We describe 7 cases of renal tubular injury in HIV-infected patients receiving an antiretroviral regimen containing tenofovir. Our patients (5 women and 2 men) developed renal tubular dysfunction, with hypophosphatemia, normoglycemic glycosuria, proteinuria, and decrease of creatinine clearance. The first biologic signs of renal toxicity were observed after duration of tenofovir treatment from 5 weeks to 16 months, and they resolved less than 4 months after discontinuation of tenofovir. Six patients had a low body weight (<60 kg). Five patients received low doses of ritonavir, and 1 received didanosine. In 5 patients, the signs resolved with the discontinuation of only the tenofovir. A renal biopsy performed in 1 patient was consistent with tubulointerstitial injury. Proximal tubulopathy appears to be a rare adverse effect of long-term tenofovir therapy. In patients with low weight or mild preexisting renal impairment, regular monitoring of tubulopathy markers could lead to early detection of this dysfunction.
We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log
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increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence.
ObjectivesThe aim of the study was to describe a new evolutionary form of visceral leishmaniasis observed in immunocompromised patients.
MethodsWe carried out long-term clinical and biological follow-up of 10 HIV-1/Leishmania-coinfected patients presenting numerous secondary visceral leishmaniasis episodes despite treatment, with the follow-up time ranging from 0.5 to 10 years.
ResultsAnalysis of polymerase chain reaction (PCR) and blood culture results demonstrated continuous multiplication and circulation of parasites despite treatment, both during asymptomatic periods and during secondary visceral leishmaniasis episodes. This condition may be termed 'chronic' because of the presence of relapses over a period of several years and 'active' because of the continuous blood circulation of the parasite.
ConclusionWe wish to define 'active chronic visceral leishmaniasis' as a novel nosological entity observed in HIV-1/Leishmania-coinfected patients.
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