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Glomerulo nephritis
 

Glomerulo nephritis

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    Glomerulo nephritis Glomerulo nephritis Presentation Transcript

    • Glomerulonephritis is an infamation of the glomerular capilaries
    • Causes of nephritic syndrome Primary glomerulonephritis – Acute GN • Post streptoccocal • Non streptococal Rappidly progressive GN Membranoproliferative GN Focal GN IgA nephropathy GN
    • Systemic disease: SLE Polyarteritis nodosa Wegener’s granulomatosis Henoch schonlein purpura cryoglobulinaemia
    • Classification of glomerular disease Primary glomerulonephritis – Acute GN • Post streptoccocal • Non streptococal Rappidly progressive GN Minimal change GN Membranous GN Membranoproliferative GN Focal GN IgA nephropathy GN Chronic GN
    • SECONDARY SYSTEMIC GLOMERULAR DISEASE Lupus nephritis Diabetic nephropathy Amyloidosis Polyarteritis nodosa Wegener’s granulomatosis Henoch schonlein purpura Goodspasture’s syndrome Systemic infectious diseases
    • Hereditary nephritis Alport’s syndrome Fabry’s disease Nail patella syndrome
    • Nephritis Caused by Circulating immune Complexes With circulating immune complexmediated 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.
    •  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.
    • 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.
    • 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.
    • 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.
    • 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.
    • 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 complementleukocyte-mediated
    •  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.
    •  Some models suggest complementdependent 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.
    • Other mediators of glomerular damage include (1)monocytes and macrophages, which infiltrate the glomerulus in antibodyand cell-mediated reactions and, when activated, release a vast number of biologically active molecules; (2) platelets, which aggregate in the glomerulus during immunemediated injury and release prostaglandins and growth factors;
    • (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.
    • 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.
    • 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.
    • 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.
    • 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.
    • TYPES OF GLOMERULONEPHRITIS:There are different types of GN It may involve either the nephrotic syndrome or nephritic syndrome Diagnosis made by C/F or by renal biopsy
    • Types of glomerulonephritis (ACUTE NON STREPTOCOCAL) Minimal change disease Is a benign disorder Frequent cause of nephrotic syndrome in children Here the glomeruli shows a diffuse effacement of podocyte foot process.
    • 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
    • CAUSES Idiopathic Systemic 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 Loss Prognosis – good, Rx is corticosteroids
    • Focal & segmental to slecrosis : Characterized by sclerosis affecting some but not all the glomeruli CAUSES Associated with HIV infection IgA nephropathy Maladaptation after nephron loss Congenital malformation in podocytes
    • PATHOGENS: Unknown Investigators have said that FSGS and MCD are continuous – MCD may transform into PSGS C/F: Variable protunuria Not responding to corticosteroids Prognosis: Poor Recurs after transplantation
    • 3. MEMBRANOUS NEPHROPATHY (MENBRANEOUS GN) Occurs between 30 & 50 years. Subepithelial deposits Causing thickening of the capillary wall. Causes: idiopathic secondary to Infections (chronic hepatitis, syphillis, malaria) Malignant tumors of lung & colon SLE & other auto immune disorders Drugs (NSAID’S)
    • C/F Heavy protenuria Does not respond to cortecosteroids They may respond to prednisolone. PROGNOSIS :Variable 30% may have spontaneous remission
    • Menbranoproliferative FN:Alteration in the GBM & mesangium Proliferation of glomerular cell TYPES: Mesengial cells are found between the endothelium & GBM Immune deposits are found in subendotheal region (SLE) (bacterial endocardites, HIV, hepatitis
    • TYPE II Is autoimmune disease called IgG autoantibodies called c3 nephretic factor Causing lipodystrophy loss of subcutaneous fat from the upper half of the body.
    • IGA NEPHROPATHY : Affects children Associated with gross hematuria Associated with loin pain Here 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
    • C/F Hematuria Red blood cell cast on urine analysis.
    • Acute glomerulonephritis
    • 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
    • Luekocyte infiltration of glomerulus Thickening of the GF membrane Scarring and loss of glomerular filtration membrane Decreased glomerular filtration rate (GFR)
    • CLINICAL MANIFESTATIONS: Hematuria Protinuria Edema Azotemia Hypertension Abdominal or flank pain Oliguria Fever, chills, weakness, pallor, anorexia, nausea and vomitting may be present.
    • Elderly patient may experience circulattory ocurroal, with dyspnea, engorged nec ceeins, cardionegely and pulmonary edema. Hypoalbuninenia and hyperlipedemia.
    • DIAGNOSTIC STUDIES: History and physical examination  Urinalysis  CBC  BUN, seum creatinine and albunmin  Complement levels and ASO titre  Renal biopsy.  Signs of overload  Periorbital edema  Edema and hypertension due to overload  Crackles  Elevated jugular venous pressure  Rashes  Pallor
    • Physical examination:
    • Lab studies: Urine analysis Complement levels Twenty-four hours urine test for total protein Anti sterptolysin O titre Dipstick test Imaging studies Renal biopsy: cellular infiltration, granular deposits of immunoglobulin.
    • Treatment: Antimicrobial therapy: Penicillin 500000 IU q6 q8 hourly Loop diuretics: Frusemide: Edema: 40-80mg to 20- 40mg 6th hourly. Hypertension: 20- 40mg bid PO bid Vasodilators: Sodium nitroprusside 0.5-8mcg/kg/mim IV infusion
    • Diet: Sodium and fluid restriction Protein restriction 0.6 – 0.75g/kg/wt Water restriction to 600ml plus the previous days urine output. Sodium restriction; 2 to 4g depending on the degree of edema. Avoid high sodium food.
    • Chronic glomerulonephritis
    • 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
    • Clinical features: Hypertension Elevated BUN Nosebleed Edema of the optic disc General symptoms like malaise, weight loss, edema, mental cloudiness, Gallop rhythm, distended neck veins, symptoms of heart failure. crackles
    • Poorly nourished Mucous membrain pale because of edema. Urine analysis shows hematuria, protienuria, scanty, dark, smoky, cola coloured, Peripheral neuropathy Confusion
    • Diagnostic findings: History collection Physical assessment Urine analysis Blood investigations Radiography Biopsy
    • Treatment: Medical care: Drug therapy: Angiotensin converting enzyme inhibitors Eg: enalapril Dose: 2.5-10 mg orally not to exceed 40mg 1 day)
    • 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 qd Calcium channel blockers: Amlodipine 2.5 – 10 mg qd.
    • Nefidipine Short acting – 10mg orally tid Long acting – 30 mg orally qd not to exceed 120 – 150 mg qd Beta adrenergic blockers Metoprolol – 50 mg oral bid Alpha adrenergic blockers Clonidine (catapress) Dose : 0.1 – 0.2 mg orally bid/tid not to exceed 2.4 mg qid
    • Surgical treatment Renal replacement therapy Hemodialysis Peritoneal dialysis Renal transplantation Diet management Protein restricted diet (0.4 – 0.6 g 1kg/d Fluid instruction to 600ml
    • Complications Metabolic acidosis Pulmonary edema Pericarditis Uremic encephalopathy Uremic nueropathy Severe anemia & hypocalemia hyperkelemia
    • 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.
    • The causes can be classified also  Primary glomerulonephrills  Minimal change disease  Membranous GN  Menbranoproliferative GN  Focal segmental glomerulosclerosis  Focal GN  IgA nephropathy
    • II. systemic disease  Diabetes mellitus  Amyloidosis  SLE III. Systemic decease  Viral infection  Bacterial infection (endocardites, syphillis, leprosy)  Protozoa & parasites (P.falciparum malaria, filariasis
    • IV. Hypersensitivity Drugs. (heavy metal compounds like gold & mercury, heroin addiction, Bee sting, snake bite, poison ivy V. Malignancy Carcinomas Myeloma Hodgkins disease
    • VI. Pregnancy Toxemia of pregnancy VII. Circulatory disturbance Renal vein thrombosis Constructive pericarditis VIII. Hereditary diseases Alports disease Fabry’s disease Nail patella syndrome
    • Clinical features Heavy protienuria Hypolepidemia Hypoalbumenemia Edema lipiduria Hercoagulability
    • Pathophysiology: Damage to the glomerular capillary membrane Loss of plasma protein Stimulate synthesis of liporotiens hypoalbuminimea Hyperlipidemia decreased oncotic press generalized edema renin angeotensin edema