IMMUNOLOGIC DISORDERS OF THE KIDNEYS P 1131 1134 GLOMERULONEPHRITIS Inflammation of the glomeruli o Affects both kidneys equally o Immunologic processes involving the urinary tract usually affect the renal glomerulus o Tubular interstital and vascular changes also occur Classification o The extent of damage diffuse or focal o Initial cause of the disorder systemic lupus erythematosus systemic sclerosis scleroderma streptococcal infection o Extent of changes minimal or widespread ETIOLOGY AND PATHOPHYSIOLOGY Antibody induced injury can initiate glomerular damage two types o Anti GBM antibodies Antibodies with specific antigens for the glomerular basement membrane GMB The reason these antibodies form is unknown Immunoglobins and complements are deposited along the basement membrane o Antibodies react with circulating nonglomeruluar antigens and are randomly deposited as immune complexes along the GMB Antigens do not come from the glomeruli but from endogenous circulating native DNA or exogenous sources bacteria viruses chemicals drugs Bacteria poststreptococcal glomerulonephritis Virus after hep B hep C and rubella measles Immune complex disease accumulation of antigen andibody and compliment tissue injury Immune complex activates complement release of chemotactic factors attract polymorphonuclear leukocytes histamine and inflammatory mediators glomerular injury CLINICAL MANIFESTATIONS Hematuria microscopic to gross Urinary excretion of RBCs WBCs casts and proteinuria Elevates serum BUN and creatinine Acute illness recovery occurs however renal tissue damage and marked renal insufficiency occurs with progressive involvement Assess exposure to drugs immunizations microbial infections and viral infections hepatitis o Also immune disorders systemic lupus erythematosus and systemic sclerosis ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS APSGN Most common in children and young adults 5 21 days after toncils pharynx or skin infection by nephrotoxic group A B hemolytic strept Antibodies produces to the streptococcal antigen antigen antibody complexes deposited in the glomeruli complement activated inflammation reaction tissue injury decreased filtration of metabolic waste from the blood and increase in glomerulus permeability to large protein molecules CLINICAL MANIFESTIONS AND COMPLICATIONS Generalized body edema HTN oliguria hematuria smoky rusty appearance and proteinuria o Decreased glomerular filtration fluid retention edema Initially periorbital then ascites and peripheral edema total body o Proteinuria dependent on severity of glomerulonephropathy o Increased extracellular fluid volume HTN Abdominal or flank pain Sometimes no symptoms found on routine urinalysis Rarely chronic glomerulonephritis or renal failure occur o 95 recover completely or improve rapidly with conservative management DIAGNOSTIC STIDUIES Determine the presence or history of group A B hemolytic streptococcus o Antistrepolysin O ASO titer Decreased complement components indicated immune mediated response May be confirmed with renal biopsy Dipstick urinalysis and urine sediment microscopy o Erythrocytes and erythrocyte casts highly suggest APSGN o Proteinuria Serum screening for BUN creatinine and albumin NURSING AND COLLABORATIVE MANAGEMENT Focuses on symptomatic relief Rest o Until inflammation proteinuria hematuria and HTN subside Sodium and fluid restriction treat edema Anti HTN therapy Adjust protein intake to level of proteinuria and uremia Diuretics treat edema DIET LOW SODIUM LOW PROTEIN LOW FLUID Good personal hygiene important to prevent cutaneous infection spread Corticosteroids and cytotoxic drugs antibiotics ONLY if strept is still present usually penicillin GOODPASTURE SYNDROME Cytotoxic type II autoimmune disease very rare o Possible factors type A flu virus hydrocarbons penicillamine and genetics Characterized by presence of circulating antibodies against glomerular and alveolar basement membrane Kidneys are the primary target organ but lungs are involved o Damage occurs due to antibodies binding and causing inflammatory reaction mediated by complement fixation and activation CLINICAL MANIFESTATION Mostly in young male smokers Flu like symptoms Pulmonary symptoms cough mild SOB hemoptysis crackles rhonchi and pulmonary insufficiency o Pulmonary hemorrhage usually occurs precedes glomerular issues by weeks months Renal symptoms hematuria weakness pallor anemia and renal failure Low H H high BUN and creatinine hematuria and proteinuria Serum anti GBM antibodies are diagnostic NURSING AND COLLABORATIVE MANAGEMENT Corticosteroids immunosuppressive drugs cyclophosphamide Cytoxan azathioprine Imuran plasmapheresis and dialysis o Plasmapheresis removes circulating anti GBM antibodies o Immunosuppressive therapy inhibits antibody production Survival rate used to be 4 months now only mortality rate 20 o Death usually due to pulmonary hemorrhage respiratory failure Once anti GBM titer decreases transplantation may be considered o May reoccur but not contraindication for transplant RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS RPGN Glomerular disease associated with acute renal failure o Rapid progressive loss of renal function over days to weeks o Renal failure occurs within weeks to month chronic glomerulonephritis over years Clinical manifestations HTN edema proteinuria hematuria and RBC casts Occurs due to o Complications of multisystemic disease systemic lupus goodpasture syndrome o Complication of inflammatory or infectious disease APSGN o Idiopathic disease o Drug use penicillamine Prompt diagnosis and treatment of fluid overload HTN uremia and inflammation kidney injury Treatment corticosteroids cytotoxic agents and plasmapheresis o Dialysis and transplant are used as maintenance o RPGN may reoccur after transplant CHRONIC GLOMERULONEPHRITIS Syndrome that reflects the end stage of glomerular inflammatory disease o glomerulonephritis and nephrotic syndrome chronic glomerulonephritis kidney failure can take up to 30 years o Characterized by proteinuria hematuria and slow uremia development Usually found due to abnormal urinalysis or new HTN o Common for patients to have no previous renal issues Renal biopsy to determine cause and nature o Ultrasound and CT generally preferred to diagnosis less specific but less invasive Treatment supportive and symptomatic o Treat UTI and HTN vigorously DIET Protein and phosphate restriction o Slows kidney disease progression NEPHOTIC SYNDROME ETIOLOGY Glomerulus is excessively