scholarly journals Kidney Damage Biomarkers and Incident Chronic Kidney Disease During Blood Pressure Reduction

2018 ◽  
Vol 169 (9) ◽  
pp. 610 ◽  
Author(s):  
William R. Zhang ◽  
Timothy E. Craven ◽  
Rakesh Malhotra ◽  
Alfred K. Cheung ◽  
Michel Chonchol ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Blood Pressure Reduction ◽  
Kidney Damage ◽  
Pressure Reduction ◽  
Incident Chronic Kidney Disease

scholarly journals Intermittent hypoxia exacerbates increased blood pressure in rats with chronic kidney disease

2018 ◽  
Vol 315 (4) ◽  
pp. F927-F941 ◽  
Author(s):  
Jennifer L. Riggs ◽  
Carolyn E. Pace ◽  
Heather H. Ward ◽  
Laura V. Gonzalez Bosc ◽  
Lynnette Rios ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Intermittent Hypoxia ◽  
Interstitial Fibrosis ◽  
Control Diet ◽  
Kidney Injury ◽  
Kidney Damage ◽  
Plasma Creatinine ◽  
Sprague Dawley

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.

scholarly journals Gender differences in adenine-induced chronic kidney disease and cardiovascular complications in rats

2014 ◽  
Vol 307 (11) ◽  
pp. F1169-F1178 ◽  
Author(s):  
Vishal Diwan ◽  
David Small ◽  
Kate Kauter ◽  
Glenda C. Gobe ◽  
Lindsay Brown
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiac Hypertrophy ◽  
Kidney Function ◽  
Cardiac Fibrosis ◽  
Kidney Damage ◽  
Plasma Testosterone ◽  
Male And Female ◽  
Males And Females

Gender contributes to differences in incidence and progression of chronic kidney disease (CKD) and associated cardiovascular disease. To induce kidney damage in male and female Wistar rats ( n = 12/group), a 0.25% adenine diet for 16 wk was used. Kidney function (blood urea nitrogen, plasma creatinine, proteinuria) and structure (glomerular damage, tubulointerstitial atrophy, fibrosis, inflammation); cardiovascular function (blood pressure, ventricular stiffness, vascular responses, echocardiography) and structure (cardiac fibrosis); plasma testosterone and estrogen concentrations; and protein expression for oxidative stress [heme oxygenase-1, inflammation (TNF-α), fibrosis (transforming growth factor-β), ERK1/2, and estrogen receptor-α (ER-α)] were compared in males and females. Adenine-fed females had less decline in kidney function than adenine-fed males, although kidney atrophy, inflammation, and fibrosis were similar. Plasma estrogen concentrations increased and plasma testosterone concentrations decreased in adenine-fed males, with smaller changes in females. CKD-associated molecular changes in kidneys were more pronounced in males than females except for expression of ER-α in the kidney, which was completely suppressed in adenine-fed males but unchanged in adenine-fed females. Both genders showed increased blood pressure, ventricular stiffness, and cardiac fibrosis with the adenine diet. Cardiovascular changes with adenine were similar in males and females, except males developed concentric, and females eccentric cardiac hypertrophy. In hearts from adenine-fed male and female rats, expression of ER-α and activation of the ERK1/2 pathway were increased, in part explaining changes in cardiac hypertrophy. In summary, adenine-induced kidney damage may be increased in males due to the suppression of ER-α.

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