<b>Objective</b> To examine long term cardiorenal outcomes associated with increased concentrations of creatinine after the start of angiotensin converting enzyme inhibitor/angiotensin receptor blocker treatment.<b>Design</b> Population based cohort study using electronic health records from the Clinical Practice Research Datalink and Hospital Episode Statistics.<b>Setting</b> UK primary care, 1997-2014.<b>Participants</b> Patients starting treatment with angiotensin converting enzyme inhibitors or angiotensin receptor blockers (n=122 363).<b>Main outcome measures</b> Poisson regression was used to compare rates of end stage renal disease, myocardial infarction, heart failure, and death among patients with creatinine increases of 30% or more after starting treatment against those without such increases, and for each 10% increase in creatinine.
The mean age to end-stage renal disease (ESRD) was 54 yr, with no significant difference between men and women and no association with the angiotensin-converting enzyme polymorphism.
Angiotensin receptor blockers are associated with lower mortality than ACE inhibitors in predialytic stage 5 chronic kidney disease: A nationwide study of therapy with renin-angiotensin system blockade.
Withdrawal of angiotensin-converting enzyme (ACE) inhibitors may affect the progression of chronic renal failure and an insertion/deletion (I/D) polymorphism of the ACE gene may influence it.
Although plasma levels of adiponectin, a recently discovered anti-inflammatory and antiatherogenic adipocytokine, are markedly elevated in ESRD, gene expression of adiponectin (ApM1) has not been analyzed in ESRD patients.
The association between the use of angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) and mortality in end-stage renal disease (ESRD) patients lacks sufficient evidence.
Our results conclude that TGF-β1 (rs1800470) may increase the risk of both ESRD and T2D in both populations, but TGF-β1 (rs1800469) provided risk for only ESRD in the population of Jammu and Kashmir.
The common mechanism is probably through lower levels of ACE, glomerular pressure and proteinuria resulting in reduced renal damage and retardation of progression to ESRF.
Both in ADPKD and IGAN groups, there was no significant difference in the frequencies of ecNOS genotypes between patients with normal renal function and age matched patients with ESRF and between patients with normal renal function and control group.
For renal outcomes, ARBs significantly reduced the risk of ESRD by 23% (odds ratio 0.77, 95%CI 0.65-0.92), while ACE inhibitors were not associated with a decreased risk of ESRD (0.69, 0.43-1.10).
Our data also suggest that an interaction effect may exist between ACE (I/D) and eNOS (G894 --> T) polymorphism in increasing the risk of vascular complications in ESRD patients.
To investigate whether the down-regulation of renal parathyroid hormone/parathyroid hormone related protein (PTH/PTHrP) receptor messenger ribonucleic acid (mRNA) expression is a general phenomenon in patients with different stages of renal disease, besides chronic renal failure.
Two hundred and forty-six end-stage renal disease (ESRD) patients on peritoneal dialysis and 183 control subjects, all of Chinese origin, were genotyped for the ACE insertion/deletion (I/D) and the AGT M235T gene polymorphisms.
The deletion polymorphism of the angiotensin-converting enzyme (ACE) gene has been considered as a risk factor for IgA nephropathy and for its progression to end-stage renal failure.
This study examined the features of different PTH fragments in stage 5 chronic kidney disease (CKD) and the effects of parathyroidectomy (PTX) on the above markers in severe secondary hyperparathyroidism (SHPT) patients.
In light of these findings, the main pathophysiological consequence of the downregulation of Klotho observed in acute and chronic renal failure may be the induction of renal FGF23 resistance.
Our results indicate that the ACE DD genotype in FSGS may be a risk factor for the poor responsiveness to steroid therapy and the development of chronic renal failure.
Six patients with steroid-resistant nephrotic syndrome went into end stage renal disease; ACE genotype was I/I in one and I/D in five, but none were D/D.