Patrícia de Fátima Lopes

Oxidative stress in the pathophysiology of metabolic syndrome: which mechanisms are involved?

Metabolic syndrome (MS) is a combination of cardiometabolic risk factors, including obesity, hyperglycemia, hypertriglyceridemia, dyslipidemia and hypertension. Several studies report that oxidative condition caused by overproduction of reactive oxygen species (ROS) plays an important role in the development of MS. Our body has natural antioxidant system to reduce oxidative stress, which consists of numerous endogenous and exogenous components and antioxidants enzymes that are able to inactivate ROS. The main antioxidant defense enzymes that contribute to reduce oxidative stress are superoxide dismutase (SOD), catalase (CAT) and gluthatione peroxidase (GPx). The high-density lipoprotein cholesterol (HDL-c) is also associated with oxidative stress because it presents antioxidant and anti-inflammatory properties. HDL-c antioxidant activity may be attributed at least in part, to serum paraoxonase 1 (PON1) activity. Furthermore, derivatives of reactive oxygen metabolites (d-ROMs) also stand out as acting in cardiovascular disease and diabetes, by the imbalance in ROS production, and close relationship with inflammation. Recent reports have indicated the gamma-glutamyl transferase (GGT) as a promising biomarker for diagnosis of MS, because it is related to oxidative stress, since it plays an important role in the metabolism of extracellular glutathione. Based on this, several studies have searched for better markers for oxidative stress involved in development of MS.

BK polyomavirus in Kidney transplant recipients: screening, monitoring and clinical management

BK polyomavirus (BKPyV) is a causal agent of nephropathy, ureteral stenosis and hemorrhagic cystitis in kidney transplant recipients, and is considered an important emerging disease in transplantation. Regular screening for BKPyV reactivation mainly during the first 2 years posttransplant, with subsequent pre-emptive reduction of immunosuppression is considered the best option to avoid disease progression, since successful clearance or reduction of viremia is achieved in the vast majority of patients within 6 months. The use of drugs with antiviral properties for patients with persistent viremia has been attempted despite unclear benefits. Clinical manifestations of BKPyV nephropathy, current strategies for diagnosis and monitoring of BKPyV infection, management of immunosuppressive regimen after detection of BKPyV reactivation and the use of antiviral drugs are discussed in this review.

Five years results after intrafamilial kidney post-transplant in a case of familial hypomagnesemia due to a claudin-19 mutation.

INTRODUCTION Familial Hypomagnesaemia with hypercalciuria and nephrocalcinosis, with severe ocular impairment secondary to claudin-19 mutation, is a rare recessive autossomic disorder. Its spectrum includes renal Mg2+ wasting, medullary nephrocalcinosis and progressive chronic renal failure in young people. OBJECTIVE To report a case of kidney transplantation father to daughter in a familial occurrence of severe bilateral nephrocalcinosis associated with ocular impairment in a non-consanguineous Brazilian family, in which two daughters had nephrocalcinosis and severe retinopathy. METHODS The index case, a 19 years-old female, had long-lasting past medical history of recurrent urinary tract infections, and the abdominal X-ray revealed bilateral multiple renal calcifications as well as ureteral lithiasis, and she was under haemodialysis. She had the diagnosis of retinitis pigmentosa in the early neonatal period. The other daughter (13 years-old) had also nephrocalcinosis with preserved kidney function, retinopathy with severe visual impairment, and in addition, she exhibited hypomagnesaemia = 0.5 mg/dL and hypercalciuria. The other family members (mother, father and son) had no clinical disease manifestation. Mutation analysis at claudin-19 revealed two heterozygous missense mutations (P28L and G20D) in both affected daughters. The other family members exhibited mutant monoallelic status. In despite of that, the index case underwent intrafamilial living donor kidney transplantation (father). CONCLUSION In conclusion, the disease was characterized by an autosomal recessive compound heterozygous status and, after five years of donation the renal graft function remained stable without recurrence of metabolic disturbances or nephrocalcinosis. Besides, donor single kidney Mg2+ and Ca2+ homeostasis associated to monoallelic status did not affect the safety and the usual living donor post-transplant clinical course.

Metabolic syndrome components and estimated glomerular filtration rate based on creatinine and/or cystatin C in young adults: A gender issue?

AIMS This work aims to identify correlations between estimated glomerular filtration rate (eGFR) based on creatinine and/or cystatin C (Cr, CysC) with metabolic syndrome (MS) components in young adults, according to gender. MATERIAL AND METHODS This is a cross sectional study, where young adults aged between 18 and 30 were matched by gender, age and body mass index. All subjects underwent clinical evaluation and blood sampling for laboratory measurements. MS was determined according to the JIS criteria. The eGFR was estimated using CKD-EPI equations (eGFRCr; eGFRCysC; eGFRCr-CysC). RESULTS We evaluated 78 subjects with a mean age of 24.5 years. 10.2% had MS, with higher incidence among males (15.4% ♂ vs. 5.1% ♀). Elevated waist circumference was the MS component most observed. Significant correlations (Pearson; p<0.05) between eGFR and metabolic markers were observed only in males. In addition, we observed a significant association between the increase of MS components and the decay of eGFRCr and eGFRCr-CysC (zero vs. two or more components, ANOVA, p<0.05) only among males. CONCLUSION eGFR decay associated with components of MS and insulin resistance in young male adults could represent a worrying specific risk and indicate that further studies are needed to better understand these findings.

Neoplasia trofoblástica gestacional após normalização espontânea da gonadotrofina coriônica humana em paciente com mola hidatiforme parcial

We report here a case of gestational trophoblastic neoplasia after spontaneous normalization of human chorionic gonadotropin in a patient with a partial hydatidiform mole. This is the second occurrence of this event to be reported and the first one with proven immunohistochemical evidence. Besides showing the treatment for this pregnancy complication, this case report discusses the possibility of reducing the duration of post-molar follow-up, as well as strategies for early recognition of gestational trophoblastic neoplasia after spontaneous remission of molar pregnancy.