scholarly journals Deficiency in Pappa2 expression reduces nephron endowment and associates with hypertension and chronic kidney disease in rats

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Vikash Kumar ◽  
Chun Yang ◽  
Terry Kurth ◽  
Aron Geurts ◽  
Allen W Cowley
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Nephron Endowment

scholarly journals Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
F. Boubred ◽  
M. Saint-Faust ◽  
C. Buffat ◽  
I. Ligi ◽  
I. Grandvuillemin ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Birth Weight ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Chronic Renal Disease ◽  
Postnatal Growth ◽  
Nephron Number ◽  
Nephron Endowment ◽  
Causes Of Mortality

Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the “early programming” of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a “factor of vulnerability” when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways.

scholarly journals Loss of miR-17~92 results in dysregulation of Cftr in nephron progenitors

2019 ◽  
Vol 316 (5) ◽  
pp. F993-F1005 ◽  
Author(s):  
Yu Leng Phua ◽  
Kevin Hong Chen ◽  
Shelby L. Hemker ◽  
April K. Marrone ◽  
Andrew J. Bodnar ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Development ◽  
The Self ◽  
Self Renewal ◽  
Nephron Endowment ◽  
Nephron Progenitors ◽  
Increased Risk ◽  
Renal Hypodysplasia

We have previously demonstrated that loss of miR-17~92 in nephron progenitors in a mouse model results in renal hypodysplasia and chronic kidney disease. Clinically, decreased congenital nephron endowment because of renal hypodysplasia is associated with an increased risk of hypertension and chronic kidney disease, and this is at least partly dependent on the self-renewal of nephron progenitors. Here, we present evidence for a novel molecular mechanism regulating the self-renewal of nephron progenitors and congenital nephron endowment by the highly conserved miR-17~92 cluster. Whole transcriptome sequencing revealed that nephron progenitors lacking this cluster demonstrated increased Cftr expression. We showed that one member of the cluster, miR-19b, is sufficient to repress Cftr expression in vitro and that perturbation of Cftr activity in nephron progenitors results in impaired proliferation. Together, these data suggest that miR-19b regulates Cftr expression in nephron progenitors, with this interaction playing a role in appropriate nephron progenitor self-renewal during kidney development to generate normal nephron endowment.

No effect of vitamin D supplementation on metabolic parameters but on lipids in patients with type 2 diabetes and chronic kidney disease

2020 ◽  
pp. 1-10
Author(s):  
Jiwoon Kim ◽  
Ji Sun Nam ◽  
Heejung Kim ◽  
Hye Sun Lee ◽  
Jung Eun Lee
Keyword(s):  
Type 2 Diabetes ◽  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Supplementation ◽  
Lipid Profiles ◽  
Metabolic Parameters ◽  
Injection Group ◽  
Different Doses

Abstract. Background/Aims: Trials on the effects of cholecalciferol supplementation in type 2 diabetes with chronic kidney disease patients were underexplored. Therefore, the aim of this study was to investigate the effects of two different doses of vitamin D supplementation on serum 25-hydroxyvitamin D [25(OH)D] concentrations and metabolic parameters in vitamin D-deficient Korean diabetes patients with chronic kidney disease. Methods: 92 patients completed this study: the placebo group (A, n = 33), the oral cholecalciferol 1,000 IU/day group (B, n = 34), or the single 200,000 IU injection group (C, n = 25, equivalent to 2,000 IU/day). 52% of the patients had less than 60 mL/min/1.73m2 of glomerular filtration rates. Laboratory test and pulse wave velocity were performed before and after supplementation. Results: After 12 weeks, serum 25(OH)D concentrations of the patients who received vitamin D supplementation were significantly increased (A, -2.4 ± 1.2 ng/mL vs. B, 10.7 ± 1.2 ng/mL vs. C, 14.6 ± 1.7 ng/mL; p < 0.001). In addition, the lipid profiles in the vitamin D injection group (C) showed a significant decrease in triglyceride and a rise in HDL cholesterol. However, the other parameters showed no differences. Conclusions: Our data indicated that two different doses and routes of vitamin D administration significantly and safely increased serum 25(OH)D concentrations in vitamin D-deficient diabetes patients with comorbid chronic kidney disease. In the group that received the higher vitamin D dose, the lipid profiles showed significant improvement, but there were no beneficial effects on other metabolic parameters.

Ankle-brachial index in chronic kidney disease

VASA ◽  
2012 ◽  
Vol 41 (3) ◽  
pp. 159-160
Author(s):  
Espinola-Klein ◽  
F. Dopheide ◽  
Gori
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ankle Brachial Index
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