Oxidative stress in autosomal dominant polycystic kidney disease: player and/or early predictor for disease progression?

Andries, Asmin; Daenen, Kristien; Jouret, François; Bammens, Bert; Mekahli, Djalila; Schepdael, Ann Van

doi:10.1007/s00467-018-4004-5

Cited by 30 publications

(24 citation statements)

References 117 publications

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“…But also in nondiabetic CKD patients, disturbed regulatory MiRNAs such as MiR21 have been reported in CKD patients and an impaired complex IVactivity has been reported [57,59]. Recent evidence also found a role for mitochondrial dysfunction in nondiabetic CKD, more specifically, autosomal dominant polycystic kidney disease, which is further discussed in the accompanying review by Andries et al in this issue [58,100].…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

Oxidative stress in chronic kidney disease

et al. 2018

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Oxidative stress (OS), defined as disturbances in the pro-/antioxidant balance, is harmful to cells due to the excessive generation of highly reactive oxygen (ROS) and nitrogen (RNS) species. When the balance is not disturbed, OS has a role in physiological adaptations and signal transduction. However, an excessive amount of ROS and RNS results in the oxidation of biological molecules such as lipids, proteins, and DNA. Oxidative stress has been reported in kidney disease, due to both antioxidant depletions as well as increased ROS production. The kidney is a highly metabolic organ, rich in oxidation reactions in mitochondria, which makes it vulnerable to damage caused by OS, and several studies have shown that OS can accelerate kidney disease progression. Also, in patients at advanced stages of chronic kidney disease (CKD), increased OS is associated with complications such as hypertension, atherosclerosis, inflammation, and anemia. In this review, we aim to describe OS and its influence on CKD progression and its complications. We also discuss the potential role of various antioxidants and pharmacological agents, which may represent potential therapeutic targets to reduce OS in both pediatric and adult CKD patients.

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Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

Oxidative stress in chronic kidney disease

et al. 2018

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“…ADPKD diagnosis is based on family history and imaging-based criteria through renal ultrasonography. When there is no family history linkage and mutation analyses, 95 both vascular endothelial dysfunction and increased arterial stiffness are important contributors to arterial dysfunction and disorders 96 OS and inflammation seem to be involved in the development of vascular dysfunction in ADPKD patients. 97 In order to study, the important role of inflammation in ADPKD, pro-inflammatory cytokines have been measured such as chemo-attractant protein-1 and osteopontin mRNA whose levels have resulted to be elevated in the cystic epithelium and IL-6 and IL-8.…”

Section: Role Of Oxidative Stress In Autosomal Dominant Polycystic Kimentioning

confidence: 99%

Pathogenesis of Congenital Malformations: Possible Role of Oxidative Stress

et al. 2020

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Objective Congenital anomalies are important causes of morbidity and mortality in children. Oxidative stress (OS) is involved in the physiopathology of pregnancy-related congenital malformations. This review summarizes the role of OS in the pathogenesis of congenital malformations; in particular, its purpose is to describe how OS influences the development of heart congenital malformations, oesophageal atresia, biliary atresia, diaphragmatic hernia, and autosomal dominant polycystic kidney disease. Study Design Systematic review of previous studies about the role of OS in pregnancy and its possible effects in developing of congenital malformations. One electronic database (PubMed) was searched and reference lists were checked. Results An imbalance between the production of reactive oxygen species (ROS) and antioxidant defense can occur early in pregnancy and continue in the postnatal life, producing OS. It may destroy the signaling pathways needed for a correct embryogenesis leading to birth defects. In fact, cell functions, especially during embryogenesis, needs specific signaling pathways to regulate the development. These pathways are sensitive to both endogenous and exogenous factors; therefore, they can produce structural alterations of the developing fetus. Conclusion Because OS plays a significant role in pathogenesis of congenital malformations, studies should be developed in order to better define their OS mechanisms and the beneficial effects of supplemental therapeutic strategies. Key Points

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“…In addition, the presence of oxidative stress in early ADPKD, with reduced nitric oxide levels, may per se aggravate endothelial dysfunction, which leads to cardiovascular events, including hypertension. Both nitric oxide reduction and the cardiovascular events may contribute to ADPKD progression . Hypertension occurs in 75% of adults with ADPKD before any loss of kidney function, with a mean age of diagnosis of 32 years in men and 34 years in women.…”

Section: Discussionmentioning

confidence: 99%

“…The beneficial effects of tolvaptan are primarily caused by the inhibition of cAMP productions. Moreover, independently of cAMP signaling, other beneficial effect may be based on its antioxidant activity . Thus, tolvaptan may activate the Nrf2/HO‐1 antioxidant pathway through phosphorylation of protein kinase RNA‐like endoplasmic reticulum kinase (PERK) .…”

Section: Discussionmentioning

confidence: 99%

Coexistence of autosomal dominant polycystic kidney disease type 1 and hereditary renal hypouricemia type 2: A model of early‐onset and fast cyst progression

et al. 2020

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Autosomal dominant polycystic kidney disease (ADPKD) is a heterogeneous inherited disease characterized by renal and extrarenal manifestations with progressive fluidfilled cyst development leading to end-stage renal disease. The rate of disease progression in ADPKD exhibits high inter-and intrafamilial variability suggesting involvement of modifier genes and/or environmental factors. Renal hypouricemia (RHUC) is an inherited disorder characterized by impaired tubular uric acid transport with severe complications, such as acute kidney injury and chronic kidney disease (CKD).However, the two disorders have distinct and well-delineated genetic, biochemical, and clinical findings. Only a few cases of coexistence of ADPKD and RHUC (type 1) in a single individual have been reported. We report a family with two members: an ADPKD 24-year-old female which presented bilateral renal cysts in utero and hypouricemia since age 5, and her mother with isolated hypouricemia. Next-generation sequencing identified two mutations in two genes PKD1 and SLC2A9 in this patient and one isolated SLC2A9 mutation in her mother, showing RHUC type 2, associated to CKD. The coexistence of these two disorders provides evidence of SLC2A9 variant could act as a modifier change, with synergistic actions, that could promote cystogenesis and rapid ADPKD progression. This is the first case of coexistence of PKD1 and SLC2A9 mutations treated with tolvaptan.

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Oxidative stress in autosomal dominant polycystic kidney disease: player and/or early predictor for disease progression?

Cited by 30 publications

References 117 publications

Oxidative stress in chronic kidney disease

Oxidative stress in chronic kidney disease

Pathogenesis of Congenital Malformations: Possible Role of Oxidative Stress

Coexistence of autosomal dominant polycystic kidney disease type 1 and hereditary renal hypouricemia type 2: A model of early‐onset and fast cyst progression

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