scholarly journals Kidney Damage Caused by Obesity and Its Feasible Treatment Drugs

2022 ◽  
Vol 23 (2) ◽  
pp. 747
Author(s):  
Meihui Wang ◽  
Zixu Wang ◽  
Yaoxing Chen ◽  
Yulan Dong

The rapid growth of obesity worldwide has made it a major health problem, while the dramatic increase in the prevalence of obesity has had a significant impact on the magnitude of chronic kidney disease (CKD), especially in developing countries. A vast amount of researchers have reported a strong relationship between obesity and chronic kidney disease, and obesity can serve as an independent risk factor for kidney disease. The histological changes of kidneys in obesity-induced renal injury include glomerular or tubular hypertrophy, focal segmental glomerulosclerosis or bulbous sclerosis. Furthermore, inflammation, renal hemodynamic changes, insulin resistance and lipid metabolism disorders are all involved in the development and progression of obesity-induced nephropathy. However, there is no targeted treatment for obesity-related kidney disease. In this review, RAS inhibitors, SGLT2 inhibitors and melatonin would be presented to treat obesity-induced kidney injury. Furthermore, we concluded that melatonin can protect the kidney damage caused by obesity by inhibiting inflammation and oxidative stress, revealing its therapeutic potential.

Author(s):  
Natalie Ebert ◽  
Elke Schaeffner

Both acute and chronic states of kidney disease have considerable healthcare impact as they can produce enormous disease burden and costs. To classify chronic kidney disease into the CKD staging system, glomerular filtration rate as an index of kidney function, as well as albuminuria as a marker of kidney damage have to be assessed as correctly as possible. Misclassification is a serious concern due to the difficulties in precise GFR assessment and correct interpretation of results. Differentiating between pure senescence and true disease among older adults can be a delicate issue. To find the right renal replacement option for individuals that progress to end-stage renal disease can be challenging, and some older patients may even benefit from conservative care without dialysis. To prevent acute kidney injury as a frequent and potentially life-threatening complication, clinicians need to develop an understanding of the common vulnerability to kidney damage among older adults.


Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3852
Author(s):  
Vassilios Liakopoulos ◽  
Evangelia Dounousi

Chronic kidney disease (CKD) constitutes a major health problem worldwide [...]


2018 ◽  
Vol 315 (4) ◽  
pp. F927-F941 ◽  
Author(s):  
Jennifer L. Riggs ◽  
Carolyn E. Pace ◽  
Heather H. Ward ◽  
Laura V. Gonzalez Bosc ◽  
Lynnette Rios ◽  
...  

Kidney injury and sleep apnea (SA) are independent risk factors for hypertension. Exposing rats to intermittent hypoxia (IH) to simulate SA increases blood pressure whereas adenine feeding causes persistent kidney damage to model chronic kidney disease (CKD). We hypothesized that exposing CKD rats to IH would exacerbate the development of hypertension and renal failure. Male Sprague-Dawley rats were fed a 0.2% adenine diet or control diet (Control) until blood urea nitrogen was >120 mg/dl in adenine-fed rats (14 ± 4 days, mean ± SE). After 2 wk of recovery on normal chow, rats were exposed to IH (20 exposures/h of 5% O2-5% CO2 7 h/day) or control conditions (Air) for 6 wk. Mean arterial pressure (MAP) was monitored with telemeters, and plasma and urine samples were collected weekly to calculate creatinine clearance as an index of glomerular filtration rate (GFR). Prior to IH, adenine-fed rats had higher blood pressure than rats on control diet. IH treatment increased MAP in both groups, and after 6 wk, MAP levels in the CKD/IH rats were greater than those in the CKD/Air and Control/IH rats. MAP levels in the Control/Air rats were lower than those in the other three groups. Kidney histology revealed crystalline deposits, tubule dilation, and interstitial fibrosis in both CKD groups. IH caused no additional kidney damage. Plasma creatinine was similarly increased in both CKD groups throughout whereas IH alone increased plasma creatinine. IH increases blood pressure further in CKD rats without augmenting declines in GFR but appears to impair GFR in healthy rats. We speculate that treating SA might decrease hypertension development in CKD patients and protect renal function in SA patients.


Author(s):  
А.Г. Борисов ◽  
С.В. Чернавский ◽  
М.А. Смирнова ◽  
А.А. Стремоухов

Статья посвящена современным подходам к терапии сахарного диабета, осложненного поражением почек. Сахарный диабет является важнейшей проблемой современной медицины, что прежде всего обусловлено высокой распространенностью заболевания среди трудоспособного населения. Диабетическая нефропатия – одно из тяжелых хронических осложнений диабета, повышающее инвалидизацию и смертность пациентов. Диабетическая нефропатия является основной причиной развития терминальной почечной недостаточности в развитых странах и со временем затрагивает около 30% пациентов. Поражение почек у больных сахарным диабетом встречается в 6-7% случаев из общего числа нефропатий у пациентов, получающих лечение в специализированном нефрологическом отделении многопрофильного стационара. Первые проявления диабетической нефропатии развиваются через 3-4 года от дебюта заболевания и достигают своего пика через 15-20 лет. Понятие «хроническая болезнь почек» включает в себя поражение почек независимо от первичного диагноза, характеризующееся такими основными диагностическими критериями, как экскреция альбумина с мочой и значения скорости клубочковой фильтрации, которые являются маркерами повреждения почек. Методы предупреждения прогрессирования диабетической нефропатии включают в себя общие мероприятия по изменению образа жизни, контроль гликемии и артериального давления, коррекцию нарушений липидного обмена в сочетании с нефропротективной терапией. В настоящее время при выборе терапии у больных сахарным диабетом 2 типа в сочетании с хронической болезнью почек наряду с приемом метформина предпочтение отдается ингибиторам натрий-глюкозного котранспортера 2-го типа и агонистам рецепторов глюкагоноподобного пептида-1, обладающим нефропротективным эффектом. The article is devoted to modern approaches to the treatment of diabetes mellitus complicated by kidney damage. Diabetes mellitus is the most important problem of modern medicine, which is primarily due to the high prevalence of the disease among the working-age population. Diabetic nephropathy is one of the severe chronic complications of diabetes, which increases the disability and mortality of patients. Diabetic nephropathy is the main cause of the development of end-stage renal failure in developed countries and eventually affects about 30% of patients. Kidney damage in patients with diabetes occurs in 6-7% of cases out of the total number of nephropathies in patients receiving treatment in a specialized nephrological department of a multidisciplinary hospital. The first manifestations of diabetic nephropathy develop 3-4 years after the onset of the disease, and reach their peak in 15-20 years. The concept of «chronic kidney disease» includes kidney damage regardless of the primary diagnosis and is characterized by such basic diagnostic criteria as urinary albumin excretion and glomerular filtration rate values, which are markers of kidney damage. Methods for preventing the progression of diabetic nephropathy include general measures to change the lifestyle, control of glycemia and blood pressure, correction of lipid metabolism disorders in combination with nephroprotective therapy. Currently, when choosing therapy in patients with type 2 diabetes mellitus in combination with chronic kidney disease, along with taking metformin, preference is given to sodium-glucose cotransporter type 2 inhibitors and glucagon-like peptide-1 receptor agonists with a nephroprotective effect.


Pharmaceutics ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 713
Author(s):  
Gracia Santos-Díaz ◽  
Ana María Pérez-Pico ◽  
Miguel Ángel Suárez-Santisteban ◽  
Vanesa García-Bernalt ◽  
Raquel Mayordomo ◽  
...  

Chronic kidney disease (CKD) is a major health problem worldwide and, in Spain, it is present in 15.1% of individuals. CKD is frequently associated with some comorbidities and patients need to be prescribed multiple medications. Polypharmacy increases the risk of adverse drug reactions (ADRs). There are no published studies evaluating the prevalence of potential drug–drug interactions (pDDIs) among CKD patients in any European country. This study was aimed to determine the prevalence, pattern, and factors associated with pDDIs among CKD patients using a drug interactions program. An observational cross-sectional study was carried out at Plasencia Hospital, located in Spain. Data were collected among patients with CKD diagnoses and pDDIs were assessed by the Lexicomp® Drug Interactions platform. Data were obtained from 112 CKD patients. A total number of 957 prescribed medications were acknowledged, and 928 pDDIs were identified in 91% of patients. Age and concomitant drugs were significantly associated with the number of pDDIs (p < 0.05). According to the results, the use of programs for the determination of pDDIs (such as Lexicomp®) is recommended in the clinical practice of CKD patients in order to avoid serious adverse effects, as is paying attention to contraindicated drug combinations.


Author(s):  
Elena Hunter ◽  
Benita Percival ◽  
Zeeshan Ahmad ◽  
Ming-Wei Chang ◽  
John A. Hunt ◽  
...  

AbstractChronic kidney disease (CKD) is a renal dysfunction that can lead to high rates of mortality and morbidity, particularly when coupled with late diagnosis. CKD has become a major health problem due to its challenging detection at early stages when clear symptoms are yet to be presented. Thus, CKD is likely to be identified when the substantive conditions of the disease are manifest. In order to address the development of the disease and provide necessary treatments at the initial stage, the investigation of new biomarkers and metabolites associated with early detection of CKD are needed. Identified metabolites could be used to confirm the presence of the disease, obtain information on its mechanism and facilitate the development of novel pharmaceutical treatments. Such metabolites may be detected from biofluids and tissues using a range of analytical techniques. There are a number of metabolites that have been identified by mass spectrometry at high sensitivities, whilst the detection of metabolites directly from biofluids using NMR could present a more rapid way to expand our understanding of this disease. This review is focused on NMR-based metabolomics associated with CKD in humans and animals.


2017 ◽  
Vol 4 (07) ◽  
pp. 1432
Author(s):  
Mahdi Mohammadian ◽  
Hamid Salehiniya ◽  
Salman Khazaei ◽  
Abdollah Mohammadian-Hafshejani

Chronic kidney disease (CKD) is known as a major health problem worldwide (Levey et al., 2007). The CKD is defined as a stage of disease in which the patient's kidney function is less than a half of normal capacity (2). If the kidney function is 10% to 15% less than the normal capacity, the patient has reached the End Stage Renal Disease (ESRD). At this stage, the kidney transplant or dialysis with hemodialysis or peritoneal dialysis is necessary for patient's survival (Levey et al., 2002).


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