Mineral metabolism in chronic kidney disease

2015 ◽  
Vol 61 (10) ◽  
pp. 425-433 ◽  
Author(s):  
Malgorzata Kochanek ◽  
Albara Said ◽  
Edgar V. Lerma
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mineral Metabolism

scholarly journals P0754FGF23 AND URINARY PHOSPHATE EXCRETION FOR ESTIMATION OF NEPHRON NUMBER: DIFFERENCES BETWEEN CHRONIC KIDNEY FAILURE AND KIDNEY TRANSPLANTATION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Marzia Pasquali ◽  
Natalia De Martini ◽  
Lida Tartaglione ◽  
Silverio Rotondi ◽  
Marta Catalfamo ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Transplantation ◽  
Kidney Disease ◽  
Mineral Metabolism ◽  
Chronic Kidney Failure ◽  
Serum Levels ◽  
Nephron Number ◽  
Phosphate Excretion ◽  
Single Nephron ◽  
The Difference

Abstract Background and Aims Assuming that FGF23 levels correlate with phosphate excretion per nephron, nephron number can be estimated by measuring FGF23 levels and urinary phosphate excretion (FEP). Kuro-O proposed that the ratio of FEP to serum FGF23 levels should correlate with nephron number and is defined as the Nephron Index (NI). The aim of the study is calculating NI as nephron number estimation in patients affected by various degree of chronic kidney disease, both transplanted and not. Method In 147 CRF patients kidney function, mineral metabolism biomarkers and NI were evaluated. Nephron Index was calculated following Kuro-o’s equation (kuro-o 2019): NI=FEP·Ps·eGFRFGF23 Observed patients were divided into two groups: patients with CKD (noTX) and transplanted ones (TX). Results noTX group was made up of 67 patients (40 males and 27 females) affected by CKD stages from G1 to G5. TX group was composed by 80 patient (49 males and 31 females) with various degree of CKD (G1T-G4T) showing mean graft age of 83,2 ± 54,8 months (range: 10,3-268,0). The two groups differed for age (mean age 59 ± 15,6 years in CKD, 55± 10,3years in TX). Mean eGFR did not differ between TX and noTX but NI was higher in TX since FEP was higher despite lower FGF23 levels in TX. The difference in FGF23 levels does not appear to depend on Klotho and PTH whose serum levels were no different between Tx and noTx. (Table1). As far as correlations are concerned, NI correlated with eGFR, FGF23, PTH and 1,25D in both group, while NI correlated with FEP only in the TX group. It's interesting that no correlation existed between FGF23 and sP, FEP, eGFR and sKlotho in TX differently from noTX (Table2). Discussion. NI could not be properly defined as nephron number estimation in TX pts. However it may represent higher function of residual nephrons, since higher FEP did not correlate to FGF23 and could be determined by compensatory hyperfiltration (increased single nephron GFR) in transplanted patients. Conclusion After kidney transplantation, high NI value could have a functional meaning rather than represent residual number of nephrons.

scholarly journals Cholecalciferol v. ergocalciferol for 25-hydroxyvitamin D (25(OH)D) repletion in chronic kidney disease: a randomised clinical trial

2016 ◽  
Vol 116 (12) ◽  
pp. 2074-2081 ◽  
Author(s):  
James B. Wetmore ◽  
Cassandra Kimber ◽  
Jonathan D. Mahnken ◽  
Jason R. Stubbs
Keyword(s):  
Clinical Trial ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mineral Metabolism ◽  
Substantial Reduction ◽  
Randomised Clinical Trial ◽  
Optimal Method ◽  
Hydroxyvitamin D ◽  
Significant Difference ◽  
25 Hydroxyvitamin D

AbstractPatients with chronic kidney disease (CKD) demonstrate complex mineral metabolism derangements and a high prevalence of vitamin D deficiency. However, the optimal method of 25-hydroxyvitamin D (25(OH)D) repletion is unknown, and trials analysing the comparative efficacy of cholecalciferol and ergocalciferol in this population are lacking. We conducted a randomised clinical trial of cholecalciferol 1250μg (50 000 IU) weekly v. ergocalciferol 1250μg (50 000 IU) weekly for 12 weeks in forty-four non-dialysis-dependent patients with stage 3–5 CKD. The primary outcome was change in total 25(OH)D from baseline to week 12 (immediately after therapy). Secondary analyses included the change in 1,25-dihydroxyvitamin D (1,25(OH)2D), parathyroid hormone (PTH), D2 and D3 sub-fractions of 25(OH)D and 1,25(OH)2D and total 25(OH)D from baseline to week 18 (6 weeks after therapy). Cholecalciferol therapy yielded a greater change in total 25(OH)D (45·0 (sd 16·5) ng/ml) v. ergocalciferol (30·7 (sd 15·3) ng/ml) from baseline to week 12 (P<0·01); this observation partially resulted from a substantial reduction in the 25(OH)D3 sub-fraction with ergocalciferol. However, following cessation of therapy, no statistical difference was observed for total 25(OH)D change from baseline to week 18 between cholecalciferol and ergocalciferol groups (22·4 (sd 12·7) v. 17·6 (sd 8·9) ng/ml, respectively; P=0·17). We observed no significant difference between these therapies with regard to changes in serum PTH or 1,25(OH)2D. Therapy with cholecalciferol, compared with ergocalciferol, is more effective at raising serum 25(OH)D in non-dialysis-dependent CKD patients while active therapy is ongoing. However, levels of 25(OH)D declined substantially in both arms following cessation of therapy, suggesting the need for maintenance therapy to sustain levels.

Imaging for detection of vascular disease in chronic kidney disease patients

2015 ◽  
Author(s):  
Paolo Raggi ◽  
Luis D’Marco
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Disease ◽  
Mineral Metabolism ◽  
Fibrous Tissue ◽  
Inflammatory Cells ◽  
Arterial System ◽  
Arterial Circulation ◽  
Atherosclerosis Risk Factors ◽  
Calcium Crystals

The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.

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