Vitamin D resistance in chronic kidney disease (CKD)

Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Parikh, Amay [verfasserIn] Chase, Herbert S Vernocchi, Linda Stern, Leonard

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Cholecalciferol Vitamin D deficiency Parathyroid hormone Chronic kidney disease Kidney transplant

Anmerkung:	© Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: BMC nephrology - London : BioMed Central, 2000, 15(2014), 1 vom: 19. März
Übergeordnetes Werk:	volume:15 ; year:2014 ; number:1 ; day:19 ; month:03

Links:	Volltext

DOI / URN:	10.1186/1471-2369-15-47

Katalog-ID:	SPR027511758

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520			\|a Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance.
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allfields	10.1186/1471-2369-15-47 doi (DE-627)SPR027511758 (SPR)1471-2369-15-47-e DE-627 ger DE-627 rakwb eng Parikh, Amay verfasserin aut Vitamin D resistance in chronic kidney disease (CKD) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. Cholecalciferol (dpeaa)DE-He213 Vitamin D deficiency (dpeaa)DE-He213 Parathyroid hormone (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Kidney transplant (dpeaa)DE-He213 Chase, Herbert S aut Vernocchi, Linda aut Stern, Leonard aut Enthalten in BMC nephrology London : BioMed Central, 2000 15(2014), 1 vom: 19. März (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:15 year:2014 number:1 day:19 month:03 https://dx.doi.org/10.1186/1471-2369-15-47 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2014 1 19 03
spelling	10.1186/1471-2369-15-47 doi (DE-627)SPR027511758 (SPR)1471-2369-15-47-e DE-627 ger DE-627 rakwb eng Parikh, Amay verfasserin aut Vitamin D resistance in chronic kidney disease (CKD) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. Cholecalciferol (dpeaa)DE-He213 Vitamin D deficiency (dpeaa)DE-He213 Parathyroid hormone (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Kidney transplant (dpeaa)DE-He213 Chase, Herbert S aut Vernocchi, Linda aut Stern, Leonard aut Enthalten in BMC nephrology London : BioMed Central, 2000 15(2014), 1 vom: 19. März (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:15 year:2014 number:1 day:19 month:03 https://dx.doi.org/10.1186/1471-2369-15-47 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2014 1 19 03
allfields_unstemmed	10.1186/1471-2369-15-47 doi (DE-627)SPR027511758 (SPR)1471-2369-15-47-e DE-627 ger DE-627 rakwb eng Parikh, Amay verfasserin aut Vitamin D resistance in chronic kidney disease (CKD) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. Cholecalciferol (dpeaa)DE-He213 Vitamin D deficiency (dpeaa)DE-He213 Parathyroid hormone (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Kidney transplant (dpeaa)DE-He213 Chase, Herbert S aut Vernocchi, Linda aut Stern, Leonard aut Enthalten in BMC nephrology London : BioMed Central, 2000 15(2014), 1 vom: 19. März (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:15 year:2014 number:1 day:19 month:03 https://dx.doi.org/10.1186/1471-2369-15-47 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2014 1 19 03
allfieldsGer	10.1186/1471-2369-15-47 doi (DE-627)SPR027511758 (SPR)1471-2369-15-47-e DE-627 ger DE-627 rakwb eng Parikh, Amay verfasserin aut Vitamin D resistance in chronic kidney disease (CKD) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. Cholecalciferol (dpeaa)DE-He213 Vitamin D deficiency (dpeaa)DE-He213 Parathyroid hormone (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Kidney transplant (dpeaa)DE-He213 Chase, Herbert S aut Vernocchi, Linda aut Stern, Leonard aut Enthalten in BMC nephrology London : BioMed Central, 2000 15(2014), 1 vom: 19. März (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:15 year:2014 number:1 day:19 month:03 https://dx.doi.org/10.1186/1471-2369-15-47 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2014 1 19 03
allfieldsSound	10.1186/1471-2369-15-47 doi (DE-627)SPR027511758 (SPR)1471-2369-15-47-e DE-627 ger DE-627 rakwb eng Parikh, Amay verfasserin aut Vitamin D resistance in chronic kidney disease (CKD) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. Cholecalciferol (dpeaa)DE-He213 Vitamin D deficiency (dpeaa)DE-He213 Parathyroid hormone (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Kidney transplant (dpeaa)DE-He213 Chase, Herbert S aut Vernocchi, Linda aut Stern, Leonard aut Enthalten in BMC nephrology London : BioMed Central, 2000 15(2014), 1 vom: 19. März (DE-627)326643672 (DE-600)2041348-8 1471-2369 nnns volume:15 year:2014 number:1 day:19 month:03 https://dx.doi.org/10.1186/1471-2369-15-47 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2014 1 19 03
language	English
source	Enthalten in BMC nephrology 15(2014), 1 vom: 19. März volume:15 year:2014 number:1 day:19 month:03
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topic_facet	Cholecalciferol Vitamin D deficiency Parathyroid hormone Chronic kidney disease Kidney transplant
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topic_title	Vitamin D resistance in chronic kidney disease (CKD) Cholecalciferol (dpeaa)DE-He213 Vitamin D deficiency (dpeaa)DE-He213 Parathyroid hormone (dpeaa)DE-He213 Chronic kidney disease (dpeaa)DE-He213 Kidney transplant (dpeaa)DE-He213
topic	misc Cholecalciferol misc Vitamin D deficiency misc Parathyroid hormone misc Chronic kidney disease misc Kidney transplant
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title_full	Vitamin D resistance in chronic kidney disease (CKD)
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author_browse	Parikh, Amay Chase, Herbert S Vernocchi, Linda Stern, Leonard
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doi_str_mv	10.1186/1471-2369-15-47
title_sort	vitamin d resistance in chronic kidney disease (ckd)
title_auth	Vitamin D resistance in chronic kidney disease (CKD)
abstract	Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Previous studies have shown that treatment with ergocalciferol in patients with CKD stage 3 + 4 is not effective with less than 33% of patients achieving a 25-OH vitamin D target of >30 ng/ml. The aim of this study was to test the response to cholecalciferol in CKD. We attempted to replete 25-OH vitamin D to a target level of 40–60 ng/ml using the response to treatment and PTH suppression as an outcome measure. Methods This retrospective cohort study identified patients (Stages 2–5 and Transplant) from 2001–2010 who registered at the Chronic Kidney Disease Clinic. Patients received cholecalciferol 10,000 IU capsules weekly as initial therapy. When levels above 40 ng/ml were not achieved, doses were titrated up to a maximum of 50,000 IU weekly. Active vitamin D analogs were also used in some Stage 4–5 CKD patients per practice guidelines. Patients reaching at least one level of 40 ng/mL were designated RESPONDER, and if no level above 40 ng/mL they were designated NON-RESPONDER. Patients were followed for at least 6 months and up to 5 years. Results 352 patients were included with a mean follow up of 2.4 years. Of the CKD patients, the initial 25-OH vitamin D in the NON-RESPONDER group was lower than the RESPONDER group (18 vs. 23 ng/ml) (p = 0.03). Among all patients, the initial eGFR in the RESPONDER group was significantly higher than the NON-RESPONDER group (36 vs. 30 ml/min/1.73 $ m^{2} $) (p < 0.001). Over time, the eGFR of the RESPONDER group stabilized or increased (p < 0.001). Over time, the eGFR in the NON-RESPONDER group decreased toward a trajectory of ESRD. Proteinuria did not impact the response to 25-OH vitamin D replacement therapy. There were no identifiable variables associated with the response or lack of response to cholecalciferol treatment. Conclusions CKD patients treated with cholecalciferol experience treatment resistance in raising vitamin D levels to a pre-selected target level. The mechanism of vitamin D resistance remains unknown and is associated with progressive loss of eGFR. Proteinuria modifies but does not account for the vitamin D resistance. © Parikh et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Vitamin D resistance in chronic kidney disease (CKD)
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