Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus-associated nephropathy (HIVAN) is a clinicopathological entity characterised by proteinuria, rapidly developing azotemia and histologically by collapsig variant of focal and segmental glomerulosclerosis with acute tubular necrosis and mild interstitial inflammation. Untreated, it may result in end stage renal disease (ESRD) in as little as four months. The incidence of HIVAN continues to increase and is the single most common cause of chronic renal disease in HIV-1 seropositive patients. It affects predominantly black individuals. Exact pathogenesis is still not clear but a great deal of progress has been made in the recent past by studies on transgenic mouse model, renal cell cultures and from study of human biopsy material. Current considerations revolve around the role of HIV or protein in renal epithelium and the effects of cytokines, including transforming growth factor-beta and basic fibroblast growth factor on renal structures. Different modalities of treatment with corticosteroids, zidovudine or angiotensin converting enzyme inhibitors have been tried with modest success.
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PMID:Human immunodeficiency virus-associated nephropathy. 1183 70

Type I membranoproliferative glomerulonephritis (MPGN) is an uncommon manifestation of human immunodeficiency virus (HIV)-associated renal disease in patients co-infected with hepatitis C virus (HCV). We describe a case of Type I MPGN in an HIV-positive diabetic man with nephrotic-range proteinuria and renal insufficiency who was not co-infected with HCV. Tubuloreticular inclusions were present but there was no evidence for either cryoglobulinemia or cryoglobulin deposits in the kidney. This finding suggests that Type I MPGN may represent a reaction of the kidney to HIV independent of the effects of HCV co-infection. Clinical suspicion must be maintained for Type I MPGN in all HIV infected patients presenting with significant proteinuria regardless of HCV infection status.
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PMID:Type I membranoproliferative glomerulonephritis in an HIV-infected individual without hepatitis C co-infection. 1186 21

Collapsing glomerulopathy (CG), an aggressive variant of focal segmental glomerular sclerosis, is a renal disease with severe proteinuria and rapidly progressive renal failure. The pathogenesis of CG is unknown. It strongly resembles human immunodeficiency virus (HIV)-associated nephropathy, but the patients are HIV negative. The characteristic glomerular lesion is capillary loop collapse with prominent podocytes filling Bowman's space. Interestingly, these glomerular changes are usually associated with severe tubulointerstitial injury, including tubular epithelial degenerative changes, microcystic dilation of several tubules, and interstitial inflammatory cell infiltrate. Recently, it became evident that the morphologic pattern of CG may appear not only in native kidneys, but also de novo in renal allografts, and that the pattern of CG in renal transplants is not always associated with severe proteinuria. Studies describing CG in renal allografts are all based on biopsies. We report 3 allograft nephrectomy specimens that showed a zonal distribution of the characteristic collapsing glomerular changes with associated tubulointerstitial injury. All 3 kidneys had obliterative vascular changes. One nephrectomy specimen had chronic obliterative transplant arteriopathy, 1 had acute vascular rejection, and 1 had thrombotic microangiopathy. None of the patients had severe proteinuria. Our cases suggest that the morphologic pattern of CG in renal allografts may not represent the same disease process as CG in native kidneys and provide further evidence that collapsing glomerular changes do not define the disease entity of CG, but rather represent a pattern of renal injury. Among other factors, hemodynamic disturbance may play a role in the development of the pattern of CG in renal allografts.
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PMID:Zonal distribution of glomerular collapse in renal allografts: possible role of vascular changes. 1205 80

Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison's disease. We report the clinical and biological conditions of 2 patients with Addison's disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison's disease.
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PMID:Focal segmental glomerular sclerosis in two patients with Addison's disease: any more than fortuitous development of glomerular disease? 1216 75

Kidney transplantation should be strongly considered for all medically suitable patients with chronic and end-stage renal disease (ESRD). Improvements in outcomes after renal transplantation have resulted in a more liberal selection of patients. High-risk category patients including human immunodeficiency virus (HIV)-positive, highly sensitized patients, T-cell positive cross-match, and ABO blood group-incompatible patients are now considered potential renal transplant candidates. Unfortunately, the demand for kidney transplants far exceeds the supply of available organs, causing a persistent increase in the number of patients on the waiting list with a parallel increase in the waiting time for a cadaveric kidney transplant. This has 2 major consequences. First, patients on the waiting list are getting sicker and older. Second, living donors have assumed increasing importance in renal transplantation. Pre-existing morbidities including malignancies, cardiovascular disease, infections, and coagulopathies should be extensively evaluated before proceeding to transplantation. Special attention should be given to cardiovascular risk factors because the leading cause of death after renal transplant is cardiovascular disease. A full immunologic evaluation with ABO blood group determination, human leukocyte antigen (HLA) typing, screening for antibody to HLA phenotypes, and cross-matching need to be gathered before transplantation to avoid antibody-mediated hyperacute rejection or to proceed with specific protocols in highly sensitized or in positive T-cell cross-match patients. With the increased rate of donation from living donors, regular follow-up evaluation of kidney donors is recommended to detect hypertension or proteinuria in those who may develop it.
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PMID:Pretransplant evaluation of renal transplant candidates. 1243 96

We have shown the possibility to modulate various anemic syndromes during acquired immunodeficiency differed in pathogenesis and induced by graft versus host reaction (GVHR). There are different variants of combined erythro- and immunopoiesis disorders in the semiallogeneic system DBA/2 --> B6D2F1: immunodeficiency plus hemolytic anemia and immunodeficiency plus hemolytic anemia plus immunocomplex glomerulonephritis. In the allogeneic system C57BL/6 --> BALB/c there is immunodeficiency plus hypoplastic anemia with reduced bone marrow erythropoiesis. Differences in pathogenesis of anemic syndrome are connected with the functional properties of macrophages and cytokine production by macrophages. There is some positive effect of chronic hypoxia on GVHR-induced immunopathology in B6D2F1 mice: it increases humoral immune response, has favorable effect on anemia and corrects early and late committed precursor number. The absence of any influence of chronic hypoxia on the secreted activity of macrophages gives an evidence to the direct influence of erythron on the humoral immune response. VM-2-84 has favorable effect on anemia (suppresses IL-1 production, reduces the number of early erythroid precursors and stimulates the amount of the granulocyte and macrophage precursors) in B6D2F1 mice with glomerulonephritis. The compound from alkancarboxylic acids - VM-2-84, up to two months decreases proteinuria and reduces proliferation of mezangiocytes and chronic inflammation with the restoration of immune system. Trecrezan, while having beneficial effect on anemia, reduces a hyperplasia of erythron in mice with immunodeficiency; it influences the production of monokines. The obtained facts about effectiveness of preparation possessing combined erythro- and immunopoiesis-modulating properties, open new ways of a target regulation of disorders of immunity.
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PMID:The Correction of Combined Immuno- and Hemopoiesis Disorders Induced by Graft-Versus-Host Reaction. 1268 18

Focal segmental glomerulosclerosis (FSGS) is defined as a clinical-pathologic syndrome manifesting proteinuria and focal and segmental glomerular sclerosis with foot process effacement. The pathologic approach to the classification of FSGS is complicated by the existence of primary (idiopathic) forms and multiple subcategories with etiologic associations, including human immunodeficiency virus (HIV)-associated nephropathy, heroin nephropathy, familial forms, drug toxicities, and a large group of secondary FSGS mediated by structural-functional adaptations to glomerular hyperfiltration. A number of morphologic variants of primary and secondary focal sclerosis are now recognized, including FSGS not otherwise specified (NOS), perihilar, cellular, tip, and collapsing variants. The defining features of these morphologic variants and of the major subcategories of FSGS are discussed with emphasis on distinguishing light microscopic patterns and clinical-pathologic correlations.
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PMID:Pathologic classification of focal segmental glomerulosclerosis. 1270 72

The authors report the first case of immunotactoid glomerulopathy (ITG) in a human immunodeficiency virus (HIV)-positive, hepatitis B- and C-negative African-American man who presented with hematuria and proteinuria. His initial presentation was compatible with HIV associated nephropathy, but on renal biopsy he was found to have ITG. He has been treated with highly active antiretroviral therapy and an angiotensin-converting enzyme inhibitor, but his proteinuria has not responded after 4 months of treatment. This case emphasizes the diverse glomerular lesions seen in HIV-positive patients and supports the use of renal biopsy to establish a diagnosis.
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PMID:Immunotactoid glomerulopathy in an HIV-positive African-American man. 1465 25

The advent of highly active antiretroviral therapy represents a significant advance in medical care for human immunodeficiency virus (HIV)-infected persons. However, not everyone has derived the expected benefits of antiretroviral therapy and HIV-associated diseases such as nephropathy still occur in at-risk populations. Currently, there are no recommendations for screening HIV-positive patients for HIV-associated nephropathy. We propose semiannual screening for proteinuria in HIV-positive African Americans and patients with a family history of renal disease, and provide an algorithm for evaluation.
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PMID:Human immunodeficiency virus-associated nephropathy: a primary care perspective. 1476 31

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


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