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)

Collapsing focal segmental glomerulosclerosis (cFSGS) is characterized by hyperplasia of glomerular epithelial cells. In a mouse model of FSGS and in a patient with recurrent idiopathic FSGS, we identified the proliferating cells as parietal epithelial cells (PECs). In the present study, we have evaluated the origin of the proliferating cells in cFSGS associated with human immunodeficiency virus (HIV) and pamidronate. We performed a detailed study of glomerular lesions in biopsies of two patients with HIV-associated cFSGS and a nephrectomy specimen of a patient with pamidronate-associated cFSGS. Glomeruli were studied by serial sectioning using light and electron microscopy and immunohistochemistry to determine the epithelial cell phenotype. We used Synaptopodin, vascular endothelial growth factor, and CD10 as podocyte markers, CK8 and PAX2 as PEC markers and Ki-67 as marker of cell proliferation. The newly deposited extracellular matrix was characterized using antiheparan sulfate single-chain antibodies. The proliferating cells were negative for the podocyte markers, but stained positive for the PEC markers and the cell proliferation marker Ki-67. The proliferating PAX-2 and CK8 positive cells that covered the capillary tuft were always in continuity with PAX-2/CK8 positive cells lining Bowman's capsule. The matrix deposited by these proliferating cells stained identically to Bowman's capsule. Our study demonstrates that PECs proliferate in HIV and pamidronate-associated cFSGS. Our data do not support the concept of the proliferating, dedifferentiated podocyte.
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PMID:Proliferating cells in HIV and pamidronate-associated collapsing focal segmental glomerulosclerosis are parietal epithelial cells. 1676 Oct 13

Since 1984, human immunodeficiency virus-associated nephropathy has been established as a clinical entity that presents with nephrotic syndrome and progressive kidney failure. The pathological description is usually consistent with a collapsing form of focal segmental glomerulosclerosis. Podocytes and renal tubular cells have been proposed as a reservoir for the human immunodeficiency virus. This nephropathy is the third leading cause of end-stage renal disease in the population of African descent. It is documented that highly active antiretroviral therapy (HAART) successfully reverses or at least controls nephropathy in HIV-positive patients. The success of the treatment of HIV nephropathy now poses 2 problems to nephrologists: (1) an increased population of HIV-positive patients with chronic kidney disease not yet on dialysis and (2) potential nephrotoxicity of antiretroviral medications as well as medications used to treat opportunistic infections. HAART is defined by the combination of 2 reverse transcriptase inhibitors with a protease inhibitor or 3 reverse-transcriptase inhibitors. Many of these antiretrovirals have well-defined nephrotoxic effects. The objective of this text is to review data pertaining to some of the most common antiretrovirals (ARTs) and include information regarding nephrotoxicity of the medications frequently used to combat opportunistic infections. ARTs included in the review are (1) nucleoside reverse-transcriptase inhibitors (zidovudine and didanosine), (2) nucleotide reverse transcriptase inhibitors (adefovir and tenofovir), (3) the protease inhibitors (indinavir and saquinavir), and (4) the HIV fusion inhibitors.
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PMID:Nephrotoxicity as a complication of antiretroviral therapy. 1681 36

Human immunodeficiency virus-associated nephropathy (HIVAN) is characterized by high-grade proteinuria and rapid progression to end-stage renal disease (ESRD). Despite the large numbers of HIV-infected cases in Asian countries, data on HIVAN in this area are limited. We report a 54-year-old Taiwanese man with HIVAN who presented with cytomegalovirus retinitis, renal insufficiency (serum creatinine, 3.8 mg/dL) and nephrotic range proteinuria with a daily protein loss of 10.8 g. Despite highly active antiretroviral therapy (HAART) for 31 months, renal failure developed requiring maintenance hemodialysis. Renal biopsy showed collapsing focal segmental glomerular sclerosis, podocyte proliferation and tubulointerstitial nephritis with mononuclear cell infiltration. These features were compatible with HIVAN. Although hemodialysis was instituted, he died 2 months later due to nosocomial pneumonia complicated with multiple organ failure. In summary, this case of HIVAN in a Taiwanese patient shows that the condition may progress to ESRD despite successful viral suppression with HAART.
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PMID:Human immunodeficiency virus-associated nephropathy. 1693 71

The number of people living with human immunodeficiency virus (HIV) worldwide was estimated to be 39.5 million in 2006, 2.6 million more than in 2004. The manifestations of HIV infection in the kidney are multiple and varied, highlighting the complexity of the disease process. There is a wide spectrum of renal disease that occurs in the course of HIV infection. Biopsy studies reveal varying frequencies of histological patterns. HIV-associated nephropathy (HIVAN) is most common. A biopsy study at Chris Baragwanath Hospital in Soweto, South Africa showed that HIVAN was present in 27% and immune complex disease in 21%. Han et al. studied HIV-positive patients in Durban, South Africa and screened for proteinuria, including microalbuminuria. They found persistent proteinuria in 6%; HIVAN in 21/30 (72.4%) and the prevalence of HIVAN in patients with persistent microalbuminuria was 85.7%. Studies in black patients have shown a higher prevalence of both severe glomerular lesions (focal glomerulosclerosis) and nephrotic range proteinuria with renal dysfunction in the presence of normo-hypotension. There have been no prospective randomised controlled studies with any form of therapy for HIVAN to date. Therapy of HIVAN has included corticosteroids, cyclosporine and antiretroviral therapy (ART). ART appears to be a logical choice in the management of HIV-associated renal disease. Regimens containing protease inhibitors have been shown to be associated with significant slowing of the decline in creatinine clearance. Both peritoneal dialysis and haemodialysis are appropriate treatment modalities for HIV-infected patients with end stage renal disease. The choice of dialysis modality between haemodialysis and peritoneal dialysis is not a factor in predicting survival, if patients are stable on ART. Preliminary short-term data in case reports and small cohorts of liver, kidney, and heart transplant recipients suggest that patient survival rates may be similar to those in HIV-uninfected transplant recipients. However, high rates of acute and chronic rejection have been observed among HIV-infected kidney transplant recipients. The Infectious Diseases Society of America (IDSA) published guidelines in 2005, recommending that all individuals be assessed for kidney disease at the time of diagnosis of HIV infection with a screening urinalysis for proteinuria and a calculated estimate of renal function. Therefore any patient with persistent proteinuria, persistent haematuria or glomerular filtration rate < 60 mL/min per 1.73 m(2) should be referred to an institution where a specialist can evaluate this patient for further investigations. An integrated plan to reduce the progression to kidney failure together with lifestyle measures, focusing also on high risk groups with effective management at all levels of chronic kidney disease remains essential.
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PMID:Chronic kidney disease in human immunodeficiency virus infection. 1762 82

Conditional transgenic mice that express one of the human immunodeficiency virus (HIV)-1 accessory genes, vpr, selectively in podocytes using a podocin promoter and a tetracycline-inducible system develop renal injuries similar to those of patients with HIV-associated nephropathy (HIVAN). We have shown that a heminephrectomy accelerates podocyte injury, which is alleviated by angiotensin II (ANG II) type 1 receptor blocker (ARB). The current study further explores the role of ANG II in the genesis of HIVAN in this murine model. With ANG II infusion, heavy proteinuria was observed at 1 wk after the initiation of doxycycline administration to induce vpr expression in podocytes. Severe morphological and phenotypical changes in the podocytes were observed at 2 wk, together with extensive glomerulosclerosis. Norepinephrine infusion, instead of ANG II, increased the systemic blood pressure to the same level as that achieved using ANG II. However, albuminuria and glomerular injury were modest in norepinephrine-infused mice. Treatment with an ARB, olmesartan, almost completely inhibited glomerular injury. In contrast, lowering the blood pressure with a vasodilator, hydralazine, partially decreased albuminuria but did not produce any histological changes. ANG II infusion alone without doxycycline resulted in a lower level of albuminuria and minimal histological changes. These data demonstrate that excessive ANG II accelerates vpr-induced podocyte injury in a mouse model of HIVAN.
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PMID:Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy. 1765 72

The incidence and prevalence of end-stage renal disease (ESRD) is increasing. Diabetic nephropathy has increased in absolute numbers and as a proportion of patients with ESRD. This is almost totally accounted for by the explosive outbreak of Type 2 diabetes mellitus (DM). The world is in the midst of an epidemic of Type 2 DM and hence this trend is likely to continue for some more time. The contribution of glomerulonephritis as a proportion of patients with chronic renal failure (CRF) has declined due to increase in other causes such as diabetes. The annual incidence of IgA nephropathy, which is also a very common cause of renal insufficiency, has not changed. The incidence of focal segmental glomerulosclerosis is increasing while that of membranoproliferative glomerulonephritis is decreasing. Peak incidence of ESRD due to hypertension has shifted to a higher age-group. The proportion of renovascular disease as a cause of ESRD is also increasing. Human immunodeficiency virus associated nephropathy is the third leading cause of ESRD in African-Americans aged 20-64 years. Other diseases such as analgesic nephropathy and lead nephropathy are slowly disappearing. The significance of elevated body lead in patients with varying degrees of renal insufficiency requires further evaluation. The incidence of CRF is significantly higher in the elderly and hence there is a "graying" of CRF population. Census projections show that this trend will continue into the foreseeable future. The incidence and prevalence of ESRD vary between different populations, countries and within countries. The reason for the variations requires further study.
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PMID:Changing profile of causes of chronic renal failure. 1765 16

Human immunodeficiency virus-associated nephropathy (HIVAN) has rarely been reported in African children. In this single-center study, we analyzed ten children diagnosed with HIVAN from January 2000 to October 2006. There were eight boys and two girls, with a male:female ratio of 4:1. Their ages were from 5 months to 15 years (mean 6.8+/-6.2 years), with a peak age of 5-9 years. The presenting complaints included generalized edema (60%) and hypertension (50%). All patients had proteinuria on urine dipstick, with four (40%) at nephrotic range (proteinuria >or=500 mg/dl). Nine (90%) patients were in renal failure, with elevated serum creatinine (6.3-24 mg/dl) and serum urea (70-120 mg/dl). Renal disease was the first manifestation of HIV infection in six patients, whereas the diagnosis was made on autopsy in three. The duration from HIV infection to development of HIVAN ranged from 5 months to 10 years. CD4(+) cell count, done in only three patients due to financial constraints, was below 200/mm(3). The kidneys were hyperechoic on abdominal ultrasound in all patients, and three (30%) showed grossly enlarged kidneys. Histology of renal tissues available by autopsy in three patients showed mainly collapsing focal segmental glomerulosclerosis. Treatments given were angiotensin-converting enzyme (ACE) inhibitors and highly active antiretroviral therapy (HAART) in four and two patients, respectively, and one patient underwent peritoneal dialysis. On outcome analysis, seven (70%) patients died, two were lost to follow-up, and one was alive on HAART therapy at the writing of this article. In conclusion, HIVAN occurs in Nigeria children, and the mortality is very high from uremia.
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PMID:Human immunodeficiency virus-associated nephropathy (HIVAN) in Nigerian children. 1798 61

Nonimmune glomerulopathies are an area of significant research. This review discusses the development of focal segmental glomerulosclerosis, with particular attention to the role of the podocyte in the initiation of glomerulosclerosis and the contribution to glomerulosclerosis from capillary hypertension and soluble factors such as transforming growth factor beta, platelet-derived growth factor, vascular endothelial growth factor, and angiotensin. The effects of these factors on endothelial and mesangial cells are also discussed. In addition, we review our current understanding of the slit diaphragm (a specialized cell junction found in the kidney), slit diaphragm-associated proteins (including nephrin, podocin, alpha-actinin-4, CD2-associated protein, and transient receptor potential channel 6), and the role of these proteins in glomerular disease. We also discuss the most recent research on the pathogenesis of collapsing glomerulosclerosis, human immunodeficiency virus associated nephropathy, Denys-Drash, diabetic nephropathy, Alport syndrome, and other diseases related to the interaction between the podocyte and the glomerular basement membrane.
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PMID:Pathogenesis of nonimmune glomerulopathies. 1803 19

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

Renal disease is a relatively common complication in patients infected with the human immunodeficiency virus (HIV). A collapsing form of focal glomerulosclerosis has been considered as the primary form of HIV nephropathy. HIV infection is also associated with an increasing number of different forms of renal disease. Acute renal failure (ARF) syndromes are frequently noted during the course of HIV infection. The most common include the following: acute and often reversible renal failure resulting from infection, hypotension, and administration of nephrotoxins used to treat opportunistic infections, and the use of highly active anti-retroviral therapy. ARF has been reported in up to 20% of hospitalized HIV infected patients compared to 3 to 5% of non-HIV infected patients. Primary HIV infection is usually symptomatic, and infected patients can present with a variety of symptoms. Although ARF syndromes are frequently noted during the course of infection, it is an uncommon presentation of primary HIV infection. We describe a 42-year-old man who presented at our hospital with acute self-limited rhabdomyolysis and who was found to have primary HIV infection. Our case and other reports suggest that a diagnosis of primary HIV infection needs to be considered in patients who present with acute rhabdomyolysis.
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PMID:Primary HIV infection presenting as non-traumatic rhabdomyolysis with acute renal failure. 1858 27


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