Background: Intradialytic hypotension is a potential complication experienced by patients with end-stage renal disease who receive hemodialysis. This complication occurs during the dialysis treatment in 15-30% of all treatments. The multiple comorbidities that exist in hemodialysis patients predispose them to recurrent intradialytic hypotension episodes. Recurrent intradialytic hypotensive episodes can result in negative short-term and long-term clinical consequences. Short-term consequences include complications such as ischemic events (e.g., heart attacks, strokes), clotting of patient dialysis access, or heart rhythm abnormalities. Long-term consequences include end-organ damage, increased cardiovascular morbidity, and a higher mortality rate. Problem Statement: Available nursing interventions used to treat intradialytic hypotension such as decreased dialysis fluid temperature, changes in the calcium and sodium concentrations in the dialysis fluid and oral medication have limited success. Another existing technological intervention called blood volume monitoring shows greater potential success but is currently underutilized. Purpose: The purpose of this literature review is to synthesize current literature on blood volume monitoring technology used to prevent intradialytic hypotension in hemodialysis patients. Methods: A literature review was conducted analyzing pertinent research articles published in the last ten years, in addition to seminal articles. Seventeen articles were retrieved and analyzed that met criteria. Results: Fourteen of the seventeen research studies reached a consensus on the successful use of blood volume monitoring to decrease intradialytic hypotension and the related symptoms. Conclusion: Results of the literature review support the use of blood volume monitoring technology as an effective nursing intervention to prevent intradialytic hypotension in hemodialysis patients.

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Chronic kidney disease is an urgent public health problem in the U.S., affecting 15% of all adults, and more than 740,000 have progressed to end-stage renal disease (ESRD), requiring life-sustaining renal replacement therapy (RRT). ESRD has devastating health, quality-of-life, and economic consequences, rendering most patients unable to maintain employment and costing Medicare $36 billion in 2017. Arguably, the most disadvantaged subgroup is the subset of patients that received no or minimal pre-ESRD nephrology care, which currently accounts for one third of the total ESRD population. This subgroup suffers increased morbidity and mortality, and has limited access to kidney transplantation, the optimal RRT. Despite this subgroup representing a large minority of the ESRD patient population, there has been no U.S.-based examination of their ESRD diagnosis experiences, coping styles and strategies, and RRT decision-making preferences. Therefore, we conducted a study that compared the ESRD diagnosis experiences, coping styles and strategies, and RRT decision-making preferences among patients with varying amounts of pre-ESRD nephrology care. We also assessed nephrologists’ current practices and perspectives on the manner and timing of RRT education for patients with varying amounts of pre-ESRD care. This mixed methods study provides a comprehensive understanding of the diagnosis experiences, coping styles and strategies, and RRT decision-making preferences of patients facing sudden and unexpected ESRD diagnosis. The study contributes important knowledge about this subgroup of patients that can influence and improve health care delivery. The results of this research will inform future intervention-based investigations to improve care for patients with minimal or no pre-ESRD nephrology care. / Public Health

Hyperhomocysteinemia (hHcys) is a widely known pathogenic factor in the progression of end-stage renal disease (ESRD) and it is also associated with an increased risk for injurious cardiovascular pathologies during ESRD. HHcys is linked to the formation and activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, characterized as a critical early mechanism initiating the inflammatory response. NADPH oxidase (NOX)-derived reactive oxygen species (ROS) mediate the activation of the NLRP3 inflammasome in podocytes in response to elevated levels of homocysteine (Hcys) in vitro and in vivo. However, it remains unknown how NLRP3 inflammasome activation is triggered by NOX. The aim of the present study sought to determine the signaling cascade that triggers glomerular injury and sclerosis during hHcys mediated by Vav2, a guanine nucleotide exchange factor (GNEF). Using both genetic and pharmacological interventions of Vav2, we first tested whether this GNEF is involved in hHcys-induced NLRP3 inflammasome activation in podocytes by its role in activation of the Rac-1-NOX complex. Further, we explored whether pharmacological targeting of Vav2 activation may regulate NLRP3 inflammasome signaling pathway during hHcys-induced glomerular injury. We found that mice with hHcys (on the FF diet) or oncoVav2 (a constitutively active form of Vav2) transfection in the kidney exhibited increased colocalization of NLRP3 with apoptosis-associated speck-like protein (ASC) or caspase-1 and elevated IL-1β levels in glomeruli, indicating the formation and activation of the NLRP3 inflammasome. This glomerular NLRP3 inflammasome activation was accompanied by podocyte dysfunction and glomerular injury, even sclerosis. Local transfection of Vav2 shRNA plasmids significantly attenuated hHcys-induced NLRP3 inflammasome activation, podocyte injury, and glomerular sclerosis. In cultured podocytes, Hcys treatment and oncoVav2 transfection increased NLRP3 inflammasome formation and activation. This NLRP3 activation was inhibited by Vav2 shRNA, associated with reduction of Rac-1 activity and ROS production. Administration of NSC23766, a Rac-1 inhibitor substantially attenuated inflammasome formation, desmin expression and decreased podocin expression in glomeruli of hHcys mice. These results suggest that elevated Hcys levels activate Vav2 and thereby increase NOX activity, leading to ROS production. ROS trigger NLRP3 inflammasome activation, podocyte dysfunction and glomerular injury. Therefore, the present study defines a novel mechanism underlying hHcys-induced NLRP3 inflammasome activation and its progression to ESRD.

A nefropatia induzida por adriamicina (ADR) em ratos é um dos modelos experimentais mais utilizados para o estudo desenvolvimento da doença renal progressiva. Uma dose única deste quimioterápico induz a proteinúria progressiva e irreversível que progride para glomeruloesclerose segmental e focal, com fusão dos processos podais e lesões tubulointersticiais. A lesão das células endoteliais glomerulares precede as alterações dos podócitos na nefropatia induzida pela ADR. A atividade física regular melhora as funções cardíacas e renais em pacientes e animais com doença renal progressiva e pode reduzir ou retardar a progressão da lesão renal. Este estudo avaliou o efeito do treinamento físico prévio na evolução da lesão renal induzida por ADR e a sua relação com o processo inflamatório, a função endotelial e angiogênese. Ratos Wistar submetidos ou não ao treinamento físico receberam ADR (2,5 mg/kg, e.v) ou solução salina fisiológica (SAL). Amostras de sangue e urina foram coletadas 60 dias após as injeções para avaliação da função renal e os rins removidos para estudos histológicos, imuno-histoquímicos, Western blot e de ELISA. Amostras de urina de 24 h, obtidas 7, 30 e 60 dias após a administração de ADR ou SAL, foram utilizadas para avaliação da albuminúria. Os ratos tratados com ADR apresentaram albuminúria progressiva, elevação dos níveis plasmáticos de creatinina e queda da taxa de filtração glomerular (TFG), lesão de podócitos, expansão da área mesangial, alargamento da área intersticial relativa no córtex renal, infiltração de macrófagos, aumento dos níveis de interleucina (IL)-1?, elevação dos níveis urinários do fator de transformação do crescimento ? (TGF-?) e dos níveis urinários de proteína quimiotática de monócitos 1 (MCP-1), diminuição de marcação de aminopeptidase P (marcador de células endoteliais) nos glomérulos e perda de capilares peritubulares corticais, que estavam associados com reduções das expressões do fator de crescimento endotelial vascular (VEGF) e da óxido nítrico sintase endotelial (eNOS) no córtex renal desses animais. Estas alterações foram menos intensas nos ratos que realizaram treinamento físico prévio ao tratamento com ADR. Em conclusão, o pré-condicionamento físico reduziu as lesões renais induzidas pela ADR. Este efeito esteve associado com as reduções do processo inflamatório, das lesões endoteliais e das alterações de fatores relacionados com o processo de angiogênese (VEGF e eNOS) no córtex renal. / Adriamycin (ADR)-induced nephropathy is one of the most experimental models of progressive kidney disease in rats. A single dose of this drug induces progressive and irreversible proteinuria that progresses to focal segmental glomerulosclerosis and tubulointerstitial lesions. The lesion of glomerular endothelial cells precedes the podocyte damage in nephropathy induced by ADR. Regular physical activity improves cardiac and renal functions in patients and animals with progressive renal disease and may reduce or delay the progress of impaired renal function. This study evaluated the effect of previous physical training in renal damage induced by ADR and the role of inflammation, endothelial lesions and angiogenesis in this process. Male Wistar rats submitted or not to previous physical training received ADR (2.5 mg/kg, i.v.) or physiological saline (SAL). Urine and plasma samples were collect 60 days after the injection in order to evaluated the renal function. The kidneys were removed for histological, immunohistochemical, Western blot and ELISA analysis. Twenty-four-hour urine samples were collected to dose albuminuria 7, 30 and 60 days after ADR or SAL injection. ADR-treated rats presented progressive albuminuria, increases in plasma creatinine levels, decreasing glomerular filtration rate (GFR), podocyte damage, mesangial expansion, enlargement of the tubular interstitial relative area of renal cortex, macrophage infiltration, higher interleukin (IL)- 1? levels in renal tissue, urinary transforming growth factor ? (TGF-?) and urinary monocyte chemoattractant protein (MCP)-1, reduction of aminopeptidase P (endothelial cell marker) in the glomeruli and cortical peritubular capillary number. Those were associated with reduction in vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expressions in renal cortex. Those alterations were less intense in the animals undergone previous exercise training. In conclusion, physical training prior to ADR injection reduced the renal damage induced by this drug. This effect was related with the reduction of the inflammatory process, endothelial lesions and with the decrease in alterations of factors related to the process of angiogenesis (VEGF and eNOS) in renal cortex.

Albumin provides the vital scaffolding for growth and tissue repair and supports oncotic blood pressure and hemodynamics. In hemodialysis patients, albumin aids with fluid removal by drawing excess fluid from edematous tissues back into the blood where it can then be removed by a dialyzer. The hyperglycemia seen in dialysis patients with Type II diabetes progressively damages kidney glomeruli, which permits albumin seepage into the urine, thus lowering serum albumin. The conceptual framework underpinning this research is the van't Hoff theory of osmotic pressure. Under this framework, the solute-solvent relationship largely contributes to the osmotic movement of fluid. The purpose of this study was to determine if albumin levels differed in Hispanics on dialysis with and without diabetes and if potential differences existed over time. Differences in diabetes incidence in Hispanics suggest albumin levels may be dissimilar. Albumin physiology is abundant in the literature; how and to what magnitude albumin levels are affected in patients with diabetes is unclear. This quantitative, retrospective cohort study employed ANOVA, Repeated Measures t tests, Spearman Correlation, and regression analysis to evaluate potential associations between the research variables. Data were extracted from CMS-2728 forms to amass the final cohort (N = 827). Differences in albumin levels at the first 2 intervals were observed (Baseline 1.29 -± 0.49 mg/dL, F = 2.28, p < .032; 3 months 0.47 -±0.41 mg/dL, F = 1.62, p < .004). Covariables (hypertension, peripheral vascular disease, and infections) were controlled for but showed inconclusive results. Lower serum albumin in Hispanic dialysis patients with diabetes provides the impetus for developing ethnic-specific albumin therapies, thus promoting positive social change.

The progression of End Stage Renal Disease (ESRD) among type II diabetics is preventable, yet complications continue to plague many. Reports show that 29.1 million people (9.3%) in the United States have diabetes, and 40% of those individuals develop ESRD. Four research questions explored the relationship between ESRD, health literacy, and healthcare. Data from 2010-2015 from the National Institute of Health (NIH) was quantitatively analyzed. The conceptual framework was the revised health service utilization theory. The target population included 3939 diverse males and females between the ages of 20-75 diagnosed with type II Diabetes. Results from Chi-square, cross-tabulation, binary, and multinomial logistic regression revealed that there is a statistically significant relationship between inadequate health literacy and ESRD (p= <0.05), inadequate health literacy and healthcare services (p= <0.05), and healthcare services and development of ESRD (p=<.001). Findings exposed significant demographic co-factor differences. Males developed ESRD more than females, and African American and Hispanic populations were almost 2 times more likely than Caucasians to develop ESRD. As participants age, odds for developing ESRD increase about 2-3 times. Both race and education were significant predictors of inadequate health literacy. African Americans and Hispanics were 3 times more likely to have inadequate health literacy than Caucasian participants. Lower education increased the odds of having inadequate health literacy approximately 7.6 times. Results show that Caucasian participants had higher education levels and private health insurance, whereas African Americans and Hispanics had lower education and no insurance or Medicaid. Implications from this research show that social determinants among vulnerable populations are impacting an individual's health literacy and ability to adequately manage their health. Evidence from this study generates social change through recognition that health literacy is fundamental when attempting to prevent chronic disease complications and promote positive health.