Cases reported "Nephritis"

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21/62. Lobar nephronia in a transplanted kidney.

    We report a patient who presented with a solid mass in her graft 15 years after renal transplantation. The appearances by ultrasound were consistent with either malignancy or lobar nephronia (focal acute bacterial nephritis). biopsy confirmed the diagnosis of a lobar nephronia with marked inflammatory infiltrate and frank pus formation. Treatment with antibiotics was associated with resolution of the mass. Lobar nephronia is a diagnosis based upon renal ultrasonography and must be considered in a patient with a solid mass in the kidney.
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22/62. Sudden late onset of gross hematuria in a previous renal transplant recipient 3 months after transplant nephrectomy.

    Causes of gross hematuria in a patient with end-stage renal disease are limited compared with those in patients with normal renal function. Given the increased likelihood of patients with end-stage renal disease developing renal cell carcinoma, the workup focuses on a careful evaluation of the collecting system. The workup for gross hematuria in a renal transplant recipient is similar; however, the focus shifts toward a more thorough evaluation of the transplanted kidney and bladder because immunosuppression increases the overall risk for malignancy. An immunosuppressed patient also is at risk for infectious processes in the transplanted kidney manifesting as gross hematuria. Concerns for chronic rejection also should be investigated, although microscopic hematuria is more common in this scenario. If this is unrevealing, then close scrutiny of the native kidneys for possible sources of bleeding is warranted. We present an interesting and unusual cause of painless gross hematuria in a patient with end-stage renal disease and transplant nephrectomy 3 months before the onset of bleeding.
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23/62. Acute multifocal bacterial nephritis complicated with acute renal failure and thrombocytopenia.

    A 50-year-old woman was transferred to our hospital because of acute renal failure and thrombocytopenia. Due to rapid enlargement of the kidney, we first suspected that she had diffuse renal invasion of anaplastic carcinoma or lymphoma of the kidney. Anti-bacterial treatment for complicated urinary tract infection and hemodialysis treatment resulted in recovery of both renal function and thrombocytopenia. Serial CT study demonstrated disappearance of kidney swelling and multiple masses within the kidney. We finally made a diagnosis of acute multifocal bacterial nephritis. Timely initiation of dialysis therapy and appropriate anti-bacterial treatment was essential to rescue this case.
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24/62. The pathogenesis of Alport syndrome involves type IV collagen molecules containing the alpha 3(IV) chain: evidence from anti-GBM nephritis after renal transplantation.

    Mutations in the COL4A5 collagen gene have been implicated as the primary defect in Alport syndrome, a heritable disorder characterized by sensorineural deafness and glomerulonephritis that progresses to end-stage renal failure. In the present study, the molecular nature of the defect in Alport glomerular basement membrane (GBM) was explored using anti-GBM alloantibodies (tissue-bound and circulating) produced in three Alport patients subsequent to renal transplantation. The alloantibodies bound to the alpha 3(IV)NC1 domain of type IV collagen and not to any other basement membrane component. In tissue sections, the alloantibodies bound specifically to peripheral GBM in normal kidney and the affected renal transplant but not to that of Alport kidney. These results establish that: the alpha 3 chain in type IV collagen molecules, the Goodpasture autoantigen, is the target alloantigen in post-transplant anti-GBM nephritis in patients with Alport syndrome, and that a molecular commonality exists in the pathogenesis of anti-GBM nephritis causing loss of renal allografts in patients with Alport syndrome and renal failure in patients with Goodpasture syndrome. These findings implicate: (1) defective assembly of type IV collagen molecules containing the alpha 3(IV) chain in Alport GBM; and (2) the existence of a mechanism linking the assembly of molecules containing the alpha 3(IV) chain with those containing the alpha 5(IV) chain.
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25/62. Different mutations in the COL4A5 collagen gene in two patients with different features of Alport syndrome.

    Alport syndrome is a hereditary renal disease in which progressive renal failure is often accompanied by sensorineural deafness and ocular abnormalities. Recently, mutations were detected in the type IV collagen alpha 5 chain gene in Alport syndrome patients. We searched for mutations in this gene in 18 unrelated patients, and in two patients abnormalities were detected. In the gene of patient BB we identified a complex deletion, which included the exons encoding the non-collagenous domain and part of the collagenous region. This patient showed early onset nephritis (end-stage renal disease at 17 years) with deafness. Within a year after receiving a kidney from an unrelated donor, he developed an antiglomerular basement membrane nephritis. In patient WJ a point-mutation was detected, changing a tryptophane into a serine in the non-collagenous domain. His clinical features are milder (renal failure at 33 years, no hearing loss), and a recent renal allograft did not provoke antiglomerular basement membrane disease. These initial data suggest that differences in the extent of disruption of the non-collagenous domain may correlate with the severity and/or heterogeneity of Alport syndrome and with the development of nephritis in renal allografts.
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26/62. The features of glomerulitis in the acute stage of panarteritis nodosa. Developmental process of glomerulitis and correlation between glomerular and vascular lesions.

    In order to determine the morphological characteristics of certain vascular and glomerular lesions and the correlation between them, we attempted three-dimensional observation using serial sections of an autopsy kidney, from a patient with panarteritis nodosa in the acute phase. Fibrinoid necrotizing vasculitis spread from arcuate arteries to arterioles in a segmental, eccentric pattern, especially occurring at bifurcations. Segmental arteriolitis often originated in extraglomerular capsular arteriole and spread into the intraglomerular capsular arteriole and glomerular capillaries, directly leading to necrotizing glomerulitis. Some of the glomerulitis connected directly with extracapsular arteriolitis was segmental and eccentric in distribution. Most of the glomerulitis had a tendency to originate in the hilar arteriole, which was near bifurcations between the arteriole and glomerular capillaries. Segmental glomerulitis was found to consist of four elements: glomerular tuft necrosis with fibrin exudation, crescents, rupture or dissolution of Bowman's capsule, and pericapsulitis. It is suggested that the segmental inflammatory attacks, repeated more than twice, give rise to widespread and almost global necrotizing glomerulitis.
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27/62. Renal transplant patient with polyoma virus bladder infection and subsequent polyoma virus nephropathy.

    Polyoma virus nephropathy (PVN) is a significant cause of renal allograft dysfunction in transplant patients. A 58-year-old male received a cadaveric renal transplant and 12 weeks later presented with fever, diarrhea, and dysuria. He was diagnosed with a polyoma virus infection of the bladder by a transurethral bladder biopsy. One year post-transplant, he presented with renal allograft dysfunction and was diagnosed by biopsy with PVN of the non-native kidney. The diagnosis of a polyoma virus infection was confirmed by immunoreactivity to the polyoma T-antigen. We suggest that polyoma virus infection of the bladder be included in the differential diagnosis of urinary dysfunction in post-transplant patients, as such infections might be an under-recognized comorbidity in individuals with PVN.
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28/62. Acute focal bacterial nephritis in an 8-year-old .

    Acute focal bacterial nephritis or acute lobar nephronia is an acute localized non-liquefactive bacterial kidney infection. Clinically, it may develop as an abscess and present as acute pyelonephritis but is distinguishable by the presence of a focal mass on imaging studies. The authors report the case of an 8-year-old girl with fever up to 39 degrees C and left flank pain of 6 days duration. On physical examination, she had nothing remarkable except tenderness and knocking pain over the left costovertebral angle. Post-contrast abdominal computed tomography revealed several wedge-shaped hypodense lesions in the left kidney. urine culture grew escherichia coli. Acute focal bacterial nephritis was diagnosed. The patient was treated with antibiotics and discharged on the 12th day of hospitalization.
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29/62. Histopathology and immunohistologic demonstration of the distribution of rickettsia typhi in fatal murine typhus.

    An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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30/62. The development of anti-glomerular basement membrane nephritis in two children with Alport's syndrome after renal transplantation: characterization of the antibody target.

    Two children with Alport's syndrome are described, who developed anti-glomerular basement membrane (GMB) antibody-mediated nephritis after renal transplantation. The reactivity of antibodies in their serum with collagenase-solubilized normal GBM was examined by SDS-PAGE with one- and two-dimensional immunoblotting. The specificity was compared with that of antibodies present in serum from a patient with Goodpasture's syndrome, and a mouse monoclonal antibody (MCA-P1), directed against the Goodpasture antigen. All reacted in a similar way with collagenase-solubilized GBM. Since abnormalities in the composition of the GBM are present in Alport's syndrome, it is proposed that differing antigen composition of GBM in the host compared with the donor kidney, together with transplant rejection, may have provoked the development of post-transplant anti-GBM antibodies.
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