Chronic Kidney Disease
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2021 ◽  
Vol 78 (6) ◽  
pp. 564-570
Hsin-Fu Lee ◽  
Yu-Wen Cheng ◽  
Jian-Rong Peng ◽  
Chiu-Yi Hsu ◽  
Chia-Hung Yang ◽  

2021 ◽  
Vol 45 ◽  
pp. 100580
Hui-Yeon Ko ◽  
Joonyoung Kim ◽  
Migyeong Geum ◽  
Ha-Jung Kim

Hypertension ◽  
2021 ◽  
Vol 78 (5) ◽  
pp. 1365-1367
Vincent D. Salvador ◽  
George L. Bakris

Cureus ◽  
2021 ◽  
Asfia Jabbar ◽  
Ruqaya Qureshi ◽  
Murtaza Dhrolia ◽  
Kiran Nasir ◽  
Aasim Ahmad

2021 ◽  
Vol 30 (4) ◽  
pp. 294-299
Maria Mattera ◽  
Nicola Veronese ◽  
Filippo Aucella ◽  
Luciana La Tegola ◽  

2021 ◽  
Vol 0 (0) ◽  
Jordana Yahr ◽  
Juan Calle ◽  
Jonathan J. Taliercio

Abstract Chronic kidney disease (CKD) affects approximately 15% of the US population and is associated with significant cardiovascular morbidity and mortality. The two leading causes of end stage kidney disease are hypertension and diabetes mellitus, both of which are modifiable risk factors. The cornerstones of CKD care include early detection, management of associated risk factors, modification of cardiovascular disease risk, slowing progression of disease, and management of complications including anemia, acid base disturbance, and mineral and bone disorders. For the last 20 years, renin-angiotensin system inhibitors were the mainstay treatment for proteinuric diabetic and nondiabetic kidney disease. Recently, new therapies such as sodium-glucose linked transporter 2 inhibitors, have emerged as powerful tools in the treatment of CKD with indications in both diabetic and nondiabetic kidney disease. In this article, we define CKD staging, review new hypertension and diabetic guidelines for CKD patients, and discuss major trials for new potential therapies in CKD, particularly diabetic kidney disease. We will provide practical guidance for primary care physicians to diagnose CKD and implement these agents early in the disease course to prevent the progression of disease and reduce the morbidity and mortality of this vulnerable population.

2021 ◽  
Vol 385 (16) ◽  
pp. e56

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3605
Ping-Huang Tsai ◽  
Hsiu-Chien Yang ◽  
Chin Lin ◽  
Chih-Chien Sung ◽  
Pauling Chu ◽  

Muscle wasting and hyperphosphatemia are becoming increasingly prevalent in patients who exhibit a progressive decline in kidney function. However, the association between serum phosphate (Pi) level and sarcopenia in advanced chronic kidney disease (CKD) patients remains unclear. We compared the serum Pi levels between advanced CKD patients with (n = 51) and those without sarcopenia indicators (n = 83). Low appendicular skeletal muscle mass index (ASMI), low handgrip strength, and low gait speed were defined per the standards of the Asian Working Group for Sarcopenia. Mean serum Pi level was significantly higher in advanced CKD patients with sarcopenia indicators than those without sarcopenia indicators (3.88 ± 0.86 vs. 3.54 ± 0.73 mg/dL; p = 0.016). Univariate analysis indicated that serum Pi was negatively correlated with ASMI, handgrip strength, and gait speed. Multivariable analysis revealed that serum Pi was significantly associated with handgrip strength (standardized β = −0.168; p = 0.022) and this association persisted even after adjustments for potential confounders. The optimal serum Pi cutoff for predicting low handgrip strength was 3.65 mg/dL, with a sensitivity of 82.1% and specificity of 56.6%. In summary, low handgrip strength is common in advanced CKD patients and serum Pi level is negatively associated with handgrip strength.

2021 ◽  
Vol 9 (F) ◽  
pp. 428-435
Gede Wira Mahadita ◽  
Ketut Suwitra

In humans, the end product of purine metabolism is uric acid. Over 70% of uric acid is excreted through the kidneys. When renal function is impaired, uric acid secretion is also impaired. This directly correlates the prevalence of hyperuricemia with the severity of chronic kidney disease (CKD). It has been reported that the prevalence of hyperuricemia in patients with Stage I-III CKD is 40–60% and up to 70% in patients with Stage IV-V CKD. Some studies found a link between serum uric acid levels and decreased glomerular filtration rate (GFR), an independent risk factor for CKD development. Because CKD and serum uric acid levels are related, the relationship between the two frequently generates controversy. As such, this review of the literature discusses the role of uric acid in the pathogenesis and progression of CKD.

2021 ◽  
Vol 11 (1) ◽  
Yusaku Hashimoto ◽  
Takahiro Imaizumi ◽  
Sawako Kato ◽  
Yoshinari Yasuda ◽  
Takuji Ishimoto ◽  

AbstractThe influence of body mass or metabolic capacity on the association between alcohol consumption and lower risks of developing chronic kidney disease (CKD) is not fully elucidated. We examined whether the body mass index (BMI) affects the association between drinking alcohol and CKD. We defined CKD as an estimated glomerular filtration rate decline < 60 mL/min/1.73 m2 and/or positive proteinuria (≥ 1+). Participants were 11,175 Japanese individuals aged 40–74 years without baseline CKD who underwent annual health checkups. Daily alcohol consumption at baseline was estimated using a questionnaire, and the participants were categorized as “infrequent (occasionally, rarely or never),” “light (< 20 g/day),” “moderate (20–39 g/day),” and “heavy (≥ 40 g/day).” Over a median 5-year observation period, 936 participants developed CKD. Compared with infrequent drinkers, light drinkers were associated with low CKD risks; adjusted hazard ratios (95% confidence intervals) were 0.81 (0.69–0.95). Stratified by BMI (kg/m2), moderate drinkers in the low (< 18.5), normal (18.5–24.9), and high (≥ 25.0) BMI groups had adjusted hazard ratios (95% confidence intervals) of 3.44 (1.60–7.42), 0.75 (0.58–0.98), and 0.63 (0.39–1.04), respectively. Taken together, the association between alcohol consumption and CKD incidence was not the same in all the individuals, and individual tolerance must be considered.

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