This graduation thesis is a narrative review for Goodpasture syndrome (GS), a rare autoimmune disease affecting the kidneys and lungs. This eponymous syndrome, first described by Goodpasture in 1919, refers to the renopulmonary vascular damage done by circulating antibodies and their subsequent post-deposition inflammatory damage. The complex pathogenesis of the disease includes genetic predisposition, central tolerance defect, glomerular basement membrane (GBM) exposure revealing a culprit epitope, subsequent antibodies production against GBM and finally, culmination with antibody deposition in the kidneys and lungs. The autoantibodies thereafter, trigger a fulminant inflammatory reaction carried by cell-mediated and complement-dependent immune processes. The symptoms that follow range in severity from dyspnea to pulmonary hemorrhage and respiratory failure in the lungs, and from oliguria and hematuria to rapidly progressive glomerulonephritis (RPGN) in the kidneys. Therefore, physicians should have a high clinical suspicion of GS with any respiratory symptoms presentation in RPGN patients. Early diagnosis is imperative for treatment and is performed through serological tests and kidney biopsy. Treatment revolves around antibodies removal through plasma exchange and immunosuppressive therapy to halt further antibodies production. Pulmonary symptoms usually resolve, while recovery of renal function is poor and patients often require renal replacement therapy. Fortunately, GS seldom recur and patients who survive the initial ailment have a favorable prognosis.