30 research outputs found
Aortic calcification in vehicle versus 185 mg/kg CaMg treated chronic renal failure (CRF) rats.
<p>*: p<0.05 vs. CRF + vehicle.</p
Circulating levels of sclerostin but not DKK1 associate with laboratory parameters of CKD-MBD
<div><p>Introduction</p><p>Mounting evidence indicates that a disturbed Wnt–β-catenin signaling may be involved in the pathogenesis of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD). Data on the impact of CKD on circulating levels of the Wnt antagonists sclerostin and Dickkopf related protein 1 (DKK1) and the relationship with laboratory parameters of CKD-MBD are incomplete.</p><p>Methods</p><p>We analyzed serum sclerostin and DKK1 in 308 patients across the stages of chronic kidney disease (kDOQI stage 1–2 n = 41; CKD stage 3 n = 54; CKD stage 4–5 n = 54; hemodialysis n = 100; peritoneal dialysis n = 59) as well as in 49 healthy controls. We investigated associations with demographics, renal function, parameters of mineral metabolism including 25(OH) vitamin D, 1,25(OH)<sub>2</sub> vitamin D, biointact fibroblast growth factor 23 (FGF23), and parathyroid hormone (PTH), and bone turnover markers.</p><p>Results</p><p>Serum sclerostin, but not DKK1, increases in more advanced stages of CKD and associates with PTH, phosphate, and 1,25(OH)<sub>2</sub> vitamin D concentrations. Bone turnover markers are highest in hemodialysis patients presenting the combination of high PTH with low sclerostin level. Serum DKK1 levels are lower in CKD patients than in controls and are not associated with laboratory parameters of mineral metabolism. Interestingly, a direct association between DKK1 and platelet count was observed.</p><p>Conclusion</p><p>In CKD, serum levels of the Wnt inhibitors DKK1 and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1, may qualify as a biomarker of CKD-MBD, particularly in dialysis patients. DKK1 serum levels, remarkably, correlate almost uniquely with blood platelet counts.</p></div
Setup of the study addressing the effect of calcium acetate/magnesium carbonate (CaMg) on bone.
<p>The three groups presented in the clear bars received a normal phosphorus diet; those presented in the hatched bars received a high phoshorus diet. Nx: 5/6<sup>th</sup> nephrectomy.</p
Calcium and magnesium content in the tibia of 5/6<sup>th</sup> nephrectomized rats on a normal (NP) or high phosphorus (HP) diet treated with either vehicle (veh), 185 or 375 mg/kg/day CaMg.
<p>Calcium and magnesium content in the tibia of 5/6<sup>th</sup> nephrectomized rats on a normal (NP) or high phosphorus (HP) diet treated with either vehicle (veh), 185 or 375 mg/kg/day CaMg.</p
Urine biochemistry over time of 5/6<sup>th</sup> nephrectomized rats receiving normal phosphorus (NP) or high phosphorus (HP) diet, in combination with vehicle (Veh), 185 or 375 mg/kg CaMg.
<p>*: p<0.05 vs NP, same dose.</p><p>°: p<0.05 vs week −4, same diet and dose.</p><p>Urine biochemistry over time of 5/6<sup>th</sup> nephrectomized rats receiving normal phosphorus (NP) or high phosphorus (HP) diet, in combination with vehicle (Veh), 185 or 375 mg/kg CaMg.</p
Static and dynamic bone parameters of 5/6<sup>th</sup> nephrectomized rats on a normal (NP) or high phosphorus (HP) diet treated with either vehicle (veh), 185 or 375 mg/kg/day CaMg.
<p>*: p<0.05 vs. NP, same dose.</p
Urinary phosphorus levels in 5/6<sup>th</sup> nephrectomized rats on a normal (NP) or high phosphorus (HP) diet treated with either vehicle (veh), 185 or 375 mg/kg/day CaMg.
<p>*: p<0.05 vs NP, same dose; #: p<0.05 vs vehicle, same diet; °: p<0.05 vs week −4, same diet and dose.</p
Bone-specific alkaline phosphatase level (Bone ALP) (A) and C-terminal telopeptide of collagen type 1 (CTX-I) (B), categorized according to PTH and sclerostin levels above [high] or below [low] the median.
<p>Groups with same indices differ significantly.</p
Demographics, biochemistry and therapy in healthy volunteers and CKD patients across stages.
<p>Demographics, biochemistry and therapy in healthy volunteers and CKD patients across stages.</p