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Journal articles on the topic 'Kidney disease'

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Author: Grafiati

Published: 4 June 2021

Last updated: 4 March 2023

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1

Verma, Dr Amit Kumar. "Periodontal Disease with Diabetes or Diabetes Kidney Disease." International Journal of Trend in Scientific Research and Development Volume-3, Issue-1 (December 31, 2018): 1043–51. http://dx.doi.org/10.31142/ijtsrd19176.

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2

S, Memon. "Hyponatremia in Chronic Kidney Disease." Open Access Journal of Urology & Nephrology 7, no. 2 (April 4, 2022): 1–7. http://dx.doi.org/10.23880/oajun-16000202.

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Introduction: There is adequate literature written on hyponatremia, but not much seen in context of Chronic Kidney Disease (CKD). Patients become prone for this electrolyte derangement when they are afflicted with organ failure especially CKD. This vulnerability becomes even worse in ageing due to impaired sensitivity to fluid intake and often burdened with multiple comorbid. For the adequate management of hyponatremia, knowledge of volume status, age of patients and associated comorbid, and duration of hyponatremia are very important. Patients and Methods: This observational study was conducted in adult CKD admitted patients. Demographic information, history, and examination finding were noted. Then each patient underwent investigation i.e., serum sodium, urea, creatinine, spot urine sodium, chloride, potassium, urine and serum osmolality, random blood sugar and echocardiography and noted in questionnaire. CKD staging was done with the help of Modified of diet and Renal disease (MDRD) equation. Diagnosis/ Impression of patient and need of hypertonic saline (3%saline) were all noted along with final outcome whether sodium improved/unimproved, discharge/expired were noted in pre-formed questionnaire. Results: Analysis was done on 171 CKD patients with female to male ratio: 1.19/1 and mean age 55.8 ± 15.16. Hypertension was most prevalent comorbid. Hypovolemia was the most common volume status seen along with moderate hyponatremia and hypertonicity were frequently observed features. 23 out of 171 patients were symptomatic, 44(25.7%) had low Left Ventricular function. Mortality was noted at 9.4%. Conclusion: Overall outcome of patient remained satisfactory despite of presence of CKD and significant number of patients were severe hyponatremic. Predominant management for hyponatremia remained conservative along with treatment for primary disease. Symptomatic hyponatremia and low LV function were found to be contributing to bad outcomes while severity of hyponatremia did not influence badly.

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3

Parmar, Dr Jigar A., Anant G. Joshi, and Dr Manish Chakrabarti. "Dyslipidemia and Chronic Kidney Disease." International Journal of Scientific Research 3, no. 5 (June 1, 2012): 396–97. http://dx.doi.org/10.15373/22778179/may2014/123.

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4

Mal, Pooran, Muhammad Nadeem Ahsan, Mehwish Bukhari, and Abdul Manan Junejo. "CHRONIC KIDNEY DISEASE." Professional Medical Journal 25, no. 09 (September 9, 2018): 1380–85. http://dx.doi.org/10.29309/tpmj/18.4360.

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5

Bollenbecker, Seth, Brian Czaya, Orlando M. Gutiérrez, and Stefanie Krick. "Lung-kidney interactions and their role in chronic kidney disease-associated pulmonary diseases." American Journal of Physiology-Lung Cellular and Molecular Physiology 322, no. 5 (May 1, 2022): L625—L640. http://dx.doi.org/10.1152/ajplung.00152.2021.

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Chronic illnesses rarely present in a vacuum, devoid of other complications, and chronic kidney disease is hardly an exception. Comorbidities associated with chronic kidney disease lead to faster disease progression, expedited dialysis dependency, and a higher mortality rate. Although chronic kidney disease is most commonly accompanied by cardiovascular diseases and diabetes, there is clear cross talk between the lungs and kidneys pH balance, phosphate metabolism, and immune system regulation. Our present understanding of the exact underlying mechanisms that contribute to chronic kidney disease-related pulmonary disease is poor. This review summarizes the current research on kidney-pulmonary interorgan cross talk in the context of chronic kidney disease, highlighting various acute and chronic pulmonary diseases that lead to further complications in patient care. Treatment options for patients presenting with chronic kidney disease and lung disease are explored by assessing activated molecular pathways and the body’s compensatory response mechanisms following homeostatic imbalance. Understanding the link between the lungs and kidneys will potentially improve health outcomes for patients and guide healthcare professionals to better understand how and when to treat each of the pulmonary comorbidities that can present with chronic kidney disease.

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Fatima, Tanveer, Aurangzeb Afzal, and Sania Ashraf. "CHRONIC KIDNEY DISEASE." Professional Medical Journal 25, no. 06 (June 9, 2018): 887–91. http://dx.doi.org/10.29309/tpmj/18.4418.

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7

Paul, Binu M., and Gregory B. Vanden Heuvel. "Kidney: polycystic kidney disease." Wiley Interdisciplinary Reviews: Developmental Biology 3, no. 6 (September 3, 2014): 465–87. http://dx.doi.org/10.1002/wdev.152.

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8

Nishi, Shinichi. "Chronic Kidney Disease and Cardiovascular Disease: Progression of Arterial Diseases in Chronic Kidney Disease." Nihon Naika Gakkai Zasshi 105, no. 5 (2016): 791–92. http://dx.doi.org/10.2169/naika.105.791.

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9

Neyra, Javier A., and Lakhmir S. Chawla. "Acute Kidney Disease to Chronic Kidney Disease." Critical Care Clinics 37, no. 2 (April 2021): 453–74. http://dx.doi.org/10.1016/j.ccc.2020.11.013.

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10

Idan, Ahmed Fadhil. "Effect of Coronavirus among Kidney Disease Patients." Journal of Communicable Diseases 54, no. 02 (June 30, 2022): 28–32. http://dx.doi.org/10.24321/0019.5138.202267.

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Background: COVID-19 is a novel coronavirus disease caused by the severe acute respiratory syndrome coronavirus 2. Chronic kidney disease (CKD) is associated with an increased risk of both inpatient and outpatient pneumonia. Objective: To describe the effect of COVID-19 virus on patients with kidney disease and renal transplants and analyse the outcomes of patients at the time of the study. Patients and Method: This is a descriptive study conducted in Baghdad Medical City, Al Shifa Center (single centre study). The study included 13 RTPCR-positive patients who were screened in the inpatient and outpatient departments. All patients received treatment according to the Iraq Ministry of Health protocol with dose adjusted as per the glomerular filtration rate (GFR). Result: The mean age of participants was 51.46 years with males more than females. Among the positive cases, 2 had acute kidney injury (15.4%), 3 had chronic kidney diseases (23.1%), 5 had end-stage renal disease (38.5%), and 3 had had renal transplants (23.1%). 6 patients out of 13 were diabetic, 11 were hypertensive, and 1 patient had heart failure. 7 (53.8%) patients were given conservative treatment, 4 were given isolated conventional haemodialysis, and only 2 patients were kept in an intensive care unit on continuous renal replacement therapy. 2 male patients died during the treatment. Conclusion: Chronic kidney disease is a risk factor for COVID-19 infection and more mortality and infection were found in male patients as compared to female patients in our study.

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11

TONELLI, Marcello, and Miguel RIELLA. "Chronic Kidney Disease and the Aging Population." Turkish Nephrology Dialysis Transplantation 23, no. 01 (January 21, 2014): 3–7. http://dx.doi.org/10.5262/tndt.2014.1001.02.

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12

Stanisic, Marijana, Rajko Hrvacevic, Zoran Paunic, and Stanko Petrovic. "Nephronophthisis and medullary cystic kidney disease complex." Vojnosanitetski pregled 62, no. 9 (2005): 683–88. http://dx.doi.org/10.2298/vsp0509683s.

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Background. Nephronophthisis and medullary cystic kidney disease complex refers to the genetic heterogeneous group of inherited tubulointerstital nephritis. Nephronophthisis comprises at last 3 clinical manifestations, has the autosomal recessive pattern of inheritance, appears early in life and is the most frequent inherited kidney disease that causes terminal renal failure in childhood, while medullary cystic kidney disease has the autosomal dominant pattern of inheritance, is less frequent, and terminal renal failure appears later in life. These two forms have similar clinical and morphological findings but extrarenal manifestations, the median ages of occurrence of terminal renal failure, and siblings presence help us distinguish these diseases. Case report. In this article we illustrated the case of a 20- years old patient with the suspicion of having complex nephornophthisis and medullary cystic kidney disease based upon mild renal failure, seen in routinely taken laboratory findings and bilateral cysts in corticomedullary region of the kidneys verified on abdominal ultrasound examination. Conclusion. This disease should rise suspicion in children or adolescents with progressive renal failure, a typical clinical manifestation, blood and urine samples results, bilateral cysts in the corticomedullary region of the kidneys seen during ultrasound examination of the kidneys and family inheritance.

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13

Przybyciński, Jarosław, Violetta Dziedziejko, Kamila Puchałowicz, Leszek Domański, and Andrzej Pawlik. "Adiponectin in Chronic Kidney Disease." International Journal of Molecular Sciences 21, no. 24 (December 9, 2020): 9375. http://dx.doi.org/10.3390/ijms21249375.

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Adiponectin is the adipokine associated with insulin sensitization, reducing liver gluconeogenesis, and increasing fatty acid oxidation and glucose uptake. Adiponectin is present in the kidneys, mainly in the arterial endothelium and smooth muscle cells, as well as in the capillary endothelium, and might be considered as a marker of many negative factors in chronic kidney disease. The last few years have brought a rising body of evidence that adiponectin is a multipotential protein with anti-inflammatory, metabolic, anti-atherogenic, and reactive oxygen species (ROS) protective actions. Similarly, adiponectin has shown many positive and direct actions in kidney diseases, and among many kidney cells. Data from large cross-sectional and cohort studies showed a positive correlation between serum adiponectin and mortality in chronic kidney disease. This suggests a complex interaction between local adiponectin action, comorbidities, and uremic milieu. In this review we discuss the role of adiponectin in chronic kidney disease.

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14

Thana, Alvionita, Fernando Corneles Moniharapon, Kristin Armis Pasaribu, Sindy Friska, and Wahyu Irawati. "THE POTENTIAL OF MICRO-CHINESE MEDICINE OSMOTHERAPY USING NANOPARTICLES AS A TREATMENT FOR CHRONIC KIDNEY DISEASE." BIOLINK (Jurnal Biologi Lingkungan Industri Kesehatan) 9, no. 1 (August 19, 2022): 1–14. http://dx.doi.org/10.31289/biolink.v9i1.6358.

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The kidneys are the most important to excretory organs because they have function to remove waste products from the body has metabolism. In the excretory system, the damage that could occur is the kidney has decreased until finally unable to perform its function properly which is called Chronic Kidney Disease (CKD). Chronic Kidney Disease caused by age, gender, and a history of diseases such as diabetes. One of the nanoparticle therapies that could be given to patients with chronic kidney disease is Micro-Chinese Medicine Osmotherapy. The purpose of this paper is to determine: 1) structure and how they work of the kidney and its relation to the urinary system, 2) causes and effects of chronic kidney disease on the urinary system, 3) mechanism of the urinary system in conditions of chronic kidney disease, and 4) mechanism and results of Micro-Chinese Medicine Osmotherapy. The research method used is a literature review from various sources which helps in reviewing the four focus of the study. Kidney is divided into three major parts, namely cortex, medulla, and renal pelvis. The excretory system has three stages, including filtration, reabsorption, and augmentation. Chronic kidney disease can be caused by age, where older age has a risk of developing CKD. Kidney disease can be divided into several stages, including normal, at risk of damage, kidneys are damaged, kidneys are not functioning properly and kidneys are no longer functioning or chronic kidney disease (CKD). The mechanism of action of Micro-Chinese Medicine Osmotherapy is divided based on its function, named as anti-inflammatory, anti-coagulation, and degradation. The results of treatment for kidney disease is Micro Medicine Osmotherapy could make all renal arteries of patients with chronic kidney disease widen and increase perfusion.

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15

Ingelfinger, Julie. "World kidney day 2016 averting the legacy of kidney disease – Focus on childhood." Paediatrics Today 12, no. 1 (March 15, 2016): 115–23. http://dx.doi.org/10.5457/p2005-114.146.

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16

Kon, Valentina, Hai-Chun Yang, Loren E. Smith, Kasey C. Vickers, and MacRae F. Linton. "High-Density Lipoproteins in Kidney Disease." International Journal of Molecular Sciences 22, no. 15 (July 30, 2021): 8201. http://dx.doi.org/10.3390/ijms22158201.

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Decades of epidemiological studies have established the strong inverse relationship between high-density lipoprotein (HDL)-cholesterol concentration and cardiovascular disease. Recent evidence suggests that HDL particle functions, including anti-inflammatory and antioxidant functions, and cholesterol efflux capacity may be more strongly associated with cardiovascular disease protection than HDL cholesterol concentration. These HDL functions are also relevant in non-cardiovascular diseases, including acute and chronic kidney disease. This review examines our current understanding of the kidneys’ role in HDL metabolism and homeostasis, and the effect of kidney disease on HDL composition and functionality. Additionally, the roles of HDL particles, proteins, and small RNA cargo on kidney cell function and on the development and progression of both acute and chronic kidney disease are examined. The effect of HDL protein modification by reactive dicarbonyls, including malondialdehyde and isolevuglandin, which form adducts with apolipoprotein A-I and impair proper HDL function in kidney disease, is also explored. Finally, the potential to develop targeted therapies that increase HDL concentration or functionality to improve acute or chronic kidney disease outcomes is discussed.

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17

&NA;. "KIDNEY DISEASE." American Journal of Nursing 96, no. 5 (May 1996): 10. http://dx.doi.org/10.1097/00000446-199605000-00006.

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18

Wilund, Kenneth. "Kidney Disease." Medicine & Science in Sports & Exercise 48 (May 2016): 971. http://dx.doi.org/10.1249/01.mss.0000487913.43414.93.

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19

&NA;. "Kidney Disease." Home Healthcare Nurse: The Journal for the Home Care and Hospice Professional 26, no. 7 (July 2008): 396. http://dx.doi.org/10.1097/01.nhh.0000326314.48477.75.

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20

Zuber, Kim, and Jane S. Davis. "Kidney Disease." Physician Assistant Clinics 1, no. 1 (January 2016): i. http://dx.doi.org/10.1016/s2405-7991(15)00019-5.

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21

EILERS, DENISE. "Kidney disease." Nursing 40, no. 1 (January 2010): 8. http://dx.doi.org/10.1097/01.nurse.0000365904.43073.f0.

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22

Zakrocka, Izabela, and Wojciech Załuska. "Kynurenine pathway in kidney diseases." Pharmacological Reports 74, no. 1 (October 6, 2021): 27–39. http://dx.doi.org/10.1007/s43440-021-00329-w.

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AbstractKidney diseases have become one of the most common health care problems. Due to a growing number of advanced aged patients with concomitant disorders the prevalence of these diseases will increase over the coming decades. Despite available laboratory tests, accurate and rapid diagnosis of renal dysfunction has yet to be realized, and prognosis is uncertain. Moreover, data on diagnostic and prognostic markers in kidney diseases are lacking. The kynurenine (KYN) pathway is one of the routes of tryptophan (Trp) degradation, with biologically active substances presenting ambiguous properties. The KYN pathway is known to be highly dependent on immunological system activity. As the kidneys are one of the main organs involved in the formation, degradation and excretion of Trp end products, pathologies involving the kidneys result in KYN pathway activity disturbances. This review aims to summarize changes in the KYN pathway observed in the most common kidney disease, chronic kidney disease (CKD), with a special focus on diabetic kidney disease, acute kidney injury (AKI), glomerulonephritis and kidney graft function monitoring. Additionally, the importance of KYN pathway activity in kidney cancer pathogenesis is discussed, as are available pharmacological agents affecting KYN pathway activity in the kidney. Despite limited clinical data, the KYN pathway appears to be a promising target in the diagnosis and prognosis of kidney diseases. Modulation of KYN pathway activity by pharmacological agents should be considered in the treatment of kidney diseases.

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23

Oh, Soo, Rabeet Khan, and Ahmed Ziada. "Polycystic kidney disease." InnovAiT: Education and inspiration for general practice 13, no. 6 (April 1, 2020): 326–35. http://dx.doi.org/10.1177/1755738020910762.

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Polycystic kidney disease (PKD) is a monogenic, hereditary disorder of the kidneys that leads to fluid-filled cysts within the renal tubes. It is one of the most common causes of end-stage renal failure. There are two types, the more common autosomal dominant (ADPKD) and the rarer autosomal recessive (ARPKD). ADPKD mostly presents in adulthood, whereas ARPKD is usually detected during antenatal screening or as a neonate. This article will focus on key points to understand and consider for the holistic management of PKD.

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24

Yee, J. "Diabetic Kidney Disease: Chronic Kidney Disease and Diabetes." Diabetes Spectrum 21, no. 1 (January 1, 2008): 8–10. http://dx.doi.org/10.2337/diaspect.21.1.8.

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25

Lanewala, AliAsghar. "Chronic kidney disease – End-stage kidney disease group." Asian Journal of Pediatric Nephrology 4, no. 1 (2021): 3. http://dx.doi.org/10.4103/ajpn.ajpn_24_21.

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26

Putri, Novita, Tria Firmanti, Andrik, Atik Wilujeng, and Ali. "Menjaga Kesehatan Ginjal dengan Konsep Kesehatan secara Holistik pada Siswa SMAN 1 Giri Banyuwangi." Journal of Health Innovation and Community Service 1, no. 1 (April 27, 2022): 31–35. http://dx.doi.org/10.54832/jhics.v1i1.13.

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Introduction: Chronic Kidney Disease (CKD) is a non-communicable disease whose prevalence is still high and is still widely found in Indonesia. Chronic kidney disease (CKD) can affect metabolism in the body and disrupt fluid and electrolyte balance. Patients who have chronic kidney disease (CKD) will have an experience dependence on kidney replacement therapies such as hemodialysis, peritoneal dialysis, or kidney transplantation. Prevention of chronic kidney disease by providing knowledge related to the importance of maintaining the kidneys can improve understanding, especially in adolescents. Purpose: Respondents can know and understand the importance of holistically maintaining kidney health. Method: The implementation of community service uses the method of lectures and discussions by providing educational materials to maintain kidney health with the concept of holistic health. Results: Students understand the importance of holistically maintaining kidney health. Conclusion: Providing education related to chronic kidney disease (CKD) is effective to increasing knowledge in the younger generation as a preventive measure of non-communicable diseases, especially chronic kidney disease.

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27

Stevens, Richard J., Julie Evans, Jason Oke, Benjamin Smart, F. D. Richard Hobbs, Elizabeth Holloway, Jeremy Horwood, et al. "Kidney age, not kidney disease." Canadian Medical Association Journal 190, no. 13 (April 2, 2018): E389—E393. http://dx.doi.org/10.1503/cmaj.170674.

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28

Philo, Dakota. "Horseshoe Kidney in Conjunction With Autosomal Dominant Polycystic Kidney Disease: A Case Report." Journal of Diagnostic Medical Sonography 37, no. 3 (February 13, 2021): 298–303. http://dx.doi.org/10.1177/8756479320988290.

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Horseshoe kidney in the presence of autosomal dominant polycystic kidney disease is a rare occurrence of two relatively common and unrelated renal findings. Visualization of multiple, bilateral cysts along with fusion of the kidneys by a midline isthmus can usually isolate these diagnoses. Accurate sonographic evaluation is essential in determining the degree of disease progression and possible complications associated with these diseases. Sonography is also useful in identifying extrarenal involvement and eliminating differential diagnoses.

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29

YANAGITA, Motoko. "Kidney Disease: Curable Disease?" TRENDS IN THE SCIENCES 16, no. 5 (2011): 122–24. http://dx.doi.org/10.5363/tits.16.5_122.

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Rahmawati, Wiwit, Heru Muryawan, and Farah Prabowo. "Renal imaging in children with chronic kidney disease." Paediatrica Indonesiana 53, no. 4 (August 31, 2013): 193. http://dx.doi.org/10.14238/pi53.4.2013.193-9.

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Background Chronic kidney failure is a cause of death inchildren. Diagnosing chronic kidney disease is often made byclinical manifestations, laboratory findings and ultrasonographyor other imaging tests. Early detection of chronic kidney diseaseis needed for education and management of the disease.Objective To describe renal imaging findings and mortality inchildren with chronic kidney disease .Methods This was a cross-sectional study on children with kidneydiseases who were inpatients at Dr. Kariadi Hospital from January2008 to June 2011. Data were taken from medical records. Chronickidney disease was confirmed by clinical manifestations, laboratoryfindings, and radiologic imaging. Renal ultrasound findings weredetermined by the radiologist responsible at that time. Resultswere presented as ft:equency distributions.Results Of 37 chronic kidney disease cases, 27 were males and 10were females. Subjects' most common complaints were dyspnea (7out of 3 7) and edema (30 out of 3 7) . Renal ultrasound imaging ofsubjects with chronic kidney disease yielded the following findings:reduced cortico-medullary differentiation (30 out of 3 7), bilateralechogenic kidneys (21 out of 3 7), reduced renal cortex thickness(4 out of 37) and small-sized kidneys (4 out of 37) . Eight of the37 children died. These 8 subjects had the following radiologicimaging findin gs: both kidneys appeared small in size (4 out ofS),reduced 'renal cortex' thickness (4 out of 8), echogenic kidneys(6 out of 8), and reduced cortico-medullary differentiation (8out of8).Conclusion Renal ultrasound imaging of pediatric subjects withchronic kidney disease revealed findings of reduced corticomedullarydifferentiation, bilateral echogenic kidneys, reducedrenal cortex thickness, and small kidneys bilaterally.

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Prkacin, Ingrid, Gordana Cavric, and Nikolina Basic-Jukic. "MicroRNA in kidney disease." BANTAO Journal 14, no. 1 (June 27, 2016): 8–10. http://dx.doi.org/10.1515/bj-2016-0002.

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AbstractClinical and laboratory findings of kidney disease in an adult may find an explanation in kidney functional and/or structural abnormalities that already existed during infancy and childhood, but that may have been missed or underdiagnosed. All the cardiovascular abnormalities that occur in adults with chronic kidney disease are also present in children with chronic kidney disease. Complications in childhood chronic kidney disease will have consequences well beyond pediatric age and influence outcomes of affected young adults with disease. Kidney dysfunction appears early in the course of kidney disease and has been observed in children and adults with chronic kidney disease, condition characterised with kidney fibrosis. Transforming growth factor beta is recognized as a major mediator of kidney fibrosis. New evidence illustrates the relationship between transforming growth factor beta signaling and microRNAs expression during kidney diseases development. MicroRNAs play important roles in kidney development and kidney diseases; they are naturally occurring, 22-nucleotide, noncoding RNAs that mediate posttranscriptional gene regulation. Dysregulation of miRNA expression is an indicator of several diseases including chronic kidney disease. Targeting microRNAs should be a therapeutic potential to ameliorate the disease related to fibrosis. The discovery that circulating miRNAs are detectable in serum and plasma, and that their expression varies as a result of disease, presents great potential to be used as biomarkers in kidney disease prevention and diagnosis.

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Mounier-Véhier, Claire, Stéphan Haulon, Patrick Devos, Christophe Lions, Olivier Jaboureck, Virginia Gaxotte, Alain Carré, and Jean-Paul Beregi. "Renal Atrophy Outcome after Revascularization in Fibromuscular Dysplasia Disease." Journal of Endovascular Therapy 9, no. 5 (October 2002): 605–13. http://dx.doi.org/10.1177/152660280200900510.

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Purpose: To assess clinical, biological, and kidney parameters before and 6 months after revascularization of renal artery stenosis due to fibromuscular dysplasia (FMD). Methods: Twenty hypertensive patients (18 women; mean age 48.7 ± 15.4 years) with unilateral de novo FMD stenosis were studied before and 6 months after revascularization (balloon angioplasty 19; bypass surgery 1). Blood pressure and creatinine clearance were measured, and renal length, cortical thickness, cortical area (CA), and medullary length (ML) were evaluated by spiral computed tomographic angiography (CTA) in 20 poststenotic and 20 contralateral kidneys. Results: Six months after revascularization, the systolic and diastolic blood pressures decreased by 19 mmHg and 10 mmHg, respectively (p=0.02), the number of antihypertensive drugs decreased by 1 (p=0.01), but the increase in creatinine clearance was not significant. At baseline, the poststenotic kidneys were significantly more atrophied than the contralateral normal kidney (ML in normal kidney 89 ± 9 mm versus 81 ± 10 mm in poststenotic kidney, p<0.001; CA in normal kidney 824 ± 149 mm versus 703 ± 156 mm in poststenotic kidney, p<0.01), which persisted at 6 months (ML in normal kidney 89 ± 10 versus 80 ± 11 in poststenotic kidney, p<0.001; CA in normal kidney 807 ± 145 mm versus 696 ± 157 mm in poststenotic kidney, p<0.01). Renal length was still within normal range in all kidneys, and the morphological parameters remained stable after revascularization. Conclusions: We demonstrated significant cortical/medullary atrophy in poststenotic kidneys compared to contralateral normal kidneys. Despite intraparenchymal disease, clinical outcome was favorable after revascularization. Cortical/medullary thinning appears to be an early marker of renal ischemia that could support revascularization in FMD disease.

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Neki, NS, Amritpal Singh, Gagandeep Singh Shergill, and Amanpreet Kaur. "Polycystic Kidney Disease – A cause for Low backache." Asian Pacific Journal of Health Sciences 3, no. 4 (November 30, 2016): 145–47. http://dx.doi.org/10.21276/apjhs.2016.3.4.23.

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34

M S, Champa, and Rekha B S. "Chronic Kidney Disease Detection Using Micro-service Architecture." International Journal of Innovative Research in Computer Science & Technology 7, no. 3 (May 2019): 84–89. http://dx.doi.org/10.21276/ijircst.2019.7.3.10.

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35

Shivraj, Shivraj, and Venugopal K. "Gastrointestinal Manifestations in Patients with Chronic Kidney Disease." Academia Journal of Medicine 2, no. 2 (July 24, 2019): 54–59. http://dx.doi.org/10.21276/ajm.2019.2.2.15.

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36

VN, Karan, and Vishwanath VN. "Clinical Profile of Patients with Chronic Kidney Disease." Academia Journal of Medicine 2, no. 2 (July 24, 2019): 175–78. http://dx.doi.org/10.21276/ajm.2019.2.2.45.

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37

(Medicine), Dr Ashok Kumar M. D. "Observation on Serum Magnesium in Chronic Kidney Disease." Journal of Medical Science And clinical Research 05, no. 05 (June 2, 2017): 20570–72. http://dx.doi.org/10.18535/jmscr/v5i5.211.

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38

Peco-Antić, Amira. "How to grow up with chronic kidney disease?" Central European Journal of Paediatrics 14, no. 1 (March 7, 2018): 37–46. http://dx.doi.org/10.5457/p2005-114.197.

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39

Moyseyenko, V., T. Nykula, and I. Burzhynskaya. "CHRONIC KIDNEY DISEASE AND VISCERAL CANDIDIASIS." Ukrainian Journal of Nephrology and Dialysis, no. 4(48) (August 25, 2015): 61–64. http://dx.doi.org/10.31450/ukrjnd.4(48).2015.11.

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Kidneys play a significant role in metabolism, detoxification, biotransformation of dietary, medicinal and other substances. The mainstay of treatment of patients with chronic kidney disease, including pyelonephritis is antibiotic therapy; of glomerulonephritis - glucocorticoids, cytostatics. The presence of comorbidities, diabetes increases the total number of drugs used. Frequent prolonged use of drugs causes secondary immunodeficiency, gastrointestinal tract dysbiosis, clinical manifestations of which are oral mucosa candidiasis; the progression of kidney damage, kidney transplant may cause visceral candidiasis. Control of immunosuppressive therapy, parenteral infusion ofantifungal agents and timely diagnosis prevent candidiasis in patients with chronic kidney disease.

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Ariton, Diana Maria, Joan Jiménez-Balado, Olga Maisterra, Francesc Pujadas, María José Soler, and Pilar Delgado. "Diabetes, Albuminuria and the Kidney—Brain Axis." Journal of Clinical Medicine 10, no. 11 (May 27, 2021): 2364. http://dx.doi.org/10.3390/jcm10112364.

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Cognitive decline and kidney disease are significant public health problems that share similar characteristics and risk factors. The pathophysiology of the kidney–brain axis is not completely understood, and studies analysing the relationship between the biomarkers of kidney damage and cognitive impairment show different results. This article focuses on the epidemiological and clinical aspects concerning the association of albuminuria, a marker for endothelial dysfunction and microvascular disease, and cognitive impairment in patients with chronic kidney disease, diabetic kidney disease and end-stage kidney disease. Most studies show a positive relationship between albuminuria and cognitive impairment in all groups, but evidence in type 2 diabetes (T2D) patients is limited. We briefly discuss the mechanisms underlying these associations, such as damage to the microvascular circulation, leading to hypoperfusion and blood pressure fluctuations, as well as increased inflammation and oxidative stress, both in the brain and in the kidneys. Further clinical and epidemiological studies developed to understand the interplay between the kidneys and brain diseases will hopefully lead to a reduction in cognitive impairment in these patients.

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41

Tomasello, Sarah. "Anemia of Chronic Kidney Disease." Journal of Pharmacy Practice 21, no. 3 (June 2008): 181–95. http://dx.doi.org/10.1177/0897190008315906.

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Chronic kidney disease may result in complete kidney failure and contribute to many other health issues. Anemia is a logical consequence of the disease because the kidneys are the primary source of erythropoietin, the hormone that acts to stimulate red blood cell production in the bone marrow. All patients with chronic kidney disease are at risk for anemia, and treating anemia is extremely important to their health and well-being. Preventing or reversing the effects of anemia on the heart may decrease morbidity and mortality and improve quality of life. Many patients fail to receive treatment for anemia before requiring renal replacement therapy for end-stage renal disease. Pharmacists can play a vital role in screening, evaluating, designing proper treatment regimens, and monitoring patients with anemia of chronic kidney disease. Current recommendations regarding anemia are reviewed, including evaluation, pharmacotherapeutic agents, monitoring parameters, and goals of therapy.

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Braga, Patrícia C., Marco G. Alves, Anabela S. Rodrigues, and Pedro F. Oliveira. "Mitochondrial Pathophysiology on Chronic Kidney Disease." International Journal of Molecular Sciences 23, no. 3 (February 4, 2022): 1776. http://dx.doi.org/10.3390/ijms23031776.

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In healthy kidneys, interstitial fibroblasts are responsible for the maintenance of renal architecture. Progressive interstitial fibrosis is thought to be a common pathway for chronic kidney diseases (CKD). Diabetes is one of the boosters of CKD. There is no effective treatment to improve kidney function in CKD patients. The kidney is a highly demanding organ, rich in redox reactions occurring in mitochondria, making it particularly vulnerable to oxidative stress (OS). A dysregulation in OS leads to an impairment of the Electron transport chain (ETC). Gene deficiencies in the ETC are closely related to the development of kidney disease, providing evidence that mitochondria integrity is a key player in the early detection of CKD. The development of novel CKD therapies is needed since current methods of treatment are ineffective. Antioxidant targeted therapies and metabolic approaches revealed promising results to delay the progression of some markers associated with kidney disease. Herein, we discuss the role and possible origin of fibroblasts and the possible potentiators of CKD. We will focus on the important features of mitochondria in renal cell function and discuss their role in kidney disease progression. We also discuss the potential of antioxidants and pharmacologic agents to delay kidney disease progression.

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Afarideh, Mohsen, Xin Zhang, Christopher M. Ferguson, James F. Glockner, Amir Lerman, Stephen C. Textor, and Lilach O. Lerman. "Peristenotic Collateral Circulation in Atherosclerotic Renovascular Disease." Hypertension 76, no. 2 (August 2020): 497–505. http://dx.doi.org/10.1161/hypertensionaha.120.15057.

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The significance of peristenotic collateral circulation (PCC) development around a stenotic renal artery is unknown. We tested the hypothesis that PCC is linked to loss of kidney function and recovery potential in patients with atherosclerotic renovascular disease (ARVD). Thirty-four patients with ARVD were assigned to medical-therapy with or without revascularization based on clinical indications. The PCC was visualized using multidetector computed tomography and defined relative to segmental arteries in patients with essential hypertension. PCC number before and 3 months after treatment was correlated with various renal parameters. Thirty-four stenotic kidneys from 30 patients were analyzed. PCC number correlated inversely with kidney volume. ARVD–stenotic kidneys with baseline PCC (collateral ARVD [C-ARVD], n=13) associated with elevated 24-hour urine protein and stenotic kidney vein level of tumor necrosis factor-α, lower single-kidney volume and blood flow, and greater hypoxia than in stenotic kidneys with no PCC (no collateral ARVD [NC-ARVD], n=17). Revascularization (but not medical-therapy alone) improved stenotic kidney function and reduced inflammation in both NC-ARVD and C-ARVD. In C-ARVD, revascularization also increased stenotic kidney volume, blood flow, and oxygenation to levels comparable to NC-ARVD, and induced PCC regression. However, revascularization improved systolic blood pressure, plasma renin activity, and filtration fraction only in NC-ARVD. Therefore, patients with C-ARVD have greater kidney dysfunction, atrophy, hypoxia, and inflammation compared with patients with NC-ARVD, suggesting that PCC does not effectively protect the stenotic kidney in ARVD. Renal artery revascularization improved in C-ARVD stenotic kidney function, but not hypertension or renin-angiotensin system activation. These observations may help direct management of patients with ARVD.

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Salsabila, Sharifa Audi, Alfian Nur Rosyid, Maulana Antiyan Empitu, Ika Nindya Kadariswantiningsih, Satriyo Dwi Suryantoro, Mutiara Rizki Haryati, Mochammad Thaha, and Yusuke Suzuki. "Kidney-Pulmonary Crosstalk from Pathophysiological Perspective." Jurnal Respirasi 8, no. 1 (January 30, 2022): 44. http://dx.doi.org/10.20473/jr.v8-i.1.2022.44-51.

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Lungs and kidneys are distant organs which are functionally related in physiological and pathological contexts. Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are common complications in acute kidney injury (AKI) or acute-on-chronic kidney disease. On the other hand, there is a considerable risk of AKI in respiratory diseases such as ARDS and chronic obstructive pulmonary disease (COPD). From a pathophysiological point of view, the kidney-lung crosstalk involves interdependency in the regulation of fluid hemodynamic, acid-base and electrolyte balance, and carbon dioxide partial pressure. Aside from the closely related function, the crosstalk may also occur by non-classical mechanisms such as through activation of systemic inflammation, excessive cytokine release, and the formation of auto-antibody which targets both kidneys and lungs. This review discussed several disease mechanisms by which kidney and lungs affect each other or are simultaneously affected by pathological processes. Particularly, this review discussed some specific mechanisms in lungs and kidneys, such as how hypoxemia and hypercapnia induced by ARDS may reduce kidney function and how distance injury on kidney may affect the development of non-cardiogenic edema lungs.

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Dell, Katherine M., Matthew Matheson, Erum A. Hartung, Bradley A. Warady, Susan L. Furth, Alvaro Muñoz, Allison Dart, et al. "Kidney Disease Progression in Autosomal Recessive Polycystic Kidney Disease." Journal of Pediatrics 171 (April 2016): 196–201. http://dx.doi.org/10.1016/j.jpeds.2015.12.079.

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Bellorin-Font, Ezequiel, Eudocia Rojas, and Kevin J. Martin. "Bone Disease in Chronic Kidney Disease and Kidney Transplant." Nutrients 15, no. 1 (December 29, 2022): 167. http://dx.doi.org/10.3390/nu15010167.

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Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcification leading to an increase in bone fractures and vascular disease, which ultimately result in high morbidity and mortality. The bone component of CKD-MBD, referred to as renal osteodystrophy, starts early during the course of CKD as a result of the effects of progressive reduction in kidney function which modify the tight interaction between mineral, hormonal, and other biochemical mediators of cell function that ultimately lead to bone disease. In addition, other factors, such as osteoporosis not apparently dependent on the typical pathophysiologic abnormalities resulting from altered kidney function, may accompany the different varieties of renal osteodystrophy leading to an increment in the risk of bone fracture. After kidney transplantation, these bone alterations and others directly associated or not with changes in kidney function may persist, progress or transform into a different entity due to new pathogenetic mechanisms. With time, these alterations may improve or worsen depending to a large extent on the restoration of kidney function and correction of the metabolic abnormalities developed during the course of CKD. In this paper, we review the bone lesions that occur during both CKD progression and after kidney transplant and analyze the factors involved in their pathogenesis as a means to raise awareness of their complexity and interrelationship.

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Sanai, Toru, Ken Okamura, Tsuyoshi Takashima, Motoaki Miyazono, and Yuji Ikeda. "Chronic kidney disease and thyroid diseases." Nihon Toseki Igakkai Zasshi 52, no. 11 (2019): 615–23. http://dx.doi.org/10.4009/jsdt.52.615.

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Dharmaratne, RW. "Exploring the role of excess fluoride in chronic kidney disease: A review." Human & Experimental Toxicology 38, no. 3 (November 25, 2018): 269–79. http://dx.doi.org/10.1177/0960327118814161.

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This review covers nearly 100 years of studies on the toxicity of fluoride on human and animal kidneys. These studies reveal that there are direct adverse effects on the kidneys by excess fluoride, leading to kidney damage and dysfunction. With the exception of the pineal gland, the kidney is exposed to higher concentrations of fluoride than all other soft tissues. Therefore, exposure to higher concentrations of fluoride could contribute to kidney damage, ultimately leading to chronic kidney disease (CKD). Among major adverse effects on the kidneys from excessive consumption of fluoride are immediate effects on the tubular area of the kidneys, inhibiting the tubular reabsorption; changes in urinary ion excretion by the kidneys disruption of collagen biosynthesis in the body, causing damages to the kidneys and other organs; and inhibition of kidney enzymes, affecting the functioning of enzyme pathways. This review proposes that there is a direct correlation between CKD and the consumption of excess amounts of fluoride. Studies particularly show immediate adverse effects on the tubular area of human and animal kidneys leading to CKD due to the consumption of excess fluoride. Therefore, it is very important to conduct more investigations on toxicity studies of excess fluoride on the human kidney, including experiments using human kidney enzymes, to study more in depth the impact of excess fluoride on the human kidney. Further, the interference of excess fluoride on collagen synthesis in human body and its effect on human kidney should also be further investigated.

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Magno, Aaron, Lakshini Herat, Revathy Carnagarin, Markus Schlaich, and Vance Matthews. "Current Knowledge of IL-6 Cytokine Family Members in Acute and Chronic Kidney Disease." Biomedicines 7, no. 1 (March 13, 2019): 19. http://dx.doi.org/10.3390/biomedicines7010019.

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Healthy kidneys are important for the efficient regulation of metabolism. However, there is an ever increasing population of patients suffering from both acute and chronic kidney diseases that disrupt this homeostasis. This review will explore the emerging roles that interleukin 6 (IL-6) cytokine family members play in the pathogenesis of kidney disease. The IL-6 family of cytokines are involved in a diverse range of physiological functions. In relation to kidney disease, their involvement is no less diverse. Evidence from both preclinical and clinical sources show that IL-6 cytokine family members can play either a deleterious or protective role in response to kidney disease. This appears to be dependent on the type of kidney disease in question or the specific cytokine. Current attempts to use or target IL-6 cytokine family members as therapies of kidney diseases will be highlighted throughout this review. Finally, the involvement of IL-6 cytokine family members in kidney disease will be presented in the context of three regularly overlapping conditions: obesity, hypertension and diabetes.

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Bahadoram, Mohammad, Saeede Labaykee, Bhaskar VKS Lakkakula, Bijan Keikhaei, Mitra Nekouei Shahraki, Soroush Mohammadi Jouabadi, Macaulay Onuigbo, Fariba Ahmadizar, Mohammad-Reza Mahmoudian-Sani, and Payam Peymani. "World Kidney Day 2021 with the theme of living well with kidney disease; a review of current concepts." Journal of Preventive Epidemiology 6, no. 1 (August 3, 2021): e08-e08. http://dx.doi.org/10.34172/jpe.2021.08.

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Since 2006, by considering one dimension of kidney disease, each year, the International Society of Nephrology (ISN) and the International Federation of Kidney Foundations (IFKF) have consistently and unanimously declared a World Kidney Day (WKD) around a specific kidney disease to increase the global awareness about kidney diseases. WKD, which is celebrated in more than 150 countries worldwide, is an international kidney health awareness campaign emphasizing the importance of the kidneys to reduce the global prevalence of kidney diseases and their related health problems by promoting patients and providing education. The present review aims to summarize the themes of previous WKD campaigns and the advocacy of the 2021 WKD campaign theme "Living well with kidney disease". The 2021 WKD Steering Committee advocates for the empowerment of CKD patients, their family members, and care partners, along with both drug and non-drug therapeutic programs to achieve better health outcomes.

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