Glomerulo Nephritis

Views:
 
Category: Education
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

Glomerulonephritis is an infamation of the glomerular capilaries:

Glomerulonephritis is an infamation of the glomerular capilaries

Causes of nephritic syndrome:

Causes of nephritic syndrome Primary glomerulonephritis Acute GN Post streptoccocal Non streptococal Rappidly progressive GN Membranoproliferative GN Focal GN IgA nephropathy GN

PowerPoint Presentation:

Systemic disease: SLE Polyarteritis nodosa Wegener’s granulomatosis Henoch schonlein purpura cryoglobulinaemia

Classification of glomerular disease:

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:

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:

Hereditary nephritis Alport’s syndrome Fabry’s disease Nail patella syndrome

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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;

PowerPoint Presentation:

(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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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.

PowerPoint Presentation:

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) :

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.

PowerPoint Presentation:

MINIMAL CHANGE DISEASE (LIPOID NEPHPOSIS) It is a begin disorder. Frequence cause of nephrotic syndrome. Different affacement of pocodeyti foot processes (they appear flattened

PowerPoint Presentation:

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

PowerPoint Presentation:

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

PowerPoint Presentation:

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

PowerPoint Presentation:

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)

PowerPoint Presentation:

C/F Heavy protenuria Does not respond to cortecosteroids They may respond to prednisolone. PROGNOSIS :- Variable 30% may have spontaneous remission

PowerPoint Presentation:

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

PowerPoint Presentation:

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.

PowerPoint Presentation:

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

PowerPoint Presentation:

C/F Hematuria Red blood cell cast on urine analysis.

PowerPoint Presentation:

Acute glomerulonephritis

PowerPoint Presentation:

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

PowerPoint Presentation:

Luekocyte infiltration of glomerulus Thickening of the GF membrane Scarring and loss of glomerular filtration membrane Decreased glomerular filtration rate (GFR)

PowerPoint Presentation:

CLINICAL MANIFESTATIONS: Hematuria Protinuria Edema Azotemia Hypertension Abdominal or flank pain Oliguria Fever, chills, weakness, pallor, anorexia, nausea and vomitting may be present.

PowerPoint Presentation:

Elderly patient may experience circulattory ocurroal, with dyspnea, engorged nec ceeins, cardionegely and pulmonary edema. Hypoalbuninenia and hyperlipedemia.

PowerPoint Presentation:

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::

Physical examination:

Lab studies::

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: :

Treatment: Antimicrobial therapy : Penicillin 500000 IU q6 q8 hourly Loop diuretics: Frusemide: Edema: 40-80mg to 20- 40mg 6 th hourly. Hypertension: 20- 40mg bid PO bid Vasodilators: Sodium nitroprusside 0.5-8mcg/kg/mim IV infusion

Diet::

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.

PowerPoint Presentation:

Chronic glomerulonephritis

Pathophysiology::

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::

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

PowerPoint Presentation:

Poorly nourished Mucous membrain pale because of edema. Urine analysis shows hematuria, protienuria, scanty, dark, smoky, cola coloured, Peripheral neuropathy Confusion

Diagnostic findings::

Diagnostic findings: History collection Physical assessment Urine analysis Blood investigations Radiography Biopsy

Treatment::

Treatment: Medical care: Drug therapy: Angiotensin converting enzyme inhibitors Eg: enalapril Dose: 2.5-10 mg orally not to exceed 40mg 1 day)

PowerPoint Presentation:

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.

PowerPoint Presentation:

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

PowerPoint Presentation:

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

PowerPoint Presentation:

Complications Metabolic acidosis Pulmonary edema Pericarditis Uremic encephalopathy Uremic nueropathy Severe anemia & hypocalemia hyperkelemia

PowerPoint Presentation:

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.

PowerPoint Presentation:

The causes can be classified also Primary glomerulonephrills Minimal change disease Membranous GN Menbranoproliferative GN Focal segmental glomerulosclerosis Focal GN IgA nephropathy

PowerPoint Presentation:

II. systemic disease Diabetes mellitus Amyloidosis SLE Systemic decease Viral infection Bacterial infection (endocardites, syphillis, leprosy) Protozoa & parasites (P.falciparum malaria, filariasis

PowerPoint Presentation:

IV. Hypersensitivity Drugs. (heavy metal compounds like gold & mercury, heroin addiction, Bee sting, snake bite, poison ivy V. Malignancy Carcinomas Myeloma Hodgkins disease

PowerPoint Presentation:

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:

Clinical features Heavy protienuria Hypolepidemia Hypoalbumenemia Edema lipiduria Hercoagulability

Pathophysiology::

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

authorStream Live Help