Renal disorders in HIV-infected patients.
(49/170)
BACKGROUND: HIV infection affects all body organs including kidney. Since the frequency of HIV-related renal disorders is unknown in Iran and the number of HIV-infected patients is increasing, this study was conducted for the first time in Iran to assess the frequency of electrolyte imbalance, renal failure, and proteinuria among HIV-infected patients. METHODS: Between April and December 2005, 65 HIV-infected patients who were receiving care at an outpatient counseling center in Tehran, participated in this study. Blood samples were collected to measure serum levels of sodium, potassium, calcium, phosphorus, blood urea nitrogen, and creatinine. Urine samples were analyzed to detect protein, red blood cells, white blood cells, and cast. RESULTS: Of the 65 HIV-infected patients, 86.2% were males. The mean age of the patients was 37+/-8.7 years, and 58.5% of the patients had a history of injecting illicit drugs. Urinalysis was normal in all patients, and serum levels of electrolytes, blood urea nitrogen, and creatinine were all in normal range. CONCLUSION: We found no electrolyte imbalance, proteinuria, or renal failure in HIV-infected patients. It seems that renal disorder is infrequent in Iranian HIV-infected patients. (+info)
Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy.
(50/170)
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. (+info)
HIV-1 and HIV-Associated Nephropathy 25 Years Later.
(51/170)
Twenty-five years after the first published description of AIDS, HIV-associated nephropathy (HIVAN) remains an important cause of kidney disease in HIV-infected patients. The pathogenesis of HIVAN involves direct HIV infection of the kidney, with both viral and host genetic factors playing an important role. The widespread use of antiretroviral therapy has influenced the epidemiology of HIV-related kidney disease, and the nephrology community should support efforts to improve access to therapy and limit HIV transmission in susceptible minority populations. This article reviews the history of HIV and HIVAN, focusing on advances in the understanding of pathogenesis, epidemiology, and treatment. (+info)
Genetic susceptibility, HIV infection, and the kidney.
(52/170)
In recent years, the sequencing of mammalian and microbial genomes has provided the opportunity to study how genetic variation in the host and pathogen influence the course of infectious disease. In the case of HIV-1 infection, such studies have led to identification of key viral proteins that determine pathogenicity, immune evasion, or drug resistance. In addition, candidate gene association studies have uncovered a large number of host genetic variants that influence the outcome of infection and some organ-specific complications. HIV-associated nephropathy (HIVAN) is a pathologically distinct complication of HIV infection. Interindividual variability in incidence, skewed ethnic distribution, and familial aggregation of HIVAN with other forms of ESRD have suggested genetic susceptibility as a major contributing factor. This article reviews the host genetic factors that influence the course of HIV-1 infection and discusses murine models that have increased the understanding of HIVAN pathogenesis and demonstrated the role of genetic background on determination of disease. (+info)
Emerging paradigms in the renal pathology of viral diseases.
(53/170)
This review considers recent information that illuminates pathogenetic mechanisms that involve three of the major viral infections that cause renal injury in the form of HIV-associated nephropathy, polyoma virus nephropathy, and hepatitis C virus-associated glomerulonephritis. (+info)
Racial differences in end-stage renal disease rates in HIV infection versus diabetes.
(54/170)
Few studies have compared the incidence of end-stage renal disease (ESRD) among individuals with the human immunodeficiency virus (HIV) and diabetes. We followed a national sample of 2,015,891 US veterans over a median peroid of 3.7 years for progression to ESRD. The age- and sex-adjusted incidence of ESRD (per 1000 person-years) among HIV-infected black patients was nearly an order of magnitude higher than among HIV-positive white patients, almost twice that of diabetic whites, and similar to that among diabetic blacks. In multivariate Cox proportional hazards analysis, diabetes was associated with an increased risk of ESRD among white patients, but HIV was not. Among black individuals, however, both HIV and diabetes conferred a similar increase in the risk of ESRD (4- to 5-fold increase compared to white individuals without HIV or diabetes). HIV and diabetes carry a similar risk of ESRD among black patients, highlighting the importance of developing strategies to prevent and treat renal disease among HIV-infected black individuals. (+info)
NPHS2 variation in sporadic focal segmental glomerulosclerosis.
(55/170)
Mutations in NPHS2, the gene that encodes podocin, are well-established causes of both familial and sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatric population, but have not been well-characterized in late-onset disease. To investigate the role of NPHS2 polymorphisms in sporadic cases of late-onset FSGS, we studied 377 biopsy-confirmed FSGS cases and 919 controls. We identified 18 single nucleotide polymorphisms (SNPs) by resequencing a subgroup of cases and controls, and subsequently genotyped African-American and European-American cases and controls for five missense SNPs, three SNPs within introns, and four SNPs in the 3' untranslated region. No homozygotes or compound heterozygotes were observed for any missense mutation. R138Q carriers were more frequent among FSGS cases relative to controls (OR = 4.9, P = 0.06), but heterozygosity for the other four missense mutations was equally distributed among FSGS cases and controls. Finally, a common haplotype of noncoding SNPs carried by 20% of African-Americans, but not observed in European-Americans, was strongly associated with a 50% reduction in risk for sporadic FSGS (OR = 0.5, P = 0.001). These results indicate that genetic variation or mutation of NPHS2 may play a role in late-onset sporadic FSGS. (+info)
Prevalence of persistent proteinuria in stable HIV/AIDS patients and its association with HIV nephropathy.
(56/170)
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. (+info)