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São José do Rio Preto, Brazil

Peixoto-Santos J.E.,University of Sao Paulo | Galvis-Alonso O.Y.,Sao Jose do Rio Preto Medical School | Velasco T.R.,University of Sao Paulo | Kandratavicius L.,University of Sao Paulo | And 5 more authors.

In the central nervous system, zinc is released along with glutamate during neurotransmission and, in excess, can promote neuronal death. Experimental studies have shown that metallothioneins I/II (MT-I/II), which chelate free zinc, can affect seizures and reduce neuronal death after status epilepticus. Our aim was to evaluate the expression of MT-I/II in the hippocampus of patients with temporal lobe epilepsy (TLE). Hippocampi from patients with pharmacoresistant mesial temporal lobe epilepsy (MTLE) and patients with TLE associated with tumor or dysplasia (TLE-TD) were evaluated for expression of MT-I/II, for the vesicular zinc levels, and for neuronal, astroglial, and microglial populations. Compared to control cases, MTLE group displayed widespread increase in MT-I/II expression, astrogliosis, microgliosis and reduced neuronal population. In TLE-TD, the same changes were observed, except that were mainly confined to fascia dentata. Increased vesicular zinc was observed only in the inner molecular layer of MTLE patients, when compared to control cases. Correlation and linear regression analyses indicated an association between increased MT-I/II and increased astrogliosis in TLE. MT-I/II levels did not correlate with any clinical variables, but MTLE patients with secondary generalized seizures (SGS) had less MT-I/II than MTLE patients without SGS. In conclusion, MT-I/II expression was increased in hippocampi from TLE patients and our data suggest that it is associated with astrogliosis and may be associated with different seizure spread patterns. © 2012 Peixoto-Santos et al. Source

Joaquim A.I.,University of Sao Paulo | De Godoy M.F.,Sao Jose do Rio Preto Medical School | Burdmann E.A.,University of Sao Paulo
Clinical Nuclear Medicine

To investigate the influence of cyclic direct radionuclide cystography (RNC) on the diagnosis of vesicoureteral reflux (VUR) in children and adults. Patients and Methods: A total of 362 examinations were performed in patients with amean age of 15.8 ± 17.2 years (2months to 76.4 years, 89.5%female). The examinations were divided into 3 groups of age: A, younger than 5 years; B, 5 years and younger than 14 years; and C, older than 14 years. Repeated cycles of bladder filling without removal of the catheter were performed. Results: VUR was diagnosed in 21%of patients based on the first cycle, 5.5% in the second cycle, and 2.5% only in the third cycle. Most examinations showing VUR corresponded to grade II. Reflux occurred in only the filling phase in 10%, only the voiding phase in 27%, and both phases in 63% of patients. There was a higher incidence of reflux in groups A and B than group C after the first cycle. The second cycle was equally effective in diagnosing VUR in all 3 groups. In group A, the third cycle was more effective compared to the other groups. Conclusions: Performing a second and a third cycle in RNC yielded an additional VUR diagnosis of 35.7%, as compared to performing only 1 cycle. The second cycle showed efficacy in all the groups, whereas the third cycle diagnosed more VUR only in group A. These results confirmed the importance of performing additional cycles in RNC for VUR diagnosis, both in children and adults. © 2015 Wolters Kluwer Health, Inc. Source

Picollo Oliveira J.F.,Sao Jose do Rio Preto Medical School | Burdmann E.A.,University of Sao Paulo
Clinical Kidney Journal

Dengue is presently the most relevant viral infection transmitted by a mosquito bite that represents a major threat to public health worldwide. Acute kidney injury (AKI) is a serious and potentially lethal complication of this disease, and the actual incidence is unknown. In this review, we will assess the most relevant epidemiological and clinical data regarding dengue and the available evidence on the frequency, etiopathogenesis, outcomes and treatment of dengue-associated AKI. © 2015 The Author. Source

Carlos C.P.,Sao Jose do Rio Preto Medical School | Mendes G.E.F.,Sao Jose do Rio Preto Medical School | Miquelin A.R.,Sao Jose do Rio Preto Medical School | Luz M.A.M.,Sao Jose do Rio Preto Medical School | And 4 more authors.

BACKGROUND.: Cyclosporine A (CsA)-induced chronic nephrotoxicity is characterized by renal dysfunction and interstitial fibrosis. Early and progressive renal macrophage influx, correlating with latter interstitial fibrotic areas, has been associated with CsA treatment. This study investigated the role of macrophages, the nitric oxide (NO) pathway, and the oxidative stress on chronic CsA nephrotoxicity. METHODS.: The macrophages were depleted by clodronate liposomes. Animals were distributed into four groups: vehicle (olive oil for 21 days), CsA 7.5 mg/kg per day (21 days), CsA plus clodronate (5 mg/mL intraperitoneally on days-4, 1, 4, 11, and 18 of CsA treatment), or vehicle plus clodronate. On day 22, glomerular filtration rate, renal blood flow, renal tubulointerstitial fibrosis, CsA blood levels, serum malondialdehyde and renal tissue immunohistochemistry for macrophages, inducible NO synthase, transforming growth factor-β, nuclear factor-kβ, α-smooth muscle actin, vimentin, and nitrotyrosine were assessed. RESULTS.: CsA-induced increase in the macrophage was prevented by clodronate. Macrophage depletion attenuated the reductions in the glomerular filtration rate and renal blood flow, the development of tubulointerstitial fibrosis, malondialdehyde increase and increases in nuclear factor-kβ, transforming growth factor-β, vimentin, inducible NO synthase, and nitrotyrosine expression provoked by CsA. Clodronate did not affect α-smooth muscle actin expression and CsA blood levels. CONCLUSIONS.: Renal macrophage influx plays an important role in CsA-induced chronic nephrotoxicity. The NO pathway and oxidative stress are likely mechanisms involved in the genesis of this form of renal injury. Copyright © 2010 by Lippincott Williams & Wilkins. Source

Araujo L.P.,Federal University of Sao Paulo | Truzzi R.R.,Sao Paulo State University | Mendes G.E.,Sao Jose do Rio Preto Medical School | Luz M.A.M.,Sao Jose do Rio Preto Medical School | And 3 more authors.
American Journal of Nephrology

Background: Tacrolimus (FK) is currently widely used in transplant immunosuppression and the treatment of autoimmune diseases. However, FK induces nephrotoxicity which is characterized by functional and structural renal injury. The ubiquitous protein annexin A1 (ANXA1) has potent anti-inflammatory effects and protects against ischemia/reperfusion injury. We investigated the effects of exogenous ANXA1 treatment in an experimental model of acute FK nephrotoxicity. Methods: Munich-Wistar rats received a low-salt diet for 1 week and were randomized to treatment with ANXA1 (Ac2-26 peptide 0.5 mg/kg/day s.c.), FK (6 mg/kg/day p.o.), association (FK+ANXA1) and vehicles (1 ml/kg/day) for 7 days. Results: FK induced a significant decrease in glomerular filtration rate and renal blood flow, and a significant increase in renal vascular resistance. In addition, FK caused extensive acute tubule-interstitial damage and an increase in anti-inflammatory ANXA1 expression in renal tissue. Exogenous ANXA1 treatment reduced FK-induced tubular dilatation and macrophage infiltration. For the first time, we observed that FK augmented ANXA1 expression in renal tissue. Conclusion: Exogenous ANXA1 treatment partially protected against FK-induced tubular injury and macrophage infiltration, and may be targeted in renal intervention strategies. Copyright © 2010 S. Karger AG, Basel. Source

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