Microvascular rarefaction and hypertension in the impaired recovery and progression of kidney disease following AKI in preexisting CKD states

Polichnowski, Aaron J.

doi:10.1152/ajprenal.00419.2018

Cited by 19 publications

(11 citation statements)

References 73 publications

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“…Decreased vessel density promotes tissue hypoxia, alters local hemodynamics, and is implicated as a contributor to disease progression, yet at the same time tubular injury can precede the rarefaction. 85,92 While the bidirectional relationship between rarefaction and kidney disease remains to be elucidated, it is clear that microvascular rarefaction, fibrosis, and vasoreactivity are related and that endothelial cell interactions with the wrapping perivascular cells (smooth muscle cells or pericytes) are critical. 93 Consider pericyte to myofibroblast differentiation during fibrosis.…”

Section: Microva Scul Ar R Arefac Tionmentioning

confidence: 99%

Microvascular dysfunction and kidney disease: Challenges and opportunities?

et al. 2020

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Kidney disease is an underappreciated public health crisis.Approximately 20% of all hospital admissions and more than half of all critically ill patients admitted to the intensive care units have acute kidney injury or AKI. 1 Further, 15% of the general population, or 1 in every 7 adults, have chronic kidney disease or CKD. 2 Kidney disease is the 9th leading cause of death and adds considerably to the cost of health care. In 2017 alone, Medicare spent $36 billion caring for patients with end-stage kidney disease on dialysis and an additional $84 billion on those with CKD. Although the kidneys are relatively small and account for only 1% of the total body weight, almost 20% of the blood flow is directed to the kidney under resting conditions. The resistance to blood flow within the renal microcirculation is intricately regulated by hormonal, paracrine, autocrine, and neural controls, to alter blood flow and glomerular filtration rate. Undoubtedly from a clinical perspective, understanding the structure and function of the renal microvasculature is important for

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Section: Microva Scul Ar R Arefac Tionmentioning

confidence: 99%

Microvascular dysfunction and kidney disease: Challenges and opportunities?

et al. 2020

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“…A positive relationship between oxidative stress and AKI has been reported in the literature 7,21 . Evidence has showed that one characteristics of AKI is tubular epithelial cell oxidative stress, which further causes microvascular dysfunction and inflammation 22,23 . The present study clearly showed that increased serum HO-1 is a positive factor to predict the extent of AKI.…”

Section: Discussionmentioning

confidence: 99%

The diagnostic and prognostic value of heme oxygenase 1 in sepsis-induced acute kidney injury: a cross-sectional observational study

Xia¹,

Zhang²,

Liu³

et al. 2019

Preprint

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Background Sepsis patients suffer from severe inflammatory and poor prognosis. Local inflammation resulted from sepsis is found to trigger organ injury, such as acute kidney injury (AKI). We conducted a cross-sectional observational study to examine the diagnostic and prognostic role of serum heme oxygenase 1 (HO-1) on sepsis-induced AKI. Methods The 83 enrolled patients were initially divided into two groups with no AKI (NAKI) and sepsis-induced AKI group (SAKI) based on whether had AKI. Then the patients were concretely divided into four groups: septic shock and AKI group (SS+AKI group), sepsis-induced AKI group (S+AKI group), septic shock group (SS group), and sepsis group (S group. The venous blood was sampled within 24 hours after diagnosis of sepsis. We detected the serum HO-1 and laboratory indicators by enzyme-linked immunosorbent assay. The 28-day survival status was observed between the HO-1 high- and low-level patients grouped by the median of HO-1 concentration 41.33U/L. Results We found that there were statistically significant results of SOFA score and admission time between SAKI and NAKI group (p<0.05). The level of HO-1 in SAKI group was obviously elevated as compared with NAKI group (p<0.05). It was remarkable to show that HO-1 level was remarkably higher in SS+AKI group than that in other three groups (p<0.05). In All groups, HO-1 positively correlates with SOFA score, Scr, Hb, APTT, Urea, and TnI (p<0.05). In SS+AKI group, HO-1 was positively associated with SOFA score, Scr, AKI stage, γ-GT, and FDP (p<0.05). In S+AKI, HO-1 level was positively related to the level of Scr, AKI stage, and ALP (p<0.05). In SS group, SOFA score was in negative correlation to HO-1 (p<0.05). The AUC of HO-1 and serum creatinine was 0.824 (95% CI: 0.703-0.944) and 0.778 (95% CI: 0.658-0.919) separately. The AUC of combined with HO-1 and serum creatinine was 0.864 (95% CI: 0.761-0.968). The survival analysis showed that sepsis patients with high HO-1 level had a higher mortality rate compared with patients with low HO-1 expression. Conclusions The findings from this study make contributions to clinical value of HO-1, suggesting that HO-1 plays a diagnostic and prognostic role in sepsis-induced AKI.

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“…In this regard AKI and CKD share a number of pathogenic processes, including inflammation and parenchymal cell death. Additionally, kidney injury during AKI may initiate or aggravate the processes of capillary rarefaction and fibrosis that characterize CKD (Kida et al, 2013;Polichnowski, 2018;Yang et al, 2018). The clinical care of patients with AKI or CKD is marred by a paucity of effective therapeutic approaches.…”

Section: Introduction: Aki and Ckdmentioning

confidence: 99%

The Contribution of Histone Crotonylation to Tissue Health and Disease: Focus on Kidney Health

et al. 2020

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Acute kidney injury (AKI) and chronic kidney disease (CKD) are the most severe consequences of kidney injury. They are interconnected syndromes as CKD predisposes to AKI and AKI may accelerate CKD progression. Despite their growing impact on the global burden of disease, there is no satisfactory treatment for AKI and current therapeutic approaches to CKD remain suboptimal. Recent research has focused on the therapeutic target potential of epigenetic regulation of gene expression, including non-coding RNAs and the covalent modifications of histones and DNA. Indeed, several drugs targeting histone modifications are in clinical use or undergoing clinical trials. Acyllysine histone modifications (e.g. methylation, acetylation, and crotonylation) have modulated experimental kidney injury. Most recently, increased histone lysine crotonylation (Kcr) was observed during experimental AKI and could be reproduced in cultured tubular cells exposed to inflammatory stress triggered by the cytokine TWEAK. The degree of kidney histone crotonylation was modulated by crotonate availability and crotonate supplementation protected from nephrotoxic AKI. We now review the functional relevance of histone crotonylation in kidney disease and other pathophysiological contexts, as well as the implications for the development of novel therapeutic approaches. These studies provide insights into the overall role of histone crotonylation in health and disease.

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Microvascular rarefaction and hypertension in the impaired recovery and progression of kidney disease following AKI in preexisting CKD states

Cited by 19 publications

References 73 publications

Microvascular dysfunction and kidney disease: Challenges and opportunities?

Microvascular dysfunction and kidney disease: Challenges and opportunities?

The diagnostic and prognostic value of heme oxygenase 1 in sepsis-induced acute kidney injury: a cross-sectional observational study

The Contribution of Histone Crotonylation to Tissue Health and Disease: Focus on Kidney Health

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