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

Human immunodeficiency virus (HIV)-related glomerular disease is a cause of end-stage renal disease, though there is no recent data from Brazil concerning this syndrome. Persistent proteinuria (PPt) is the main marker for glomerular disease, especially levels above 1.5 g. We examined the prevalence of and associated risk factors for PPt, along with the prevalence of HIV-associated nephropathy (HIVAN) among AIDS patients. We interviewed 411 patients who were attended at the HIV/AIDS section of the Clinical Hospital of the Federal University of Pernambuco (Brazil) from January through June 2004. PPt was defined as a positive urine dipstick exam on at least two occasions. The analyzed risk factors were: black race, a low CD4 lymphocyte count (<200 cells/mm(3)), an HIV RNA level of >100,000 copies/mL and patients on highly-active antiretroviral therapy (HAART). The patients were classified according to urinary protein/creatinine ratio (Up/Uc) < 1.0, 1.0-3.0 and > 3.0. Patients with Up/Uc >3.0 were submitted to renal biopsy. Among the 411 HIV/AIDS patients, the mean age was 37 years, 70% were male, 37.5% were black, the mean CD4 count was 363 cells/mm(3) (+/- 95), the mean RNA HIV count was 44,475 copies/mL (+/- 40,369), and 92% were on HAART. The prevalence of PPt was 5.6% (95% CI = 3.6 to 8.3%), and it was significantly associated with a low CD4 lymphocyte count (p<0.048). HIVAN was found in just one patient, and two patients improved after HAART.
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PMID:Prevalence of persistent proteinuria in stable HIV/AIDS patients and its association with HIV nephropathy. 1796 69

The AIDS epidemic with severe opportunistic infections has put a heavy demand to health workers. The existence of associated renal disorder--acute renal failure or rapidly progressive azotaemia with histological lesion of focal and segmental glomerulosclerosis complicates it even more. We treated a 29-year-old male patient with AIDS (Gr.IV/C-2), who was intravenous heroin abuser with progressed azotaemia, anaemia and thrombocytopenia. Because of unsolved questions of acute renal disease or chronic damage, treatment was started with peritoneal dialysis, including all other conservative measures. Results were good, and during the seven month therapy no episode of peritonitis was observed. Such a result is satisfactory for patients with initial renal disease, and excellent for a person with acquired immunodeficiency syndrome. The cause of death was not connected with renal disease and dialysis, but was due to AIDS. According to middle proteinuria, hypertension and rapid progession of azotaemia our patient probably belonged to the group of patient with chornic renal disease due to AIDS.
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PMID:[Case report of a patient with AIDS and renal failure treated with continuous ambulatory peritoneal dialysis]. 1797 26

In order to determine the pattern of renal disease and risk factors for renal disease in HIV-infected Nigerians, we studied 400 consecutive HIV/AIDS patients (210 males, 190 females) aged between 18 and 65 years (mean +/- SD; 34.6 +/- 9.4 years), and examined renal disease factors attributable to the infection. Diagnosis of renal disease was based on the consistent presence of at least 1+ albuminuria and/or elevated serum creatinine (>132 micromol/l) as well as the absence of other identifiable causes of chronic kidney disease (CKD). We determined socio-demography and clinical findings, as well as full laboratory work-ups including haemogram, CD4+ cell count, serum electrolytes, urea, creatinine, protein, cholesterol and urine analysis. Renal biopsies were taken in 10 patients who had moderate to massive proteinuria and had consented to the procedure. Finally, we compared HIV/AIDS cases with and without renal disease to determine the risk factors for nephropathy. We observed a high prevalence of renal disease (proteinuria and/or elevated serum creatinine), which was present in 152 (38%) of the patients. This subgroup included 74 males and 78 females with a M:F ratio of 1:1. The mean age (+/-SD) was 35.8 (+/-10.01) years. Systolic and/or diastolic hypertension was seen in 13.2% of these patients while the mean (+/- SD) body mass index (BMI) and packed cell volume (PCV) were 18.5 (+/-3.1) kg/m(2) and 25.26 (+/-6.81)%, respectively. The mean (+/-SD) CD4+ count was 246.49 (+/-192.8) cells/microl, while the mean (+/-SD) serum creatinine and 24-h urine protein excretion rates were 210.11 (+/-337.8) micromol/l and 2.57 (+/- 2.42) g/day, respectively. In subjects with and without nephropathy, there were significant differences in age, BMI, serum cholesterol, serum albumin and CD4+ counts, suggesting that these parameters may be risk factors for nephropathy. Histology revealed mainly focal glomerulosclerosis (FGS) with glomerular collapse. We conclude that the prevalence of proteinuria in HIV-seropositive patients is high in Nigeria. Such subjects show an equal male:female distribution, and glomerular histology revealed that a majority of biopsied patients had the collapsing FSGS variant. The risk factors for renal disease included severity of the HIV infection (inferred from the generally low CD4+ count), anaemia, malnutrition and increasing age.
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PMID:Renal disease in HIV-seropositive patients in Nigeria: an assessment of prevalence, clinical features and risk factors. 1806 7

A rhesus macaque (Macaca mulatta) infected with simian-human immunodeficiency virus (SHIV) while undergoing AIDS research, required a comprehensive physical examination when it presented with slight peripheral edema, hypoalbuminemia, and proteinuria. Many of the clinical findings were consistent with nephrotic syndrome, which is an indication of glomerular disease, but the possibility of concurrent disease needed to be considered because lentiviral induced immune deficiency disease manifests multiple clinical syndromes. The animal was euthanized when its condition deteriorated despite supportive care that included colloidal fluid therapy. Histopathology confirmed membranoproliferative glomerulonephritis, the result of immune complex deposition most likely due to chronic SHIV infection. Clinical symptoms associated with this histopathology in SHIV-infected macaques have not previously been described. Here we offer suggestions for the medical management of this condition, which entails inhibition of the renin-angiotensin-aldosterone system and diet modifications.
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PMID:Peripheral edema with hypoalbuminemia in a nonhuman primate infected with simian-human immunodeficiency virus: a case report. 1821 Sep 98

Childhood human immunodeficiency virus-associated nephropathy (HIVAN) is defined by the presence of proteinuria associated with mesangial hyperplasia and/or global-focal segmental glomerulosclerosis, in combination with the microcystic transformation of renal tubules. This review discusses the pathogenesis of childhood HIVAN and explores how the current pathological paradigm for HIVAN in adults can be applied to children. The Human Immunodeficiency Virus-1 (HIV-1) induces renal epithelial injury in African American children with a genetic susceptibility to develop HIVAN. The mechanism is not well understood, since renal epithelial cells harvested from children with HIVAN do not appear to be productively infected. Children with HIVAN show a renal up-regulation of heparan sulphate proteoglycans and a recruitment of circulating heparin-binding growth factors, chemokines, and mononuclear cells. Macrophages appear to establish a renal HIV-reservoir and transfer viral particles to renal epithelial cells. All of these changes seem to trigger an aberrant and persistent renal epithelial proliferative response. The paradigm that viral products produced by infected renal epithelial cells per se induce the proliferation of these cells is not supported by data available in children with HIVAN. More research is needed to elucidate how HIV-1 induces renal epithelial injury and proliferation in HIV-infected children.
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PMID:Taking a hard look at the pathogenesis of childhood HIV-associated nephropathy. 1928 42

Human immunodeficiency virus (HIV)-infected children are at risk of developing several types of renal diseases, including HIV-associated nephropathy (HIVAN), which is usually seen during late stages of infection in children with a high viral load. This disease is defined by the presence of proteinuria associated with mesangial hyperplasia and/or global-focal segmental glomerulosclerosis combined with microcystic transformation of the renal tubules. Because HIVAN can have an insidious clinical onset, renal biopsy is the only definitive way of establishing a diagnosis. Given the risk of performing this procedure in HIV-infected children with other AIDS-defining illness, we sought to identify informative biomarkers such as growth factors in the urine of 55 HIV-infected children that might be predictive of the extent and activity of the renal lesions characteristic of HIVAN. We found that the levels of epidermal growth factor were lower in the urine of children with renal disease, whereas levels of fibroblast growth factor-2 and metalloproteinase-2 were higher as compared with those levels in infected children without renal disease. Similar changes were observed in HIV-Tg26 mice correlating with the progression of renal disease in this model of HIVAN. Our findings suggest that this urinary growth factor profile may be useful in facilitating the diagnosis of HIV-infected children at risk of developing HIVAN when interpreted in the appropriate clinical setting.
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PMID:A urinary biomarker profile for children with HIV-associated renal diseases. 1956 54

Few urinary screening studies have been performed to determine the incidence of urinary abnormalities in antiretroviral therapy-naive, HIV-infected outpatients. From published data, the incidence appears to be high, particularly when compared with populations outside sub-Saharan Africa. In South Africa, urinary screening in antiretroviral therapy clinics is not routinely practiced. The aim of this descriptive study was to screen antiretroviral therapy-naive, HIV-infected outpatients attending the HIV clinic for urinary abnormalities, namely leukocyturia, microscopic hematuria, and microalbuminuria/proteinuria. This study showed that 84% of the screened population had AIDS (CD4 count < 200 cells/ mm3), and the incidence of abnormalities on urinary dipstick testing was high: 30% had leukocyturia, 33% had microscopic hematuria, and 44% had microalbuminuria/proteinuria. In patients with leukocyturia, an infective organism was cultured in only 29.1% of cases, predominantly Escherichia coli (70%) with sterile leukocyturia comprising the remainder. There may be an association with tuberculosis (TB) or sexually transmitted infections (STI) in the sterile leucocyturia group, but this remains to be confirmed. In those with a culture positive result the most common organism was E. coli (70%), which exhibited 90% resistance to cotrimoxazole, demonstrating that cotrimoxazole prophylaxis is not effective to prevent urinary tract infection in this group. On the basis of these findings, it has been proposed that urinary screening be considered standard of care in HIV clinics in South Africa. An algorithm has been proposed for use in antiretroviral therapy clinics in South Africa to guide clinicians regarding the cost-effective management of urinary dipstick abnormalities.
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PMID:Urinary screening abnormalities in antiretroviral-naive HIV-infected outpatients and implications for management--a single-center study in South Africa. 1948 82

Because both renal disease and immune activation predict progression to acquired immunodeficiency syndrome (AIDS), we evaluated the associations between proteinuria>or=1+, as determined by dipstick analysis (7 [7%] of 1012 subjects); creatinine clearance of <90 mL/min (195 [18%] of 1071 subjects); and percentages of peripheral activated CD8 cells (CD8+CD38+HLA-DR+ cells) in antiretroviral-naive, human immunodeficiency virus (HIV)-infected subjects who were enrolled in AIDS Clinical Trials Group studies 384 and A5095. Proteinuria, but not creatinine clearance, was associated with higher percentages of CD8+CD38+HLA-DR+ cells (55% vs. 50%; P=.01), with even more pronounced differences noted among men and among blacks and Hispanics. Proteinuria may be a surrogate measurement of greater immune activation in HIV-infected patients initiating antiretroviral therapy.
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PMID:Proteinuria, creatinine clearance, and immune activation in antiretroviral-naive HIV-infected subjects. 1959 72

With improved survival afforded by highly active antiretroviral therapy (HAART), CKD has emerged as one of the primary comorbid conditions affecting HIV-infected individuals. Although CKD in HIV-infected individuals is classically thought of as a consequence of advanced HIV infection such as in the case of HIV-associated nephropathy, several factors likely contribute to the development CKD in HIV infection. These factors include genetic predisposition, age-related decline in kidney function, HAART-related metabolic changes, exposure to multiple nephrotoxic medications, and concurrent conditions such as hepatitis C or illicit drug use. Similar to the general population, proteinuria and impaired kidney function are associated with faster progression to acquired immune deficiency syndrome and death. Given the prevalence and impact of kidney disease on the course of HIV infection and its management, current guidelines recommend screening all HIV-infected individuals for kidney disease. This review focuses on the current guidelines for kidney disease screening and discusses traditional as well as promising strategies for detecting CKD in this vulnerable population.
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PMID:Screening for chronic kidney disease in HIV-infected patients. 2000 86

The objective of the present study was to determine the prevalence of electrolyte disturbances in AIDS patients developing acute kidney injury in the hospital setting, as well as to determine whether such disturbances constitute a risk factor for nephrotoxic and ischemic injury. A prospective, observational cohort study was carried out. Hospitalized AIDS patients were evaluated for age; gender; coinfection with hepatitis; diabetes mellitus; hypertension; time since HIV seroconversion; CD4 count; HIV viral load; proteinuria; serum levels of creatinine, urea, sodium, potassium and magnesium; antiretroviral use; nephrotoxic drug use; sepsis; intensive care unit (ICU) admission, and the need for dialysis. Each of these characteristics was correlated with the development of acute kidney injury, with recovery of renal function and with survival. Fifty-four patients developed acute kidney injury: 72% were males, 59% had been HIV-infected for >5 years, 72% had CD4 counts <200 cells/mm(3), 87% developed electrolyte disturbances, 33% recovered renal function, and 56% survived. ICU admission, dialysis, sepsis and hypomagnesemia were all significantly associated with nonrecovery of renal function and with mortality. Nonrecovery of renal function was significantly associated with hypomagnesemia, as was mortality in the multivariate analysis. The risks for nonrecovery of renal function and for death were 6.94 and 6.92 times greater, respectively, for patients with hypomagnesemia. In hospitalized AIDS patients, hypomagnesemia is a risk factor for nonrecovery of renal function and for in-hospital mortality. To determine whether hypomagnesemia is a determinant or simply a marker of critical illness, further studies involving magnesium supplementation in AIDS patients are warranted.
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PMID:Hypomagnesemia is a risk factor for nonrecovery of renal function and mortality in AIDS patients with acute kidney injury. 2040 40


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