epithelial cell antigens; by toxins, certain cytokines; or by still poorly characterized factors, as in some cases of focal and segmental glomerulosclerosis.
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Such injury is reflected by morphologic changes in the podocytes, which include effacement of foot processes, vascularization, and retraction and detachment of cells from the GBM, and functionally by proteinuria.
In most forms of glomerular injury, loss of normal slit diaphrangms is key in the development of proteinuria.
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Nephron Loss. Once any renal disease,
glomerular or otherwise, destroys sufficient functioning nephrons to reduce the GFR to 30% to 50% of normal progression to end-stage renal failure often proceeds. develop proteinuria, and their kidneys show widespread glomerulosclerosis.
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These remaining glomeruli undergo hypertrophy to maintain renal function.
This is associated with hemodynamic
changes, including increases in single nephron, GFR, blood flow, and transcapillary pressure.
These adaptations in the intact glomeruli are ultimately maladaptive and lead to further endothelial and epithelial cell injury, increased glomerular permeability to proteins, and accumulation of proteins and lipids in the mesangial matrix.
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TYPES OF GLOMERULONEPHRITIS:-There are different types of GNIt may involve either the nephrotic
syndrome or nephritic syndromeDiagnosis made by C/F or by renal
biopsy
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Types of glomerulonephritis (ACUTE NON STREPTOCOCAL)
Minimal change diseaseIs a benign disorderFrequent cause of nephrotic
syndrome in childrenHere the glomeruli shows a diffuse
effacement of podocyte foot process.
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1. MINIMAL CHANGE DISEASE (LIPOID NEPHPOSIS)
It is a begin disorder. Frequence cause of nephrotic
syndrome. Different affacement of pocodeyti
foot processes (they appear flattened
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CAUSESIdiopathicSystemic disease (hodgkins disease,
HIV infection) & drug therapy (NSAID)
PATHOGONESIS:
Protenuria has been attributed to T cell derived factor that cause podoeyte enjury & affacement.
C/F:- Protein LossPrognosis – good, Rx is corticosteroids
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Focal & segmental to slecrosis :Characterized by sclerosis
affecting some but not all the glomeruli
CAUSESAssociated with HIV infectionIgA nephropathyMaladaptation after nephron lossCongenital malformation in
podocytes
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PATHOGENS:UnknownInvestigators have said that FSGS
and MCD are continuous – MCD may transform into PSGS
C/F:Variable protunuriaNot responding to corticosteroids
Prognosis: PoorRecurs after transplantation
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3. MEMBRANOUS NEPHROPATHY (MENBRANEOUS GN)
Occurs between 30 & 50 years.Subepithelial depositsCausing thickening of the capillary wall.
Causes:idiopathic secondary toInfections (chronic hepatitis, syphillis,
malaria)Malignant tumors of lung & colonSLE & other auto immune disordersDrugs (NSAID’S)
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C/FHeavy protenuriaDoes not respond to
cortecosteroidsThey may respond to prednisolone.
PROGNOSIS :-Variable30% may have spontaneous
remission
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Menbranoproliferative FN:-Alteration in the GBM & mesangiumProliferation of glomerular cell
TYPES:Mesengial cells are found between
the endothelium & GBMImmune deposits are found in
subendotheal region
(SLE)
(bacterial endocardites, HIV, hepatitis
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TYPE IIIs autoimmune disease called
IgG autoantibodies called c3 nephretic factor
Causing lipodystrophy loss of subcutaneous fat from the upper half of the body.
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IGA NEPHROPATHY :Affects childrenAssociated with gross hematuriaAssociated with loin painHere there is deposition of IgA is
mesangium (due to IgA production & clearance abnormal)
It is due to some infection is to respiratory or GI tract.
These activates the alternative complement pathway
Glomerular injury
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C/FHematuriaRed blood cell cast on urine
analysis.
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Acute glomerulonephritis
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PATHOPHYSIOLOGY:Antigen (group A seta – hemolylic
streptococcus
Antigen – antibody products
Deposition of antigen – antibody complexes in glomerulers
Increase production of epithelial cells lining the glonerulus
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Luekocyte infiltration of glomerulus
Thickening of the GF membrane
Scarring and loss of glomerular filtration membrane
Decreased glomerular filtration rate (GFR)
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CLINICAL MANIFESTATIONS:HematuriaProtinuriaEdemaAzotemiaHypertensionAbdominal or flank painOliguriaFever, chills, weakness, pallor,
anorexia, nausea and vomitting may be present.
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Elderly patient may experience circulattory ocurroal, with dyspnea, engorged nec ceeins, cardionegely and pulmonary edema.
Hypoalbuninenia and hyperlipedemia.
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DIAGNOSTIC STUDIES:-History and physical examinationUrinalysisCBC BUN, seum creatinine and albunminComplement levels and ASO titreRenal biopsy.Signs of overloadPeriorbital edemaEdema and hypertension due to overloadCracklesElevated jugular venous pressureRashesPallor
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Physical examination:
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Lab studies:Urine analysisComplement levelsTwenty-four hours urine test for
total proteinAnti sterptolysin O titreDipstick testImaging studiesRenal biopsy: cellular infiltration,
granular deposits of immunoglobulin.
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Treatment: Antimicrobial therapy:Penicillin 500000 IU q6 q8 hourlyLoop diuretics:Frusemide:Edema: 40-80mg to 20- 40mg 6th
hourly.Hypertension: 20- 40mg bid PO bidVasodilators:Sodium nitroprusside0.5-8mcg/kg/mim IV infusion
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Diet:
Sodium and fluid restrictionProtein restriction 0.6 – 0.75g/kg/wtWater restriction to 600ml plus the
previous days urine output.Sodium restriction; 2 to 4g
depending on the degree of edema.Avoid high sodium food.
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Chronic glomerulonephritis
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Pathophysiology:Acute GN (repeated episodes)
Cause hardening of renal arteries
Reducing the size
Scar tissue formation (numerous glomerulus and branches of renal
arteries are thickened)
Severe glomerular damage
End stage renal failure
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Clinical features:HypertensionElevated BUNNosebleedEdema of the optic discGeneral symptoms like malaise,
weight loss, edema, mental cloudiness,
Gallop rhythm, distended neck veins, symptoms of heart failure.
crackles
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Poorly nourishedMucous membrain pale because of
edema.Urine analysis shows hematuria,
protienuria, scanty, dark, smoky, cola coloured,
Peripheral neuropathyConfusion
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Diagnostic findings:
History collectionPhysical assessmentUrine analysisBlood investigationsRadiographyBiopsy
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Treatment:
Medical care:
Drug therapy:
Angiotensin converting enzyme inhibitors
Eg: enalapril
Dose: 2.5-10 mg orally not to exceed 40mg 1 day)
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Diuretics:
Fruosimide (lasix)
1-2 mg. 1kg oral/IV/bid not to exceed 600 mg /d
0.1-0.4 mg/kg/hour continuous iv infusion
Metdazone
5-20 mg orally qdCalcium channel blockers:
Amlodipine
2.5 – 10 mg qd.
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NefidipineShort acting – 10mg orally tidLong acting – 30 mg orally qd not
to exceed 120 – 150 mg qd
Beta adrenergic blockersMetoprolol – 50 mg oral bidAlpha adrenergic blockersClonidine (catapress)
Dose : 0.1 – 0.2 mg orally bid/tid not to exceed 2.4 mg qid
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Surgical treatmentRenal replacement therapyHemodialysisPeritoneal dialysisRenal transplantation
Diet managementProtein restricted diet (0.4 – 0.6 g
1kg/dFluid instruction to 600ml
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ComplicationsMetabolic acidosisPulmonary edema PericarditisUremic encephalopathyUremic nueropathySevere anemia & hypocalemiahyperkelemia
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NEPHTOTIC SYNDROME
Nephrotic syndrome is a cluster of clinical findings, including
Marked increase in protein (particularly albumin) in the urine (protienuria)
Decreased in albumin in the blood (hypoalbuminenia)
Edema, hypercholesterolemia & normal renal function.
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The causes can be classified also Primary glomerulonephrills Minimal change disease Membranous GN Menbranoproliferative GN Focal segmental
glomerulosclerosis Focal GN IgA nephropathy
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II. systemic disease Diabetes mellitus Amyloidosis SLE
III. Systemic decease Viral infection Bacterial infection (endocardites,
syphillis, leprosy) Protozoa & parasites
(P.falciparum malaria, filariasis
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IV. HypersensitivityDrugs. (heavy metal compounds
like gold & mercury, heroin addiction,
Bee sting, snake bite, poison ivy
V. MalignancyCarcinomasMyelomaHodgkins disease
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VI. PregnancyToxemia of pregnancy
VII. Circulatory disturbanceRenal vein thrombosisConstructive pericarditis
VIII. Hereditary diseasesAlports diseaseFabry’s diseaseNail patella syndrome
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Clinical features
Heavy protienuriaHypolepidemiaHypoalbumenemiaEdemalipiduriaHercoagulability
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Pathophysiology:Damage to the glomerular capillary
membrane
Loss of plasma protein
Stimulate synthesis hypoalbuminimea
of liporotiens
Hyperlipidemia decreased oncotic press
generalized edema
renin angeotensin
edema