Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Idiopathic collapsing glomerulopathy is an aggressive variant of focal segmental glomerulosclerosis (FSGS) seen primarily in adults. Its etiology is unknown. Nearly identical pathology is seen in association with nephrotic syndrome in human immunodeficiency virus type 1 (HIV-1)-infected patients, raising the possibility that viral infection plays a role in pathogenesis. This is supported by the recent discovery of parvovirus B19 DNA in some cases of idiopathic collapsing glomerulopathy. We report a case of collapsing glomerulopathy in a 16-year-old girl who presented with steroid-resistant nephrotic syndrome and pulmonary tuberculosis. In the absence of the usual associations (adult age group, African-American race, or history of intravenous drug abuse), infection is the sole known risk factor in this case. This lends support to the hypothesis that immune dysregulation due to infection per se, rather than infection by specific viral agents, may lead to collapsing glomerulopathy in susceptible individuals.
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PMID:Collapsing glomerulopathy in a 16-year-old girl with pulmonary tuberculosis: the role of systemic inflammatory mediators. 1517 56

Clinical and morphologic features of human immunodeficiency virus (HIV)-associated nephropathy (HIVAN), such as proteinuria, sclerosing glomerulopathy, tubular degeneration, and interstitial disease, have been modeled in mice bearing an HIV proviral transgene rendered noninfectious through a deletion in gag/pol. Exploring the genetic basis of HIVAN, HIV transgenic mice bearing mutations in either or both of the accessory genes nef and vpr were created. Proteinuria and focal glomerulosclerosis (FGS) only developed in mice with an intact vpr gene. Transgenic mice bearing a simplified proviral DNA (encoding only Tat and Vpr) developed renal disease characterized by FGS in which Vpr protein was localized to glomerular and tubular epithelia by immunohistochemistry. The dual transgenic progeny of HIV[Tat/Vpr] mice bred to HIV[DeltaVpr] proviral transgenic mice displayed a more severe nephropathy with no apparent increase in Vpr expression, implying that multiple viral genes contribute to HIVAN. However, the unique contribution of macrophage-specific Vpr expression in the development of glomerular disease was underscored by the induction of FGS in multiple murine lines bearing a c-fms/vpr transgene.
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PMID:Focal glomerulosclerosis in proviral and c-fms transgenic mice links Vpr expression to HIV-associated nephropathy. 1506 18

Leishmaniasis is a zoonosis caused by an intracellular parasite belonging to the genus Leishmania. In Europe, Africa, South America and China, visceral leishmaniasis is caused by L. infantum. The vectors of leishmaniasis are phlebotomine sandflies belonging to the genera Phlebotomus. According to the World Health Organization there are 2 million new cases each year and 1/10 of the world's population is at risk of infection. Leishmaniasis is considered a zoonosis and human are generally accidental hosts. The animal reservoir includes rodents, dog and other mammals. Several studies have indicate that half of the dogs with antileishmanial antibodies have no signs of disease although, animal with subclinical infections are potentially infectious to sand flies. The factors determining susceptibility or resistence to visceral leishmaniasis remain unclear, but the genetics of the host may play a major role. Clinical signs are: intermittent fever, hepatosplenomegaly, skin lesions and ulcers, alopecia, onychogryphosis, anemia, thrombocytopenia and hypergammaglobulinemia. In mice, the outcome of infection depends on the polarized activation of one of two subsets of CD4+ T cells, Th1 or Th2, the subdivision into Th1 and Th2 cells is based on the pattern of cytokines that they produce. Th1 cells produce gamma interferon (IFN-gamma) and interleukin -2 (IL-2), whereas Th2 cells produce IL-4, IL-5, and IL-10. An important difference between susceptible and resistant mice is that the resistant mice are able to switch to a Th1 profile and control the disease. An important factor in the "decision" to form a Th1 or Th2 phenotype is the early cytokine environment, and IL-12 is one of the cytokines that contributes significantly to the establishment of the Th1 phenotype. Canine leishmaniosis is endemic in the Mediterranean basin and, in most cases is caused by the parasite Leishmania infantum. The main clinical findings are skin lesions, local or generalized lymphoadenopathy, loss of body weight, glomerulopathy, ocular lesions, epistaxis and lameness. Non pruritic skin lesions are the usual manifestation and several forms have been described, such as exfoliative dermatitis and alopecia, and ulcerative, nodular and pustular dermatitis. Seroepidemiological studies of canine leishmaniasis have revealed a large number of asymptomatic seropositive animals. Moreover in areas where leishmaniasis is highly endemic, high proportion of apparently healthy animals show low levels of anti-Leishmania antibodies. Others have regressive forms of the desease, and their antibody levels will decrease in the following months or years; still others maintain low levels of antibodies without developing the desease for many years. However, the total number of infected animals is unknown. Canine leishmaniasis is a major zoonosic parasitic disease, enzootic in the Mediterranean area, caused by the intracellular protozoan Leishmania infantum. The dog is the main reservoir host of the parasite. However, most infected dogs do not present any clinical signs, and there is evidence that Leishmania infection prevalence rates in areas of endemicity are higher than those ascertained by serological studies. Visceral leishmaniasis is becoming a real problem of public health because it is an opportunistic infection in immunocompromised patients and in human immunodeficiency virus-positive subjects. The detection of the extent of the infection, particularly among asymptomatic dogs, is of great importance for the control of leishmaniasis. PCR has been applied successfully in recent years to detect Leishmania spp. even in the cases with any of the clinical manifestation of leishmaniasis. Very recently, real-time PCR for Leishmania has been applied to evaluate the parasitic load of dog tissues both at the time of the diagnosis and during follow-up of the therapy and to measure cytokine mRNA levels in different clinical samples of infected and uninfected dogs.
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PMID:[Interpretation of laboratory data during cryptic leishmaniasis in dog]. 1530 23

Hemophagocytic syndrome (HPS) is defined by bone marrow and organ infiltration by activated, nonmalignant macrophages, which phagocytose blood cells. The clinical spectrum of HPS is broad, but renal involvement has rarely been investigated. We report a previously unknown renal manifestation of HPS: nephrotic syndrome. This multicentric retrospective study included patients fulfilling the following criteria: (i) no history of nephropathy; (ii) HPS diagnosis with histologic evidence of hemophagocytosis; (iii) occurrence of nephrotic syndrome during HPS; and (iv) available renal histology. Using the same criteria, we also searched the literature for additional cases. We identified nine patients retrospectively and found two additional cases in the literature (five males and six females, whose mean age was 34 +/- 27 years). Black African patients predominated (63.6%). HPS was due to lymphoma (six cases), infectious disease (three cases), and autoimmune disease (one case), and was primary in one patient. Acute renal failure was associated with nephrotic syndrome in 10/11 cases. Renal histology showed acute tubular necrosis associated with collapsing glomerulopathy in five patients (all Africans with negative human immunodeficiency virus serology), minimal change glomerulopathy in four, and thrombotic-microangiopathy with abnormal podocytes in two. Death occurred in seven cases. Nephrotic syndrome should be included among the renal complications of HPS with acute renal failure. We postulate that abnormal T-cell activation and/or high pro-inflammatory cytokine levels during HPS might cause podocyte injuries, especially among African patients with a susceptible genetic background.
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PMID:Nephrotic syndrome associated with hemophagocytic syndrome. 1655 22

Math6 is a tissue-restricted member of the Atonal family of basic helix-loop-helix (bHLH) transcription factors and has been implicated in specification and differentiation of cell lineages in the brain. We identify here Math6 as a podocyte-expressed bHLH protein that was down-regulated in human immunodeficiency virus-associated nephropathy (HIVAN); a collapsing glomerulopathy characterized by podocyte dedifferentiation. Early in metanephric development, Math6 was expressed in metanephric mesenchyme but not ureteric bud-derived cells, with overall Math6 expression most abundant in the nephrogenic zone, including developing glomeruli. In adult kidney, Math6 expression was restricted to podocytes. In adult podocyte cell lines and kidneys from the transgenic mouse model of HIVAN, Math6 podocyte expression was reduced concurrent with previously reported reductions in Nephrin and Synaptopodin expression, suggesting a correlation between the loss of Math6 expression and typical podocyte terminal differentiation markers. These studies suggest that Math6 may participate in kidney development and may be a permissive factor for podocyte differentiation.
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PMID:Math6 expression during kidney development and altered expression in a mouse model of glomerulosclerosis. 1693 70

Glomerular lesions that complicate patients with human immunodeficiency virus (HIV) infection include HIV-associated nephropathy, membranous glomerulopathy, and immune-complex glomerulonephritides. This case series presents 3 patients with clinically significant renal disease and positive test results for anti-glomerular basement membrane (anti-GBM) antigen. Characteristic histological findings that would suggest anti-GBM antibodies have a significant role in the pathological state of each patient's kidney disease were absent. In addition, each patient recovered without specific treatment for anti-GBM disease. This case series suggests that anti-GBM antibodies likely are related to the B-cell expansion previously described in patients with HIV infection. We propose that clinicians interpret results of anti-GBM antibody tests carefully for patients with HIV infection, considering biopsy before empiric therapy, particularly in a clinical presentation that is atypical for Goodpasture disease.
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PMID:The uncertain significance of anti-glomerular basement membrane antibody among HIV-infected persons with kidney disease. 1699 46

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

To correlate CD 4 counts with albuminuria and glomerular lesions in patients infected with human immunodeficiency virus (HIV), we studied 104 HIV positive patients (68 males, 36 females) of whom 100 patients were infected by heterosexual contact, 3 by transfusion, and 1 by i.v. drug abuse. We screened over nine months for albuminuria by urine dip stick method, and performed renal biopsy on patients with albuminuria 2+ or more. Histological examination was accomplished by light microscopy in all and by electron microscopy when it was feasible. Albuminuria was observed in 29 (27%) patients, and it revealed a significant negative correlation with CD4 count (p<0.01). Patients with CD4 cells <350 cells/mm(3) disclosed a 3.5 fold increased risk of albuminuria as compared with patients with CD4 >350 cells/mm(3). There was no significant correlation between proteinuria and the duration of infection from the time of diagnosis. Albuminuria also demonstrated a significant negative correlation with the levels of hemoglobin (p<0.05). In addition, low numbers of CD4 cells were associated with lower levels of hemoglobin (p<0.001). Only 10 patients received renal biopsies, and the results revealed HIV-associated nephropathy (HIVAN) in 7 (70%) patients, chronic tubulointerstitial nephritis in 1, membranous glomerulopathy in 1, and diffuse proliferative glomerulonephritis in 1. Acute renal failure was present in 5 patients, of whom four had a pre renal component and one had multiorgan dysfunction syndrome. We conclude that our study demonstrates that both proteinuria and HIVAN are common in HIV infected patients. Proteinuria has a negative correlation with the CD4 counts and hemoglobin levels.
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PMID:Correlation of CD4 counts with renal disease in HIV positive patients. 1858 20

Collapsing glomerulopathy (CG) is a distinct clinicopathological entity characterized by high levels of nephrotic range proteinuria, rapidly progressive renal failure, marked parenchymal injury, and poor response to present therapeutic regimens. Growing awareness has led to the identification of associated conditions other than human immunodeficiency virus (HIV) and idiopathic. We report a case of CG from India in a HIV-negative young female, presenting with heavy proteinuria and rapidly progressing renal failure preceded by a febrile illness.
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PMID:A case of collapsing glomerulopathy associated with febrile illness. 1900 78

Immune complex glomerulonephritis is a common diagnosis in renal biopsy series of human immunodeficiency virus (HIV)-infected patients. There are a variety of glomerulonephritides associated with HIV infection, including IgA nephropathy, membranoproliferative glomerulonephritis, membranous nephropathy, lupus-like glomerulonephritis, immunotactoid glomerulopathy, and fibrillary glomerulonephritis. In addition, HIV-related proteins may be implicated in circulating immune complexes directly related to a response to the infection. In some cases, the relationship of the HIV infection to the glomerulonephritis is unclear. HIV infection is associated with the development of polyclonal hypergammaglobulinemia, which can promote the development of circulating immune complexes. It is not clear if HIV-associated glomerulonephritis is caused by the passive trapping of these circulating immune complexes or the in situ deposition of antibodies binding to HIV viral antigens. Some renal lesions that are seen in the setting of HIV infection more likely may be related to the presence of a co-infection such as hepatitis C virus infection. The optimal therapy for immune complex glomerulonephritis in the setting of HIV infection is unknown. Because of the underlying immunosuppressed state of many HIV-infected patients, caution with traditional cytotoxic therapies is advised. The role of antiretroviral therapy in modifying the course of these renal lesions is unclear.
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PMID:Immune complex renal disease and human immunodeficiency virus infection. 1901 24


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