Active vitamin D and its analogue, 22-oxacalcitriol, ameliorate puromycin aminonucleoside-induced nephrosis in rats

Matsui, Isao; Hamano, Takayuki; Tomida, Kodo; Inoue, Kazunori; Takabatake, Yoshitsugu; Nagasawa, Yasuyuki; Kawada, Noritaka; Ito, Takahito; Kawachi, Hiroshi; Rakugi, Hiromi; Imai, Enyu; Isaka, Yoshitaka

doi:10.1093/ndt/gfp117

Cited by 55 publications

(50 citation statements)

References 42 publications

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“…Previous literature documented that active vitamin D therapy attenuated kidney injury by protecting podocytes (41) and by suppressing renin transcription (42), mesangial proliferation, and interstitial fibrosis (43). Clinical studies have also confirmed its antiproteinuric effects (44).…”

Section: Discussionmentioning

confidence: 92%

Combined Use of Vitamin D Status and FGF23 for Risk Stratification of Renal Outcome

Nakano

Hamano

Fujii

et al. 2012

Clinical Journal of the American Society of Nephrology

115

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SummaryBackground and objectives Hyperphosphatemia, vitamin D deficiency, hyperparathyroidism, and high serum fibroblast growth factor 23 (FGF23) levels, when studied separately, were found to predict the progression of CKD. However, studies with simultaneous measurement of mineral bone disorder (MBD)-related factors were scarce. This study aimed to identify factors predicting renal outcome independent of other factors.Design, setting, participants, & measurements This was a prospective cohort study of 738 Japanese predialysis outpatients in the nephrology departments of two hospitals. The outcome was defined as a doubling of serum creatinine or initiation of dialysis.Results Mean estimated GFR (eGFR) was 35 ml/min per 1.73 m 2 . At enrollment, the increase in intact FGF23 with decreasing eGFR was the earliest among changes in MBD-related factors, followed by 1,25-dihydroxyvitamin D decrease, parathyroid hormone increase, and phosphate increase. Conclusions Combined use of two markers is useful for the risk stratification of renal outcome.

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Section: Discussionmentioning

confidence: 92%

Combined Use of Vitamin D Status and FGF23 for Risk Stratification of Renal Outcome

Nakano

Hamano

Fujii

et al. 2012

Clinical Journal of the American Society of Nephrology

115

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“…We hypothesize that the discordant associations of 25(OH)D and 1,25(OH) 2 D with increased albuminuria may be explained by autocrine/paracrine activation of 25(OH)D. This is supported by the fact that 1a-hydroxylase is expressed by various cell types other than tubular epithelial cells, including podocytes, with subsequent local activation of VDRs (44)(45)(46) and circulating levels of 25(OH)D exceeding 1,25(OH) 2 D by approximately 400-fold in our study.…”

Section: Discussionmentioning

confidence: 96%

Plasma Vitamin D Level and Change in Albuminuria and eGFR According to Sodium Intake

Keyzer¹,

Lambers-Heerspink²,

Joosten

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Low circulating 25-hydroxyvitamin D [25(OH)D] and high sodium intake are both associated with progressive albuminuria and renal function loss in CKD. Both vitamin D and sodium intake interact with the renin-angiotensin-aldosterone system. We investigated whether plasma 25(OH)D or 1,25-dihydroxyvitamin D [1,25(OH) 2 D] is associated with developing increased albuminuria or reduced renal function and whether these associations depend on sodium intake.Design, setting, participants, & measurements Baseline plasma 25(OH)D and 1,25(OH) 2 D were measured by liquid chromatography tandem mass spectrometry, and sodium intake was assessed by 24-hour urine collections in the general population-based Prevention of Renal and Vascular End-Stage Disease cohort (n=5051). Two primary outcomes were development of urinary albumin excretion .30 mg/24 h and eGFR (creatinine/cystatin C-based CKD Epidemiology Collaboration) ,60 ml/min per 1.73 m 2 . Participants with CKD at baseline were excluded. In Cox regression analyses, we assessed associations of vitamin D with developing increased albuminuria or reduced eGFR and potential interaction with sodium intake.Results During a median follow-up of 10.4 (6.2-11.4) years, 641 (13%) participants developed increased albuminuria, and 268 (5%) participants developed reduced eGFR. Plasma 25(OH)D was inversely associated with increased albuminuria (fully adjusted hazard ratio [HR] per SD higher, 0.86; 95% confidence interval [95% CI], 0.78 to 0.95; P=0.003) but not reduced eGFR (HR, 0.99; 95% CI, 0.87 to 1.12; P=0.85). There was interaction between 25(OH)D and sodium intake for risk of developing increased albuminuria (P interaction =0.03). In participants with high sodium intake, risk of developing increased albuminuria was inversely associated with 25(OH)D (lowest versus highest quartile: adjusted HR, 1.81; 95% CI, 1.20 to 2.73, P,0.01), whereas this association was nonsignificant in participants with low sodium intake (HR, 1.29; 95% CI, 0.94 to 1.77; P=0.12). Plasma 1,25(OH) 2 D was not significantly associated with increased albuminuria or reduced eGFR.Conclusions Low plasma 25(OH)D is associated with higher risk of developing increased albuminuria, particularly in individuals with high sodium intake, but not of developing reduced eGFR. Plasma 1,25(OH)2D is not associated with risk of developing increased albuminuria or reduced eGFR.

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“…Interestingly, this anti-proteinuric action of vitamin D analogs is also reported in several clinical studies in patients with chronic renal insufficiency, 19,20,24,30 as well as in other animal models of proteinuric kidney diseases. [31][32][33][34][35] Therefore, it is becoming clear that vitamin D analogs may represent a class of anti-proteinuric agents that are quite effective in alleviating podocyte injury and proteinuria in different circumstances.…”

Section: Discussionmentioning

confidence: 99%

Blockade of Wnt/β-Catenin Signaling by Paricalcitol Ameliorates Proteinuria and Kidney Injury

Kang

Dai

et al. 2011

Journal of the American Society of Nephrology

249

229

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Recent studies implicate Wnt/␤-catenin signaling in podocyte dysfunction. Because vitamin D analogs can inhibit ␤-catenin in other tissues, we tested whether the vitamin D analog paricalcitol could ameliorate podocyte injury, proteinuria, and renal fibrosis in adriamycin (ADR) nephropathy. Compared with vehicle-treated controls, paricalcitol preserved expression of nephrin, podocin, and WT1; prevented proteinuria; and reduced glomerulosclerotic lesions induced by ADR. Paricalcitol also inhibited expression of proinflammatory cytokines, reduced renal infiltration of monocytes/macrophages, hampered activation of renal myofibroblasts, and suppressed expression of the fibrogenic TGF-␤1, CTGF, fibronectin, and types I and III collagen. Selective suppression of renal Wnt4, Wnt7a, Wnt7b, and Wnt10a expression after ADR accompanied these renoprotective effects of paricalcitol. Significant upregulation of ␤-catenin, predominantly in podocytes and tubular epithelial cells, accompanied renal injury; paricalcitol largely abolished this induction of renal ␤-catenin and inhibited renal expression of Snail, a downstream effector of Wnt/␤-catenin signaling. Administration of paricalcitol also ameliorated established proteinuria. In vitro, paricalcitol induced a physical interaction between the vitamin D receptor and ␤-catenin in podocytes, which led to suppression of ␤-catenin-mediated gene transcription. In summary, these findings suggest that paricalcitol prevents podocyte dysfunction, proteinuria, and kidney injury in adriamycin nephropathy by inhibiting Wnt/␤-catenin signaling.

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Active vitamin D and its analogue, 22-oxacalcitriol, ameliorate puromycin aminonucleoside-induced nephrosis in rats

Abstract: We demonstrated the breakdown of the vitamin D activation system in podocyte injury, and established a preventative role for vitamin D in podocyte injury.

Cited by 55 publications

References 42 publications

Combined Use of Vitamin D Status and FGF23 for Risk Stratification of Renal Outcome

Combined Use of Vitamin D Status and FGF23 for Risk Stratification of Renal Outcome

Plasma Vitamin D Level and Change in Albuminuria and eGFR According to Sodium Intake

Blockade of Wnt/β-Catenin Signaling by Paricalcitol Ameliorates Proteinuria and Kidney Injury

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