From eDNA to decisions using a multi-method approach to restoration planning in streams.

Reintroduction efforts are increasingly used to mitigate biodiversity losses, but are frequently challenged by inadequate planning and uncertainty. High quality information about population status and threats can be used to prioritize reintroduction and restoration efforts and can transform ad hoc approaches into opportunities for improving conservation outcomes at a landscape scale. We conducted comprehensive environmental DNA (eDNA) and visual encounter surveys to determine the distribution of native and non-native aquatic species in two high-priority watersheds to address key uncertainties-such as the distribution of threats and the status of existing populations-inherent in restoration planning. We then used these occurrence data to develop a menu of potential conservation actions and a decision framework to benefit an endangered vertebrate (foothill yellow-legged frog, Rana boylii) in dynamic stream systems. Our framework combines the strengths of multiple methods, allowing managers and conservation scientists to incorporate conservation science and site-specific knowledge into the planning process to increase the likelihood of achieving conservation goals.

Household food insecurity among child and adolescent athletics practitioners: A cross-sectional, descriptive, and exploratory study.

OBJECTIVE: The aim of the study was to explore the prevalence of food insecurity among child and adolescent athletics practitioners and to investigate factors associated with exercise performance, dietary habits, body composition, sleep, and socioeconomic status based on food security status. METHODS: This was a cross-sectional, descriptive, and exploratory study conducted in Campinas, São Paulo, Brazil, between June and July 2023. The convenience sample included children and adolescents (7-17 y old) of both sexes. We evaluated exercise performance, household food insecurity (HFI), dietary-related parameters, and other body composition, lifestyle, and social-related variables. Exercise performance was assessed using the counter movement jump (CMJ), squat jump (SJ), horizontal long jump (HLJ), 50-m sprint test (50-m ST) and throwing strength test (TST). The assessment of HFI was conducted using the food insecurity experience scale (FIES). Comparisons and associations were investigated based on food security status. RESULTS: The total sample size was comprised of 138 children (n = 42; 30.4%) and adolescents (n = 96; 69.6%). We found an association between food security status and sex (X2(138,1) = 4.42; P = 0.036). SJ was higher in the food security group than in the HFI group (t(117) = 2.112; P = 0.037; ES = 0.39). Sleep- and dietary-related factors did not differ between the groups. CONCLUSIONS: In summary, the prevalence of HFI among child and adolescent athletics participants was approximately 40%. Regarding exercise performance, SJ was better in the food security group than in the HFI group. Concerning dietary-related data, the HFI group had a lower number of meals per day than the food security group, and other dietary data did not differ between the groups. Body composition and sleep-related parameters were similar between the groups.

Muscle-specific, liver-detargeted adeno-associated virus gene therapy rescues Pompe phenotype in adult and neonate Gaa-/- mice.

Pompe disease (PD) is a neuromuscular disorder caused by acid α-glucosidase (GAA) deficiency. Reduced GAA activity leads to pathological glycogen accumulation in cardiac and skeletal muscles responsible for severe heart impairment, respiratory defects, and muscle weakness. Enzyme replacement therapy with recombinant human GAA (rhGAA) is the standard-of-care treatment for PD, however, its efficacy is limited due to poor uptake in muscle and the development of an immune response. Multiple clinical trials are ongoing in PD with adeno-associated virus (AAV) vectors based on liver- and muscle-targeting. Current gene therapy approaches are limited by liver proliferation, poor muscle targeting, and the potential immune response to the hGAA transgene. To generate a treatment tailored to infantile-onset PD, we took advantage of a novel AAV capsid able to increase skeletal muscle targeting compared to AAV9 while reducing liver overload. When combined with a liver-muscle tandem promoter (LiMP), and despite the extensive liver-detargeting, this vector had a limited immune response to the hGAA transgene. This combination of capsid and promoter with improved muscle expression and specificity allowed for glycogen clearance in cardiac and skeletal muscles of Gaa-/- adult mice. In neonate Gaa-/- , complete rescue of glycogen content and muscle strength was observed 6 months after AAV vector injection. Our work highlights the importance of residual liver expression to control the immune response toward a potentially immunogenic transgene expressed in muscle. In conclusion, the demonstration of the efficacy of a muscle-specific AAV capsid-promoter combination for the full rescue of PD manifestation in both neonate and adult Gaa-/- provides a potential therapeutic avenue for the infantile-onset form of this devastating disease.

The possible role of physical activity in the modulation of gut microbiota in chronic kidney disease and its impact on cardiovascular risk: a narrative review.

Chronic degenerative non-communicable diseases (CDNCDs), in particular chronic kidney disease, induce gut microbiota (GM) dysbiosis, which, in turn, worsens the progression of CDNCDs and patients' quality of life. We analyzed literature studies to discuss the possible positive and beneficial impact of physical activity on GM composition and CV risk in CKD patients. Regular physical activity seems to be able to positively modulate the GM, reducing the systemic inflammation and consequently the production of uremic gut-derived toxins, which are directly correlated with the increase of cardiovascular risk. In particular, the accumulation of indoxyl sulphate (IS) seems to be able to induce vascular calcifications, vascular stiffness and cardiac calcifications, while p-Cresyl sulphate (p-CS) seems to be able to exert a cardiotoxic action through metabolic pathways, capable of inducing oxidative stress. In addition, trimethylamine N-oxide (TMAO) can alter lipid metabolism, inducing the production of foam cells and causing an accelerated atherosclerosis process. In this context, a regular physical activity program seems to represent an adjuvant non-pharmacological approach to the clinical management of CKD patients.

Screening of Fabry Disease of patients in renal replacement therapy in a population from Lazio (Italy).

OBJECTIVE: Fabry's disease (FD) is a genetic disorder of lysosomal storage characterized by the intralysosomal accumulation of globotriaosylceramide (Gb3). This genetic mutation causes a total or partial deficit of the α-galactosidase (GAL) enzyme activity. FD has an incidence of 1:40000-60000 born alive. Its prevalence is higher in specific pathological conditions like chronic kidney disease (CKD). The aim of this study was to evaluate the FD prevalence in Italian renal replacement therapy (RRT) patients from Lazio region. PATIENTS AND METHODS: 485 patients in RRT (hemodialysis, peritoneal dialysis, and kidney transplantation) were recruited. The screening test was performed on venous blood sample. The latter was analyzed using specific FD diagnostic kit, based on the analysis of dried blood spots on filter paper. RESULTS: We found 3 cases of positivity to FD (1 female and 2 males). In addition, 1 male patient was identified with biochemical alteration indicative of GAL enzyme deficiency with a genetic variant of the GLA gene of unknown clinical significance. The FD prevalence in our population was 0.60% (1 case out 163), it rises to 0.80% (1 case out of 122) if the genetic variant of unknown clinical significance is considered. Comparing the three subpopulations, we observed a statistically significant difference in GAL activity in transplanted patients compared to dialysis patients (p<0.001). CONCLUSIONS: Considering the presence of an enzyme replacement therapy able to modify FD clinical history, it is essential to try to implement FD early diagnoses. However, the screening is too expensive to be extended on large scale, due to the low prevalence of the pathology. The screening should be performed on high-risk populations.

Novel therapeutic approaches based on the pathological role of gut dysbiosis on the link between nonalcoholic fatty liver disease and insulin resistance.

The growing global epidemic of obesity and type 2 diabetes mellitus has determined an increased prevalence of NAFLD (non-alcoholic fatty liver disease), making it the most common chronic liver disease in the Western world and a leading cause of liver transplantation. In the last few years, a rising number of studies conducted both on animal and human models have shown the existence of a close association between insulin resistance (IR), dysbiosis, and steatosis. However, all the mechanisms that lead to impaired permeability, inflammation, and fibrosis have not been fully clarified. Recently, new possible treatment modalities have received much attention. To reach the review purpose, a broad-ranging literature search on multidisciplinary research databases was performed using the following terms alone or in combination: "NAFLD", "gut dysbiosis", "insulin resistance", "inflammation", "probiotics", "Chinese herbs". The use of probiotics, prebiotics, symbiotics, postbiotics, fecal microbiota transplant (FMT), Chinese herbal medicine, antibiotics, diet (polyphenols and fasting diets), and minor therapies such as carbon nanoparticles, the MCJ protein, water rich in molecular hydrogen, seems to be able to improve the phenotypic pattern in NAFLD patients. In this review, we provide an overview of how IR and dysbiosis contribute to the development and progression of NAFLD, as well as the therapeutic strategies currently in use.

A literature review of hypertensive retinopathy: systemic correlations and new technologies.

OBJECTIVE: Hypertensive retinopathy (HR) is the most common ocular manifestation of systemic arterial hypertension. This paper aims to summarize the current knowledge of HR, reviewing its classical features, such as epidemiology, pathophysiology, clinical manifestations, classifications, management and the most significant systemic correlations. We also provide an update on the latest advances in new technologies focusing on novel instrumental classifications. MATERIALS AND METHODS: A literature search was performed to identify articles regarding HR listed in Embase, PubMed, Medline (Ovid) and Scopus database up to 1 December 2021. The reference lists of the analyzed articles were also considered a source of literature information. The following keywords were used in various combinations: hypertensive retinopathy, hypertension and eye, hypertensive retinopathy and systemic correlations, optical coherence tomography (OCT) and hypertensive retinopathy, optical coherence tomography angiography (OCTA) and hypertensive retinopathy, adaptive optics (AO) and hypertensive retinopathy. The authors analyzed all English articles found using the aforementioned keywords. All the publications were thoroughly reviewed to create a detailed overview of this issue. RESULTS: HR signs have a significative association with cardiovascular, cerebrovascular and other systemic diseases. Patients with arteriosclerotic changes and, at the same time, severe HR, are at increased risk for coronary disease, peripheral vascular disease, stroke and dementia. HR is even now diagnosed and classified by its clinical appearance on a fundoscopic exam that is limited by interobserver variability. New technologies, like OCT, OCTA, AO and artificial intelligence may be used to develop a new instrumental classification that could become an objective and quantitative method for the evaluation of this disease. They could be useful to evaluate the subclinical retinal microvascular changes due to hypertension that may reflect the involvement of other vital organs. CONCLUSIONS: The eye is the only organ in the human body where changes in the blood vessels due to systemic hypertension can be studied in vivo. All doctors should be familiar with this disease because it has been largely demonstrated that signs of HR are correlated to patient's health and mortality. Researchers should develop a new common, standardized, and objective method to assess hypertensive retinal changes; new technologies may have a significant role in this field. This review takes most of the literature published so far, including the OCTA studies in order to stimulate new points of reference to standardize parameters and new diagnostic markers of this disease.

Link between gut microbiota dysbiosis and chronic kidney disease.

During chronic kidney disease (CKD), typical alterations in the gut microbiota are observed. The kidney no longer plays the role of the main excretory organ as this function is performed by the intestine. In CKD patients, an alteration of intestinal permeability and a degradation of the protective mucous layer are observed. These changes in the intestinal barrier allow the passage of bacterial material from the intestine to the bloodstream through the intestinal wall. This phenomenon contributes to the induction of the chronic inflammatory state, typical of CKD. In nephropathic patients, there is an increase in circulation of p-cresyl sulfate (p-CS), indoxyl sulphate (IS), indole-3 acetic acid (IAA) and trimethylamine-N-oxide (TMAO), all gut-derived uremic toxins. The changes in gut microbiota composition are related to CKD stage and this phenomenon is exacerbated in hemodialysis (HD) adult and pediatric patients. Interestingly, it is observed a positive shift in gut microbiota composition after renal transplantation and at the same time a reduction of circulating gut-derived uremic toxins. Either gut dysbiosis or uremic toxins accumulation contribute to the CKD onset and progression.

Risk factors for diabetic foot ulcers: an Albanian retrospective study of inpatients with type 2 diabetes.

OBJECTIVE: The aim of this study was to assess the impact of glucose control, diabetes-related complications and cardiometabolic risk factors on the risk of diabetic foot ulcers (DFUs) and DFU complications in Albanian adult inpatients with T2D. PATIENTS AND METHODS: We conducted a retrospective case-control study on 482 Albanian adult inpatients with T2D. DFU was defined as a full-thickness skin lesion requiring ≥14 days for healing and was classified at the time of hospital admission. Demographic and biochemical parameters of the study participants, the presence of comorbidities and diabetes-related complications at the time of hospital admission were evaluated through a retrospective chart review. RESULTS: Mean age of study participants was 54.8±10.7 years. Participants (284 males and 198 females) were divided into two groups: DFU (cases; n=104) and non-DFU (controls; n=378). Multivariate analysis (performed by a logistic regression model) revealed that the most relevant independent variables associated with DFU were BMI [OR=0.62; p=0.007], HDL-cholesterol [OR=0.00; p<0.0001], triglycerides [OR=7.48; p=0.0004], cigarette smoking [OR=26.46; p=0.005], duration of diabetes [OR=1.53; p<0.0001], fasting plasma glucose (FPG) [OR=1.06; p<0.0001], systolic blood pressure (SBP) [OR=1.13; p=0.0004] and insulin therapy alone [OR=0.11; p=0.02]. ROC curve analysis showed that FPG (AUC=0.83), glycated hemoglobin (HbA1c) (AUC=0.75), triglycerides (AUC=0.78) and HDL-cholesterol (AUC=0.82) were the most reliable biomarkers able to detect DFU. In the DFU group, the most relevant independent variables associated with previous minor lower-extremity amputations (LEAs) were represented by HbA1c [OR=1.47; p=0.03], age <55 years [OR=0.12; p=0.05] and female sex [OR=4.18; p=0.03]; whereas the most relevant independent variables associated with diabetic peripheral neuropathy (DPN) were HbA1c [OR=1.70; p=0.006], SBP [OR=1.08; p=0.05], BMI [OR=1.20; p=0.03] and lack of cigarette smoking [OR=0.07; p=0.01]. Correlation analysis (performed through the nonparametric Spearman's rank correlation test or through the parametric Pearson test, as appropriate) revealed a significant positive relationship between HbA1c and FPG (r=0.58; p<0.0001), ulcer surface area (r=0.50; p<0.0001), ulcer grade (r=0.23; p=0.02), minor LEAs (r=0.20; p=0.04), DPN (r=0.41; p<0.0001), and metformin therapy alone (r=0.72; p<0.0001). There was a significant inverse correlation between HbA1c and insulin therapy alone (r=-0.31; p=0.01) and combined metformin and insulin therapy (r=-0.60; p<0.0001). Both DFU and non-DFU groups exhibited suboptimal mean LDL-cholesterol levels (>100 mg/dl) and mean HbA1c values >7.5%. Moreover, in DFU group HbA1c values were markedly elevated (≥10%) particularly in patients with a grade 3 ulcer and an ulcer surface area ≥4 cm2, as well as in patients with history of minor LEAs and in patients affected by DPN. CONCLUSIONS: The present study suggested that longer duration of diabetes, cigarette smoking, lower HDL-cholesterol levels, poor glucose control, and elevated triglyceride and SBP values may all represent major risk factors for the development of DFU in Albanian patients with T2D. Thus, community interventions and health policies aimed to improve the management of diabetes and related cardiometabolic risk factors should be urgently implemented in Albania, in order to prevent DFUs and other diabetes complications in patients with T2D.

Free-amino acid metabolic profiling of visceral adipose tissue from obese subjects.

Interest in adipose tissue pathophysiology and biochemistry have expanded considerably in the past two decades due to the ever increasing and alarming rates of global obesity and its critical outcome defined as metabolic syndrome (MS). This obesity-linked systemic dysfunction generates high risk factors of developing perilous diseases like type 2 diabetes, cardiovascular disease or cancer. Amino acids could play a crucial role in the pathophysiology of the MS onset. Focus of this study was to fully characterize amino acids metabolome modulations in visceral adipose tissues (VAT) from three adult cohorts: (i) obese patients (BMI 43-48) with metabolic syndrome (PO), (ii) obese subjects metabolically well (O), and (iii) non obese individuals (H). 128 metabolites identified as 20 protein amino acids, 85 related compounds and 13 dipeptides were measured by ultrahigh performance liquid chromatography-tandem mass spectroscopy (UPLC-MS/MS) and gas chromatography-/mass spectrometry GC/MS, in visceral fat samples from a total of 53 patients. Our analysis indicates a probable enhanced BCAA (leucine, isoleucine, valine) degradation in both VAT from O and PO subjects, while levels of their oxidation products are increased. Also PO and O VAT samples were characterized by: elevated levels of kynurenine, a catabolic product of tryptophan and precursor of diabetogenic substances, a significant increase of cysteine sulfinic acid levels, a decrease of 1-methylhistidine, and an up regulating trend of 3-methylhistidine levels. We hope this profiling can aid in novel clinical strategies development against the progression from obesity to metabolic syndrome.

A Panoply of Rheumatological Manifestations in Patients with GATA2 Deficiency.

PURPOSE: To characterize rheumatological manifestations of GATA2 deficiency. METHODS: Single-center, retrospective review of 157 patients with GATA2 deficiency. Disease course, laboratory results, and imaging findings were extracted. In-person rheumatological assessments were performed on selected, available patients. A literature search of four databases was conducted to identify additional cases. RESULTS: Rheumatological findings were identified in 28 patients, out of 157 cases reviewed (17.8%). Twenty-two of those patients (78.6%) reported symptom onset prior to or in conjunction with the molecular diagnosis of GATA2 deficiency. Notable rheumatological manifestations included: piezogenic pedal papules (PPP), joint hyperextensibility, early onset osteoarthritis, ankylosing spondylitis, and seronegative erosive rheumatoid arthritis. In peripheral blood of patients with rheumatological manifestations and GATA2 deficiency, CD4+ CD3+ helper T cells and naïve CD3+ CD4+ CD62L+ CD45RA+ helper T cell subpopulation fractions were significantly lower, while CD8+ cytotoxic T cell fractions were significantly higher, compared to those without rheumatological manifestations and with GATA2 deficiency. No changes in CD19, CD3, or NK populations were observed. CONCLUSION: GATA2 deficiency is associated with a broad spectrum of rheumatological disease manifestations. Low total helper T lymphocyte proportions and low naïve helper T cell proportions are associated with those most at risk of overt rheumatological manifestations. Further, PPP and joint hyperextensibility may explain some of the nonimmunologically-mediated joint problems encountered in patients with GATA2 deficiency. This catalogue suggests that rheumatological manifestations and immune dysregulation are relatively common in GATA2 deficiency.

Evidence for the involvement of TNF-α, IL-1ß and IL-10 in the antinociceptive and anti-inflammatory effects of indole-3-guanylhydrazone hydrochloride, an aromatic aminoguanidine, in rodents.

BACKGROUND: Indole-3-guanylhydrazone hydrochloride (LQM01) is a new derivative of aminoguanidine hydrochloride, an aromatic aminoguanidine. METHODS: Mice were treated with LQM01 (5, 10, 25 or 50 mg/kg, i.p.), vehicle (0.9% saline i.p.) or a standard drug. The mice were subjected to carrageenan-induced pleurisy, abdominal writhing induced by acetic acid, the formalin test and the hot-plate test. The model of non-inflammatory chronic muscle pain induced by saline acid was also used. Mice from the chronic protocol were assessed for withdrawal threshold, muscle strength and motor coordination. LQM01 or vehicle treated mice were evaluated for Fos protein. RESULTS: LQM01 inhibits TNF-α and IL-1ß production, as well as leukocyte recruitment during inflammation process. The level of IL-10 in LQM01-treated mice increased in pleural fluid. In addition, LQM01 decreased the nociceptive behavior in the acetic acid induced writhing test, the formalin test (both phases) and increased latency time on the hot-plate. LQM01 treatment also decreased mechanical hyperalgesia in mice with chronic muscle pain, with no changes in muscle strength and motor coordination. LQM01 reduced the number of Fos positive cells in the superficial dorsal horn. This compound exhibited antioxidant properties in in vitro assays. CONCLUSIONS: LQM01 has an outstanding anti-inflammatory and analgesic profile, probably mediated through a reduction in proinflammatory cytokines release, increase in IL-10 production and reduction in neuron activity in the dorsal horn of the spinal cord in mice. GENERAL SIGNIFICANCE: Beneficial effects of LQM01 suggest that it has some important clinical features and can play a role in the management of 'dysfunctional pain' and inflammatory diseases.

Imaging of subclinical haemopoiesis after stem-cell transplantation in patients with haematological malignancies: a prospective pilot study.

BACKGROUND: Haemopoietic stem-cell transplantation (HSCT) eradicates host haemopoiesis before venous infusion of haemopoietic stem cells (HSCs). The pathway to cellular recovery has been difficult to study in human beings because of risks associated with interventions during aplasia. We investigated whether 18F-fluorothymidine (18F-FLT) imaging was safe during allogenic HSCT and allowed visualisation of early cellular proliferation and detection of patterns of cellular engraftment after HSCT. METHODS: Eligible patients were aged 18-55 years, had high-risk haematological malignancies. All patients underwent myeloablation followed by HSCT. The imaging primary endpoint was detection of early subclinical engraftment after HSCT with 18F-FLT PET or CT. Imaging was done 1 day before and 5 or 9, and 28 days, and 1 year after HSCT. This study is registered with ClinicalTrials.gov, number NCT01338987. FINDINGS: Between April 1, 2014, and Dec 31, 2015, 23 patients were enrolled and assessable for toxic effects after completing accrual. 18F-FLT was not associated with any adverse events or delayed engraftment. 18F-FLT imaging objectively identified subclinical bone-marrow recovery within 5 days of HSC infusion, which was up to 20 days before engraftment became clinically evident. Quantitatively, 18F-FLT intensity differed significantly between myeloablative infusion before HSCT and subclinical HSC recovery (p=0·00031). 18F-FLT biodistribution over time revealed a previously unknown path of cellular recovery of haemopoiesis in vivo that mirrored fetal ontogeny. INTERPRETATION: 18F-FLT allowed quantification and tracking of subclinical bone-marrow repopulation in human beings and revealed new insights into the biology of HSC recovery after HSCT. FUNDING: National Institutes of Health, Ben's Run/Ben's Gift, Albert and Elizabeth Tucker Foundation, Mex Frates Leukemia Fund, Jones Family fund, and Oklahoma Center for Adult Stem Cell Research.

New perspectives for chronic pain treatment: a patent review (2010-2016).

INTRODUCTION: Chronic pain is a major problem of public health worldwide and is responsible for the increase in health costs. The therapeutic options available in the market for the treatment of chronic pain are often rather ineffective due to; the high number of adverse reactions, tolerance and dependence, reducing the quality of life, pharmacotherapy adherence and functional capacity. Hence, several studies have been conducted in the search for new treatment alternatives for chronic pain syndromes. Areas covered: This review brings together the therapeutic patents published over the past six years reporting the discovery of new drugs for the treatment of chronic pain, based on the perspective that these compounds are candidates for the management of chronic pain conditions. Expert opinion: Over the past 6 years, several pharmaceutical companies, as well as universities and researchers, have synthesized a series of compounds, which have been shown to be effective in controlling chronic pain in preclinical studies. These findings nurture the hope of discovering new therapeutic options for chronic pain. However, such studies are in early stages and there is a long and hard path to be followed until these compounds can become chemical entities available to the public.

Arterial ageing: from endothelial dysfunction to vascular calcification.

Complex structural and functional changes occur in the arterial system with advancing age. The aged artery is characterized by changes in microRNA expression patterns, autophagy, smooth muscle cell migration and proliferation, and arterial calcification with progressively increased mechanical vessel rigidity and stiffness. With age the vascular smooth muscle cells modify their phenotype from contractile to 'synthetic' determining the development of intimal thickening as early as the second decade of life as an adaptive response to forces acting on the arterial wall. The increased permeability observed in intimal thickening could represent the substrate on which low-level atherosclerotic stimuli can promote the development of advanced atherosclerotic lesions. In elderly patients the atherosclerotic plaques tend to be larger with increased vascular stenosis. In these plaques there is a progressive accumulation of both lipids and collagen and a decrease of inflammation. Similarly the plaques from elderly patients show more calcification as compared with those from younger patients. The coronary artery calcium score is a well-established marker of adverse cardiovascular outcomes. The presence of diffuse calcification in a severely stenotic segment probably induces changes in mechanical properties and shear stress of the arterial wall favouring the rupture of a vulnerable lesion in a less stenotic adjacent segment. Oxidative stress and inflammation appear to be the two primary pathological mechanisms of ageing-related endothelial dysfunction even in the absence of clinical disease. Arterial ageing is no longer considered an inexorable process. Only a better understanding of the link between ageing and vascular dysfunction can lead to significant advances in both preventative and therapeutic treatments with the aim that in the future vascular ageing may be halted or even reversed.

Is low-protein diet a possible risk factor of malnutrition in chronic kidney disease patients?

Chronic kidney disease (CKD) is becoming increasingly widespread in the world. Slowing its progression means to prevent uremic complications and improve quality of life of patients. Currently, a low-protein diet (LPD) is one of the tools most used in renal conservative therapy but a possible risk connected to LPD is protein-energy wasting. The aim of this study is evaluate the possible correlation between LPD and malnutrition onset. We enrolled 41 CKD patients, stages IIIb/IV according to K-DIGO guidelines, who followed for 6 weeks a diet with controlled protein intake (recommended dietary allowance 0.7 g per kilogram Ideal Body Weight per day of protein). Our patients showed a significant decrease of serum albumin values after 6 weeks of LDP (T2) compared with baseline values (T0) (P=0.039), whereas C-reactive protein increased significantly (T0 versus T2; P=0.131). From body composition analysis, a significant impairment of fat-free mass percentage at the end of the study was demonstrated (T0 versus T2; P=0.0489), probably related to total body water increase. The muscular mass, body cell mass and body cell mass index are significantly decreased after 6 weeks of LDP (T2). The phase angle is significantly reduced at the end of the study compared with basal values (T0 versus T2; P=0.0001, and T1 versus T2; P=0.0015). This study indicated that LPD slows down the progression of kidney disease but worsens patients' nutritional state.

Obesity and kidney disease: Beyond the hyperfiltration.

In industrialized countries, overweight and obesity account for approximately 13.8% and 24.9% of the kidney disease observed in men and women, respectively. Moreover, obesity-associated glomerulopathy is now considered as "an emerging epidemic." Kidney function can be negatively impacted by obesity through several mechanisms, either direct or indirect. While it is well established that obesity represents the leading risk factor for type 2 diabetes and hypertension, awareness that obesity is associated with direct kidney damage independently of hypertension and diabetes is still not widespread. In this paper we will discuss the emerging role of adipose tissue, particularly in the visceral depot, in obesity-induced chronic kidney damage.