Pathophysiology Glomerulonephritis is an infection of the glomerular membrane which impairs proper function. In the kidney, this membrane is responsible for the filtration of water and associated solutes out of the body while simultaneously keeping plasma proteins in the cardiovascular system. When an alteration occurs, the permeability of the membrane decreases, thus decreasing the overall glomerular filtration rate (GFR) of the kidney and leading to complications associated with low GFR. Glomerulonephritis can be caused by primary or secondary glomerular injuries. Primary injury to the glomerulus include damage from immunologic responses, ischemia, free radicals, drugs, toxins, vascular disorders (BOOK REF). Secondary injuries to
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The main differentiator when diagnosis Goodpasture syndrome is the presence of anti-GBM-Abs in the blood, as classically this has been an indicator of the amount of antibody in the renal tissue (Kalluri et al., 1995). Recently, however, a study demonstrated that circulation tests of anti-GBM-Abs can conclude with false-positives by not detecting IgG4 autoantibodies (Ohlsson et al., 2014). New findings such as these highlight the necessity for a renal biopsy to officially diagnose with Goodpasture syndrome. Renal biopsy can reveal particular patterns associated with anti-glomerular basement antibody disease. Specifically, extensive formations of crescents and glomerulonephritis can be found with interstitial inflammation, diffuse inflammation of the glomerulus, and necrosis to surrounding tissue (Silvarino, Noboa, & Cervera, 2014). Renal biopsies will also allow histologic information to be gained about the types of antibodies interacting with the glomerular basement membrane. Common differential diagnoses can be assessed with the presence of anti-neutrophil cytoplasmic antibodies (ANCAs).
Subjective Findings Subjective findings for Goodpasture syndrome include general malaise, lower back pain, dysuria, fatigue, and exertional dyspnea (Dammacco, Battaglia, Gesualdo, & Racanelli, 2013). Lower back pain, dysuria and malaise would be associated with the renal complications of the disease, while exertional dyspnea and historical conveyance of hemoptysis would be associated with pulmonary complications of the disease. Subjective findings would help in the diagnosis of the disease with the addition of objective findings.
The main differentiator when diagnosis Goodpasture syndrome is the presence of anti-GBM-Abs in the blood, as classically this has been an indicator of the amount of antibody in the renal tissue (Kalluri et al., 1995). Recently, however, a study demonstrated that circulation tests of anti-GBM-Abs can conclude with false-positives by not detecting IgG4 autoantibodies (Ohlsson et al., 2014). New findings such as these highlight the necessity for a renal biopsy to officially diagnose with Goodpasture syndrome. Renal biopsy can reveal particular patterns associated with anti-glomerular basement antibody disease. Specifically, extensive formations of crescents and glomerulonephritis can be found with interstitial inflammation, diffuse inflammation of the glomerulus, and necrosis to surrounding tissue (Silvarino, Noboa, & Cervera, 2014). Renal biopsies will also allow histologic information to be gained about the types of antibodies interacting with the glomerular basement membrane. Common differential diagnoses can be assessed with the presence of anti-neutrophil cytoplasmic antibodies (ANCAs).
Subjective Findings Subjective findings for Goodpasture syndrome include general malaise, lower back pain, dysuria, fatigue, and exertional dyspnea (Dammacco, Battaglia, Gesualdo, & Racanelli, 2013). Lower back pain, dysuria and malaise would be associated with the renal complications of the disease, while exertional dyspnea and historical conveyance of hemoptysis would be associated with pulmonary complications of the disease. Subjective findings would help in the diagnosis of the disease with the addition of objective findings.