Vitamin D deficiency aggravates ischemic acute kidney injury in rats

Bragança, Ana Carolina de; Volpini, Rildo Aparecido; Canale, Daniele; Gonçalves, Janaína Garcia; Shimizu, Maria Heloísa Massola; Sanches, Talita Rojas; Seguro, Antônio Carlos; Andrade, Lúcia

doi:10.14814/phy2.12331

Cited by 39 publications

(49 citation statements)

References 46 publications

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“…125,126 In animal models, pre-administration of 1,25D attenuated AKI resulting from a variety of nephrotoxic insults, including ischemia-reperfusion injury, [127][128][129] gentamicin, 130 cyclosporine, 131 cisplatin, 132 glomerulonephritis, 133 and obstruction. 134 Furthermore, de Braganca et al 135 investigated the effects of dietary-induced 25D deficiency on the severity of AKI in rats. They found that rats fed a vitamin D−free diet had a more severe decrease in glomerular filtration rate, greater urinary protein excretion, and increased tubular necrosis after ischemia-reperfusion injury compared with rats fed a standard diet.…”

Section: Vitamin D Metabolites As Novel Therapies In Aki and Criticalmentioning

confidence: 99%

Dysregulated Mineral Metabolism in AKI

Leaf

Christov

2019

Seminars in Nephrology

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Dysregulated mineral metabolism is a nearly universal sequalae of acute kidney injury (AKI). Abnormalities in circulating mineral metabolites observed in patients with AKI include hypocalcemia, hyperparathyroidism, hyperphosphatemia, decreased vitamin D metabolite levels, and increased fibroblast growth factor 23 levels. We review the pathophysiology of dysregulated mineral metabolism in AKI with a focus on calcium, phosphate, parathyroid hormone, and vitamin D metabolites. We discuss how mineral metabolite levels can serve as novel prognostic markers for incident AKI and other related outcomes in various clinical settings. Finally, we discuss how vitamin D metabolites potentially could be used as novel therapeutic agents for AKI prevention and treatment.

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Section: Vitamin D Metabolites As Novel Therapies In Aki and Criticalmentioning

confidence: 99%

Dysregulated Mineral Metabolism in AKI

Leaf

Christov

2019

Seminars in Nephrology

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“…VD may also modulate oxidative stress and inflammation, reducing fibroblast activation and interstitial inflammation [74,75,77,109] Moreover, CKD progression and lower expression of megalin have been associated with lower 25(OH)-VD reuptake and therefore reducing intracrine 1,25(OH) 2 -VD production in the renal proximal tubules (Figure 2b) [50,51,110]. On the other hand, increasing levels of proteinuria may perpetuate VDD.…”

Section: Vd and Ckd: Human Studiesmentioning

confidence: 99%

Vitamin D Deficiency in Chronic Kidney Disease: Recent Evidence and Controversies

Gois

Wolley

Ranganathan

et al. 2018

IJERPH

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Vitamin D (VD) is a pro-hormone essential for life in higher animals. It is present in few types of foods and is produced endogenously in the skin by a photochemical reaction. The final step of VD activation occurs in the kidneys involving a second hydroxylation reaction to generate the biologically active metabolite 1,25(OH)2-VD. Extrarenal 1α-hydroxylation has also been described to have an important role in autocrine and paracrine signaling. Vitamin D deficiency (VDD) has been in the spotlight as a major public healthcare issue with an estimated prevalence of more than a billion people worldwide. Among individuals with chronic kidney disease (CKD), VDD prevalence has been reported to be as high as 80%. Classically, VD plays a pivotal role in calcium and phosphorus homeostasis. Nevertheless, there is a growing body of evidence supporting the importance of VD in many vital non-skeletal biological processes such as endothelial function, renin-angiotensin-aldosterone system modulation, redox balance and innate and adaptive immunity. In individuals with CKD, VDD has been associated with albuminuria, faster progression of kidney disease and increased all-cause mortality. Recent guidelines support VD supplementation in CKD based on extrapolation from cohorts conducted in the general population. In this review, we discuss new insights on the multifactorial pathophysiology of VDD in CKD as well as how it may negatively modulate different organs and systems. We also critically review the latest evidence and controversies of VD monitoring and supplementation in CKD patients.

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“…Thus, low levels of vitamin D can be deleterious and impair the recovery of renal diseases and/or even accelerate the progression of renal disease. In a previous study, we showed that vitamin D deficiency exerted a pivotal role on the aggravation of acute kidney injury (AKI) after ischemia/reperfusion (I/R) insult ( 9 ). We also demonstrated that vitamin D deficiency favored renal capillary rarefaction, and increased renal fibrosis and inflammation ( 10 ).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Deficiency Aggravates the Renal Features of Moderate Chronic Kidney Disease in 5/6 Nephrectomized Rats

et al. 2018

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The pathogenesis of chronic kidney disease (CKD) involves a very complex interaction between hemodynamic and inflammatory processes, leading to glomerular/vascular sclerosis, and fibrosis formation with subsequent evolution to end-stage of renal disease. Despite efforts to minimize the progression of CKD, its incidence and prevalence continue to increase. Besides cardiovascular diseases and infections, several studies demonstrate that vitamin D status could be considered as a non-traditional risk factor for the progression of CKD. Therefore, we investigated the effects of vitamin D deficiency (VDD) in the course of moderate CKD in 5/6 nephrectomized rats (Nx). Adult male Wistar rats underwent Sham surgery or Nx and were subdivided into the following four groups: Sham, receiving standard diet (Sham); Sham VDD, receiving vitamin D-free diet (VDD); Nx, receiving standard diet (Nx); and VDD+Nx, receiving vitamin D-free diet (VDD+Nx). Sham or Nx surgeries were performed 30 days after standard or vitamin D-free diets administration. After validation of vitamin D depletion, we considered only Nx and VDD+Nx groups for the following studies. Sixty days after surgeries, VDD+Nx rats exhibited hypertension, a greater decline in renal function and plasma FGF-23 levels, renal hypertrophy, as well as higher plasma levels of PTH and aldosterone. In addition, those animals presented more significant chronic tubulointerstitial changes (cortical interstitial expansion/inflammation/fibrosis), higher expression of collagen IV, fibronectin and α-smooth muscle actin, and lower expressions of JG12 and M2 macrophages. Also, VDD+Nx rats had greater infiltration of inflammatory cells (M1 macrophages and T-cells). Such changes were accompanied by higher expression of TGF-β1 and angiotensinogen and decreased expression of VDR and Klotho protein. Our observations indicate that vitamin D deficiency impairs the renal function and worsens the renovascular and morphological changes, aggravating the features of moderate CKD in 5/6 nephrectomized rats.

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Vitamin D deficiency aggravates ischemic acute kidney injury in rats

Cited by 39 publications

References 46 publications

Dysregulated Mineral Metabolism in AKI

Dysregulated Mineral Metabolism in AKI

Vitamin D Deficiency in Chronic Kidney Disease: Recent Evidence and Controversies

Vitamin D Deficiency Aggravates the Renal Features of Moderate Chronic Kidney Disease in 5/6 Nephrectomized Rats

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