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Phosphate Binding by Sucroferric Oxyhydroxide Ameliorates Renal

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Phosphate Binding by Sucroferric Oxyhydroxide Ameliorates Renal www.nature.com/scientificreports OPEN Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model Received: 3 September 2018 Yoshikazu Nemoto1, Takanori Kumagai1, Kenichi Ishizawa1, Yutaka Miura2, Takeshi Shiraishi1, Accepted: 27 December 2018 Chikayuki Morimoto1, Kazuhiro Sakai1, Hiroki Omizo1, Osamu Yamazaki1, Yoshifuru Tamura1, Published: xx xx xxxx Yoshihide Fujigaki1, Hiroshi Kawachi3, Makoto Kuro-o2, Shunya Uchida 1 & Shigeru Shibata 1,4 Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal phosphate binding by sucroferric oxyhydroxide (SF) ameliorates renal injury in the rat remnant kidney model. Sprague-Dawley rats received 5/6 nephrectomy (RK) and had a normal chow or the same diet containing SF (RK + SF). RK rats showed increased plasma FGF23 and phosphate levels, which were suppressed by SF administration. Of note, albuminuria in RK rats was signifcantly ameliorated by SF at both 4 and 8 weeks. SF also attenuated glomerulosclerosis and tubulointerstitial injury. Moreover, several diferent approaches confrmed the protective efects on podocytes, explaining the attenuation of glomerulosclerosis and albuminuria observed in this study. As a possible mechanism, we found that SF attenuated renal infammation and fbrosis in RK rats. Interestingly, von Kossa staining of the kidney revealed calcium phosphate deposition in neither RK nor RK + SF rats; however, plasma levels of calciprotein particles were signifcantly reduced by SF. These data indicate that latent positive phosphate balance accelerates CKD progression from early stages, even when overt ectopic calcifcation is absent. Chronic kidney disease (CKD) is a public health problem worldwide, contributing to deaths from end-stage renal disease and cardiovascular disorders1,2. Because the precise mechanisms for the CKD progression remain largely undetermined, the identifcation and intervention against major risk factors, including hypertension, proteinuria, and impaired glucose tolerance, are the mainstay to prevent the decline in kidney function. Several clinical studies indicate that phosphate overload may deteriorate kidney function3. Previously, we also reported that hyperphos- phatemia is an independent risk factor for CKD progression4. Remarkably, higher plasma phosphate levels, even within the normal ranges, were associated with the decline in estimated glomerular fltration rate (GFR) in CKD patients4. However, the causal role of phosphate overload in CKD progression remains undetermined. Mineral and bone disorders (MBD) are frequently associated with CKD. Reduced phosphate excretion from the kidney and its accumulation in the body stimulate the production of a phosphaturic hormone fbroblast growth factor 23 (FGF23) namely in osteocytes5,6. FGF23 then decreases phosphate reabsorption by inhibiting 5,7,8 sodium-dependent phosphate transporters NaPi-2a and NaPi-2c . FGF23 also reduces 1,25(OH)2 vitamin D levels by inducing the expression of 25-hydroxyvitamin D-24-hydroxylase, thereby decreasing intestinal phos- phate absorption. Besides FGF23, parathyroid hormone (PTH) is also stimulated by high extracellular phosphate levels, which increases renal phosphate excretion by inhibiting NaPi transporters6,9. However, these mechanisms cannot fully compensate for the reduced renal phosphate excretion in advanced CKD, resulting in phosphate accumulation and hyperphosphatemia. In addition, secondary hyperparathyroidism aggravates hyperphos- phatemia through excessive bone absorption10. Previous studies indicate that high phosphate levels in the blood can signifcantly afect cardiovascular func- tion5,6,11. Phosphate accumulation in advanced CKD patients results in extensive vascular calcifcation11, which 1Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan. 2Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Tokyo, Japan. 3Department of Cell Biology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. 4Division of Clinical Epigenetics, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan. Correspondence and requests for materials should be addressed to S.S. (email: shigeru. [email protected]) SCIENTIFIC REPORTS | (2019) 9:1732 | https://doi.org/10.1038/s41598-018-38389-3 1 www.nature.com/scientificreports/ 0 week 4 week 8 week Group Control RK RK + SF Control RK RK + SF Control RK RK + SF Systolic BP (mmHg) 100 ± 1 106 ± 2 107 ± 3 100 ± 2 126 ± 3a 127 ± 4a 100 ± 2 131 ± 6b 115 ± 4c BW (g) 179 ± 1 185 ± 4 187 ± 4 364 ± 4 400 ± 12 310 ± 22d 511 ± 5 465 ± 17 341 ± 31b,e CCr (ml/min/100 g) n.d. n.d. n.d. n.d. n.d. n.d. 0.72 ± 0.05 0.24 ± 0.03b 0.29 ± 0.01b FeP (%) n.d. n.d. n.d. n.d. n.d. n.d. 4.14 ± 0.30 13.13 ± 1.89b 0.34 ± 0.08c Urinary Ca (mg/day) 1.92 ± 0.62 2.38 ± 0.38 3.47 ± 0.70 0.75 ± 0.14 0.82 ± 0.15 3.93 ± 0.77b,c 0.57 ± 0.15 0.62 ± 0.07 3.95 ± 0.90b,c BUN (mg/dl) n.d. n.d. n.d. n.d. n.d. n.d. 20.3 ± 0.7 86.4 ± 21.7b 46.9 ± 3.1 Plasma Ca (mg/dl) n.d. n.d. n.d. n.d. n.d. n.d. 10.6 ± 0.2 11.1 ± 0.1 13.2 ± 0.2b,e Hb (g/dl) n.d. n.d. n.d. n.d. n.d. n.d. 12.9 ± 0.2 11.2 ± 0.8 12.8 ± 0.7 intact PTH (pg/ml) n.d. n.d. n.d. n.d. n.d. n.d. 146.8 ± 21.6 866.7 ± 376.7 5.9 ± 0.8c b,e 1,25(OH)2 VitD (pg/ml) n.d. n.d. n.d. n.d. n.d. n.d. 132 ± 12.3 160 ± 37.1 405 ± 41.3 Ca × P n.d. n.d. n.d. n.d. n.d. n.d. 59.0 ± 3.9 80.1 ± 5.0b 33.5 ± 2.2b,e Table 1. Biological parameters at 0, 4, and 8 weeks. BP, blood pressure; HR, heart rate; BW, body weight; FeP, fractional excretion of phosphate; Hb, hemoglobin; VitD, vitamin D. aP < 0.01 versus control at 4 weeks; bP < 0.01 versus control at 8 weeks; cP < 0.05 versus RK at 8 weeks; dP < 0.01 versus RK at 4 weeks; eP < 0.01 versus RK at 8 weeks. plays a critical role in high cardiovascular mortality in these patients. Moreover, when the vascular smooth muscle cells are exposed to high extracellular phosphate, these cells transit to osteoblast-like cells and express osteogenic genes including Runx2, BMP-2, and Msx28,11,12, further contributing to the progression of calcium deposition. Similarly, calcium phosphate deposition in the renal parenchyma can also deteriorate kidney func- tion11,13–16. However, the injurious efects of phosphate in the kidney that are independent of ectopic calcifcation are not well characterized. In the plasma, mineral binding proteins such as fetuin-A sequesters a CaPi nanopar- ticle by binding and forming the complex with the mineral core (calciprotein particle; CPP)8,17,18. Tese particles primarily act to prevent the growth of CaPi crystals. Nonetheless, its accumulation in pathological conditions can induce pro-infammatory responses and apoptotic pathways8,19,20. Given that plasma CPP levels increase with CKD progression21,22, it has been postulated that CPP may deteriorate kidney function in CKD subjects8. Based on these observations, we here tested whether the latent positive phosphate balance at an early stage of the rat remnant kidney (RK) model can facilitate kidney damage. In this study, we show that the intervention against the disturbed phosphate metabolism by sucroferric oxyhydroxide (SF), a phosphate binder, ameliorates the progression of kidney dysfunction. Results Efects of sucroferric oxyhydroxide (SF) on phosphate metabolism in remnant kidney (RK) rats. Male Sprague-Dawley rats received 5/6 nephrectomy and were randomly assigned to RK or RK with sucroferric oxyhydroxide (50 mg/g chow; RK + SF) group and were maintained for 8 weeks. Rats without 5/6 nephrectomy served as control. All the groups received normal diet. RK and RK + SF rats showed signifcant reduction in creatinine clearance (CCr) compared with control rats (Table 1). BUN was signifcantly increased in RK group compared with control rats; there were no signifcant diference in BUN levels between RK and RK + SF. Plasma phosphate levels were modestly but signifcantly elevated (Fig. 1a), whereas the levels of phosphaturic hormone FGF23 were highly increased in RK rats (Fig. 1b). Urinary phosphate levels were similar between control and RK rats (Fig. 1c). However, fractional excretion of phosphate was increased in RK rats (Table 1). In RK + SF rats, plasma phosphate and FGF-23 levels were signifcantly lower than RK rats (Fig. 1). SF administration also reduced urinary phosphate excretion, confrming the ability of SF to prevent phosphate absorption in the intes- tine. Levels of plasma calcium and 1,25(OH)2 vitamin D were signifcantly higher in RK + SF rats (Table 1), which can be explained by the suppression of FGF23. Blood pressure levels were similar between RK and RK + SF rats at baseline. Interestingly, however, blood pressure elevation was partially attenuated by SF at 8 weeks (but not at 4 weeks). Hemoglobin levels were not signifcantly diferent among three groups. Administration of SF ameliorates glomerulosclerosis and tubulointerstitial injury in RK rats. To evaluate whether SF exerted protective efects on renal injury in RK rats, we measured urinary albumin levels at 0, 4, and 8 weeks. Urinary albumin levels were comparable among groups at baseline. RK rats showed a marked increase in urinary albumin levels at 4 weeks and at 8 weeks (Fig. 2). Compared with RK group, urinary albumin levels were signifcantly decreased in RK + SF group at both 4 and 8 weeks (Fig.
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