Brights Disease Lab Report Sample
Abstract Background C3 glomerulopathy C3G is a recent disease classification that is characterized by the presence of glomerular deposits composed of C3 in the absence of significant amounts of immunoglobulin and comprises dense deposit disease and C3 glomerulonephritis C3GN. Most C3GN manifests as membranoproliferative, mesangial proliferative glomerulonephritis patterns via light microscopy. Case presentation A year-old woman was admitted to a local hospital with elevated serum creatinine for two weeks.
Background
Blood biochemistry analysis Brghts the following concentrations: albumin, The serum C3 level was 0. The direct Coombs test was positive. Immunofluorescence testing revealed only diffuse, finely Brights Disease Lab Report Sample depositions of C3 along the glomerular capillary walls in frozen and paraffin-embedded tissue sections. Electron microscopy demonstrated the presence of subepithelial electron-dense deposits, similar to those that are observed in membranous nephropathy. Corticosteroid and cyclophosphamide were administered, with a subsequent improvement in renal function. C3GN with ANCA positivity may be represented by more crescents, severe renal dysfunction and more extrarenal manifestations.
More cases are needed to elucidate the clinicopathologic features and read article treatments of these patients.
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Peer Review reports Background C3 glomerulopathy C3G is a recent disease classification that is characterized by the presence of glomerular deposits composed of C3 in the absence of significant amounts of immunoglobulin Ig [ 12 ]. C3G results from the dysregulation of the alternative complement pathway, which may be caused by an acquired or genetic dysfunction of complement regulating proteins [ 3 ].
The appearance of intramembranous electron-dense deposits corresponding to the C3 deposits is characteristic of DDD. Most C3GN manifests as membranoproliferative, mesangial proliferative glomerulonephritis patterns in light microscopy. Electron microscopy shows nondense, intramembranous, mesangial, subendothelial or subepithelial deposits of C3 in C3GN [ 24 ]. Isolated subepithelial deposits of C3 are rarely reported. Anti-neutrophil cytoplasmic antibodies ANCAs have been proven to cause pauci-immune necrotizing and crescentic GN and vasculitis [ 5 ].
ANCA has become the serologic biomarker for these disorders, with the test having good sensitivity [ 6 ]. The intrinsic mechanism of these symptoms are discussed and detailed. Case presentation A year-old Chinese woman was admitted with elevated serum creatinine for two weeks.
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She noticed lower back pain and went to a Labb hospital two weeks prior. There were no symptoms of gross hematuria, foamy urine, frequent urination, urination urgency, urination pain, chills or fever. Therefore, she was transferred to our hospital. No special medication was previously taken by the patient.
Physical examination showed prominent features of facial pallor.
There were no palpable lymph nodes. The results of chest and abdominal exams were within normal limits, and mild edema of the lower extremities was noticed.]
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