scholarly journals Influence of angiotensin converting enzyme (ACE) gene rs4362 polymorphism on the progression of kidney failure in patients with autosomal dominant polycystic kidney disease (ADPKD)

2016 ◽  
Vol 143 (6) ◽  
pp. 748
Author(s):  
BhaskarV.K.S. Lakkakula ◽  
Gnanasambandan Ramanathan ◽  
Santu Ghosh ◽  
Ramprasad Elumalai ◽  
Soundararajan Periyasamy
Keyword(s):  
Kidney Disease ◽  
Angiotensin Converting Enzyme ◽  
Polycystic Kidney Disease ◽  
Kidney Failure ◽  
Autosomal Dominant ◽  
Converting Enzyme ◽  
Polycystic Kidney ◽  
Ace Gene ◽  
Autosomal Dominant Polycystic Kidney

Effect of statin and angiotensin-converting enzyme inhibition on structural and hemodynamic alterations in autosomal dominant polycystic kidney disease model

2007 ◽  
Vol 293 (3) ◽  
pp. F854-F859 ◽  
Author(s):  
Iram Zafar ◽  
Yunxia Tao ◽  
Sandor Falk ◽  
Kimberly McFann ◽  
Robert W. Schrier ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Angiotensin Converting Enzyme ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Combined Treatment ◽  
Ace Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney

Autosomal dominant polycystic kidney disease (ADPKD) is the most common life-threatening hereditary disease and is the fourth most common cause of end-stage kidney disease. Preclinical studies to identify effective interventions to prevent or slow progression of PKD nephropathy are therefore direly needed. Heterozygous Han:SPRD rats are an autosomal dominant PKD model with many of the characteristics of ADPKD in humans. In the present study, parameters known to antedate the decrease in renal function, namely, renal structure, renal blood flow (RBF), and mean arterial pressure (MAP), were evaluated with three different interventions, namely, HMG-CoA reductase inhibition with lovastatin, angiotensin-converting enzyme (ACE) inhibition with enalapril, and a combination of these two treatments. The statin therapy demonstrated structural and functional benefits, including increased RBF and decreased BUN, independently of a change in MAP, while the ACE inhibition therapy demonstrated structural benefit in association with a decrease in MAP. An enhancement of these protective interventions in this autosomal dominant PKD model was not demonstrated with the combined treatment.

scholarly journals Evaluation of common polymorphisms of eNOS gene and ACE gene in autosomal dominant polycystic kidney disease patients and their association with hypertension and renal failure

2019 ◽  
Vol 10 (1) ◽  
pp. e04-e04
Author(s):  
Tahereh Malakoutian ◽  
Bahareh Madadi ◽  
Ahmad Ebrahimi
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Enos Gene ◽  
Polycystic Kidney ◽  
Ace Gene ◽  
Control Subjects ◽  
Significant Difference ◽  
Autosomal Dominant Polycystic Kidney

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is the most hereditary renal disease that leads to end-stage renal disease (ESRD). Objectives: Since there is no available parameter to assess the clinical course of ADPKD and its outcome, yet, the aim of our study was evaluation of the association of common polymorphisms of eNOS and ACE genes with clinical manifestations (kidney failure and hypertension) in ADPKD. Patients and Methods: Seventy-five ADPKD patients and 100 control subjects participated in our study. Around 7.5 cc of whole blood was taken from each participant and sent to the genetic laboratory. DNA was obtained from them by the phenol chloroform extraction and ethanol precipitation techniques. Then genotyping for I/D polymorphism of ACE gene and Glu298 ASP and T786C polymorphisms of eNOS gene was performed by PCR electrophoresis and molecular evaluation by special primers for two genes. Results: The frequency of DD polymorphism of ACE gene and TC polymorphism of T786C of eNOS were considerably elevated in ADPKD individuals than control subjects. No significant difference between groups regarding Glu298 ASP polymorphisms of eNOS gene was detected. In ADPKD patients, 29 patients (39%) had hypertension, 5 patients (6.7%) had diabetes and 43 patients (57%) had glomerular filtration rate (GFR) below 60 mL/min/1.73 m2 . The polymorphisms of ACE and eNOS genes were not meaningfully different regarding diabetes, high blood pressure, GFR and plasma creatinine in ADPKD individuals (P>0.05). Conclusion: In our study, we could not find any association between polymorphisms of ACE and eNOS genes with renal insufficiency and hypertension in ADPKD patients.

scholarly journals Asymptomatic Pyuria as a Prognostic Biomarker in Autosomal Dominant Polycystic Kidney Disease

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0004292021
Author(s):  
Brian E. Jones ◽  
Yaman G. Mkhaimer ◽  
Laureano J. Rangel ◽  
Maroun Chedid ◽  
Phillip J. Schulte ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Disease Progression ◽  
Polycystic Kidney Disease ◽  
Kidney Function ◽  
Kidney Failure ◽  
Autosomal Dominant ◽  
Prognostic Biomarker ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney

Background: Autosomal dominant polycystic kidney disease (ADPKD) has phenotypic variability only partially explained by established biomarkers that do not readily assess pathologically important factors of inflammation and kidney fibrosis. We evaluated asymptomatic pyuria, a surrogate marker of inflammation, as a biomarker for disease progression. Methods: We performed a retrospective cohort study of adult patients with ADPKD. Patients were divided into asymptomatic pyuria (AP) and no pyuria (NP) groups. We evaluated the effect of pyuria on kidney function and kidney volume. Longitudinal models evaluating kidney function and kidney volume rate of change with respect to incidences of asymptomatic pyuria were created. Results: There were 687 included patients (347 AP, 340 NP). The AP group had more female (65.1% vs 49.4%). Median age at kidney failure was 86 and 80 years in NP and AP groups, respectively (Log-rank, p=0.49) for patients with Mayo Imaging Class (MIC)1A-1B as compared to 59 and 55 years for patients with MIC1C-1D-1E (Log-rank, p=0.02). Compared to NP group, the rate of kidney function (ml/min/1.73m2/year) decline shifted significantly after detection of asymptomatic pyuria in models including all patients (-1.48, p<0.001), MIC 1A-B patients (-1.79 , p<0.001), MIC 1C-1D-1E patients (-1.18, p<0.001), and PKD1 patients (-1.04, p<0.001). Models evaluating kidney volume rate of growth showed no change after incidence of asymptomatic pyuria as compared to NP group. Conclusions: Asymptomatic pyuria is associated with kidney failure and faster kidney function decline irrespective of the ADPKD gene, cystic burden, and cystic growth. These results support asymptomatic pyuria as an enriching prognostic biomarker for the rate of disease progression.-

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