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21/52. Minimal change disease in a patient receiving IFN-alpha therapy for chronic hepatitis c virus infection.

    Chronic hepatitis c virus (HCV) infection is associated with several extrahepatic syndromes. The principal types of renal disorders associated with chronic HCV infection are cryoglobulinemia or noncryoglobulinemic membranoproliferative glomerulonephritis (MPGN). interferon-alpha (IFN-alpha) may precipitate or exacerbate the occurrence of MPGN. Our patient was a 32-year-old man who tested positive for HCV in July 1997. The patient was treated with IFN-alpha in another medical center for 6 months because his liver biopsy showed chronic active hepatitis. In December 1998, he applied to our clinic for a follow-up examination. The level of aspartate aminotransferase (AST) was 44 U/L, and that of alanine aminotransferase (ALT) was 69 U/L. HCV rna was positive in serum, and chronic HCV infection was detected by liver biopsy. IFN-alpha therapy (5 million U/day) was administered for 6 months longer. In May 1999, the patient came to our polyclinic with edema of the feet and legs. We detected proteinuria, serum cholesterol of 269 mg/dl, AST of 50 U/L, ALT of 41 U/L, serum total protein of 3.4 g/dl, serum albumin of 1.2 g/dl, positive cryoglobulin, and urine protein of 9.84 g/day. Cryoglobulinemic MPGN was suspected and kidney biopsy was performed, resulting in a diagnosis of minimal change disease (MCD).
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22/52. Renal angiomyolipoma in association with pulmonary lymphangioleiomyomatosis.

    The authors report on a premenopausal female hemodialysis patient with relapsing pneumothorax, in whom the diagnosis of pulmonary lymphangioleiomyomatosis (LAM) was made. Ten years earlier, she had retroperitoneal bleeding from a kidney tumor corresponding to an angiomyolipoma (AML). The association between renal AML and pulmonary LAM is reviewed. Renal AML represents the most frequent extrapulmonary manifestation of pulmonary LAM. It is found in 32% to 60 % of cases in which a systematic search with abdominal computed tomography (CT) scan is done. The latter approach is advised to help avoid complications caused by renal AML. Therapeutic recommendations for renal AML are based on tumor size or presence of symptoms. Conversely, premenopausal women presenting with AML should be investigated for associated pulmonary LAM with high-resolution CT scan. Because LAM is very likely estrogen dependent, one of the several proposed antiestrogen therapies should be considered. Finally, there is significant overlap between renal AML, pulmonary LAM, and tuberous sclerosis. The latter should therefore be actively searched for in case of either AML or LAM.
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23/52. familial mediterranean fever and glomerulonephritis and review of the literature.

    familial mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent and self-limited attacks of fever usually accompanied by polyserositis. amyloidosis is its most common renal complication. A number of reports have shown vasculitic diseases such as polyarteritis nodosa and Henoch-Schonlein purpura affecting the kidney in FMF. Here we present a patient with FMF and membranoproliferative glomerulonephritis and analyze the data published on these two entities.
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24/52. Membranoproliferative glomerulonephritis associated with multicentric angiofollicular lymph node hyperplasia. Case report and review of the literature.

    A 14-year-old boy presented with fever, anemia, hepatosplenomegaly, generalized lymphadenopathy and nephrotic syndrome. Lymph node biopsy showed angiofollicular lymph node hyperplasia (generalized Castleman's disease) of the plasma cell type. Kidney biopsy showed membranoproliferative glomerulonephritis type 1. Complete remission was achieved with corticosteroid treatment and repeat kidney biopsy 22 months later showed complete resolution of the renal pathology. The association between membranoproliferative glomerulonephritis and multicentric angiofollicular lymph node hyperplasia, plasma cell type, has not previously been reported.
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25/52. Autosomal dominant polycystic kidney disease complicated by glomerulonephritis.

    Two patients with autosomal dominant polycystic kidney disease (ADPKD) and concurrent glomerulonephritis are described. Both developed nephrotic-range proteinuria and one showed a concomitant acceleration in the rate of decline of renal function. Subsequent open renal biopsy revealed membrano-proliferative type-1 and mesangio-proliferative glomerulonephritis, respectively. Nephrotic-range proteinuria in the presence of ADPKD, with or without an accompanying decline in renal function, should prompt further investigation to exclude coexisting glomerular disease.
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keywords = kidney disease, kidney
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26/52. Horseshoe kidney with mesangioproliferative glomerulonephritis and goiter.

    Horseshoe kidney is a relatively common renal anomaly with which many structural and developmental anomalies have been shown to be associated. However, there are only a few case reports regarding the association of membranous glomerulonephritis and focal sclerosing glomerulonephritis in patients with horseshoe kidneys. We report a girl who was evaluated for hematuria and proteinuria, and found to have horseshoe kidney. Renal biopsy demonstrated mesangioproliferative glomerulonephritis. She also had simple diffuse goiter.
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27/52. Heterozygous and homozygous factor h deficiencies associated with hemolytic uremic syndrome or membranoproliferative glomerulonephritis: report and genetic analysis of 16 cases.

    Factor H (FH) is the major regulatory protein of the complement alternative pathway, with a structure consisting of a tandem array of 20 homologous units, called short consensus repeats (SCR). Reported are 16 FH-deficient patients. Among six patients with homozygous deficiency, four presented with membranoproliferative glomerulonephritis, and two with atypical hemolytic uremic syndrome (HUS). The ten other patients had heterozygous FH deficiency and developed atypical HUS. HUS onset occurred from birth to midadulthood, and disease progression was variable. Four children with homozygous or heterozygous FH deficiency and HUS underwent renal transplantation, which was successful in three but failed as a result of recurrence of HUS in one patient. All but one patient exhibited alternative pathway-mediated complement consumption, with no detectable FH antigenic levels or with 50% immunochemical or functional FH levels in the case of complete or partial deficiency, respectively. The molecular mechanisms of the deficiency were documented in all cases by exon-specific sequencing analysis. These mechanisms included nucleotide substitutions, insertion, or deletion located in SCR 2, 7, 11, 13, 15, and 20, leading to an amino acid substitution or to a stop codon. This report emphasizes the variability in the clinical progression of kidney diseases associated with FH deficiencies. Genetic analysis reveals the molecular abnormalities associated with FH deficiencies to be polymorphous.
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keywords = kidney disease, kidney
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28/52. A male with angioimmunoblastic T-cell lymphoma and proliferative glomerulonephritis.

    In this article we present the case report of a 67-year-old male with a nephrotic syndrome due to a proliferative glomerulonephritis, associated with an angioimmunoblastic T-cell lymphoma. diagnosis was made on an axillary lymph node biopsy and showed expanded T-cell areas with multiple blood vessels, small mature lymphocytes, eosinophils, and plasma cells. A kidney biopsy was suggestive for a proliferative glomerulonephritis with intra- and extracapillary proliferation. Hypercellular glomeruli were seen, as well as multiple floride crescents. Interstitial edema and fibrosis were absent. Immunohistochemical reactions were negative; there was some mesangial reaction with IgM in the glomeruli. Treatment with high-dose corticosteroids was initiated, with clinical improvement, and was immediately followed by therapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP), which induced complete remission with a follow-up of 1 year. To our knowledge, the association of angioimmunoblastic T-cell lymphoma and proliferative glomerulonephritis has only been described twice. It concerned elderly men who developed acute renal failure a couple of months after the diagnosis of an angioimmunoblastic T-cell lymphoma. In both, immunoglobulin-containing dense deposits within glomeruli were observed, which was not the case in our patient, where only some mesangial colorization of the IgM in the glomeruli was seen.
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29/52. Activation of the alternative pathway of complement by monoclonal lambda light chains in membranoproliferative glomerulonephritis.

    Immunopathological evidence suggests that activation of the alternative pathway of complement (AP) is involved in membranoproliferative glomerulonephritis (MPGN) and in immunoglobulin a nephropathy. In this report we describe an AP dysfunction-associated factor that was isolated from the serum and urine of a patient with hypocomplementemic MPGN. Extensive glomerular deposits of C3, properdin, and of the terminal complement components were observed in the kidney of the patient. In her serum the AP hemolytic activity was virtually absent. When mixed with fresh normal serum, the patient's serum induced a 96% C3 conversion during a 30-min incubation at 37 degrees C. This activity was found to be due to a circulating factor that by immunochemical characterization proved to be a 46-kD monoclonal immunoglobulin lambda light (L) chain dimer (lambda L). Purified lambda L, but not control lambda or kappa L chains from patients with L chain disease, activated the AP in a dose- and ionic strength-dependent manner. Functionally, lambda L was differentiated from C3 nephritic factor (an autoantibody against the AP C3 convertase, C3bBb) by its inability to bind to and stabilize the C3bBb enzyme. Instead, lambda L was observed to interact directly with the AP control factor H. Thus, lambda L represents a novel type of immunoglobulin-related AP-activating factor with the capacity to initiate alternative complement pathway activation in the fluid phase.
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30/52. Membranoproliferative glomerulonephritis.

    glomerulonephritis (GN) encompasses a wide variety of primary and secondary diseases that cause injury to the functioning unit of the kidney, the glomerulus. The many classifications of GN sometimes lead to confusion. This case study describes an individual with membranoproliferative GN and includes discussion of classification, treatment, and prognosis of this disease.
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