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Journal articles on the topic 'Chronic heart and renal failures'

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Author: Grafiati
Published: 11 March 2023

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1

El-Belbessi, Sami, Nachman Brautbar, Kenneth Anderson, Vito M. Campese, and Shaul G. Massry. "Effect of Chronic Renal Failure on Heart." American Journal of Nephrology 6, no. 5 (1986): 369–75. http://dx.doi.org/10.1159/000167193.

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2

Parker, J., F. Valle, and D. Cherney. "RENAL OXYGEN CONSUMPTION IN CHRONIC HEART FAILURE." Canadian Journal of Cardiology 34, no. 10 (October 2018): S92—S93. http://dx.doi.org/10.1016/j.cjca.2018.07.478.

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3

Haffner, S. M., K. K. Gruber, G. Aldrete, P. A. Morales, M. P. Stern, and K. R. Tuttle. "Increased lipoprotein(a) concentrations in chronic renal failure." Journal of the American Society of Nephrology 3, no. 5 (November 1992): 1156–62. http://dx.doi.org/10.1681/asn.v351156.

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Subjects with chronic renal failure have a greatly increased risk of coronary heart disease and dyslipidemia. Relatively few studies have examined the relationship of chronic renal failure to lipoprotein (Lp)(a) concentrations, an important risk factor for coronary heart disease. Diabetic subjects have been reported to have both increased Lp(a) concentrations and an increased risk of renal failure, thereby possibly confounding the Lp(a)-renal failure association. The association between Lp(a) and chronic renal failure in 359 control subjects and 111 subjects with renal failure was examined. Lp(a) (in milligrams per deciliter) was elevated in subjects with chronic renal failure, regardless of ethnicity (Mexican Americans, 19.8 +/- 2.7 versus 14.1 +/- 1.3; P = 0.03; non-Hispanic white patients, 24.9 +/- 3.0 versus 16.3 +/- 1.2; P = 0.006;). These differences persisted after adjustment for diabetes and ethnicity (P < 0.001). The type of treatment for chronic renal failure (diet, hemodialysis, or peritoneal dialysis) did not have an effect on Lp(a) concentrations. Lp(a) levels were not correlated with the level of creatinine in subjects with chronic renal failure. Thus, the elevation of Lp(a) levels in renal failure must occur early in renal failure, or alternatively, elevated Lp(a) levels may promote progression to chronic renal failure. These results indicate that Lp(a) concentrations are increased in chronic renal failure and may increase the risk for coronary heart disease in these subjects.
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4

Boran, Mediha, M. Kamil Göl, Erol Şener, Oğuz Taşdemir, and Kemal Bayazit. "Open Heart Surgery in Patients with Chronic Renal Failure." Asian Cardiovascular and Thoracic Annals 3, no. 3-4 (September 1995): 112–16. http://dx.doi.org/10.1177/021849239500300405.

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Coronary and valvular heart diseases are the main causes of mortality and morbidity among the long-term survivors of chronic renal failure. Despite the additional risk factors, open heart surgical procedures have recently been attempted with high rates of success in some patients with chronic renal failure. Forty-three patients with chronic renal failure that have undergone open heart surgery are included in this study. Ten of the patients were female and the mean age was 53.1 ± 11.2 (26 to 71). Twenty-five patients underwent aortocoronary bypass operations and 18 others underwent heart valve replacements. In this group of patients, 38 (88.3%) were in the compensated retention stage of chronic renal failure and 5 (11.7%) were in the end stage. The decompensated chronic renal failure patients were on regular hemodialysis and continued to receive hemodialysis in the preoperative and postoperative period. Sixteen patients of the compensated chronic renal failure group needed hemodialysis postoperatively. Early mortality rate was 7.8% (n = 3). Mean stay in the intensive care unit after the operation was 3.0 ± 3.3 days (2 to 22 days). In the long-term follow-up 3 patients underwent successful renal transplantations within 9 to 18 months after the cardiac operations. Two of these patients had valve replacements and 1 had concomitant valve replacement and coronary artery bypass grafting prior to renal transplantation. We conclude that coronary angiography, catheterization, myocardial revascularization, and valve replacements can be safely performed and should be considered if indicated in chronic renal failure patients.
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5

Voronkov, L. G., A. V. Liashenko, N. A. Tkach, and L. P. Paraschenyuk. "Chronic heart failure as multimorbid state." Ukrainian Journal of Cardiology 26, no. 4 (October 8, 2019): 90–101. http://dx.doi.org/10.31928/1608-635x-2019.4.90101.

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Regulatory, structural and functional disturbances of other organs and systems (kidney, hepar, vessels, skeletal muscles, brain etc) play the substantial role in CHF. These disturbances may be the conseguences of pre-existing states (hypertension, diabetes, hypo- or hyperthyreoidism etc) and from, other side, may reflect the progressive inherent changes in chronic heart failure (CHF) per se. In particular, currently relevant comorbidities in this syndrome are insulin resistance, diabetes mellitus, renal dysfunction, cognitive impairment, depression peripheral myopathy. Every of them demonstrate the close pathophysiologic interplay with CHF which results in clinical prognosis impairment and in decrease of life quality. Prevalence of renal dysfunction described in 39 % of patients with CHF in our research. Renal dysfunction connected with older age, high class of NYHA, diabetes mellitus, arterial hypertension, higher level of citrulline and uric acid in patients with CHF. Patients with iron deficiency characterized with high class of NYHA, low functionality and poor quality of life. In patients with iron deficiency noted high level of mortality and many critical clinical events. Prevalence of cognitive impairment described in 85 % of patients with CHF in our research. Cognitive dysfunction associated with older age, high class of NYHA, diabetes mellitus, arterial hypertension, bad life quality, high level of ceruloplasmin in patients with CHF. Taking to account above-mentioned comorbidities in quideline-recommended management of CHF and the use of additional therapeutic approaches targeted to its treatment represent the contemporary strategy of personalized treatment in this syndrome.
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6

Курлянская, Е. К. "Renal Denervation in Patients with Chronic Heart Failure." Кардиология в Беларуси, no. 4 (September 26, 2022): 456–68. http://dx.doi.org/10.34883/pi.2022.14.4.008.

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Цель. Проанализировать отдаленные результаты денервации почечных артерий у пациентов с хронической сердечной недостаточностью (ХСН).Материалы и методы. В исследование включен 61 пациент с ХСН III–IV ФК по NYHA, которому выполнена катетерная абляция симпатических нервов почечных артерий. До поступления в стационар и в клинике пациенты находились на оптимальной медикаментозной терапии в соответствии с рекомендациями и протоколами по ведению пациентов с ХСН. Оценка клинико-анамнестических, инструментально-диагностических и лабораторных параметров выполнялась до ДПА, а также через 6 и 12 месяцев после абляции. Респондерами ДПА считали пациентов с уменьшением КСО по данным ЭхоКГ на 15% и более относительно значений до выполнения ДПА. Через 12 месяцев после ДПА были сформированы 2 группы: группа 1 – респондеры ДПА (39 пациентов), группа 2 – нереспондеры ДПА (22 пациента). Номинальные данные представлены в виде абсолютной (n) и относительной частот (доля, выраженная в %), количественные данные – в виде медианы (Me) и межквартильного диапазона (LQ; UQ).Результаты. У пациентов с ХСН ФК III–IV положительный эхокардиографический ответ на ДПА сопровождался значимым увеличением ФВ ЛЖ (р=0,008), снижением ИЛС (р=0,035), среднего показателя продольной деформации миокарда ЛЖ (р=0,012), ДЛА (р=0,018), концентрации в крови NT-proBNP (р=0,017), тканевого ингибитора ММП (р=0,028) и СРБ (р=0,028), а также уменьшением суточного количества групповых ЖЭС (р=0,048). Независимо от эхокардиографического ответа на интервенционное лечение качество жизни и результаты теста 6-минутной ходьбы в течение 6 месяцев улучшились у всех пациентов, но через 12 месяцев у респондеров ДПА количество баллов по Миннесотскому опроснику было меньше (р=0,046), а пройденная за 6 минут дистанция – больше (р=0,048), чем у нереспондеров ДПА. Эхокардиографический эффект ДПА у пациентов с ХСН связан с исходным суточным количеством групповых желудочковых экстрасистол (р=0,048), концентрацией в крови ST2 (р=0,020) и ТИММП (р=0,020).Выводы. Катетерная ДПА у пациентов с ХСН ФК III–IV способствует улучшению внутрисердечной гемодинамики, снижению суточного количества ЖЭС и снижению уровня лабораторных маркеров, ассоциированных с фиброзом миокарда. Обратное ремоделирование ЛЖ в течение 12 месяцев после ДПА ассоциировано с суточным количеством желудочковых экстрасистол, концентрацией в крови ST2 и ТИММП до интервенционного вмешательства. Purpose. To analyze long-term results of renal denervation (RND) in patients with chronic heart failure.Materials and methods. The study enrolled 61 patients with chronic heart failure class III–IV according to NYHA who underwent catheter ablation of the sympathetic nerves of the renal arteries. Before admission and during their in-patient stay, the patients were on optimal drug therapy in line with the recommendations and protocols for CHF management. Evaluation of clinical and anamnestic, instrumental, diagnostic and laboratory parameters was performed before RND, as well as 6 and 12 months after ablation. The patients with 15% or more reduction of ESV according to Echo compared with the parameters before cardiac output were considered as responders. Two groups were formed 12 months after RND: group 1 – RND responders (39 patients), group 2 – nonresponders (22 patients). Nominal data are presented as absolute (n) and relative frequencies (fraction in percentage terms), quantitative data as median (Me) and interquartile range (LQ; UQ).Results. The positive echocardiographic response to RND in patients with CHF class III–IV was accompanied by a significant increase in LV EF (p=0.008), decrease in WMSI (p=0.035), mean LV myocardial longitudinal strain (p=0.012), pulmonary arterial pressure (p=0.018), NT-proBNP concentration (p=0.017), TIMP (p=0.028) and CRP (p=0.028), and a decrease in daily group VPB (p=0.048). Regardless of the echocardiographic response to interventional treatment, quality of life and 6-minute walk test scores improved at 6 months in all patients, but at 12 months, responders to the RND had a lower Minnesota Questionnaire score (p=0.046) and a greater distance walked in 6 minutes (p=0.048) than nonresponders to the RND. The echocardiographic effect of RND in patients with CHF was associated with baseline daily number of group ventricular premature beats (p=0.048), ST2 concentration in blood (p=0.020), and TIMP (p=0.020).Conclusions. Catheter RND in patients with CHF class III–IV improves intracardiac hemodynamics, reduces the daily number of VPB and decreases the level of laboratory markers associated with myocardial fibrosis. Reversible LV remodeling within 12 months after RND was associated with the daily number of ventricular premature beats, ST2 concentration in blood, and TIMP prior to interventional treatment.
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7

van der Meer, P., and D. J. van Veldhuisen. "Anaemia and renal dysfunction in chronic heart failure." Heart 95, no. 21 (October 14, 2009): 1808–12. http://dx.doi.org/10.1136/hrt.2008.151258.

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8

Waldum, Bård, Arne S. Westheim, Leiv Sandvik, Berit Flønæs, Morten Grundtvig, Lars Gullestad, Torstein Hole, and Ingrid Os. "Renal Function in Outpatients With Chronic Heart Failure." Journal of Cardiac Failure 16, no. 5 (May 2010): 374–80. http://dx.doi.org/10.1016/j.cardfail.2010.01.001.

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9

Omar, Sabry, and Ahmed Zedan. "Cardiorenal syndrome." Southwest Respiratory and Critical Care Chronicles 1, no. 1 (January 30, 2013): 11. http://dx.doi.org/10.12746/swrccc.v1i1.24.

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Cardiovascular disease is the leading cause of death in patients with chronic kidney disease. Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcomes in patients with cardiovascular disorders. Renal impairment with any degree of albuminuria has been increasingly recognized as an independent risk factor for cardiovascular events and heart failure hospitalizations, while chronic heart failure may cause chronic kidney disease. The bidirectional nature of these disorders contributes to the complexity and the composite definitions of cardiorenal syndromes. However, the most important clinical trials in heart failure tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in heart failure are not known, and several pathways could contribute to the ‘‘vicious heart/kidney circle.’’ Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin aldosterone pathway, and arginine-vasopressin release. These mechanisms cause fluid and sodium retention, peripheral vasoconstriction, and volume overload. Therapy to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardiorenal syndrome.
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10

Unic-Stojanovic, Dragana, Miroslav Milicic, Petar Vukovic, Srdjan Babic, and Miomir Jovic. "Heart surgery in patients on chronic dialysis." Medical review 66, no. 1-2 (2013): 64–69. http://dx.doi.org/10.2298/mpns1302064u.

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Introduction. Patients on dialysis for end-stage renal failure are subjected to cardiac surgery with increasing frequency. End-stage renal failure is known to be an important risk factor for complications of cardiac operations performed with cardiopulmonary bypass. The aim of this study was to determine the impact of preoperative clinical status and operative variables on perioperative morbidity and mortality in hemodialysis dependent patients subjected to a cardiac surgery. Material and Methods. The following operative variables were examined: urgency, type and duration of surgery and duration of extracorporeal circulation. The study is a retrospective analysis of consecutive patients with end-stage renal failure dependent on maintenance hemodialysis who underwent cardiac surgery during four years. Results. The study included 46 patients. Operations performed included isolated coronary artery bypass grafting (CABG, n = 24), valve surgery alone (n = 6), and combined valve surgery or coronary artery bypass grafting and valve surgery (n = 16). The perioperative mortality rate was 13% with four fatal outcomes in patients who had undergone combined cardiac surgery. We found age > 70 years, preoperative New York Heart Association class IV, preoperative anemia, combined surgery and emergent surgery to be associated with a higher relative risk for perioperative death. Conclusion. Patients on dialysis have an increased morbidity and mortality following cardiac surgery; however, we believe that end-stage renal failure should not be regarded as a contraindication to cardiac surgery or cardiopulmonary bypass.
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11

Diaconu, Camelia C. "Chronic heart failure and chronic kidney disease." Romanian Medical Journal 63, no. 1 (March 31, 2016): 35–38. http://dx.doi.org/10.37897/rmj.2016.1.8.

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Introduction. Renal dysfunction is one of the most common comorbidity of heart failure and may complicate its evolution. Aim. To analyze the frequency of chronic kidney disease in patients with decompensated chronic heart failure hospitalized in the Internal Medicine Clinic of the Clinical Emergency Hospital of Bucharest over a period of one year. Material and method. We retrospectively analyzed the data registered in hospital’s database between June 1st, 2014 – June 1st, 2015. Between 01.06.2014-01.06.2015, 609 patients with the diagnosis of chronic heart failure were hospitalized. Of these, 109 (17.89%) were diagnosed with chronic kidney disease (CKD) and represented our group of study. Distribution of chronic kidney disease in patients with chronic heart failure, depending on the stage of chronic kidney disease, was: no patient with stage 1, 26.61% with stage 2, 33.94% with stage 3A, 28.44% in stage 3B, 8.26% with stage 4 and 2.75% with stage 5. Distribution of NYHA class in the study group was: 20.18% NYHA class II, 40.37% NYHA class III, 39, 45% NYHA IV. 37 of the 109 patients (33.94%) with chronic heart failure and CKD had type 2 diabetes. Other important comorbidities in the group of study have been hypertension and anemia. Conclusions. Most patients with chronic heart failure admitted to our clinic were men, had heart failure NYHA class III and presented CKD class 3. A significant proportion of patients had risk factors for both BRC and heart failure: essential hypertension, diabetes and anemia.
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12

Pliquett, Rainer U. "Cardiorenal Syndrome: An Updated Classification Based on Clinical Hallmarks." Journal of Clinical Medicine 11, no. 10 (May 20, 2022): 2896. http://dx.doi.org/10.3390/jcm11102896.

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Cardiorenal syndrome (CRS) is defined as progressive, combined cardiac and renal dysfunction. In this mini review, a historical note on CRS is presented, the pathomechanisms and clinical hallmarks of both chronic heart failure and chronic kidney disease are discussed, and an updated classification of CRS is proposed. The current consensus classification relies on the assumed etiology and the course of the disease, i.e., acute or chronic CRS. Five types are described: type-I CRS presenting as acute cardiac failure leading to acute renal failure; type-II CRS presenting as chronic cardiac failure leading to chronic renal failure; type-III CRS presenting as acute kidney injury aggravating heart failure; type-IV CRS presenting as chronic kidney failure aggravating heart failure; and type-V CRS presenting as concurrent, chronic cardiac and renal failure. For an updated classification, information on the presence or absence of valvular heart disease and on the presence of hyper- or hypovolemia is added. Thus, CRS is specified as “acute” (type-I, type-III or type-V CRS) or “chronic” (type-II, type-IV or type-V) CRS, as “valvular” or “nonvalvular” CRS, and as “hyper-” or “hypovolemia-associated” CRS if euvolemia is absent. To enable the use of this updated classification, validation studies are mandated.
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13

Nasybullina, A. A., O. V. Bulashova, V. M. Gazizyanova, M. I. Malkova, E. E. Mustafin, and G. R. Khusnutdinova. "Markers of inflammation in patients with heart failure in association with chronic kidney disease." Kazan medical journal 97, no. 6 (December 15, 2016): 881–87. http://dx.doi.org/10.17750/kmj2016-881.

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Aim. Evaluation of markers of systemic inflammation in patients with chronic heart failure in comorbidity with chronic kidney disease.Methods. The study included 188 patients with heart failure and kidney disease including control group (76 patients) with heart failure with preserved renal function aged 38 to 83 years (mean age 66.8±10.1 years), with the duration of heart failure of about 8 years. Quantitative measurement of C-reactive protein and proteins of blood serum and daily excretion of protein with urine were performed.Results. Glomerular filtration rate in patients without renal pathology was 71.1±11.7 ml/min/1.73 m2, and in the group with heart failure associated with kidney dysfunction it was 51.5±19.1 ml/min/1.73 m2. C-reactive protein, γ-globulin, albumin and total serum protein in patients with chronic kidney disease differed from those in patients with heart failure without kidney damage.Conclusion. C-reactive protein and γ-globulin in the serum significantly increase in patients with heart failure and chronic kidney disease and can be used as markers of cardiac as well as renal events.
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14

Yaqoob, Naveed, Muhammad Ahmad Raza Butt, Faiza Nafees Khan, Muhammad Ilyas, Muhammad Haidar Zaman, and Fahad Khalid. "Prevalance of Renal and Electrolyte Disorders in Chronic Heart Failure Patients." Pakistan Journal of Medical and Health Sciences 16, no. 9 (September 30, 2022): 658–60. http://dx.doi.org/10.53350/pjmhs22169658.

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Objective: To determine the prevalence of renal and electrolyte disorders in patients presented with chronic heart failure. Study Design: Cross sectional/Observational Place & Duration of Study: Data was collected from the different tertiary care hospitals of Pakistan, including Rawal Institute of Health Sciences, Islamabad and Department of Cardiology, Rashid Latif Medical College, Lahore During the period from January, 2022 to June, 2022. Methods: Total 210 patients of both genders with ages 25 to 75 years presented with chronic heart failure were analyzed. Patients detailed demographic were recorded after taking written consent. Blood samples of all the patients were collected to examine the serum electrolyte and serum creatinine. Prevalence of renal dysfunction and electrolyte disorders were recorded.ae Results: One hundred and fifty two (72.38%) patients were males while 58 (27.62%) patients were females. 85 (40.48%) patients were ages 25 to 50 years and 125 (59.52%) were ages between 51 to 75 years. Renal dysfunction was found in 61 (29.05%) patients, 56 (26.67%) patients had hypokalemia and hyponatremia was found in 59 (28.10%) patients. Conclusion: The incidence of renal dysfunction and electrolyte disorders in patients with chronic heart failure was high. Patients with ages above 50 years had high rate of renal dysfunction, hypokalemia and hyponatremia. Keywords: Chronic Heart Failure, Renal Dysfunction, Hyponatremia, Hypokalemia
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15

Артифексова, A. Artifeksova, Зубеева, G. Zubeeva, Харламова, O. Kharlamova, Суслова, et al. "Structural and morphological aspects of heart failure in chronic renal failure." Journal of New Medical Technologies. eJournal 8, no. 1 (November 5, 2014): 0. http://dx.doi.org/10.12737/7377.

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The purpose of the study was to identify the structural and morphological characteristics of myocardium in patients with chronic renal insufficiency with clinical signs of heart failure and coronary heart disease. Surveyed 141 patients with chronic renal insufficiency 0, I, II, III stages. An eсhocardioscopiс study were held on the Vivid S6, General Electric, United States, which was of course-diastolic left ventricular cavity transverse dimension, thickness of the ventricular septal and posterior wall of the left ventricle, the length of the left ventricle in diastolic phase. Calculation is made of left ventricular myocardial mass index, index of the sphericity of the eccentricity. Determined the content of creatinine, CK-MB, troponin I and myoglobin. Morphological study on myocardial autopsic material 46 deaths of patients with chronic renal failure of varying degrees of severity. The Results. Initial displays remodeling appear in patients in the early stages of the disease. The loading phase of the disease is growing concentric hypertrophy of the left ventricle, there has been a progression of remodeling in increasing the frequency of occurrence of spherisation the cavity of the left ventricle. Dialysis reduces the severity of concentric hypertrophy of the left ventricle. As a result of the microscopic study of the heart was installed correlative dependence of structural changes in the myocardium of symptoms of chronic kidney failure.
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16

Demikhova, Nadiia, Yuliia Smiianova, and Irina Vilkhova. "FP106CORRECTION OF CHRONIC HEART FAILURE IN RENAL HYPERTENSIVE PATIENTS." Nephrology Dialysis Transplantation 30, suppl_3 (May 2015): iii101. http://dx.doi.org/10.1093/ndt/gfv169.30.

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17

Rostand, Stephen G., and Edwin A. Rutsky. "Ischemic Heart Disease in Chronic Renal Failure: Management Considerations." Seminars in Dialysis 2, no. 2 (October 1, 2007): 98–101. http://dx.doi.org/10.1111/j.1525-139x.1989.tb00566.x.

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18

Sezgin, A., Ş. Mercan, A. Taşdelen, H. Atalay, and S. Aşlamacı. "Open Heart Surgery in Patients With Chronic Renal Failure." Transplantation Proceedings 30, no. 3 (May 1998): 784–85. http://dx.doi.org/10.1016/s0041-1345(98)00047-5.

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19

Vergaro, Giuseppe, and Massimo Iacoviello. "Is there a “renal paradox” in chronic heart failure?" International Journal of Cardiology 267 (September 2018): 139–40. http://dx.doi.org/10.1016/j.ijcard.2018.05.081.

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20

Maxwell, A. Peter, Hean Y. Ong, and D. Paul Nicholls. "Influence of progressive renal dysfunction in chronic heart failure." European Journal of Heart Failure 4, no. 2 (March 2002): 125–30. http://dx.doi.org/10.1016/s1388-9842(01)00238-0.

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21

Dimkovic, Nada. "Cardiovascular diseases in patients with chronic renal diseases." Srpski arhiv za celokupno lekarstvo 136, Suppl. 2 (2008): 135–41. http://dx.doi.org/10.2298/sarh08s2135d.

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The risk of cardiovascular disease in patients with chronic renal disease appears to be far greater than in the general population and the risk of cardiovascular death is much higher than the risk of eventually requiring renal replacement therapy. Heart failure is important finding and it is evident even before the initiation of dialysis; the frequency of heart failure is 10 to 30 times higher in patients on dialysis than in the general population. Left ventricular hypertrophy has incidence of nearly 75-80% and is closely related to heart failure, ventricular arrhythmias, fatal myocardial infarction, aortic root dilatation and cerebrovascular event. Ischaemic heart disease is usually the consequence of coronary artery disease, but 27% of haemodialysis patients may have symptoms without atherosclerotic changes in coronary arteries. Silent myocardial ischemia is more frequent in dialysis population. Hypertension is present in 80-85% of patients and its prevalence is linearly related to glomerular filtration rate. Patients with end-stage renal disease are more likely to have an increase in pulse pressure and isolated systolic hypertension and they may not demonstrate the normal nocturnal decline in blood pressure. Patients on dialysis are prone to calcification of media and intima due to disbalance of promoters and inhibitors of calcification process. Now, there are no valid data about the privilege of one dialysis method over another in cardiovascular morbidity and mortality. Numerous traditional and non-traditional risk factors urge for preventive measures for cardiovascular diseases in patients with chronic renal diseases.
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22

SILVERBERG, DONALD S., DOV WEXLER, ADRIAN IAINA, and DORON SCHWARTZ. "Anemia, chronic renal disease and chronic heart failure: the cardiorenal anemia syndrome." Transfusion Alternatives in Transfusion Medicine 10, no. 4 (December 2008): 189–96. http://dx.doi.org/10.1111/j.1778-428x.2008.00120.x.

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23

Héliès-Toussaint, Cécile, Christophe Moinard, Carole Rasmusen, Imène Tabbi-Anneni, Luc Cynober, and Alain Grynberg. "Aortic banding in rat as a model to investigate malnutrition associated with heart failure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 5 (May 2005): R1325—R1331. http://dx.doi.org/10.1152/ajpregu.00320.2004.

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Heart failure is a severe pathology, which has displayed a dramatic increase in the occurrence of patients with chronic heart disease in developed countries, as a result of increases in the population's average age and in survival time. This pathology is associated with severe malnutrition, which worsens the prognosis. Although the cachexia associated with chronic heart failure is a well-known complication, there is no reference animal model of malnutrition related to heart failure. This study was designed to evaluate the nutritional status of rats in a model of loss of cardiac function obtained by ascending aortic banding. Cardiac overload led to the development of cardiac hypertrophy, which decompensates to heart failure, with increased brain natriuretic peptide levels. The rats displayed hepatic dysfunction and an associated renal hypotrophy and renal failure, evidenced by the alteration in renal function markers such as citrullinemia, creatininemia, and uremia. Malnutrition has been evidenced by the alteration of protein and amino acid metabolism. A muscular atrophy with decreased protein content and increased amino acid concentrations in both plasma and muscle was observed. These rats with heart failure displayed a multiorgan failure and malnutrition, which reflected the clinical situation of human chronic heart failure.
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24

Ripley, Toni L. "Valsartan in Chronic Heart Failure." Annals of Pharmacotherapy 39, no. 3 (March 2005): 460–69. http://dx.doi.org/10.1345/aph.1e327.

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OBJECTIVE: To evaluate the evidence for valsartan in the treatment of heart failure and determine its need for formulary inclusion. DATA SOURCES: OVID and PubMed databases were searched (1983–June 2004) using the key words angiotensin-receptor blocker, heart failure, valsartan, Diovan, and angiotensin-converting enzyme inhibitor. Only English-language literature was selected. STUDY SELECTION AND DATA EXTRACTION: Pharmacology and pharmacokinetic evaluations for valsartan were selected. Prospective, randomized clinical trials investigating the use of valsartan and other angiotensin-receptor blockers (ARBs) in chronic heart failure were evaluated. DATA SYNTHESIS: Valsartan, a selective antagonist for angiotensin receptor subtype 1, is the first ARB to be approved for use in chronic heart failure. Clinical trial data support valsartan as an alternative to angiotensin-converting enzyme (ACE) inhibitors in ACE inhibitor—intolerant patients with chronic heart failure. Valsartan is generally well tolerated, with renal impairment, elevated serum creatinine and potassium levels, and dizziness being the most common adverse effects; consequently, patients experiencing those adverse events while taking ACE inhibitors are likely to experience them with valsartan. Although further study is needed, differences in effectiveness among races may exist with use of valsartan; however, at this time, valsartan is recommended as an alternative to ACE inhibitors regardless of race. Candesartan and losartan have been studied in similar settings. Candesartan's data support its use in heart failure; however, losartan's data have been less consistent. CONCLUSIONS: Valsartan is a safe and effective alternative for heart failure patients intolerant of ACE inhibitors. Valsartan has not been shown to be safe and effective when used in combination with ACE inhibitors.
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25

Koning, Anne M., Wouter C. Meijers, Isidor Minović, Adrian Post, Martin Feelisch, Andreas Pasch, Henri G. D. Leuvenink, Rudolf A. de Boer, Stephan J. L. Bakker, and Harry van Goor. "The fate of sulfate in chronic heart failure." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 3 (March 1, 2017): H415—H421. http://dx.doi.org/10.1152/ajpheart.00645.2016.

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New leads to advance our understanding of heart failure (HF) pathophysiology are urgently needed. Previous studies have linked urinary sulfate excretion to a favorable cardiovascular risk profile. Sulfate is not only the end product of hydrogen sulfide metabolism but is also directly involved in various (patho)physiological processes, provoking scientific interest in its renal handling. This study investigates sulfate clearance in chronic HF (CHF) patients and healthy individuals and considers its relationship with disease outcome. Parameters related to renal sulfate handling were determined in and compared between 96 previously characterized CHF patients and sex-matched healthy individuals. Among patients, sulfate clearance was analyzed for associations with clinical and outcome parameters. In CHF patients, plasma sulfate concentrations are significantly higher, whereas 24-h urinary excretion, fractional excretion, and clearance of sulfate are significantly lower, compared with healthy individuals. Among patients, sulfate clearance is independently associated with diuretics use, creatinine clearance and 24-h urinary sodium excretion. Sulfate clearance is associated with favorable disease outcome [hazard ratio per SD increase 0.38 (95% confidence interval 0.23–0.63), P < 0.001]. Although significance was lost after adjustment for creatinine clearance, the decrease of sulfate clearance in patients is independent of this parameter, indicating that sulfate clearance is not merely a reflection of renal function. This exploratory study reveals aberrant sulfate clearance as a potential contributor to CHF pathophysiology, with reduced levels in patients and a positive association with favorable disease outcome. Further research is needed to unravel the nature of its involvement and to determine its potential as a biomarker and target for therapy. NEW & NOTEWORTHY Sulfate clearance is decreased in chronic heart failure patients compared with healthy individuals. Among patients, sulfate clearance is positively associated with favorable disease outcome, i.e., a decreased rehospitalization rate and increased patient survival. Hence, decreased sulfate clearance may be involved in the pathophysiology of heart failure.
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Gilbert, Cameron, David Z. I. Cherney, Andrea B. Parker, Susanna Mak, John S. Floras, Abdul Al-Hesayen, and John D. Parker. "Hemodynamic and neurochemical determinates of renal function in chronic heart failure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 310, no. 2 (January 15, 2016): R167—R175. http://dx.doi.org/10.1152/ajpregu.00190.2015.

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Abnormal renal function is common in acute and chronic congestive heart failure (CHF) and is related to the severity of congestion. However, treatment of congestion often leads to worsening renal function. Our objective was to explore basal determinants of renal function and their response to hemodynamic interventions. Thirty-seven patients without CHF and 59 patients with chronic CHF (ejection fraction; 23 ± 8%) underwent right heart catheterization, measurements of glomerular filtration rate (GFR; inulin) and renal plasma flow (RPF; para-aminohippurate), and radiotracer estimates of renal sympathetic activity. A subset (26 without, 36 with CHF) underwent acute pharmacological intervention with dobutamine or nitroprusside. We explored the relationship between baseline and drug-induced hemodynamic changes and changes in renal function. In CHF, there was an inverse relationship among right atrial mean pressure (RAM) pressure, RPF, and GFR. By contrast, mean arterial pressure (MAP), cardiac index (CI), and measures of renal sympathetic activity were not significant predictors. In those with CHF there was also an inverse relationship among the drug-induced changes in RAM as well as pulmonary artery mean pressure and the change in GFR. Changes in MAP and CI did not predict the change in GFR in those with CHF. Baseline values and changes in RAM pressure did not correlate with GFR in those without CHF. In the CHF group there was a positive correlation between RAM pressure and renal sympathetic activity. There was also an inverse relationship among RAM pressure, GFR, and RPF in patients with chronic CHF. The observation that acute reductions in RAM pressure is associated with an increase in GFR in patients with CHF has important clinical implications.
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Egers, Max, and Marijane Hynes. "Sodium-glucose co-transporter 2 inhibitors in 2022: mechanisms of cardiorenal benefit." Journal of Kidney Care 7, no. 5 (September 2, 2022): 216–24. http://dx.doi.org/10.12968/jokc.2022.7.5.216.

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The use of sodium-glucose co-transporter 2 (SGLT2) inhibitors has evolved over the past decade, from their initial indication as an adjunctive oral medication to treat hyperglycaemia in diabetics, to becoming part of guideline-directed therapy for the treatment of chronic kidney disease, heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. This transition was driven by data from large cardiovascular and renal outcome trials, which repeatedly demonstrated that SGLT2 inhibitors improve important endpoints in chronic kidney disease and heart failure. In chronic kidney disease, SGLT2 inhibition reduces decline in glomerular filtration rate, risk of progression to end-stage renal disease and death from renal causes. With respect to their use in heart failure, SGLT2 inhibitors decrease risk of major adverse cardiac events, hospitalisation for heart failure and death from cardiovascular causes. While the benefits of these medications have been demonstrated, the mechanisms by which they are conferred are less clear. Extensive investigation into potential mechanisms of benefits has been pursued internationally and current hypotheses include increased natriuresis and osmotic diuresis, improved glomerular haemodynamic, reduced body mass and reduced adipose tissue mediated inflammation, in addition to others. This review discusses the physiology underlying the therapeutic benefit of SGLT2 inhibition in chronic kidney disease and heart failure.
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Szlagor, Magdalena, Jill Dybiec, Ewelina Młynarska, Jacek Rysz, and Beata Franczyk. "Chronic Kidney Disease as a Comorbidity in Heart Failure." International Journal of Molecular Sciences 24, no. 3 (February 3, 2023): 2988. http://dx.doi.org/10.3390/ijms24032988.

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Heart failure (HF) is one of the greatest problems in healthcare and it often coexists with declining renal function. The pathophysiology between the heart and the kidneys is bidirectional. Common mechanisms leading to the dysfunction of these organs result in a vicious cycle of cardiorenal deterioration. It is also associated with difficulties in the treatment of aggravating HF and chronic kidney disease (CKD) and, as a consequence, recurrent hospitalizations and death. As the worsening of renal function has an undeniably negative impact on the outcomes in patients with HF, searching for new treatment strategies and identification of biomarkers is necessary. This review is focused on the pathomechanisms in chronic kidney disease in patients with HF and therapeutic strategies for co-existing CKD and HF.
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29

Shigehara, Rihiro, Marohito Murakami, Takashi Araki, Hideyo Oguchi, Kaori Kanbe, and Suzuka Koike. "Tolvaptan therapy for chronic renal failure in a patient with chronic ischemic heart failure." Nihon Toseki Igakkai Zasshi 47, no. 11 (2014): 691–96. http://dx.doi.org/10.4009/jsdt.47.691.

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30

Kamilova, Umida, Charos Abdullaeva, Gulnoza Zakirova, Dilyafruz Masharipova, and Dilnoza Tagaeva. "Assessment of Kidney Dysfunction in Patients with Chronic Heart Failure." Open Access Macedonian Journal of Medical Sciences 10, B (September 10, 2022): 2093–97. http://dx.doi.org/10.3889/oamjms.2022.10241.

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BACKGROUND: Heart failure and kidney disease share common pathophysiological pathways which can lead to mutual dysfunction, known as cardiorenal syndrome. The formation of cardiorenal syndrome in patients with chronic heart failure (CHF) is a natural manifestation of a functionally interconnected process at the organ level. Renal dysfunction is a common and independent factor in the progression of the disease, a high incidence of cardiovascular events, and death in the population. AIM: The aim of the study of the relationship between kidney dysfunction and the clinical course of the disease, quality of life, and indicators of the left ventricular systolic function in patients with CHF. MATERIALS AND METHODS: The study involved 150 patients with CHF I–III functional class according to the New York Heart Association. Exercise tolerance (6 min walk test) was assessed, the clinical condition was assessed using the clinical assessment scale, and the quality of life of patients with CHF (QoL) was assessed according to the Minnesota QOL questionnaire. An assessment of the functional state of the kidneys was carried out: The level of serum creatinine was determined; glomerular filtration rate (GFR) was calculated using the calculation formulas CKD-EPI. The assessment of renal blood flow was carried out using the ultrasound apparatus “SONOACEX6” (Korea). The structural and functional state of the myocardium and the process of left ventricle (LV) remodeling were assessed using the “MEDISON ACCUVIX V20” echocardiograph (Korea), using a 3.25 MHz transducer in standard echocardiographic positions, by the transthoracic method in accordance with the recommendations of the American Association of Echocardiography. RESULTS: The results of the study of physical performance according to 6 min walk test in patients of Group I with CHF GFR >60 ml/min/1.73 m2 were 363.59 ± 7.6 m, respectively. The decrease in the distance traveled according to the 6 min walk test data in Group II of patients with eGFR ≤60 ml/min/1.73 m2, exercise tolerance was more pronounced than in patients of Group I and this figure was 248.7 ± 11.0 m, which was 46.2% lower than the results of Group I of the study (p < 0.001). Analysis of the parameters of clinical manifestations according to the data of the clinical assessment scale showed that in patients of Group I, the total score was 5.5 ± 0.13 points. In CHF patients with renal dysfunction, changes were also noted at the level of the lobar and segmental renal arteries, characterized by a significant increase in pulsatility index and resistance index, there was a decrease in speed indicators during diastole, systole, and the average blood flow velocity. Further analysis of the parameters of LV systolic function ejection fraction (EF), as well as fractional shortening of the LV in systole (Fs%), showed that in Group II, these indicators had significant differences with Group I. There was a significant difference in EF by 10.5% and 25.4% and Fs% by 11.2% (p < 0.001). CONCLUSION: In CHF patients with impaired renal function, changes in renal blood flow were characterized by a significant increase in pulsatile and resistive indices, a decrease in the rate of renal blood flow at the level of the lobar and segmental renal arteries.
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31

Kamilova, U. K., and I. T. Alikulov. "KIDNEY DYSFUNCTION EVALUATION IN CHRONIC HEART FAILURE PATIENTS." Cardiovascular Therapy and Prevention 13, no. 2 (April 20, 2014): 51–54. http://dx.doi.org/10.15829/1728-8800-2014-2-51-54.

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Aim. To study the signs of kidney dysfunction in chronic heart failure (CHF).Material and methods. We included 96 patients with postinfarction cardiosclerosis and CHF with the age of 40–60 years. Patients were divided into two groups by functional class (FC) of CHF according to NYHA. In all patients the levels of serum creatinine and MDRD glomerular filtration rate (GFR), urine alanine transferase, aspartat transferase, alkaline phosphatase and cholinaestherase by spectrophotometric method were measured.Results. In 33,3% of patients with II FC NYHA and in 66,67% with III FC NYHA we found GFR less than 60 ml/min/1,73 sq.m. Investigation of fermenturia levels in those according to renal functioning showed more prevalent increase of urine enzymes in lower GFR, in whom the patients with III FC NYHA consisted 66,67%. The level of ALT was 39% (p<0,01) higher and AP 35% (p<0,001) higher comparing to subjects without renal dysfunction.Conclusion. In patients with chronic heart failure as the diseases progresses there is kidney dysfunction developing with the decrease of GFR, increase of resdual nitrogen and enzimes in urine. Enzyme levels testing in urine of CHF patients can be a part of diagnostic approach to kidney dysfunction diagnostic at earlier stages.
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32

Koepke, J. P., and G. F. DiBona. "Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders." American Journal of Physiology-Renal Physiology 252, no. 5 (May 1, 1987): F865—F871. http://dx.doi.org/10.1152/ajprenal.1987.252.5.f865.

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Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.
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33

Bereda, Gudisa. "Pathophysiology and Management Chronic Heart Failure." South Asian Research Journal of Biology and Applied Biosciences 4, no. 2 (May 6, 2022): 26–36. http://dx.doi.org/10.36346/sarjbab.2022.v04i02.001.

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Chronic heart failure refers to a clinical state of systemic and pulmonary congestion resulting from inability of the heart to pump as much blood as required for the adequate metabolism of the body. The commonest causes of heart failure are coronary artery disease, hypertension and diabetes, however, hypertension and diabetes have been found to be stronger risk factors in elderly women and coronary artery disease and smoking are stronger risk factors in elderly men. Pathophysiologically, heart failure is either an inadequate cardiac output for the organism’s metabolic demands or an adequate cardiac output that is due to neurohormonal compensation, which means the inability of the heart to supply blood to the tissues according to their needs without additional strain. The pharmacological treatment of chronic heart failure with reduced ejection fraction is now based on four classes of drugs that have been proven to reduce mortality among heart failure patients such as angiotensinogen converting enzyme inhibitors or angiotensin II receptor blockers, beta-blockers, aldosterone antagonists and sodium-glucose co-transporter 2 inhibitors. Angiotensinogen converting enzyme inhibitors or angiotensin II receptor blocker therapy should be initiated at a low dose with very gradual up titration, monitoring renal function and serum potassium levels closely. Chronic heart failure treatment with direct inhibitors of aldosterone receptors brought about a significant improvement in terms of survival and hospitalizations.
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34

Margulies, K. B., D. M. Heublein, M. A. Perrella, and J. C. Burnett. "ANF-mediated renal cGMP generation in congestive heart failure." American Journal of Physiology-Renal Physiology 260, no. 4 (April 1, 1991): F562—F568. http://dx.doi.org/10.1152/ajprenal.1991.260.4.f562.

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Previous studies have demonstrated that the biological actions of atrial natriuretic factor (ANF) are mediated via increases in its intracellular second messenger guanosine 3',5'-cyclic monophosphate (cGMP). Because cGMP egresses rapidly from target cells after ANF binding to particulate guanylate cyclase-linked receptors, extracellular cGMP may be a useful biological marker for the action of ANF in vivo under pathophysiological conditions. The present studies tested the hypothesis that the avid sodium retention and renal ANF resistance characteristic of chronic congestive heart failure (CHF) are associated with attenuated renal cGMP responses to ANF. We assessed the natriuretic and cGMP responses to endogenous and exogenous ANF during the evolution of CHF produced by 6 days of rapid ventricular pacing in conscious dogs (n = 6). Simultaneous measurement of plasma and urinary cGMP concentrations allowed determination of the net renal generation of cGMP, an indicator of the renal contribution to total urinary cGMP excretion. In early CHF, increased sodium excretion and renal cGMP production were observed in association with increases in plasma ANF. Exogenous ANF administration (10 micrograms/kg iv) before CHF also produced parallel increases in sodium excretion and renal cGMP production. In more advanced CHF produced by 6 days of pacing, we observed avid sodium retention in association with reversal of earlier increases in renal cGMP production despite progressive increases in circulating ANF. Natriuretic and renal cGMP responses to exogenous ANF were similarly attenuated in chronic CHF. These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF.
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35

Efremova, E. V., A. M. Shutov, A. S. Podusov, and M. P. Markevich. "Biomarkers of myocardial and renal dysfunction in chronic heart failure." Nephrology and Dialysis 22, no. 2 (2020): 181–88. http://dx.doi.org/10.28996/2618-9801-2020-2-181-188.

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36

Böhm, Michael, Sebastian Ewen, and Felix Mahfoud. "Renal Denervation for Chronic Heart Failure: Background and Pathophysiological Rationale." Korean Circulation Journal 47, no. 1 (2017): 9. http://dx.doi.org/10.4070/kcj.2016.0231.

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37

Damman, Kevin, Serge Masson, Hans L. Hillege, Aldo P. Maggioni, Adriaan A. Voors, Cristina Opasich, Dirk J. van Veldhuisen, et al. "Clinical outcome of renal tubular damage in chronic heart failure†." European Heart Journal 32, no. 21 (June 11, 2011): 2705–12. http://dx.doi.org/10.1093/eurheartj/ehr190.

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38

Damman, Kevin, Paul R. Kalra, and Hans Hillege. "PATHOPHYSIOLOGICAL MECHANISMS CONTRIBUTING TO RENAL DYSFUNCTION IN CHRONIC HEART FAILURE." Journal of Renal Care 36 (May 2010): 18–26. http://dx.doi.org/10.1111/j.1755-6686.2010.00172.x.

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39

Abraham, William T., Tatiana Tsvetkova, Brian D. Lowes, Debra A. Ferguson, E. Michael Gilbert, and Michael R. Bristow. "Carvedilol improves renal hemodynamics in patients with chronic heart failure." Journal of Cardiac Failure 4, no. 3 (September 1998): 3. http://dx.doi.org/10.1016/s1071-9164(98)90008-2.

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40

Al-Hesayen, Abdul, and John D. Parker. "Renal handling of endothelin in patients with chronic heart failure." American Journal of Cardiology 95, no. 4 (February 2005): 532–34. http://dx.doi.org/10.1016/j.amjcard.2004.10.027.

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41

Damman, Kevin, Serge Masson, Hans L. Hillege, Adriaan A. Voors, Dirk J. van Veldhuisen, Patrick Rossignol, Gianni Proietti, et al. "Tubular Damage and Worsening Renal Function in Chronic Heart Failure." JACC: Heart Failure 1, no. 5 (October 2013): 417–24. http://dx.doi.org/10.1016/j.jchf.2013.05.007.

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42

Naafs, M. A. B., C. van der Hoek, S. van Duin, G. Koorevaar, W. Schopman, and J. Silberbusch. "Decreased renal clearance of digoxin in chronic congestive heart failure." European Journal of Clinical Pharmacology 28, no. 3 (May 1985): 249–52. http://dx.doi.org/10.1007/bf00543318.

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43

Silverberg, Donald, Dov Wexler, Miriam Blum, Doron Schwartz, and Adrian Iaina. "The association between congestive heart failure and chronic renal disease." Current Opinion in Nephrology and Hypertension 13, no. 2 (March 2004): 163–70. http://dx.doi.org/10.1097/00041552-200403000-00004.

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44

Löffler, Adrián Ignacio, Thomas P. Cappola, James Fang, Scott J. Hetzel, Andrew Kadlec, Brad Astor, and Nancy K. Sweitzer. "Effect of Renal Function on Prognosis in Chronic Heart Failure." American Journal of Cardiology 115, no. 1 (January 2015): 62–68. http://dx.doi.org/10.1016/j.amjcard.2014.09.055.

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45

Reddy KV, Charan. "Clinical significance of NT-proBNP levels in Chronic Kidney Disease Patients with or without Heart Failure: An Indian Perspective." Cardiology Research and Reports 3, no. 1 (March 16, 2021): 01–03. http://dx.doi.org/10.31579/2692-9759/012.

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Objective: N-terminal pro-brain natriuretic peptide (NT-proBNP) levels are extremely useful in detecting heart failure (HF). However, the effects of renal inadequacy on NT-proBNP levels in patients presenting with or without HF remains less clear. We sought to examine the correlation of NT-proBNP levels in all CKD patients and cut-off values of NT pro-BNP level for the diagnosis of HF in stable CKD patients as well as CKD patients who are on haemodialysis (HD). Material and Methods: The study comprises 141 CKD patients of both sexes who presented with or without dyspnea to casualty of Lilavati Hospital, Mumbai, India, were prospectively enrolled, and blood samples collected to estimate NT-proBNP level. Results: NT-proBNP cut-off level of 1850 pg/mL for stable CKD patients not on dialysis has a sensitivity of 95% and specificity of 80 %. NT-proBNP cut-off level of 8000pg/ml for CKD patients on HD has a sensitivity of 87 % and specificity of 79%. NT-proBNP cut-off level of 4200 pg/mL for all CKD patients has a sensitivity of 85% and specificity of 81%, for diagnosis of HF. Conclusion: The clinical use of NT-proBNP is a valuable tool for the evaluation of dyspneic patients with suspected HF, irrespective of renal function. We recommend the above NT-proBNP cut-off levels for diagnosing HF patients in the presence of impaired renal function. Evaluation of the correlation between NT-proBNP levels in CKD is important to identify and to design treatment modalities in order to reduce CVD .Therefore, NT-proBNP measurement can be a valuable tool for diagnosis and evaluation of dyspneic patients for early initiation of HF treatment.
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Rosansky, S. J., K. L. Johnson, C. Hutchinson, and S. Erdel. "Blood pressure changes during daytime sleep and comparison of daytime and nighttime sleep-related blood pressure changes in patients with chronic renal failure." Journal of the American Society of Nephrology 4, no. 5 (November 1993): 1172–77. http://dx.doi.org/10.1681/asn.v451172.

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Blood pressure has a diurnal pattern primarily related to activity and sleep. Chronic renal failure patients may lack the normal nocturnal decline in blood pressure during sleep. In 33 subjects (14 with normal renal function and 19 with renal dysfunction), the relationship between depth of daytime sleep, as determined by electroencephalographic sleep phase, and change in mean arterial blood pressure (MAP) and heart rate measured oscillometrically, was correlated. In 15 chronic renal failure patients, the effect of daytime and nighttime sleep on MAP and heart rate was compared. The percent change in night asleep versus day awake MAP and heart rate was measured (with Space Labs ambulatory blood pressure monitors) and compared with the percent change in daytime sleep-related MAP and heart rate measured during a daytime sleep electroencephalographic study. During daytime sleep, MAP changes are not significantly different in the normal versus renal dysfunction groups. In the 33 study subjects, MAP declines progressively from the upright position to Phase 3/4 sleep (118 +/- 3.6 to 106 +/- 3.6 mm Hg). The largest decline occurs between the upright to recumbent position, before sleep. Heart rate declines moving from the upright to recumbent position, 76 +/- 2.3 to 70 +/- 2.1 beats/min, but does not decline further with sleep. In 15 chronic renal failure patients, heart rate (10.8 +/- 2.8%; P < 0.05), but not MAP, declines during nighttime sleep. Both MAP (7.7 +/- 3.3%) and heart rate (5.4 +/- 1.9%) decline significantly during daytime sleep. The responses of MAP and heart rate to daytime and nighttime sleep were in opposite directions in 3 of 15 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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François, Karlien, Claudio Ronco, and Joanne M. Bargman. "Peritoneal Dialysis for Chronic Congestive Heart Failure." Blood Purification 40, no. 1 (2015): 45–52. http://dx.doi.org/10.1159/000430084.

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Maladaptive responses between a failing heart and the kidneys ultimately lead to permanent chronic kidney disease, referred to as cardiorenal syndrome type 2. In this narrative review, we discuss the pathophysiological pathways in the progression of cardiorenal failure and review the current evidence on peritoneal dialysis as a treatment strategy in cardiorenal syndrome type 2. A patient with heart failure can present with clinical symptoms related to venous congestion even in the absence of end-stage renal disease. Diuretics remain the cornerstone for the treatment of fluid overload related to heart failure. However, with chronic use, diuretic resistance can supervene. When medical therapy is no longer able to relieve congestive symptoms, ultrafiltration might be needed. Patients with heart failure tolerate well the gentle rate of fluid removal through peritoneal dialysis. Recent publications suggest a positive impact of starting peritoneal dialysis in patients with cardiorenal syndrome type 2 on the hospitalisation rate, functional status and quality of life.
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Putra, I. Gede Bagus Gita Pranata, Samuel Widodo, I. Wayan Wita, I. Made Bakta, and I. Wayan Sudarsa. "The Comparison of Lipid Profile in Heart Failure Patients with and without Acute Renal Dysfunction." Biomedical and Pharmacology Journal 15, no. 4 (December 20, 2022): 2323–29. http://dx.doi.org/10.13005/bpj/2571.

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The incidence of heart failure (particularly heart failure with reduced ejection fraction/HFREF) is increasing over time, especially in developing nations. Based on the most recent data from Riset Kesehatan Dasar 2020 (RISKESDAS/Baseline Health Research), heart failure has become the highest etiology of mortality for patients with heart disease in Bali. Moreover, in patients with chronic kidney disease that have already undergone hemodialysis, the incidence of heart failure is increasing to more than 80% of the population. The correlation between renal dysfunction and heart failure has been known extensively with the term “Cardiorenal syndrome”. However, there is a paucity of literature regarding the prevention of renal dysfunction in heart failure patients and the control of dyslipidemia risk factors for preventing renal dysfunction. Renal dysfunction is not only a cause of morbidity but also a risk factor for heart failure patients' mortality; therefore, prevention is essential for improving heart failure patients' prognosis. We conduct research to compare the lipid profiles of patients with acute renal dysfunction and those without acute renal dysfunction who have heart failure. Based on the results of the lipid profile, we enrolled 70 consecutive heart failure patients with dyslipidemia or non-dyslipidemia. The incidence of renal failure in the group with dyslipidemia is 84.2%. We found that acute renal dysfunction patients had a statistically significant (p<0.05) increase in dyslipidemia compared to non-renal dysfunction patients, particularly with high LDL levels. The association between statin therapy and a low incidence of acute renal failure in patients with heart failure was statistically significant (p<0.05), according to additional findings from our study.
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Kimak, Elzbieta, Marcin Dziedzic, Aleksandra Kimak, Kamila Stachyra, Andrzej Prystupa, and Janusz Solski. "Can chronic heart failure induce kidney function damage?" Current Issues in Pharmacy and Medical Sciences 29, no. 1 (April 1, 2016): 28–32. http://dx.doi.org/10.1515/cipms-2016-0007.

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Abstract Accelerated atherosclerosis and increased cardiovascular events have been extensively documented in patients with end stage chronic kidney disease. The aim of our work was to find evidence supporting the theory that chronic heart failure (CHF) induces renal function damage. In our work, lipids, apolipoprotein (apo)AI, NTproBNP, hsCRP, lipid hydroperoxide (LPO) and creatinine levels were determined in patients with CHF. A total of 37 patients who were diagnosed with CHF, as well as 15 healthy persons, were recruited for the study. The patients were placed into 2 groups: patients with NYHA class 2 and NYHA class 3. Using routine laboratory methods, NT-proBNP level, and lipids were measured by way of employing a Cobas Integra analyser, while the concentration of hs-CRP was measured by immunonephelometric methods. Moreover, serum LPO concentration was measured using Cayman’s Assay Kit (LPO). The statistical analysis of the obtained results was performed using the nonparametric Kruskal-Wallis test and Spearman’s correlation analysis. Our work demonstrated that the CHF patients had significantly decrease concentration of HDL cholesterol and apoAI, but increased NT-pro-BNP, hsCRP and LPO levels. In all CHF patients, a significant positive correlation between NT-proBNP concentration and creatinine levels, and a significant negative correlation between NT-proBNP concentration and apoAI levels, as well as between concentration of creatinine and apoAI levels, was shown. The study results suggest that variation in the concentration of NT-proBNP, LPO, hsCRP, apoAI, creatinine, in addition to chronic heart failure progression, gradually accompany the progress of chronic renal failure. What is more, the disorders may lead to the occurrence of cardiovascular events, consequently, to patient death.
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50

Totsune, Kazuhito, Kazuhiro Takahashi, Osamu Murakami, Fumitoshi Satoh, Masahiko Sone, and Toraichi Mouri. "Elevated Plasma C-Type Natriuretic Peptide Concentrations in Patients with Chronic Renal Failure." Clinical Science 87, no. 3 (September 1, 1994): 319–22. http://dx.doi.org/10.1042/cs0870319.

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1. C-type natriuretic peptide is a neuropeptide, which is also produced by the vascular endothelial cells. Plasma immunoreactive C-type natriuretic peptide concentrations in patients with various diseases have not yet been studied. 2. Plasma immunoreactive C-type natriuretic peptide concentrations were studied by radioimmunoassay in normal subjects, patients with congestive heart failure, non-dialysed patients with chronic renal failure and haemodialysis patients with chronic renal failure. The C-type natriuretic peptide levels were compared with the levels of atrial natriuretic peptide and brain natriuretic peptide. 3. Plasma immunoreactive C-type natriuretic peptide concentrations were greatly elevated in patients with chronic renal failure [non-dialysed, 13.0 ± 4.2 pmol/l (mean ± SEM), n = 9, P < 0.01) compared with normal subjects (4.4 ± 0.4 pmol/l, n = 26); haemodialysis, 16.1 ± 2.1 pmol/l, n = 13, P < 0.01], but not in patients with congestive heart failure (New York Heart Association Class II-IV, 3.0 ± 0.7 pmol/l, n = 11, P > 0.05). Plasma immunoreactive atrial natriuretic peptide and brain natriuretic peptide concentrations were elevated both in patients with congestive heart failure and in haemodialysis patients with chronic renal failure. 4. Reverse-phase high performance liquid chromatography showed that immunoreactive C-type natriuretic peptide in plasma from normal subjects and haemodialysis patients was eluted in the positions of C-type natriuretic peptide −22 and −53. 5. These findings suggest that C-type natriuretic peptide is a non-cardiac circulating hormone and participates in the cardiovascular regulation in a different manner from atrial natriuretic peptide and brain natriuretic peptide.
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