Up to 80% of individuals with Goodpasture syndrome exhibit both respiratory and renal symptoms. Acute presentation of symptoms occurs more frequently than chronic symptoms. An individual may initially complain of loss of appetite, fatigue and weakness. Renal involvement is accompanied by blood in urine, difficulty while urination, nausea, pallor and edema of extremities. Pulmonary involvement includes dry cough with shortness of breath and coughing out blood .
Other tests are used to confirm symptoms such as tests for serum BUN and creatnine levels, chest X-rays, arterial blood gas analysis are carried out. Kidney biopsies are preferred over lung biopsies to assist in diagnosis as signs of crescent formation, glomerular membrane damage, interstitial fibrosis and tubular atrophy can determine extent of renal injury  .
Plasmapharesis is carried out to purify the blood and remove anti-GPDM antibodies from the plasma .
Goodpasture syndrome is characterized by the presence of autoantibodies that target the α3, α4 and α5 chain of non collagenous 1 (NC1) domain of type IV collagen found within the glomerular and pulmonary basement membrane layers   .
Individuals carrying alleles HLA-DRW2, HLA-DRB4 and HLA-DRB1 within the Major Histocompatibility Complex (MHC) locus are susceptible to events that trigger autoantibody activation   . The events implicated include inhalation of cigarette smoke, metal dust or drugs such as cocaine, exposure to hydrocarbons and infectious diseases such as influenza A2 that also affect the respiratory system     .
Goodpasture syndrome is rare in occurrence with approximately one case reported per two million individuals in Europe3. A study conducted on patients with end stage renal disease (ESRD) in Australia and New Zealand noted that 0.8 percent individuals suffered from Goodpasture syndrome .
Demographically, young and elderly adult Caucasian and Asian males have a higher incidence of developing this syndrome5. Younger males show symptoms of lung hemorrhage prior to renal disease while older and elderly males will initially present with renal disease  .
The basement membrane layer serves as a foundation for epithelial cell organization. It is formed by the polymerization of agrin, laminin and Type IV collagen fibers to various glycoprotein molecules . In the renal glomerulus, the basement membrane is flanked by fenestrated endothelial cells of the glomerular capillary and podocytes. This layer provides mechanical support to the capillary wall, provide a base for receptor ligand interaction and assists in the ultrafiltration process of the kidney . Three novel collagen IV chains α3,α4 and α5 first identified by scientists in 1987, serve as epitopes for binding of autoantibodies.
Researchers hypothesize that in the presence of triggering factors such as cigarette smoke or hydrocarbon exposure in susceptible individuals damage the basement membrane. This results in a conformational change of the collagen IV molecule that then exposes the α3,α4 and α5 epitopes to both CD4+ reactive T cells and B cells    . These antibodies are highly specific and have been observed in serum samples of patients suspected of Goodpasture’s disease .
Downstream effects that occur after antibody target interaction results in activation of complements, cytokines and proteases interferes with the glomerular filtration process resulting in glomerulonephritis, identified by crescent formation and proteinuria. Continued antibody assault will result in migration of macrophages and neutrophils into the kidney leading to interstitial nephritis and fibrosis in kidney. 2-D electrophoresis and western blot analysis of collagen domains isolated from human alveolar basement membrane also showed a positive reaction to anti-glomerular basement membrane antibodies  .
The alveolar basement membrane is impervious to anti-glomerular basement membrane antibodies under normal circumstances. However, environmental factors damage the alveolar basement layer especially in susceptible individuals and expose the epitopes to antibody binding .
There are no guidelines for prevention of Goodpasture syndrome.
It is named after Dr. Ernest Goodpasture (1886-1960), an American physician and pathologist. During the influenza pandemic in 1919, he observed that some infected patients suffered acute symptoms of renal failure along with hemoptysis or coughing up blood .
Goodpasture syndrome is a rare autoimmune disease. Individuals with acute renal failure and pulmonary hemorrhage should be evaluated for this condition. Presence of anti-glomerular basement membrane antibodies in sera of affected patients is diagnostically relevant.
Plasmapharesis and steroids are usually recommended for treatment. The prognosis is good when diagnosed and treated promptly. However, delay in treatment will lead to complications such as renal failure and death.