Screening for decreased glomerular filtration rate and associated risk factors in a cohort of HIV-infected patients in a middle-income country.

With the introduction of combined active antiretroviral therapy and the improved survival of HIV-infected patients, degenerative diseases and drug toxicity have emerged as long-term concerns. We studied the prevalence of decreased glomerular filtration rate (GFR) and associated risk factors in a cohort of HIV-infected patients from a middle-income country. Our cross-sectional study included all adult patients who attended an urban outpatient clinic in 2008. GFR was estimated using the CKD-EPI equation. The prevalence ratio (PR) of decreased GFR (defined as <60 mL/min/1.73 m(2)) was estimated using generalizing linear models assuming a Poisson distribution. We analyzed data from 1,970 patients, of which 82.9% had been exposed to ART. A total of 249 patients (12.6%) had a GFR between 60 and 89 mL/min/1.73 m(2), 3.1% had a GFR between 30 and 59, 0.3% had a GFR between 15 and 29, and 0.4% had a GFR <15. Decreased GFR was found in only 74 patients (3.8%). In the multivariate regression model, the factors that were independently associated with a GFR below 60 mL/min/1.73 m(2) were as follows: age ≥ 50 years (PR = 3.4; 95% CI: 1.7-6.8), diabetes (PR = 2.0; 95% CI: 1.2-3.4), hypertension (PR = 2.0; 95% CI: 1.3-3.2), current CD4+ cell count <350 cells/mm3 (PR = 2.1; 95% CI: 1.3-3.3), past exposure to tenofovir (PR = 4.7; 95% CI: 2.3-9.4) and past exposure to indinavir (PR =1.7; 95% CI: 1.0-2.8). As in high-income countries, CKD was the predominant form of kidney involvement among HIV-infected individuals in our setting. The risk factors associated with decreased glomerular filtration were broad and included virus-related factors as well as degenerative and nephrotoxic factors. Despite the potential for nephrotoxicity associated with some antiretroviral drugs, in the short-term, advanced chronic renal disease remains very rare.

Changes in the small intestine of Schistosoma mansoni-infected mice fed a high-fat diet.

The consumption of a high-fat diet modifies both the morphology of the small intestine and experimentally tested effects of schistosomiasis mansoni. However, whether a schistosomiasis infection associated with a high-fat diet causes injury to the small intestine has never been investigated. Mice were fed either a high-fat or a standard-fat diet for 6 months and were then infected with Schistosoma mansoni cercariae. Physical characteristics of the intestinal tissue (mucosal thickness, small intestinal villi length and height, and abundance of goblet cells and enterocytes on the villous surface) and the distribution of granulomas along the intestinal segments and their developmental stage were measured at the time of sacrifice (9 or 17 weeks post-infection). The group fed a high-fat diet exhibited different granuloma stages, whereas the control group possessed only exudative granulomas. The chronically infected mice fed a high-fat diet exhibited higher granuloma and egg numbers than the acutely infected group. Exudative, exudative/exudative-productive and exudative-productive granulomas were present irrespective of diet. Computer-aided morphometric analysis confirmed that villus length, villus width, muscular height and submucosal height of the duodenal and jejunal segments were affected by diet and infection. In conclusion, a high-fat diet and infection had a significant impact on the small intestine morphology and morphometry among the animals tested.

Histopathological features of keratocystic odontogenic tumor: a descriptive study of 177 cases from a Brazilian population.

The aim of this study was to describe the clinicopathologic features of 177 keratocystic odontogenic tumors (KCOTs) diagnosed in a Brazilian population. A total of 177 KCOTs were reviewed and affected 158 patients with ages ranging from 5 to 79 years (mean age = 32 years) with a slight female predominance. Mandible was the most common affected site (69.3%), and a unilocular radiolucency was the most common radiographic image. Microscopically, all cases showed at least focal areas of classic KCOT, but several histological aspects were also observed, including diffuse and focal epithelial lining hyperplasia (48.6%), epithelial budding (12.4%), reactive cytological alterations (11.3%), dystrophic calcification (7.9%), daughter cysts (7.8%), odontogenic epithelial remnants (4.5%), focal areas of orthokeratinization (2.8%), and ameloblastomatous epithelium (1.7%). These variations may make KCOT diagnosis challenging in some cases, so careful full-sample analysis and knowledge of these uncommon histological features associated with KCOT are essential for correct diagnosis.