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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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Renal vein thrombosis: initial manifestation of Goodpasture's syndrome
From CHEST, 1/1/91 by Andrew Gottehrer

Goodpasture's syndrome is an immunologic disorder characterized by glomerulonephritis, pulmonary hemorrhage and anti-glomerular basement membrane (GBM) antibody formation. [1] Although most patients have some degree of proteinuria, frank nephrosis is distinctly unusual. [1,2] Furthermore, renal vein thrombosis has not been reported, to our knowledge, as the initial presentation of Goodpasture's syndrome.

We report a patient who presented with renal vein thrombosis and nephrosis that progressed to pulmonary hemorrhage and renal failure. Results of renal biopsy and serum anti-GBM assay confirmed the diagnosis of Goodpasture's syndrome. This unique presentation contributed to the delay in correct diagnosis and initiation of appropriate therapy.


A 23-year-old woman presented with leg edema and left flank tenderness. Serum blood urea nitrogen was 13 mg/dl, creatinine 1.4 mg/dl, albumin 2.2 g/dl and cholesterol 276 g/dl. Urinalysis revealed 4+ proteinuria. A renal venogram demonstrated left renal vein thrombosis (Fig 1). Chest radiograph showed subtle bilateral alveolar infiltrates, which were ascribed to nephrosis and volume overload. Renal vein thrombosis secondary to the nephrotic syndrome was diagnosed and the patient was treated with intravenous heparin that was converted to coumadin at discharge.

Two weeks later, the patient was readmitted with severe dyspnea, anasaca, oliguria, cough productive of blood-tinged sputum, and nausea. A chest radiograph showed bilateral alveolar infiltrates most marked in the lower and mid lung zones (Fig 2). Blood urea nitrogen was 111 mg/dl; creatinine, 10 mg/dl; potassium, 7.2 mmol/L; and hematocrit, 10.7 percent. Urinalysis revealed 4+ proteinuria and hematuria. The patient was intubated because of progressive hypoxemia and transferred to the Medical University of South Carolina. Endotracheal secretions were blood-tinged and contained numerous hemosiderin-laden macrophages.

Following stabilization with hemodialysis, a renal biopsy specimen was obtained that showed 75 percent of glomeruli involved with crescentic glomerulonephritis and linear deposition of IgG and [C.sub.3] in basement membranes. Serum anti-GBM titer by radioimmunoassay was 1:256. The patient was treated with corticosteroids, cyclophosphamide and plasmapheresis with resolution of pulmonary infiltrates and respiratory failure. Three weeks later, she was discharged, requiring chronic hemodialysis for oliguric renal failure.


Renal vein thrombosis is a well-recognized complication of nephrotic syndrome. Although the precise mechanism is unknown, vascular thrombosis appears to be a consequence of the hypercoagulable state that accompanies nephrosis rather than a cause, as was previously suspected, of the renal lesions. [3-5] in adults, renal vein thrombosis most commonly occurs with membranous and membranoproliferative glomerulonephritis, [6,8] and associations with renal sarcoidosis, amyloidosis, [3] lupus nephritis [3,8] and sickle cell anemia [9] have also been described. To our knowledge, renal vein thrombosis has not been previously reported in a patient with nephrosis associated with Goodpasture's syndrome.

We suspect that renal vein thrombosis in our patient resulted from anti-GBM-related nephrosis that preceded the more typical features of Goodpasture's syndrome, such as frank alveolar hemorrhage and azotemia. Nepthrotic syndrome has been noted infrequently as a complication of Goodpasture's syndrome, probably because of the typically fulminant course of renal insufficiency that occurs in anti-GBM disease. [1] This rapid course may also underlie the apparent rarity of renal vein thrombosis in patients with Goodpasture's syndrome.

Other etiologies of pulmonary hemorrhage and glomerulonephritis have been described. These include Wegener's granulomatosis, systemic lupus erythematosus, Henoch-Schonlein purpura, and cryoglobulinemia. Although there is an immunologic basis to these disorders, circulating anti-GBM antibodies have not been demonstrated. [10]

This unique presentation of Goodpasture's syndrome contributed to the delay in correct diagnosis of the present patient. Furthermore, the administered anticoagulation therapy for renal vein thrombosis may have exacerbated the pulmonary hemorrhage and eventual degree of respiratory failure.

In summary, renal vein thrombosis secondary to nephrosis is an unusual but important initial presentation of Goodpasture's syndrome. Failure to detect the underlying disorder may prompt initiation of inappropriate therapy for thrombosis, such as anticoagulant drugs, thereby aggravating the degree of respiratory failure from subsequent alveolar hemorrhage.


[1] Glassock RJ, Cohen AH, Adler, SG. Secondary glomerular diseases. In: Brenner BM, Rector Jr, RJ, eds. The kidney. 3rd ed. Philadelphia: W.B. Saunders, Co.; 1986:1032-36

[2] Robinson T, Rabinowitz JG. The nephrotic syndrome. Radiol Clin North Am 1972; 10:495-510

[3] Llach F, Papper S, Massry SG. The clinical spectrum of renal vein thrombosis: acute and chronic. Am J Med 1980; 69:819-27

[4] Harrington JT, Kassirer JP. Renal vein thrombosis. Ann Rev Med 1982; 33:255-62

[5] Humphreys JT, Alfrey AC. Vascular diseases of the kidney. In: Brenner BM, Rector Jr, RJ, eds. The kidney, 3rd ed. Philadelphia: W.B. Saunders, 1986:1180-84

[6] Llach F, Arieff AI, Massry SG. Renal vein thrombosis and nephrotic syndrome. A prospective study of 36 adult patients. Ann Intern Med 1975; 83:8-14

[7] Llach F, Koffler A, Finck E, Massry SG. On the incidence of renal vein thrombosis in the nephrotic syndrome. Arch Intern Med 1977; 137:333-36

[8] Appel GB, Williams GS, Meltzer JI, Pirani CL. Renal vein thrombosis, nephrotic syndrome, and systemic lupus erythematosus. Ann Intern Med 1976; 85:310-17

[9] Strom T, Muehrcke RC, Smith RD. Sickle cell anemia with the nephrotic syndrome and renal vein obstruction. Arch Intern Med 1972; 129:104-08

[10] Albelda SM, Gefter WB, Epstein D, Miller WT. Diffuse pulmonary hemorrhage: a review and classification. Radiology 1985; 154:289-97

COPYRIGHT 1991 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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