scholarly journals Impact of achieved blood pressure on renal function decline and first stroke in hypertensive patients with chronic kidney disease

2017 ◽  
Vol 33 (3) ◽  
pp. 409-417 ◽  
Author(s):  
Youbao Li ◽  
Min Liang ◽  
Chongfei Jiang ◽  
Guobao Wang ◽  
Jianping Li ◽  
...  
2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Salma Naouaoui ◽  
Meriem Chettati ◽  
Wafaa Fadili ◽  
Inass Laouad

Abstract Background and Aims High blood pressure is a leading cause of end stage renal disease (ESRD). However; early detection of chronic kidney disease (CKD) delays progression of kidney failure and reduces the risk of cardiovascular complications. Therefore, the aim of our study was to assess the attitudes and practices of interns and residents regarding screening for chronic kidney disease in patients with high blood pressure at a Moroccan University hospital. Methods A cross-sectional survey was conducted among 100 medical interns and residents at Mohammed VI university hospital of Marrakesh. Results Overall, 82% of the trainees who responded (response rate 89%) stated that they were sensitized to screening for chronic kidney disease in patients with high blood pressure, mainly during their medical studies. However, trainees who systematically monitor renal function in their hypertensive patients did not exceed 13%. While 34% of respondents preferred to refer them to a cardiologist or a nephrologist, and 35% looked for renal impairment only in special situations, dominated by the presence of diabetes or severe hypertension. The main tests used by the participants for monitoring kidney function were represented by blood renal function (100%) and 24h urine protein (61%). Microalbuminuria was mentioned by only 23% of the trainees. The major limits reported by the surveyed physicians were the lack of experience and the non- compliance of patients. Conclusion Our findings revealed inappropriate practices among our training doctors concerning the screening of CKD in hypertensive patients. Therefore, more educational workshops and courses are recommended, especially in low-income countries where access to dialysis is not always affordable.


2012 ◽  
Vol 30 ◽  
pp. e218 ◽  
Author(s):  
Kouichi Tamura ◽  
Mai Yanagi ◽  
Tetsuya Fujikawa ◽  
Hiromichi Wakui ◽  
Tomohiko Kanaoka ◽  
...  

2014 ◽  
Vol 16 (5) ◽  
pp. 362-366 ◽  
Author(s):  
Kei Yokota ◽  
Masamichi Fukuda ◽  
Yoshio Matsui ◽  
Kazuomi Kario ◽  
Kenjiro Kimura

Author(s):  
Qiao Qin ◽  
Fangfang Fan ◽  
Jia Jia ◽  
Yan Zhang ◽  
Bo Zheng

Abstract Purpose An increase in arterial stiffness is associated with rapid renal function decline (RFD) in patients with chronic kidney disease (CKD). The aim of this study was to investigate whether the radial augmentation index (rAI), a surrogate marker of arterial stiffness, affects RFD in individuals without CKD. Methods A total of 3165 Chinese participants from an atherosclerosis cohort with estimated glomerular filtration rates (eGFR) of ≥ 60 mL/min/1.73 m2 were included in this study. The baseline rAI normalized to a heart rate of 75 beats/min (rAIp75) was obtained using an arterial applanation tonometry probe. The eGFRs at both baseline and follow-up were calculated using the equation derived from the Chronic Kidney Disease Epidemiology Collaboration. The association of the rAIp75 with RFD (defined as a drop in the eGFR category accompanied by a ≥ 25% drop in eGFR from baseline or a sustained decline in eGFR of > 5 mL/min/1.73 m2/year) was evaluated using the multivariate regression model. Results During the 2.35-year follow-up, the incidence of RFD was 7.30%. The rAIp75 had no statistically independent association with RFD after adjustment for possible confounders (adjusted odds ratio = 1.12, 95% confidence interval: 0.99–1.27, p = 0.074). When stratified according to sex, the rAIp75 was significantly associated with RFD in women, but not in men (adjusted odds ratio and 95% confidence interval: 1.23[1.06–1.43], p = 0.007 for women, 0.94[0.76–1.16], p = 0.542 for men; p for interaction = 0.038). Conclusion The rAI might help screen for those at high risk of early rapid RFD in women without CKD.


2021 ◽  
Vol 22 (12) ◽  
pp. 6270
Author(s):  
Chia-Ter Chao ◽  
Shih-Hua Lin

The accumulation of uremic toxins (UTs) is a prototypical manifestation of uremic milieu that follows renal function decline (chronic kidney disease, CKD). Frailty as a potential outcome-relevant indicator is also prevalent in CKD. The intertwined relationship between uremic toxins, including small/large solutes (phosphate, asymmetric dimethylarginine) and protein-bound ones like indoxyl sulfate (IS) and p-cresyl sulfate (pCS), and frailty pathogenesis has been documented recently. Uremic toxins were shown in vitro and in vivo to induce noxious effects on many organ systems and likely influenced frailty development through their effects on multiple preceding events and companions of frailty, such as sarcopenia/muscle wasting, cognitive impairment/cognitive frailty, osteoporosis/osteodystrophy, vascular calcification, and cardiopulmonary deconditioning. These organ-specific effects may be mediated through different molecular mechanisms or signal pathways such as peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), mitogen-activated protein kinase (MAPK) signaling, aryl hydrocarbon receptor (AhR)/nuclear factor-κB (NF-κB), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Runt-related transcription factor 2 (RUNX2), bone morphogenic protein 2 (BMP2), osterix, Notch signaling, autophagy effectors, microRNAs, and reactive oxygen species induction. Anecdotal clinical studies also suggest that frailty may further accelerate renal function decline, thereby augmenting the accumulation of UTs in affected individuals. Judging from these threads of evidence, management strategies aiming for uremic toxin reduction may be a promising approach for frailty amelioration in patients with CKD. Uremic toxin lowering strategies may bear the potential of improving patients’ outcomes and restoring their quality of life, through frailty attenuation. Pathogenic molecule-targeted therapeutics potentially disconnect the association between uremic toxins and frailty, additionally serving as an outcome-modifying approach in the future.


2012 ◽  
Vol 50 (1) ◽  
pp. 147-155 ◽  
Author(s):  
S. Chakrabarti ◽  
H. M. Syme ◽  
C. A. Brown ◽  
J. Elliott

Chronic kidney disease is common in geriatric cats, but most cases have nonspecific renal lesions, and few studies have correlated these lesions with clinicopathological markers of renal dysfunction. The aim of this study was to identify the lesions best correlated with renal function and likely mediators of disease progression in cats with chronic kidney disease. Cats were recruited through 2 first-opinion practices between 1992 and 2010. When postmortem examinations were authorized, renal tissues were preserved in formalin. Sections were evaluated by a pathologist masked to all clinicopathological data. They were scored semiquantitatively for the severity of glomerulosclerosis, interstitial inflammation, and fibrosis. Glomerular volume was measured using image analysis; the percentage of glomeruli that were obsolescent was recorded. Sections were assessed for hyperplastic arteriolosclerosis and tubular mineralization. Kidneys from 80 cats with plasma biochemical data from the last 2 months of life were included in the study. Multivariable linear regression ( P < .05) was used to assess the association of lesions with clinicopathological data obtained close to death. Interstitial fibrosis was the lesion best correlated with the severity of azotemia, hyperphosphatemia, and anemia. Proteinuria was associated with interstitial fibrosis and glomerular hypertrophy, whereas higher time-averaged systolic blood pressure was associated with glomerulosclerosis and hyperplastic arteriolosclerosis.


Hypertension ◽  
2010 ◽  
Vol 55 (5) ◽  
pp. 1110-1115 ◽  
Author(s):  
Martin L. Ford ◽  
Laurie A. Tomlinson ◽  
Thomas P.E. Chapman ◽  
Chakravarthi Rajkumar ◽  
Stephen G. Holt

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