Purification and characterization of the biological effects of phospholipase A(2) from sea anemone Bunodosoma caissarum

Sea anemones contain a variety of biologically active substances. Bunodosoma caissarum is a sea anemone from the Cnidaria phylum, found only in Brazilian coastal waters. The aim of the present work was to study the biological effects of PLA(2) isolated from the sea anemone B. caissarum on the isolated perfused kidney, the arteriolar mesenteric bed and on insulin secretion. Specimens of B. caissarum were collected from the Sao Vicente Channel on the southern coast of the State of São Paulo, Brazil. Reverse phase HPLC analysis of the crude extract of B. caissarum detected three PLA(2) proteins (named BcPLA(2)1, BCPLA(2)2 and BcPLA(2)3) found to be active in B. caissarum extracts. MALDI-TOF mass spectrometry of BcPLA(2)1 showed one main peak at 14.7 kDa. The N-terminal amino acid sequence of BcPLA(2)1 showed high amino acid sequence identity with PLA(2) group III protein isolated from the Mexican lizard (PA23 HELSU, HELSU, PA22 HELSU) and with the honey bee Apis mellifera (PLA(2) and 1POC_A). In addition, BcPLA(2)1 also showed significant overall homology to bee PLA(2). The enzymatic activity induced by native BCPLA(2)1 (20 mu g/well) was reduced by chemical treatment with p-bromophenacyl bromide (p-BPB) and with morin. BcPLA(2)1 strongly induced insulin secretion in presence of high glucose concentration. In isolated kidney, the PLA(2) from B. caissarum increased the perfusion pressure, renal vascular resistance, urinary flow, glomerular filtration rate, and sodium, potassium and chloride levels of excretion. BcPLA(2)1, however, did not increase the perfusion pressure on the mesenteric vascular bed. In conclusion, PLA(2), a group III phospholipase isolated from the sea anemone B. caissarum, exerted effects on renal function and induced insulin secretion in conditions of high glucose concentration. (C) 2009 Elsevier Ltd. All rights reserved.

Purification and biological effects of a C-type lectin isolated from Bothrops moojeni

Snake venom proteins from the C-type lectin family have very distinct biological activities despite their highly conserved primary structure, which is homologous to the carbohydrate recognition region of true C-type lectins. We purified a lectin-like protein (BmLec) from Bothrops moojeni venom and investigated its effect on platelet aggregation, insulin secretion, antibacterial activity, and isolated kidney cells. The BmLec was purified using two chromatographic steps: affinity chromatography and reverse phase high performance liquid chromatography (HPLC). BmLec showed a dose-dependent platelet aggregation and significantly decreased the bacterial growth rate in approximately 15%. During scanning electron microscopy, the profile of Xanthomonas axonopodis pv. passiflorae treated with lectin disclosed a high vesiculation and membrane rupture. BmLec induced a strong and significant increase in insulin secretion at 2.8 and 16.7 mM glucose concentrations, and this effect was seen in the presence of EGTA in both experiments. BmLec (10 mu g/mL) increased the perfusion pressure, renal vascular resistance and urinary flow. The glomerular filtration rate and percentages of sodium, potassium and chloride tubular transport were reduced at 60 minutes of perfusion. Renal alterations caused by BmLec were completely inhibited by indomethacin in all evaluated parameters. In conclusion, the C-type lectin isolated from Bothrops moojeni affected platelet aggregation, insulin secretion, antibacterial activity and isolated kidney function.

Renal and vascular effects of the natriuretic peptide isolated from Crotalus durissus cascavella venom

Crotalus durissus cascavella is a snake that is usually found in the scrublands of northeast Brazil. The components of its venom may have effects on the vascular and renal systems. Recently, a new bradykinin inhibitory peptide has been identified in the venom of the Crotalinae family. The aim of the present study was to investigate the renal and vascular effects of the natriuretic peptide isolated from the venom of Crotalus durissus cascavella (NP2_Casca). The chromatographic profile showed the fractionation of substances identified as convulxin, gyroxin, crotoxin and crotamine, as well as fractions V and VI. The electrophoretic profile of fraction V consisted of several bands ranging from approximately 6 kDa to 13 kDa, while fraction VI showed only two main electrophoretic bands with molecular weights of approximately 6 and 14 kDa. Reverse-phase chromatography showed that NP2_Casca corresponds to about 18% of fraction VI and that this fraction is the main natriuretic peptide. NP2_Casca was compared to other natriuretic peptides from other sources of snake venom. All amino acid sequences that were compared showed a consensus region of XGCFGX, XLDRIX and XSGLGCX. The group treated with NP2-Casca showed an increase in perfusion pressure, renal vascular resistance, urinary flow and glomerular filtration rate. The percent of total and proximal tubular transport of sodium was reduced significantly after administration of the peptide. The mean arterial pressure showed a dose-dependent decrease after infusion of NP2_Casca, and an increase in nitrite production. In the aortic ring assay, NP2_Casca caused a relaxant effect in endothelium-intact thoracic aortic rings precontracted with phenylephrine in the presence and absence of isatin. NP2_Casca failed to relax the aortic rings precontracted with an isosmotic potassium Krebs-Henseleit solution. In conclusion, the natriuretic peptide isolated from Crotalus durissus cascavella venom produced renal and vascular effects. NP2_Casca reduced total and proximal sodium tubular transport, leading to an increase in sodium excretion, thereby demonstrating a diuretic action. A hypotensive effect was displayed in an arterial pressure assay, with an increase in nitrite production, suggesting a possible vasoactive action. (C) 2008 Elsevier Ltd. All rights reserved.

Renal- and calcium-dependent vascular effects of Polybia paulista wasp venom

In the present study, the effects of Polybia paulista venom (PPV) on renal and vascular tissues were investigated. Isolated kidneys perfused with PPV (1 and 3 mu g/mL) had increased perfusion pressure, renal vascular resistance, urinary flow, and glomerular filtration rate; and reduced sodium tubular transport. Histological evaluation demonstrated deposits of proteins in Bowman's space and tubular lumen, and focal areas of necrosis. The venom promoted a cytotoxic effect on Madin-Darby canine kidney (MDCK) cells. A significant increase in lactic dehydrogenase levels was observed in response to venom exposure. In isolated mesenteric vascular beds, pressure and vascular resistance augmented in a dose-dependent manner. PPV increased the contractility of aortic rings maintained under basal tension. This contractile response was inhibited when preparations were maintained in Ca2+-free medium. Likewise, verapamil, a voltage-gated calcium channel blocker, also inhibited the contractile response. In this study, phentolamine, a blocker of a-adrenergic receptor blocker, significantly reduced the contractile effect of PPV in the aortic ring. In conclusion, PPV produced nephrotoxicity, which suggests a direct effect on necrotic cellular death in renal tubule cells. The vascular contractile effect of PPV appears to involve calcium influx through voltage-gated calcium channels via adrenergic regulation.

Renal and cardiovascular effects of Bothrops marajoensis venom and phospholipase A(2)

Bothrops marajoensis is found in the savannah of Marajo Island in the State of Par S and regions of Amapa State, Brazil. The aim of the work was to study the renal and cardiovascular effects of the B. marajoensis venom and phospholipase A(2) (PLA(2)). The venom was fractionated by Protein Pack 5PW. N-terminal amino acid sequencing of sPLA(2) showed amino acid identity with other lysine K49sPLA(2)s of snake venom. B. marajoensis venom (30 mu g/mL) decreased the perfusion pressure, renal vascular resistance, urinary flow, glomerular filtration rate and sodium tubular transport. PLA(2) did not change the renal parameters. The perfusion pressure of the mesenteric bed did not change after infusion of venom. In isolated heart, the venom decreased the force of contraction and increased PP but did not change coronary flow. In the arterial pressure, the venom and PLA(2) decreased mean arterial pressure and cardiac frequency. The presence of atrial flutter and late hyperpolarisation reversed, indicating QRS complex arrhythmia and dysfunction in atrial conduction. In conclusion, B. marajoensis venom and PLA(2) induce hypotension and bradycardia while simultaneously blocking electrical conduction in the heart. Moreover, the decrease in glomerular filtration rate, urinary flow and electrolyte transport demonstrates physiological changes to the renal system. (C) 2009 Elsevier Ltd. All rights reserved.

Expression and Role of CD166 in the Chronic Kidney Disease

Background: CD166, an adhesion molecule of the immunoglobulin superfamily, is one of the crucial effectors that traffic lymphocytes into tissues. Till now, the expression and role of CD166 in the chronic kidney disease remains unknown. Objectives: In the present study, we are to examine the expression of CD166 in the chronic kidney disease, and to explore its function with CD4+ T cells. Materials and Methods: CD166 expression was tested by Flow Cytometry (FACS) in the primary macrophages stimulated with LPS. In vivo, the expression of CD166 and CD4 were examined in the kidney tissues of adriamycin-induced nephropathy (AN) mice by immnohistochemistry. Macrophages and lymphocytes were co-cultured, the interaction between CD166 and CD4 was tested by immunofluorescent staining. Furthermore, the effects of CD166 on the activation and proliferation of T cells were explored. Results: In this study, CD166 expression was found to be upregulated on activated macrophages and glomerular endothelia in the adriamycin-induced nephropathy (AN) mice and CD4+ T cells were increased with CD166 expression in the AN mice. The interaction between macrophages and CD4+ T cells indicated that CD166 played a key role in the recruitment of lymphocytes in the chronic kidney disease, and neither proliferation nor activation of T cells was affected by CD166. Conclusions: CD166 expressed on macrophages and endothelia in AN kidney, and the function was related to the recruitment of CD4+ T cells into inflamed kidney, indicating that CD166 may be a potential target for reducing the inflammatory infiltrates in the chronic kidney disease.

Clinical effects of sirolimus treatment in patients with increased serum creatinine levels after renal transplant

Purpose: To observe the clinical effects of sirolimus (SRL) immunosuppressive therapy in patients with progressively increasing levels of serum creatinine (Scr) after renal transplant. Methods: In total, 180 patients whose Scr levels had been rising after renal transplant were given an oral calcineurin inhibitor (CNI): either cyclosporine A (CsA) or tacrolimus (FK506). All patients were treated at People’s Hospital of Zhengzhou, China, between January 2011 and December 2013, and were given SRL-based conversion treatment. Scr level and glomerular filtration rate (GFR) were observed before and 1, 3, and 6 months after treatment initiation. In addition, liver function, blood glucose, blood lipid levels, rejection reaction incidence, and mortality were recorded to evaluate the effects of SRL. Results: Scr levels were 116.60 ± 30.60 μmol/L and 119.00 ± 24.60 μmol/L, and GFR was 70.00 ± 19.70 mL/min and 75.90 ± 15.60 mL/min, at 3 and 6 months after treatment, respectively. The 3- and 6- month Scr and GFR values were statistically different (p < 0.05) compared to pre-treatment levels (Scr: 144.10 ± 61.70 μmol/L vs and GFR: 59.10 ± 16.20 mL/min. Acute rejection (AR) occurred in 20 patients (13.30 %) within 6 months of treatment initiation, but rejection was reversed with conventional methylprednisolone therapy. Twenty-one patients (11.70 %) developed lung infections, but all were cured. There were no significant differences in liver function before and after treatment. Conclusion: SRL-based immunosuppressive therapy is effective in treating patients with increased Scr levels after renal transplant.

Histopatologia de fígado, rim e baço de piaractus mesopotamicus, prochilodus lineatus e pseudoplatystoma fasciatum parasitados por myxosporídios, capturados no Rio Aquidauana, Mato Grosso do Sul, Brasil

Este estudo descreveu a histopatologia de rim, baço e fígado de Piaractus mesopotamicus, Prochilodus lineatus e Pseudoplatystoma fasciatum, parasitados por mixosporídios, capturados no Rio Aquidauana, MS. Após necropsia, amostras do fígado, rim cefálico e baço foram colhidas, fixadas em formalina a 10 % tamponada e processadas de acordo com a rotina histológica. Os cortes foram feitos à espessura de 5 μm e corados com hematoxilina-eosina. Foram encontrados Myxobolus porofilus em P. lineatus, M. colossomatis em P. mesopotamicus e Myxobolus spp. nas três espécies de hospedeiros. Cistos de mixosporídios no exame histopatológico foram vistos no fígado e baço de P. mesopotamicus. Mais de 50% das amostras de fígado de P mesopotamicus e P lineatus apresentou hepatodistrofia difusa. Mais de 80 % das amostras de fígado de P. fasciatum apresentou formações hialinas concêntricas e esteatose em 50% das amostras. em 95,23 % das amostras de rins de P. mesopotamicus, foram observadas alterações teciduais, e em mais de 60 % dos casos nefrodistrofia difusa moderada e congestão de sinusóides glomerulares. Alterações teciduais nas amostras de rins de P. lineatus foram observadas em menos de 20 % da amostra. No baço dos peixes ora examinados não foram encontradas lesões dignas de relato.

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013

Background: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution. Methods: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian metaregression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol. Findings: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa. Interpretation: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks.

Deficiency in apoptosis-inducing factor recapitulates chronic kidney disease via aberrant mitochondrial homeostasis

Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein with dual roles in redox signaling and programmed cell death. Deficiency in AIF is known to result in defective oxidative phosphorylation (OXPHOS), via loss of complex I activity and assembly in other tissues. Because the kidney relies on OXPHOS for metabolic homeostasis, we hypothesized that a decrease in AIF would result in chronic kidney disease (CKD). Here, we report that partial knockdown of Aif in mice recapitulates many features of CKD, in association with a compensatory increase in the mitochondrial ATP pool via a shift toward mitochondrial fusion, excess mitochondrial reactive oxygen species production, and Nox4 upregulation. However, despite a 50% lower AIF protein content in the kidney cortex, there was no loss of complex I activity or assembly. When diabetes was superimposed onto Aif knockdown, there were extensive changes in mitochondrial function and networking, which augmented the renal lesion. Studies in patients with diabetic nephropathy showed a decrease in AIF within the renal tubular compartment and lower AIFM1 renal cortical gene expression, which correlated with declining glomerular filtration rate. Lentiviral overexpression of Aif1m rescued glucose-induced disruption of mitochondrial respiration in human primary proximal tubule cells. These studies demonstrate that AIF deficiency is a risk factor for the development of diabetic kidney disease.

L’évaluation des déterminants des paramètres hémodynamiques centraux à l’aide de la cohorte populationnelle CARTaGENE.

Les maladies cardiovasculaires ont un impact considérable sur la vie des Canadiens, et de nombreux efforts ont permis d’identifier différents facteurs de risque associés à cette condition. L’hypertension artérielle représente un de ces facteurs modifiables les plus importants. Quoique l’hypertension est définie à l’aide de mesures de pression artérielle en périphérie, il devient de plus en plus apparent que la mesure de pression centrale et de ses composantes auraient des avantages au niveau de la prédiction de la survenue d’événements cardiovasculaires. Le présent mémoire vise à mieux caractériser deux déterminants de cette pression centrale, le traitement antihypertenseur à base de bêtabloqueurs et l’insuffisance rénale chronique précoce. En utilisant les données recueillies dans la banque de données populationnelle CARTaGENE, il a été possible à l’aide d’analyses statistiques par appariement basé sur le coefficient de propension de démontrer que l’utilisation d’agents antihypertensifs de type bêtabloqueurs était associée à un profil hémodynamique central défavorable. Ainsi, les individus recevant ces agents avaient une pression centrale et une amplification artérielle plus élevées que des individus du groupe contrôle apparié et ce, malgré une pression périphérique identique. Cet effet semblait être incomplètement expliqué par la réduction du rythme cardiaque associé à l’utilisation de bêtabloqueurs. Aussi, il a été démontré que l’insuffisance rénale chronique de stade 3 (débit de filtration glomérulaire estimé entre 30 et 60 mL/min/1.73m2) n’était pas associée à une élévation des paramètres hémodynamiques centraux, contrairement à ce qui avait déjà été décrit chez des individus avec insuffisance rénale chronique plus avancée. De plus, le niveau d’albuminurie ne serait également pas associé à un changement du profil central dans un sous-groupe de la cohorte CARTaGENE.

Rôle de l’urée dans la dysfonction de la cellule bêta-pancréatique au cours de l’insuffisance rénale chronique

L’insuffisance rénale chronique (IRC) se définit par un défaut de filtration glomérulaire et est associée à plusieurs désordres. La perturbation de l’homéostasie glucidique en fait partie. L’homéostasie glucidique est contrôlée principalement par l’insuline, soit l’hormone sécrétée en réponse au glucose par les cellules bêta-pancréatiques contenues dans les îlots de Langerhans. La préservation de la fonction de la cellule bêta est essentielle au maintien de l’homéostasie glucidique. Il a été démontré que la sécrétion de l'insuline est altérée au cours l'IRC, cependant les mécanismes demeurent peu connus. Au cours de l’IRC, l’accumulation chronique de toxines urémiques pourrait contribuer à la défaillance de la cellule bêta. L’urée est une toxine urémique majeure et sa toxicité a été récemment rapportée dans plusieurs tissus. Le but de ce mémoire était donc de vérifier le rôle de l’urée dans la dysfonction de la cellule bêta-pancréatique au cours de l’IRC. Nous avons démontré que l’exposition des îlots de souris à des concentrations pathologiques d’urée entraîne une diminution de la sécrétion d’insuline via l’augmentation du stress oxydant et des O-glycosylations. Ce défaut est dû à une perturbation du métabolisme intracellulaire du glucose. Entre autres, nous avons observé une baisse de la glycolyse associée à la réduction de l’activité enzymatique de la phosphofructokinase-1. Ces résultats démontrent un effet toxique direct de l’urée sur la sécrétion d’insuline et permettent de mieux comprendre le mécanisme de dysfonction de la cellule bêta-pancréatique au cours de l’IRC.

L’évaluation des déterminants des paramètres hémodynamiques centraux à l’aide de la cohorte populationnelle CARTaGENE

Les maladies cardiovasculaires ont un impact considérable sur la vie des Canadiens, et de nombreux efforts ont permis d’identifier différents facteurs de risque associés à cette condition. L’hypertension artérielle représente un de ces facteurs modifiables les plus importants. Quoique l’hypertension est définie à l’aide de mesures de pression artérielle en périphérie, il devient de plus en plus apparent que la mesure de pression centrale et de ses composantes auraient des avantages au niveau de la prédiction de la survenue d’événements cardiovasculaires. Le présent mémoire vise à mieux caractériser deux déterminants de cette pression centrale, le traitement antihypertenseur à base de bêtabloqueurs et l’insuffisance rénale chronique précoce. En utilisant les données recueillies dans la banque de données populationnelle CARTaGENE, il a été possible à l’aide d’analyses statistiques par appariement basé sur le coefficient de propension de démontrer que l’utilisation d’agents antihypertensifs de type bêtabloqueurs était associée à un profil hémodynamique central défavorable. Ainsi, les individus recevant ces agents avaient une pression centrale et une amplification artérielle plus élevées que des individus du groupe contrôle apparié et ce, malgré une pression périphérique identique. Cet effet semblait être incomplètement expliqué par la réduction du rythme cardiaque associé à l’utilisation de bêtabloqueurs. Aussi, il a été démontré que l’insuffisance rénale chronique de stade 3 (débit de filtration glomérulaire estimé entre 30 et 60 mL/min/1.73m2) n’était pas associée à une élévation des paramètres hémodynamiques centraux, contrairement à ce qui avait déjà été décrit chez des individus avec insuffisance rénale chronique plus avancée. De plus, le niveau d’albuminurie ne serait également pas associé à un changement du profil central dans un sous-groupe de la cohorte CARTaGENE.

Rôle de l’urée dans la dysfonction de la cellule bêta-pancréatique au cours de l’insuffisance rénale chronique

L’insuffisance rénale chronique (IRC) se définit par un défaut de filtration glomérulaire et est associée à plusieurs désordres. La perturbation de l’homéostasie glucidique en fait partie. L’homéostasie glucidique est contrôlée principalement par l’insuline, soit l’hormone sécrétée en réponse au glucose par les cellules bêta-pancréatiques contenues dans les îlots de Langerhans. La préservation de la fonction de la cellule bêta est essentielle au maintien de l’homéostasie glucidique. Il a été démontré que la sécrétion de l'insuline est altérée au cours l'IRC, cependant les mécanismes demeurent peu connus. Au cours de l’IRC, l’accumulation chronique de toxines urémiques pourrait contribuer à la défaillance de la cellule bêta. L’urée est une toxine urémique majeure et sa toxicité a été récemment rapportée dans plusieurs tissus. Le but de ce mémoire était donc de vérifier le rôle de l’urée dans la dysfonction de la cellule bêta-pancréatique au cours de l’IRC. Nous avons démontré que l’exposition des îlots de souris à des concentrations pathologiques d’urée entraîne une diminution de la sécrétion d’insuline via l’augmentation du stress oxydant et des O-glycosylations. Ce défaut est dû à une perturbation du métabolisme intracellulaire du glucose. Entre autres, nous avons observé une baisse de la glycolyse associée à la réduction de l’activité enzymatique de la phosphofructokinase-1. Ces résultats démontrent un effet toxique direct de l’urée sur la sécrétion d’insuline et permettent de mieux comprendre le mécanisme de dysfonction de la cellule bêta-pancréatique au cours de l’IRC.

Evaluación de la función renal en pacientes con enfermedad renal crónica (ERC) sin tratamiento sustitutorio, tras un programa de intervención nutricional (PIN): estudio aleatorizado

La Enfermedad Renal Crónica (ERC) se define como la disminución de la función renal, donde se reduce el filtrado glomerular (FG) estimado < 60 ml/min/1,73m2 o como la presencia de daño renal de forma persistente durante al menos tres meses. La enfermedad renal crónica (ERC) es una patología progresiva que afecta cada vez más a la población, el daño renal aumenta con el paso del tiempo, siendo su resultado el tratamiento renal sustitutivo, trasplante o incluso la muerte, el gran problema es que en ocasiones no hay síntomas hasta que esta instaurada. Las causas de la ERC son complejas e incluyen enfermedades comunes, como la hipertensión, el síndrome metabólico (conjunto de varios factores como HTA, obesidad), la diabetes y otras patologías que afectan al riñón. Desde la clasificación de ERC en 5 fases, los clínicos pueden diagnosticar precozmente, incluso en estadios iniciales. Para frenar la progresión de la enfermedad es recomendable la disminución de ingesta de proteica. El objetivo de este estudio es evaluar una intervención nutricional (PIN) sobre la función renal, valorando la ingesta, vigilando el estado renal y nutricional en pacientes con enfermedad renal crónica sin tratamiento sustitutorio. Se siguieron los criterios de las quías KDIGO/KDOQI, y los diferentes Documentos de Consenso de las Sociedades Científicas. Se diseñó un estudio longitudinal aleatorizado de 86 participantes, de los 43 que componían el grupo estudio (E) finalizaron el programa de intervención nutricional 90,69% de la muestra inicial, y 38 de los participantes del grupo control (C) (88,37%). La duración del ensayo fue de 12 meses. El estado nutricional se evaluó mediante la valoración global subjetiva (VSG), datos antropométricos, dietéticos y analíticos. Se realizó los análisis estadísticos con el programa SPSS. A los doce meses, se ha observado un aumento de FG y una disminución de otros parámetros que agravan la enfermedad. Además, se ha producido un control de la ingesta proteica y de la ingesta energética. Conclusión: Mediante una intervención nutricional mantenida en el tiempo, se puede controlar el estado nutricional y se evita la progresión de la enfermedad renal, influyendo positivamente en algunos parámetros de riesgo. Por lo que podemos concluir que la utilización de programas de intervención nutricional (PIN) en las consultas de enfermería nefrológica para pacientes con enfermedad renal crónica, podría evitar, en ocasiones, el paso del paciente a diálisis, trasplante o a la muerte.