scholarly journals Renal anaemia: the role of haemoglobin control in patients with chronic kidney disease

2010 ◽  
Vol 64 (3-4) ◽  
pp. 137-143
Author(s):  
Viktorija Kuzema ◽  
Aivars Pētersons ◽  
Harijs Čerņevskis ◽  
Aivars Lejnieks
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Retrospective Chart Review ◽  
Chronic Glomerulonephritis ◽  
Advanced Degree ◽  
Renal Anaemia ◽  
Erythropoiesis Stimulating Agents ◽  
The Impact

Renal anaemia: the role of haemoglobin control in patients with chronic kidney disease Chronic kidney disease (CKD) is a significant and prevalent health problem in the world. Anaemia is one of the most common manifestations in patients with CKD. The correction of anaemia with erythropoietin normalises haemoglobin level and improves quality of life. Many aspects of the impact of anaemia treatment with erythropoiesis-stimulating agents on the progression of CKD remain unresolved and disputable. The present study is a retrospective chart review of 1654 outpatients with CKD. The data were collected from the Centre of Nephrology between 1 January 2002 and 31 December 2006. The aims of the study were to assess the causes of CKD; the prevalence of anaemia based on the current guidelines for anaemia management in CKD (Kidney Disease Dialysis Outcomes Quality Initiative; K/DOQI); to evaluate haemoglobin (Hb), systolic and diastolic blood pressure (SBP and DBP), glomerular filtration rate (GFR) at the first referral to a nephrologist and at the start of renal replacement therapy (RRT). The most common causes of CKD were arterial hypertension (17.2%), chronic glomerulonephritis (17.2%), chronic intersticial nephritis (13.3%), and diabetes (12.8%). Twenty-three percent of end-stage renal disease (ESRD) patients had diabetes mellitus. At the first visit in the renal department, 16% of the patients had an advanced degree of CKD (GFR <30 ml/min). The proportion of patients under an observation in the kidney centre for a period of six months and more was only 34% (554 of 1654). Hypertension was recorded in 72% of study subjects. The blood pressure (BP) values in patients at the first visit (n = 1633) vs. at the start of RRT (n = 154) were: mean SBP 147.4 ± 24.8 mm Hg vs. 152.2 ± 23.0 mm Hg (P < 0.05); mean DBP 88.8 ± 13.6 mm Hg vs. 88.4 ± 12.0 mm Hg (P 0.05). Anaemia was recorded in 41% of study subjects, estimated using K/DOQI recommendations. The prevalence of anaemia was increased from 30.2% to 44.8% of study patients with a rise of BP (from normal BP to hypertension; P < 0.05). The mean Hb level at the start of RRT was 9.8 ± 2.1 g/dl. Only 18% of patients with renal anaemia had used erythropoiesis-stimulating agents before RRT (28 of 155). Anaemia is the prevalent condition at moderate degrees of CKD. The severity of anaemia in the CKD population is determined by evidence of diabetes, cardiovascular disease, and renal function. Anaemia may often be unrecognised or untreated.

The Role of Systemic Blood Pressure in the Progression of Chronic Kidney Disease

2015 ◽  
Vol 9 (5) ◽  
Author(s):  
Karen A Griffin ◽  
Krishna Pothugunta ◽  
Aaron J Polichnowski ◽  
Anil K Bidani
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Systemic Blood Pressure ◽  
Systemic Blood

P2641Renal and cardiovascular benefits of treatment with angiotensin receptor blockers in patients with hypertension and chronic kidney disease: A systematic review and meta-analysis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Burnier ◽  
L R Ruilope ◽  
G B Bader ◽  
S D Durg ◽  
P B Brunel
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Meta Analysis ◽  
Risk Of Bias ◽  
Forest Plot ◽  
Cardiovascular Morbidity And Mortality ◽  
Increased Risk ◽  
Receptor Blockers ◽  
The Impact

Abstract Background Blood pressure (BP) control is critical in delaying the progression of chronic kidney disease (CKD), which otherwise results in an increased risk of cardiovascular morbidity and mortality. Angiotensin II receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors, are recommended by several guidelines as first-line treatment for patients with hypertension and CKD. Purpose We reviewed and analysed the effect of ARB treatment on BP and renal outcomes (estimated glomerular filtration rate (eGFR), serum creatinine (SCr), creatinine clearance (CrCl) or proteinuria) in patients with hypertension and CKD with or without diabetes, including large clinical trials such as RENAAL and IDNT. Methods MEDLINE, EMBASE, and BIOSIS databases were searched for literature from the earliest available date to July 2017. Randomised (parallel-group) controlled trials of ≥8 weeks assessed the impact of ARBs on systolic/diastolic BP (SBP/DBP), eGFR, SCr, CrCl or proteinuria were included in the analysis. Meta-analysis (post- versus pre-treatment) and meta-regression were conducted in R-statistical software (v3.4.1) using meta- and metafor-packages. Mean difference (MD, generic inverse variance) with 95% confidence intervals (CIs) was used to pool data for an outcome in a single forest plot. The risk of bias (quality) of included studies was assessed by the six items of the Cochrane instrument. Results Of the 165 articles assessed for eligibility, 24 studies were included in the analysis (19 evaluated ARBs as monotherapy, 4 evaluated ARBs in combination with other antihypertensives and 1 evaluated ARBs both as mono- and combination therapy). Treatment with ARBs as monotherapy for ≥8 weeks to <1 year significantly reduced mean office SBP (MD, −12.60 mmHg; 95% CI, −18.53 to −6.67)/DBP (−6.52 mmHg; −11.27 to −1.77) (p<0.01). BP reduction was also significant (p<0.01) with ARB monotherapy for ≥1 year SBP (−14.84 mmHg; −17.82 to −11.85)/DBP (−10.27 mmHg; −12.26 to −8.27). ARBs also significantly reduced SBP/DBP when combined with other antihypertensive treatments for ≥8 weeks to <1 year as well as for ≥1 year (Figure). Moreover, ARBs induced significant reductions (p<0.01) in proteinuria (≥8 weeks to <1 year [MD, −0.6 g/L; 95% CI, −0.93 to −0.26; ≥1 year [−0.9 g/L; −1.22 to −0.59]), but no significant changes in eGFR, CrCl or SCr levels. The beneficial effect of ARBs was maintained overtime with no significant additional impact on SBP change (estimate: 0.025; 95% CI, –0.14 to 0.19) or eGFR (estimate: 0.068; 95% CI, −0.14 to 0.28; p=0.53). The overall risk of bias was judged to be low. Effect of ARBs on blood pressure changes Conclusion Treatment with ARBs effectively and sustainably lowered BP and proteinuria with no significant change in eGFR in patients with hypertension and CKD with or without diabetes.

scholarly journals The quality of life of chronic kidney disease patients with hypertension treated with angiotensin system-related agents

2020 ◽  
Vol 11 (4) ◽  
pp. 6633-6639
Author(s):  
Mohammed Salim KT ◽  
Saravanakumar RT ◽  
Dilip C ◽  
Amrutha KP
Keyword(s):  
Quality Of Life ◽  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Antihypertensive Drugs ◽  
Angiotensin Receptor Blockers ◽  
Converting Enzyme Inhibitors ◽  
Angiotensin System ◽  
The Impact

The chronic kidney disease (CKD) co-exist with hypertension in approximately 80 to 85 per cent of patients. The CKD stages can be defined by glomerular filtration rate (GFR), and the deterioration of kidney function or reduction in GFR has observed in those with uncontrolled blood pressure (BP). We had conducted a prospective study to analyse the impact of the angiotensin system-related agents on the quality of life of CKD patients with hypertension. The SF-36 questionnaire, direct patients interview and medical records were the sources for retrieval of information. We observed that male patients were more prone to CKD than female. Hypertension was the primary (77.8%) aetiology behind the incidence of CKD. The angiotensin-converting enzyme inhibitors (ACEI) was responsible for very low (58%) and low (44%) health disabilities to the patients. In contrast, the angiotensin receptor blockers (ARB) even though it has a limited adverse effect, the patients complained of medium (9%) and high disabilities than the ACEIs. The discontinuation of the antihypertensive drugs by the CKD patients was almost negligible (3.4%). The study concludes that a balanced diet and reasonable blood pressure control is essential to prevent the progression of CKD and to improve the quality of life.

scholarly journals Hyperuricemia and chronic kidney disease

2021 ◽  
pp. 77-81
Author(s):  
Olga Kompaniets
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Clinical Studies ◽  
Review Of The Literature ◽  
Relationship Of ◽  
The Impact ◽  
The Relationship

The article is devoted to a review of the literature on the impact of hyperuricemia on the development and progression of chronic kidney disease (CKD). The tendency of changes of views on the role of uric acid in the pathogenesis of CKD is demonstrated. An analysis of experimental, epidemiological and clinical studies on the effects of uric acid on the physiology of the nephron and endothelial tissues, the relationship of hyperuricemia with metabolic and cardiorenal syndromes.

scholarly journals Chronic kidney disease and cardiovascular events: a focus on central blood pressure

2017 ◽  
Vol 14 (1) ◽  
pp. 58-60
Author(s):  
I T Murkamilov ◽  
K A Aitbaev ◽  
I S Sabirov ◽  
V V Fomin ◽  
F A Yusupov
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Renal Dysfunction ◽  
Cardiovascular Events ◽  
Vascular Complications ◽  
Vascular Wall ◽  
Cardio Vascular

The purpose of the review - to present the literature on the role of central arterial pressure (CAP) and arterial stiffness progression cardio-vascular complications (CVC) and renal dysfunction in patients with chronic kidney disease (CKD). The main provisions. In this review we discuss the pathogenetic questions damaging effect of increasing CAP and arterial stiffness on the vascular wall, the development of arteriosclerosis, atherosclerosis and destabilization of atherosclerotic plaque in the blood vessels of the kidneys. All this is the direct cause of the CVC and renal dysfunction in CKD.

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