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Goodpasture's syndrome

Goodpasture’s syndrome (also known as Goodpasture’s disease and anti-glomerular basement membrane disease or anti-GBM disease) was first described by Ernest Goodpasture in 1919. It is an rare condition characterised by rapid destruction of the kidneys and haemorrhaging of the lungs. Although many diseases can present with these symptoms, the name Goodpasture’s syndrome is usually reserved for the autoimmune disease produced when the patient’s immune system attacks cells presenting the Goodpasture antigen, which are found in the kidney and lung, causing damage to these organs. more...

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Signs and symptoms

Most patients present with both lung and kidney disease, however, some patients present with one of these diseases alone. The first lung symptoms usually develop days to months before kidney damage is evident.

Lung disease

Lung damage may cause nothing more serious than a dry cough and minor breathlessness and such mild symptoms may last for many years before more severe ones develop. At its most serious, however, lung damage may cause severe impairment of oxygenation so that intensive care is required. Deterioration between the two extremes may occur very rapidly, often at the same time as rapid deterioration in the kidney. The patient often does not seek medical attention until he or she begins coughing up blood. The patient may be anaemic due to loss of blood through lung haemorrhaging over a long period. In Goodpasture’s syndrome, unlike many other conditions that cause similar symptoms, lung haemorrhaging most often occurs in smokers and those with damage from lung infection or exposure to fumes.

Kidney disease

The kidney disease mostly affects the glomeruli causing a form of nephritis. It is usually not detected until a rapid advance of the disease occurs so that kidney function can be completely lost in a matter of days. Blood leaks into the urine causing haematuria, the volume urinated decreases and urea and other products usually excreted by the kidney are retained and build up in the blood. This is acute renal failure. Renal failure does not cause symptoms until more than 80% of kidney function has been lost. Symptoms include loss of appetite and sickness at first and then, when the damage is more advanced, breathlessness, high blood pressure and oedema (swelling caused by fluid retention).


Because of the vagueness of early symptoms and rapid progression of the disease, diagnosis is often not reached until very late in the course of the disease. Kidney biopsy is often the fastest way to secure the diagnosis and gain information about the extent of the disease and likely effect of treatment. Tests for anti-GBM antibodies may also be useful, combined with tests for antibodies to neutrophil cytoplasmic antigens, which are also directed against the patient’s own proteins.


As with many autoimmune conditions, the precise cause of Goodpasture’s Syndrome is not yet known. It is believed to be a type II hypersensitivity reaction to Goodpasture’s antigens on the cells of the glomeruli of the kidneys and the pulmonary alveoli, whereby the immune system wrongly recognises these cells as foreign and attacks and destroys them, as it would an invading pathogen.


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Pulmonary renal syndrome seropositive for both antineutrophil cytoplasmic autoantibodies and anti-glomerular basement membrane autoantibodies
From CHEST, 10/1/05 by Matthew C. Exline

INTRODUCTION: Pulmonary renal syndrome (PRS) confers a high mortality in the critical care setting. Prompt diagnosis and appropriate treatment are keys to preventing long term morbidity. However, there may be considerable overlap both symptomatically and serologically between the various etiologies of PRS, making initial treatment decisions difficult. We present a case of a patient with the antineutrophil cytoplasmic autoantibodies (ANCA)-positive Goodpasture's Overlap Syndrome, defined as PRS seropositive for both ANCA and anti-glomerular basement membrane autoantibodies (anti-GBM).

CASE PRESENTATION: A 41 year-old white male, previously healthy smoker, presented with two weeks of increasing dyspnea, diffuse myalgias, and hemoptysis. On presentation the patient was profoundly hypoxemic with respiratory distress requiring intubation in the emergency room. On exam, he was afebrile, tachycardic, and hypotensive. Lungs had diminished breath sounds at bases and bilateral rhonchi. Laboratory studies were significant for elevated creatinine and blood urea nitrogen, leukocytosis and eosinophilia. Chest x-ray revealed bilateral pulmonary infiltrates. The patient developed progressive renal failure needing dialysis, shock requiring pressor support, and persistent hypoxemia. A bronchoscopy was preformed with bronchoaveolar lavage demonstrating alveolar hemorrhage with 23% macrophages, 30% neutrophils, and 46% eosinophils. Serum quantitative immunoglobulins were significant for IgE of 1043 mg/dl. A sinus CT showed right maxillary and ethmoid sinusitis. Based on the clinical picture, elevated IgE, and peripheral / BAL eosinophilia a diagnosis of Churg-Strauss was made and the patient initiated on prednisone therapy without improvement for five days. Subsequent serologic evaluation was positive for rheumatoid factor (1:80), C-ANCA (1:512), and anti-GBM at 106 EU/ml. The patient was then initiated on plasmapheresis for presumed Goodpasture's disease. A renal biopsy displayed anti-glomerular basement membrane antibody and C-ANCA positive focal crescentric and necrotizing glomerulonephritis consistent with ANCA-positive Goodpasture's Overlap Syndrome. He was continued on plasma exchange until his anti-GBM titers normalized, and treated with high dose prednisone and cyclophosphamide. The patient was successfully liberated from mechanical ventilation and hemodialysis. He was discharged home on prednisone and mycophenolate mofetil. He continues to be dialysis independent at one year follow-up.

DISCUSSIONS: Pulmonary renal syndrome, initially described by Goodpasture in 1919, is usually associated with either ANCA (60-70%) or anti-GBM (20%) antibodies. It has recently been recognized that patients may present as both ANCA and anti-GBM antibody positive. Approximately 5% of ANCA positive sera is also anti-GBM positive and 32% of anti-GBM positive sera is ANCA positive. However there are only a few case series that correlate these serological findings with the clinical progression of these patients. There is still debate on the prognosis of these patients, in part due to a lack of clear diagnostic criteria and differences in treatment modalities. Some studies suggest these dually positive patients have a similar clinical course to ANCA vasculitis with many (75%) recovering renal function. Others suggest near universal renal failure in these patients similar to those with Goodpasture's syndrome.

CONCLUSION: It is vital to differentiate ANCA-positive anti-GBM patients from other causes of PRS in order to deliver appropriate treatment in a timely fashion. Plasma exchange, while a mainstay of therapy in Goodpasture's syndrome, is not thought to be beneficial for ANCA positive vasculitis and may not be routinely offered unless an diagnosis of Overlap Syndrome is considered. Prompt and aggressive plasmapheresis for ANCA positive anti-GBM positive patients may portend a greater likelihood of renal recovery as in our patient.



(1) Gallagher H et al. Pulmonary renal syndrome: a 4-year, single-center experience. Am J Kidney Dis 2002; 39(1):42-47.

(2) Levy JB et al. Clinical features and outcome of patients with both ANCA and anti-GBM antibodies. Kidney Int 2004; 66(4):1535-1540.

(3) Hellmark T et al. Comparison of anti-GBM antibodies in sera with or without ANCA. J Am Soc Nephrol 1997; 8(3):376-385.

DISCLOSURE: Matthew Exline, None.

Matthew C. Exline MD * John G. Mastronarde MD The Ohio State University, Columbus, OH

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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