scholarly journals Sodium Thiosulfate Improves Hypertension in Rats with Adenine-Induced Chronic Kidney Disease

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 147
Author(s):  
Chien-Ning Hsu ◽  
Chih-Yao Hou ◽  
Guo-Ping Chang-Chien ◽  
Sufan Lin ◽  
Hung-Wei Yang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Oral Administration ◽  
Sodium Thiosulfate ◽  
Renin Angiotensin System ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Targeting Therapy ◽  
Sprague Dawley Rats

Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2S-based therapy, can exert a protective effect against hypertension in an adenine-induced CKD rat model. Eight-week-old male Sprague–Dawley rats were fed with 0.5% adenine chow for 3 weeks to induce CKD. After 1 week, the rats were divided into two groups: one without and one with STS (2 g/kg body weight/day) in drinking water for 2 weeks. Treatment with STS lowered systolic and diastolic blood pressure by 7 and 9 mm Hg, respectively. Renal H2S-generating enzyme expression was inhibited by CKD, while STS therapy increased plasma levels of H2S and thiosulfate. Additionally, restoration of nitric oxide bioavailability and rebalance of the renin–angiotensin system may contribute to the protective effects of STS. Our data suggest that the oral administration of STS improves hypertension in an adenine-induced CKD model, which brings us closer to the clinical translation of H2S-targeting therapy in CKD-induced hypertension.

scholarly journals Effect of sodium bicarbonate supplementation on the renin-angiotensin system in patients with chronic kidney disease and acidosis: a randomized clinical trial

2020 ◽  
Author(s):  
Dominique M. Bovée ◽  
Lodi C. W. Roksnoer ◽  
Cornelis van Kooten ◽  
Joris I. Rotmans ◽  
Liffert Vogt ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Sodium Chloride ◽  
Kidney Disease ◽  
Sodium Bicarbonate ◽  
Renin Angiotensin System ◽  
Ammonium Excretion ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Endothelin 1 ◽  
Plasma Bicarbonate

Abstract Background Acidosis-induced kidney injury is mediated by the intrarenal renin-angiotensin system, for which urinary renin is a potential marker. Therefore, we hypothesized that sodium bicarbonate supplementation reduces urinary renin excretion in patients with chronic kidney disease (CKD) and metabolic acidosis. Methods Patients with CKD stage G4 and plasma bicarbonate 15–24 mmol/l were randomized to receive sodium bicarbonate (3 × 1000 mg/day, ~ 0.5 mEq/kg), sodium chloride (2 × 1,00 mg/day), or no treatment for 4 weeks (n = 15/arm). The effects on urinary renin excretion (primary outcome), other plasma and urine parameters of the renin-angiotensin system, endothelin-1, and proteinuria were analyzed. Results Forty-five patients were included (62 ± 15 years, eGFR 21 ± 5 ml/min/1.73m2, plasma bicarbonate 21.7 ± 3.3 mmol/l). Sodium bicarbonate supplementation increased plasma bicarbonate (20.8 to 23.8 mmol/l) and reduced urinary ammonium excretion (15 to 8 mmol/day, both P < 0.05). Furthermore, a trend towards lower plasma aldosterone (291 to 204 ng/L, P = 0.07) and potassium (5.1 to 4.8 mmol/l, P = 0.06) was observed in patients receiving sodium bicarbonate. Sodium bicarbonate did not significantly change the urinary excretion of renin, angiotensinogen, aldosterone, endothelin-1, albumin, or α1-microglobulin. Sodium chloride supplementation reduced plasma renin (166 to 122 ng/L), and increased the urinary excretions of angiotensinogen, albumin, and α1-microglobulin (all P < 0.05). Conclusions Despite correction of acidosis and reduction in urinary ammonium excretion, sodium bicarbonate supplementation did not improve urinary markers of the renin-angiotensin system, endothelin-1, or proteinuria. Possible explanations include bicarbonate dose, short treatment time, or the inability of urinary renin to reflect intrarenal renin-angiotensin system activity. Graphic abstract

scholarly journals Treatment with patiromer decreases aldosterone in patients with chronic kidney disease and hyperkalemia on renin-angiotensin system inhibitors

2016 ◽  
Vol 90 (3) ◽  
pp. 696-704 ◽  
Author(s):  
Matthew R. Weir ◽  
George L. Bakris ◽  
Coleman Gross ◽  
Martha R. Mayo ◽  
Dahlia Garza ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Stopping Renin-Angiotensin System Inhibitors in Chronic Kidney Disease: Predictors of Response

2011 ◽  
Vol 119 (4) ◽  
pp. c348-c354 ◽  
Author(s):  
Anderson Roman Gonçalves ◽  
Arif Khwaja ◽  
Aimune K. Ahmed ◽  
Mohsen El Kossi ◽  
Meguid El Nahas
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Predictors Of Response

scholarly journals Short-Term High Fat Intake Does Not Significantly Alter Markers of Renal Function or Inflammation in Young Male Sprague-Dawley Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Catherine Crinigan ◽  
Matthew Calhoun ◽  
Karen L. Sweazea
Keyword(s):  
Kidney Disease ◽  
Renal Mass ◽  
Early Stage ◽  
Young Male ◽  
Protective Effects ◽  
Sprague Dawley ◽  
High Fat ◽  
Short Term ◽  
Sprague Dawley Rats ◽  
The Impact

Chronic high fat feeding is correlated with diabetes and kidney disease. However, the impact of short-term high fat diets (HFD) is not well-understood. Six weeks of HFD result in indices of metabolic syndrome (increased adiposity, hyperglycemia, hyperinsulinemia, hyperlipidemia, hyperleptinemia, and impaired endothelium-dependent vasodilation) compared to rats fed on standard chow. The hypothesis was that short-term HFD would induce early signs of renal disease. Young male Sprague-Dawley rats were fed either HFD (60% fat) or standard chow (5% fat) for six weeks. Morphology was determined by measuring changes in renal mass and microstructure. Kidney function was measured by analyzing urinary protein, creatinine, and hydrogen peroxide (H2O2) concentrations, as well as plasma cystatin C concentrations. Renal damage was measured through assessment of urinary oxDNA/RNA concentrations as well as renal lipid peroxidation, tumor necrosis factor alpha (TNFα), and interleukin 6 (IL-6). Despite HFD significantly increasing adiposity and renal mass, there was no evidence of early stage kidney disease as measured by changes in urinary and plasma biomarkers as well as histology. These findings suggest that moderate hyperglycemia and inflammation produced by short-term HFD are not sufficient to damage kidneys or that the ketogenic HFD may have protective effects within the kidneys.

P0178COMPARATIVE EFFECTIVENESS OF RENIN-ANGIOTENSIN SYSTEM INHIBITORS AND CALCIUM CHANNEL BLOCKERS IN INDIVIDUALS WITH ADVANCED CHRONIC KIDNEY DISEASE: A NATIONWIDE COHORT STUDY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Edouard L Fu ◽  
Catherine M Clase ◽  
Marie Evans ◽  
Bengt Lindholm ◽  
Joris Rotmans ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Lower Risk ◽  
Renin Angiotensin System ◽  
Channel Blockers ◽  
Angiotensin System ◽  
Advanced Chronic Kidney Disease ◽  
Risk Of Mortality ◽  
Similar Risk

Abstract Background and Aims There is a lack of data that could help to guide the choice of antihypertensive agents in patients with advanced chronic kidney disease (CKD). We evaluated whether initiating treatment with a renin-angiotensin system inhibitor (RASi) is superior to calcium channel blockers (CCB) in preventing mortality, major adverse cardiovascular events (MACE) or kidney replacement therapy (KRT) in patients with advanced CKD. Method Observational study from the Swedish Renal Register, 2007-2017. We identified all nephrologist-referred patients in Sweden who initiated RASi or CCB treatment and had non-dialysis dependent advanced CKD (eGFR &lt;30 ml/min/1.73m2). The associations between RASi vs CCB initiation, mortality, MACE and KRT were assessed by Cox regression. Analyses were adjusted with propensity score weighting for a wide range of confounders, including demographics, blood pressure, laboratory measures, comorbidities and medications. As a positive control we evaluated new use of the same drugs in patients with CKD G3 (N = 2608; eGFR between 30-60 ml/min/1.73m2). Furthermore subgroup, as-treated and competing risk analyses were performed. Results The propensity-score weighted cohort included 2479 RASi and 2327 CCB initiators who were well-matched for baseline confounders (all standardized differences &lt;0.1). Median follow-up was 4.1 years, with a maximum follow-up of over 10 years. Compared to CCB, initiation of RASi was associated with a similar risk of mortality (adjusted HR 0.94; 95% CI 0.85-1.03) and MACE (0.99; 0.87-1.13), but with a lower risk of KRT (0.87; 0.78-0.98). Results were consistent across subgroups, in as-treated analyses and after accounting for the competing risk of death. In the control cohort of patients with CKD G3, initiation of RASi (versus CCB) was associated with lower KRT risk (adjusted HR 0.67; 0.47-0.96), and similar risk of mortality (0.91; 0.76-1.08) and MACE (1.06; 0.82-1.35). Conclusion Compared with CCB, initiation of RASi in patients with advanced CKD was associated with a lower risk of KRT, but no different risk of mortality or MACE.

Peripheral and central angiotensin II regulates expression of genes of the renin-angiotensin system

1992 ◽  
Vol 262 (5) ◽  
pp. E651-E657 ◽  
Author(s):  
K. Kohara ◽  
K. B. Brosnihan ◽  
C. M. Ferrario ◽  
A. Milsted
Keyword(s):  
Northern Blot Analysis ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Expression Of Genes ◽  
Sprague Dawley Rats ◽  
Renin Mrna ◽  
Lower Brain Stem

We investigated whether angiotensin (ANG) II has the potential to regulate expression of genes of the renin-angiotensin system (RAS) in peripheral and central tissues. ANG II (0.1 or 6.0 nmol/h) was infused by osmotic minipump into male Sprague-Dawley rats (225-250 g) for 5 days, either intravenously or intracerebroventricularly. We measured angiotensinogen mRNA in liver, adrenal glands, and brain (hypothalamus and lower brain stem), renin mRNA in the kidney, and angiotensin-converting enzyme (ACE) mRNA in the lung and testis by Northern blot analysis. We demonstrated that plasma ANG II increases the levels of liver angiotensinogen mRNA, decreases kidney renin mRNA, and decreases lung ACE mRNA. Intracerebroventricular administration of ANG II resulted in a different pattern of responses of the peripheral RAS components. Liver angiotensinogen mRNA was increased, and kidney renin mRNA was decreased by both doses of ANG II, whereas lung ACE mRNA remained unresponsive at either dose. Centrally mediated influences of ANG II are most likely indirect since plasma ANG II concentration was not changed. This study has revealed that ANG II has profound diverse effects that influence the regulation of its formation. Further, results indicate that genes of the RAS responded to exogenous ANG II in both tissue- and route-specific ways.

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