Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Viral infections can be the causative agent in many glomerular diseases, and diagnostic criteria include clinical and laboratory data and tissue molecular analysis. Hepatitis B virus (HBV) is a well known cause of membranous glomerulonephritis (MGN), membranoproliferative GN (MPGN) and IgA nephropathy (IgAN), frequently in Asian populations. Hepatitis C virus (HCV), besides cryoglobulinemia-mediated glomerulonephritis (GN), is reported to cause other forms of GN. Human immunodeficiency virus (HIV) infection is closely related to a collapsing focal segmental glomerulosclerosis (FSGS), a distinct disease that affects mainly Africans and African-Americans. In the course of HIV infection other immune complex (IC) GN can occur, most frequently in whites. Nephrotic syndrome and progression to renal insufficiency are the main clinical manifestations. HIV-HCV co-infection is related to an IC glomerular disease, sometimes with immunotactoid deposits. Recent reports emphasize the role of parvovirus B19 (PV B19) for "idiopathic" collapsing FSGS and ICGN, and of Coxsackie B virus for IgAN. Renal biopsy is useful for defining virus-related glomerular lesions and a guide for prognostic and therapeutic evaluation.
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PMID:Virus-related glomerular diseases: histological and clinical aspects. 1245 12

Collapsing glomerulopathy (CG), a variant of idiopathic focal segmental glomerulosclerosis (FSGS), can occur in both human immunodeficiency virus (HIV)-positive and HIV-negative patients. Idiopathic membranous glomerulonephritis (MGN) has been reported to coexist with FSGS, but rarely with CG. We report 3 HIV-negative patients (2 men, 1 woman) who developed nephrotic syndrome secondary to MGN complicated by CG, with relatively rapid disease progression despite aggressive therapy.
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PMID:Collapsing glomerulopathy coexisting with membranous glomerulonephritis in native kidney biopsies: a report of 3 HIV-negative patients. 1295 90

Virus associated glomerulonephritis is considered to be a para- or post-infectious autoimmune phenomena. The disease is mediated by immune complexes which usually contain the viral antigen. Virus associated glomerulonephritis due to chronic viral infection with hepatitis B or C virus, or with human immunodeficiency virus (HIV) shows a typical histomorphological picture for each virus. Hepatitis B virus usually leads to a membranous glomerulonephritis, while hepatitis C virus is associated with a membranoproliferative glomerulonephritis due to cryoglobulins, and HIV is associated with a focal segmental sclerosing glomerulonephritis. Knowledge of the relationship between the primary viral infection and secondary glomerulonephritis is important, as a primary immunosuppressive therapy might lead to more severe viral disease. On the other hand, a primary reduction in the viral load due to antiviral therapy with immunostimulants or inhibitors of viral replication could lead to an amelioration of the secondary glomerulonephritis.
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PMID:[Virus associated glomerulonephritis]. 1456 63

The proliferative response of podocytes to injury determines the histological phenotype. Moreover, an apparent lack of podocyte proliferation may underlie the development of glomerulosclerosis. Podocyte proliferation is closely linked with its state of differentiation. However, the mechanisms regulating these processes are not fully elucidated. Because D-type cyclins have been shown to be important in the regulation of proliferation and differentiation, we examined their expression in podocytes in vitro and in vivo. The glomerular expression of cyclins D1 and D3 was examined in vitro in cultured immortalized podocytes by immunostaining and Western blot analysis, and in embryonic mice and rats, the passive Heymann nephritis model of experimental membranous nephropathy in rats, and human immunodeficiency virus (HIV)-transgenic mice. Kidneys from cyclin D1 knockout mice were also examined. Cyclin D1 was abundant in cultured proliferating podocytes, but not in quiescent differentiated podocytes. In contrast, cyclin D3 was abundant in differentiated, but not proliferating podocytes. Cyclin D1 was expressed in embryonic mouse and rat glomeruli during the S- and comma-shaped stages, and was absent in podocytes at the capillary loop stage and in mature rodent glomeruli. Cyclin D1 protein increased after injury in passive Heymann nephritis rats and in HIV-transgenic mice. Cyclin D3 was constitutively and specifically expressed in podocytes in normal rodent glomeruli, and decreases during dedifferentiation and proliferation in HIV-transgenic mice. Kidneys from cyclin D1-/- mice were normal with the podocytes expressing specific differentiation markers. Cyclin D1 is not necessary for the terminal differentiation of podocytes, and expression coincides with cell-cycle entry. In contrast, cyclin D3 expression coincides with podocyte differentiation and quiescence.
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PMID:Differential expression of d-type cyclins in podocytes in vitro and in vivo. 1503 29

Clinical disorders with an isolated lack of monocytes have not been reported hitherto. The authors describe the case of a 38-year-old woman with pulmonary alveolar proteinosis and nephrotic syndrome caused by membranous nephropathy and widespread papillomatosis of the vulva. Immunologic studies showed normal levels of immunoglobulins and C2, C3c, and C4. Cryoglobulins and paraproteins were not detected. Antinuclear antibodies, antineutrophil cytoplasmic antibodies, and antiglomerular basement membrane antibodies were not detectable. Circulating immune complexes containing C1q, immunoglobulin G, and immunoglobulin M were elevated. The patient showed immunodeficiency that was characterized by complete anergy to intracutaneously administered recall antigens in vivo and to recall antigens in vitro. The immunodeficiency was accompanied by the absence of monocytes in the peripheral blood as well as in bone marrow cultures. In parallel, long-term bone marrow cultures and colony-forming cell assays did not result in the growth of monocytes. Mitogenic agents that require the presence of monocytes induced almost no T-cell proliferation (Concanavalin A: 5,841 counts per minute [cpm]), whereas agents that act directly on T cells induced intense T-cell proliferation (phytohemagglutinin: 110,001 cpm; OKT 3: 120,616 cpm; and pokeweed mitogen: 89,474 cpm). These data suggest that the pulmonary renal syndrome in this patient results from the lack of monocytes and the consecutive defect of antigen presentation and antigen clearance.
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PMID:A patient without monocytes who had pulmonary renal syndrome. 1533 29

Infections can be the causative agent in secondary nephrotic syndrome and diagnostic criteria include clinical and laboratory data and tissue molecular analysis. As for bacterial infections, some of patients with poststreptococcal glomerulonephritis or methicillin-resistant Staphylococcus aureus-related glomerulonephritis present nephrotic syndrome. Hepatitis B virus (HBV) is a well known cause of membranous glomerulonephritis and membranoproliferative glomerulonephritis. Hepatitis C virus (HCV), besides cryoglobulinemia-mediated glomerulonephritis, is reported to cause other forms of glomerulonephritis. Human immunodeficiency virus (HIV) infection is closely related to a collapsing focal segmental glomerulonephritis. Some of patients with these viral infections present nephrotic syndrome. There were a few reports on secondary nephrotic syndrome induced by cytomegalovirus, Epstein-Barr virus and parvovirus B19.
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PMID:[Secondary nephrotic syndrome induced by infection]. 1550 Jan 41

Epstein-Barr virus (EBV) infection can cause diverse renal manifestations ranging from microscopic hematuria to acute renal failure. Membranous nephropathy (MN) is an uncommon and usually secondary cause of nephrotic syndrome in children, and has been reported after chronic infections and antigenemia. We report two pediatric cases of secondary MN associated with acute and chronic systemic EBV infection. Patient 1 had a liver transplant for cirrhosis due to biliary atresia and developed chronic EB viremia. Membranous nephropathy occurred 3 years later and with aggressive therapy has partially subsided, in temporal association with a drop in blood EBV PCR levels. The other patient had a primary immunodeficiency and developed a lymphoproliferative disorder attributed to EBV. Nephrotic syndrome developed at initial presentation and was associated with MN on biopsy. The patient cleared the virus from blood, which was associated with eventual resolution of the MN. We postulate that EB viremia in patients lacking a fully competent immune system, but without a renal allograft, may create a susceptible environment for chronic systemic EB antigenemia that can then lead to immune-complex MN in the kidney. The association of EBV with renal histological changes consistent with MN has been suggested but not directly described before.
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PMID:Systemic Epstein-Barr virus infection associated with membranous nephropathy in children. 1655 Jul 46

Schimke immuno-osseous dysplasia is a rare autosomal recessive multi-system disorder, with clinical features of growth retardation, spondylo-epiphyseal dysplasia, nephrotic syndrome and immunodeficiency beginning in childhood. Here, we report a new case, in a 10-year-old boy with characteristic symptoms of Schimke immuno-osseous dysplasia. The patient presented with short stature and, later, developed nephrotic syndrome and peritonitis. In addition, he had perinuclear anti-neutrophilic cytoplasmic antibody (p-ANCA)-positive arthritis. Renal pathology of the patients with this disease usually show focal segmental glomerulonephritis, whereas our patient had membranous nephropathy, which has not previously been reported.
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PMID:Membranous nephropathy in Schimke immuno-osseous dysplasia. 1657 Feb 1

Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is the most common finding on renal biopsy in HIV-infected black patients and is also the commonest cause of end-stage renal disease in these patients. Early detection of HIVAN may be beneficial in evaluating early treatment. This study examined the pattern of renal diseases in HIV-infected South Africans and also attempted to diagnose HIVAN at an early stage. In this single-center cross-sectional study, 615 HIV-infected patients were screened for proteinuria. Thirty patients with varying degrees of proteinuria underwent renal biopsy. Patients with diabetes mellitus, uncontrolled hypertension, known causes of chronic kidney disease, and serum creatinine above 250 mumol/l were excluded. Patients in this study were not on antiretroviral therapy. HIVAN was found in 25 (83%) patients. Six of them (24%) had microalbuminuria. Altogether, seven patients with persistent microalbuminuria were biopsied and six (86%) showed HIVAN. Other biopsy findings included membranoproliferative nephropathy in two (7%) and interstitial nephritis in three (10%). Four patients with HIVAN had associated membranous nephropathy. HIVAN is the commonest biopsy finding among our study patients with HIV infection who present with varying degrees of proteinuria. Microalbuminuria is a manifestation of HIVAN in our study patients. Therefore, microalbuminuria may be an early marker of HIVAN, and screening for its presence may be beneficial. Renal biopsy may be considered in seropositive patients who present with persistent microalbuminuria, especially with low CD4 counts irrespective of good renal function. This will allow diagnosis and treatment of HIVAN at an early stage and may prevent further disease progression.
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PMID:A cross-sectional study of HIV-seropositive patients with varying degrees of proteinuria in South Africa. 1667 14

Hepatitis C virus (HCV) may have a pathogenic role in several forms of immune complex glomerulonephritis (ICGN), including cryoglobulinemic membrano-proliferative glomerulonephritis (MPGN) and membranous nephropathy. HCV infection may also be related indirectly (e.g. secondary to HCV-related liver disease) or coincidentally to glomerulonephritis. These include cases of fibrillary/immunotactoid glomerulopathy, MPGN arising in allografts, allograft glomerulopathy, rapidly progressive glomerulo-nephritis, focal and segmental glomerulosclerosis, and ICGN arising in individuals co-infected with human immunodeficiency virus (HIV). This review summarizes the clinical and pathologic features of HCV-associated glomerular disease, particularly immune complex glomerulonephritis, and discusses possible pathogenic mechanisms.
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PMID:Immune complex glomerulonephritis in patients with hepatitis C. 1820 31


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