hematuria/protease

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Enzymolysis of glomerular immune deposits in vivo with dextranase/protease ameliorates proteinuria, hematuria, and mesangial proliferation in murine experimental IgA nephropathy.

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The therapeutic effects of saccharolytic and proteolytic enzymes were investigated in models of IgA nephropathy. Mesangial glomerulonephritis was induced in mice by intravenous injection of preformed soluble immune complexes of dextran sulfate and either IgA (J 558) or IgM (MOPC 104 E) anti-dextran

IgA1 Protease Treatment Reverses Mesangial Deposits and Hematuria in a Model of IgA Nephropathy.

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IgA nephropathy (IgAN), characterized by mesangial IgA1 deposits, is a leading cause of renal failure worldwide. IgAN pathogenesis involves circulating hypogalactosylated IgA1 complexed with soluble IgA Fc receptor I (sCD89) and/or anti-hypogalactosylated-IgA1 autoantibodies, but no specific

Protease inhibitor-induced urolithiasis.

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OBJECTIVE To describe protease inhibitor-induced urinary stone disease in patients with human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS) who are taking indinavir sulfate (Crixivan), a protease inhibitor, for the treatment of AIDS. METHODS Patients with HIV/AIDS and

Impact of protease inhibitors on the evolution of urinary markers: Subanalyses from an observational cross-sectional study.

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Kidney injury (defined as the presence of albuminuria, proteinuria, glycosuria [without hyperglycemia], hematuria, and/or renal hypophosphatemia) is an emerging problem in human immunodeficiency virus (HIV)-infected patients, although few data are available on the role of protease inhibitors (PIs)

Mutation analysis and clinical implications of von Willebrand factor-cleaving protease deficiency.

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BACKGROUND The pentad of thrombocytopenia, hemolytic anemia, mild renal dysfunction, neurologic signs, and fever, classically characterizes the syndrome of thrombotic thrombocytopenic purpura (TTP). TTP usually occurs in adults as an acquired form but a congenital form in children has also been

Risk factors for urological symptoms in a cohort of users of the HIV protease inhibitor indinavir sulfate: the ATHENA cohort.

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BACKGROUND Nephrolithiasis is a well-known complication of indinavir treatment and may result in urological symptoms ranging from renal colic to renal insufficiency. OBJECTIVE To obtain further knowledge regarding the incidence and risk factors of urological symptoms associated with indinavir

Urolithiasis associated with protease inhibitors.

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OBJECTIVE We evaluated the radiographic characteristics as well as the clinical management of urolithiasis induced by systemic therapy with indinavir sulfate, a protease inhibitor utilized in the treatment of HIV infection. METHODS Fifteen consecutive HIV-positive male patients (average age 41.3

[Effect of protease inhibitor on primary glomerulonephritis and the mechanism of the effect].

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Effect of serine protease inhibitor Camostat Mesilate (Foipan) on primary glomerulonephritis and it's mechanism were evaluated. Forty-two patients having primary glomerulonephritis (13 cases of IgA nephropathy, 11 cases of membranous nephropathy and others), aged 18 to 81 years were selected for

[Indications and contraindications for protease inhibitors].

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Clinical interest in protease inhibitors was maximal at a time when it was believed that acute bleeding tendency in some situations was due to "primary hyperfibrinolysis". Progress in diagnostic procedures resulted in better knowledg of the true nature of such dramatic hemorrhagic diatheses, which

[Atypical hemolytic and uremic syndrome associated with von Willebrand factor-cleaving protease (ADAMTS 13) deficiency in children].

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Hemolytic and uremic syndrome (HUS) is a classical form of thrombotic microangiopathies characterized by the association of hemolytic anemia with schizocytes, thrombocytopenia, and acute renal failure. Two forms of HUS have been described: the typical form that occurs after ingestion of a strain of

A phase I/II study of the protease inhibitor indinavir in children with HIV infection.

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BACKGROUND Indinavir, an inhibitor of the human immunodeficiency virus type 1 (HIV-1) protease, is approved for the treatment of HIV infection in adults when antiretroviral therapy is indicated. We evaluated the safety and pharmacokinetic profile of the indinavir free-base liquid suspension and the

The calcium-dependent protease of Loxosceles gaucho venom acts preferentially upon red cell band 3 transmembrane protein.

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Eighty micrograms red blood cell (RBC) ghosts from patients who had previously exhibited the cutaneous form of loxoscelism (presenting localized dermonecrosis) and the viscerocutaneous form of loxoscelism (presenting dermonecrosis, hemoglobinuria, hematuria, and jaundice) and from controls were

Switching from ritonavir to cobicistat in HIV patients with renal impairment who are virologically suppressed on a protease inhibitor.

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BACKGROUND Cobicistat (COBI) is a pharmacoenhancer and one of the components of ECF/TDF (elvitegravir/cobicistat/emtricitabine/tenofovir DF), which is approved in treatment-naïve HIV patients with creatinine clearance (CrCl) ≥70 mL/min. Study 118 assessed the renal safety of COBI-containing regimens

Case series of thrombotic thrombocytopenic purpura in children and adolescents.

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Thrombotic thrombocytopenic purpura (TTP) is a well-described entity in adults but is rarely observed in children. The authors describe a series of seven children with suspected acquired TTP. Clinical findings included petechiae, purpura, or jaundice ( 6), central nervous system events ( 5), fever (

Imaging characteristics of indinavir calculi.

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OBJECTIVE Indinavir sulfate is an effective protease inhibitor of the human immunodeficiency virus type 1. Use is associated with a significant incidence of crystallization and stone formation in the urinary tract, and these calculi are not visible on plain radiographs. Previously all urinary

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