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![Native Vitamin D Epidemiology
Definition
• Insufficiency: [25(OH)D] < 30 ng/mL
• Deficiency: [25(OH)D] < 10-15 ng/mL
Causes
• CKD is associated with 25OH VitaminD deficiencies
Prevalence
• Differences with age, ethnicity, latitude, culture and seasons
• In US HD Patients:
• Insufficiency: 78%, Deficiency: 18%](https://image.slidesharecdn.com/ckdmbdgcc2017final2-190412163306/85/CKD-MBD-2017-34-320.jpg)
![FGF23 and CKD
lotho levelsof CKD patients have been
ein thevery early stagesof CKD and to
KD progresses [36]. In a rodent CKD
vels in plasma, urine, and kidney were
se in parallel [36], but the relationship
elsin CKD patientsremainsto bedeter-
ore, almost all modelsof CKD, includ-
avebeen createdbyrenal tissueablation,
tis, nephrotoxin, diabetic nephropathy,
e kidney damage, are characterized by
wnregulation of Klotho mRNA and pro-
ey and by low plasma or urine-soluble
]. Plasma soluble Klotho levels are also
early stagesof CKD [58].Pavik et al.[63]
dingthatsolubleKlothoand1,25(OH)2D
nd FGF23 levels increase in the early
nd that PTH levelsincreasein themore
Akimoto et al. [64] haverecently shown
Klotho levels of CKD patients, rather
Klotholevels,arelinked totheir number
phrons.Sakan et al.[65] recentlyreport-
renal α-Klotho levelsweresignificantly
um FGF23 levels were significantly ele-
d intermediate CKD, serum P levelsre-
he normal range. Despite falling renal
heincreasein FGF23 enhanced urinary
d serum 1,25(OH)2D levelsin early and
D, though not in advanced CKD. In ad-
ubleKlotho levelsfell significantly over
overlapping distinct mechanisms of initiation and pro-
gression [68, 69].Vascular calcification isadynamicpro-
Fig. 5. Timeprofileof changesinplasmaFGF23,Klotho,activevi-
taminD,andphosphatelevelsasCKDprogresses. Thedecreasein
Klothoproteininthebloodisanearlyevent inCKDandisprogres-
sivelyreducedalongwiththedeclineof renal function.LowKlotho
partiallyinducesFGF23resistance,causinganinitial compensatory
increasein blood FGF23tomaintain Phomeostasis. Theincrease
inFGF23decreasesactivevitaminDlevelsandisfollowedbyeleva-
tion of PTH. Hyperphosphatemia is relatively late event in ad-
vancedCKD[reprintedwithpermissionfrom 60].
Colorversionavailableonline](https://image.slidesharecdn.com/ckdmbdgcc2017final2-190412163306/85/CKD-MBD-2017-63-320.jpg)
![FGF23 and CKD
havebeen found to predict mortality not only among di-
alysispatientsbut amongpredialysisCKD patientsaswell
[22].
tial to facilitate thebinding of FG
The potential role of soluble Klo
in vivo remainsunknown at this
Fig. 2. Plasma FGF23 levels in thefour CKD stage groups. Boxes
represent the interquartile range with the upper and lower edges
representing the75th and 25th percentiles, respectively. Thereisa
statistically significant linear increase in plasma FGF23 levels
acrossthefour CKD groupsdivided by eGFR[reprinted with per-
mission from 21].
Fig. 3. Klotho family showing theth
themammalian genome. Homologo
mainsareconserved. Solubleformso
byalternativesplicingof itstranscrip
of thetransmembraneformbyβ-secr
Colorversionavailableonline](https://image.slidesharecdn.com/ckdmbdgcc2017final2-190412163306/85/CKD-MBD-2017-65-320.jpg)
More Related Content
CKD MBD 2017
- 1. CKD-MBD 2017 Professor MeguidEl Nahas Global Kidney Academy Sheffield, UK
- 2.
- 3.
- 4. The QUIZ Which ofthe following is not associated with higher mortality in CKD: a. Low serum Phosphorus b. Low PTH c. Low Vitamin D d. Low FGF23 e. Low Magnesium
- 5.
- 6. HT/Osteitis Fibrosa LT:ABD MIXED ………???? CKD-MBD
- 7. HT/Osteitis Fibrosa LT:ABD MIXED Osteoporosis CKD-MBD
- 8. Ca,Pi, ALP ALP,PTH VitaminD ……..????? CKD-MBD
- 9. Ca,Pi, ALP ALP,PTH VitaminD FGF23 CKD-MBD
- 10. Ca,Pi, ALP ALP, PTH VitaminDFGF23 CKD-MBD ……..?????
- 11. CASE 1 • 74year old with CKD 4, also suffers from Crohn’s Disease with frequent diarrhea • Severe weakness, tremor and depressive mood • eGFR = 20 ml/min • sCa: 2.1mmol/, sPi: 2.5 mmol/l, ALP: 600iU/L, PTH: 335pg/ml HOW WOULD YOU MANAGE?
- 12. CASE 1 • 74year old with CKD 4, also suffers from Crohn’s Disease with frequent diarrhea • Severe weakness, tremor and depressive mood • eGFR = 20 ml/min • sCa: 1.9 mmol/, sPi: 2.5 mmol/l, ALP: 600iU/L, PTH: 335pg/ml • TTT: Alfacalcidol: 250ng/qd, Calcium Carbonate supplementation:1g/qid
- 13. CASE 1 • 74year old with CKD 4, also suffers from Crohn’s Disease with frequent diarrhea • Severe weakness, tremor and depressive mood • eGFR = 20 ml/min • 3 months later: • sCa: 1.9 mmol/, sPi: 1.8 mmol/l, ALP: 600iU/L, PTH: 335pg/ml WHAT WOULD YOU DO NEXT?
- 14. Ca,Pi, ALP ALP, PTH VitaminDFGF23 CKD-MBD ……..?????
- 15. Ca,Pi, ALP ALP, PTH VitaminDFGF23 CKD-MBD ……..?????
- 16. CASE 1 • 74year old with CKD 4, also suffers from Crohn’s Disease with frequent diarrhea • Severe weakness, tremor and depressive mood • eGFR = 20 ml/min • 3 months later: • sCa: 1.9 mmol/, sPi: 1.8 mmol/l, ALP: 600iU/L, PTH: 335pg/ml, • Vitamin D: 67ng/ml (NR >30ng/ml) WHAT WOULD YOU DO NEXT?
- 17. Ca,Pi, ALP ALP, PTH VitaminDFGF23 CKD-MBD ……..?????
- 18. CASE 1 • 74year old with CKD 4, also suffers from Crohn’s Disease with frequent diarrhea • Severe weakness, tremor, and depressive mood • eGFR = 20 ml/min • 3 months later: • sCa: 2.1mmol/, sPi: 1.8 mmol/l, ALP: 600iU/L, PTH: 335pmol/l, Vitamin D: 67ng/ml • sMg: 0.35mmol/l (NR: 0.7-1mmol/l)
- 19. Hypomagnesemia Which is NOTcaused by hypomagnesemia? a. Hypercalcemia b. Hypertension c. Arrhythmias d. Diabetes Mellitus
- 20. (ARIC) cohort, whichincluded >14,000 participants, reported an independent association between low mag- nesium levelsand incident heart failure.11 Patientswith than on changesin magnesium metabo CKD.Asaresult of thepaucity of availa Kidney Disease: ImprovingGlobal Out on CKD–mineral and bonedisorder (C not elaboratespecificdiagnosticand the mendationswith respect to magnesium thoseprovided for calcium and phosph Theattention paid to thisneglected c with CKD is, however, increasing. Sev thisincreased interest exist, including studiesthat suggest linksbetween low sium levels, theincidenceand progress and adverse outcomes in patients wit or acutekidney injury;18 intervention possiblebenefitsof oral magnesium sup patientswith CKD;19,20 and experimenta inginhibitoryeffectsof magnesium on v tion in normal and/or uraemicanimals21 models.24,25 Theintroduction of anew binder formulation for patientsreceiv combinesamagnesium salt with acalci led to increased interest in theeffectsof In thisReview, weexamineevidencefr tal studiesand clinical investigationsth of magnesium in thehigh frequency o diseasein patientswith CKD. In vitro experimental data Magnesium exertsdirect and indirect a and vascular tissues. Although thebes relateto vascular calcification, direct ac sium on arterial function viaeffectson musclecells(VSMCs) and theendothe likely (Figure 1). Vascular calcification In micewithCKD,themagnesium conte isreportedlyelevatedsimilar tothat of ca phate.28 Magnesium can theoretically in diovascular calcification byindirect actio binding in theintestinal lumen, by sys CKD–MBD-associatedfactors,andbydir level of vascular tissues. Consistent with Table 1 | Manifestations of hypomagnesaemia70,96 and hypermagnesaemia97 Disorder Serum magnesium level (mmol/ l) Manifestation(s) Severe hypomagnesemia <0.35 Ataxia, tremors, tetany, depression Muscle brillation Psychotic behaviour Irritability Mild to moderate hypomagnesemia 0.35–0.70 Anorexia, nausea Hyper-re exia, irritability, weakness; vertigo Electrocardiographic changes (QT prolongation, ST segment shortening) Increase in myocardial irritability, reduced myocardial contractility Positive Trousseau and Chvostek signs Abnormal skeletal muscle function Hypertension Hypokalaemia, hypocalcaemia Reduced PTH level, resistance to PTH action Increased renin and aldosterone secretion Increased incidence of osteoporosis None (normal magnesium balance) 0.10–1.00 None Hypermagnesaemia ≤2 mmol/ l 1.00–2.00 Usually asymptomatic Mild hypermagnesaemia 2.00–3.00 Drowsiness Lethargy Hypore exia Moderate hypermagnesaemia 3.00–5.00 Somnolence Are exia Hypocalcaemia Hypotension Bradycardia Electrocardiographic changes (prolongation of PR and QT intervals, increase in QRS duration) Severe hypermagnesaemia >5.00 Muscle paralysis Quadriplegia Apnoea Complete heart block Cardiac arrest Abbreviation: PTH, parathyroid hormone. Modified with permission from Wiley © Navarro-Gonzalez, J. F. et al. Clinical implications of disordered magnesium homeostasis in chronic renal failure and dialysis. Semin. Dial. 22, 37–44 (2009). 0.7-1 Massy and Drueke, 2015
- 21. Magnesium in CKD washighlysignificant. Similarly, astudy of 515patients on long-term haemodialysiswith 51 month follow-up reportedsignificantlyhigher mortalityamongthosewith baselinemagnesium levels<1.14mmol/l (2.77mg/dl) than in thosewith higher magnesium levels.86 A multi- variateCox proportional hazard analysisof thesedata showed that serum magnesium wasasignificant, inde- pendent predictor of all-causemortalityafter adjustment for potential confounders,includingpatient age,gender, haemodialysisvintageanddiabetesstatus.Notably,lower serum magnesium levelswereassociated with increased mortality from non-cardiovascular causesbut not from cardiovascular causes. Theresearchersstated that the reason for theassociation between lowmagnesium levels and noncardiovascular death isunknown,but suggested that associationsof low magnesium levelswith inflam- mation, immune deficiency and neoplasia might be amongseveral possibleexplanations. Thepotential association between hypomagnesaemia and mortality wasalso investigated in alargeregistry- based cohort study that included 142,555 patients receiving haemodialysis in Japan.87 The researchers reported 11,454 deaths, of which 4,774 weresecondary to cardiovascular disease, during the1-year follow-up period. Followingappropriateadjustmentsfor relevant clinical factors(such asdemographics, CKD-associated mineral and bone abnormalities and malnutrition– inflammation–atherosclerosiscomplex-related factors) they observed a J-shaped association between serum magnesium levelsand theoddsratioof all-causemortal- Nature Reviews | NephrologyAdjustedORforall-causemortallity Serum magnesium (mmol/ l) 0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 0.04 0.09 0.08 0.10 0.07 0.06 0.05 Figure 4 | Fully adjusted association between serum magnesium level and all-cause mortality in patients on long-term haemodialysis. Data obtained from a Japanese registry-based cohort study of 142,555 patients. The dashed lines represent the 95%confidence interval. Permission obtained from Nature Publishing Group © Sakaguchi, Y. et al. Kidney Int. 85, 174–181 (2014). REVIEWSJapanese HD Population
- 22.
- 23. Types of VascularCalcifications in CKD Uremic arteriopathy Atherosclerosis
- 24. Control of VascularCalcifications SMC Osteoblast Inhibitors Fetuin A MGlaP Osteoprotegerin Osteopontin Activators Phosphorus Uremic toxins PTH VitaminD OxLDL - + UREMIA
- 25.
- 26. Control of VascularCalcifications SMC Osteochondroblast Inhibitors Fetuin A MGlaP Osteoprotegerin Osteopontin Activators Phosphorus Uremic toxins PTH VitaminD OxLDL - + UREMIA Mg
- 27. Ca,Pi, Mg, ALP ALP,PTH VitaminD FGF23 Mg
- 28. CASE 2 • 54year old woman with CKD 3b • eGFR = 38 ml/min • sCa: 2.1mmol/, sPi: 1.8 mmol/l, Mg:1.5mmol/l, ALP: 600iU/L, PTH: 335pg/ml • In spite of treatment with alfacalcidol: 1ug/day and CaCO3: 1g/qid (between meals) WHAT WOULD YOU DO NEXT?
- 29. CASE 2 • 54year old woman with CKD 3b • eGFR = 38 ml/min • sCa: 2.1mmol/, sPi: 1.8 mmol/l, Mg: 1.5mmol/l, ALP: 600iU/L, PTH: 335pg/ml, 25Vit D: 15ng/ml • In spite of treatment with alfacalcidol: 1ug/day and CaCo3: 1g/qid (between meals) WHAT WOULD YOU DO NEXT?
- 30. CASE 2 How wouldyou Manage? • Vitamin 25D supplementation • 1-25D Supplementation • Increase calcium Supplementation • PTH (Terapatide) injections
- 31. CASE 2 How wouldyou Manage? • Vitamin 25D supplementation: • Loading: 20,000iU/week x12 w = ~ 300,000iU • 800iU/day maintenance • 1-25D Supplementation • Increase calcium Supplementation • PTH (Teriparatide) injections
- 32. What does KDIGOsay?
- 33. Few significant dietary sources UVB(290-315 nm) 7-dehydrocholesterol Pre-vitamin D3 Vitamin D3 (cholecalciferol) intestine skin Vitamin D2 (ergocalciferol) (extremely) few significant dietary sources 25OHD 1,25OH2D PTH + parathyroids intestine bone Classical Endocrine effects 1 alpha hydroxylase 24,25OH2D calcitroic acid 24- hydroxylase liver P et Ca - Souberbielle, Cavalier, 2013
- 34. Native Vitamin DEpidemiology Definition • Insufficiency: [25(OH)D] < 30 ng/mL • Deficiency: [25(OH)D] < 10-15 ng/mL Causes • CKD is associated with 25OH VitaminD deficiencies Prevalence • Differences with age, ethnicity, latitude, culture and seasons • In US HD Patients: • Insufficiency: 78%, Deficiency: 18%
- 35. VITAMIN D isa Pleotropic Hormone Vitamin D Depletion: • Progression of CKD: No effect • Hospitalisations: Increase • Mortality: Increase Vitamin D Treatment: • Bood Pressure: Reduce • LVH (PRIMO, OPERA): Reduce • Proteinuria (VITAL): Reduce
- 36. Vit D &CKD-MVD
- 37. Vitamin D andVascular Pathology Massy and Drueke, 2012 LOW HIGH
- 38. Vitamin D andVascular Pathology Massy and Drueke, 2012
- 39. Ca,Pi, Mg ALP ALP,PTH VitaminD 25D 1,25D FGF23
- 40. CASE 3 • 72year old female with IgA nephropathy • Started haemodialysis in 2010. Good access dialyses 4x week • On alfacalcidol 0.5ug od, calcium acetate, amlodipine, lisinopril, EPO • Between 2010 and 2012 gradual rise in PTH to >600 pg/ml • LFTs normal but alkaline phosphatase persistently elevated • Vitamin D level >50ng/ml • Calcium 2.48 mmol/l (normal range 2.2-2.6mmol/l). Phosphorus 1.7 mmol/l (0.8 to 1.5 mmol/l) What would you do?
- 41. What does KDIGOsay?
- 42. Vitamin(s) D andPTH VitD v Placebo Old v New Oral v IV
- 43. CASE 3 • 72year old female with IgA nephropathy • Started haemodialysis in 2010. Good access dialyses 4x week • On alfacalcidol 2ug iv x3 /week • Between 2012 and 2014 gradual rise in PTH to >1000 pg/ml • LFTs normal but alkaline phosphatase persistently elevated • Vitamin D level >50ng/ml • Calcium 2.68 mmol/l (normal range 2.2-2.6mmol/l). Phosphorus 2.1 mmol/l (0.8 to 1.5 mmol/l) What would you do next?
- 44. How would youManage SHPT? • Increase alfacalcidol dose • Switch alfacalcidol to paracalcitol • Add cinacalcet to alfacalcidol • Parathyroidectomy • Do nothing – leave alone
- 45. How would youManage SHPT? • Increase alfacalcidol dose • Switch alfacalcidol to paracalcitol • Add cinacalcet to alfacalcidol • Parathyroidectomy • Do nothing – leave alone
- 46.
- 47. EVOLVE Study –Cinacalcet in chronic haemodialysis patients EVOLVE INVESTIGATORS NEJM.2012.367;2482-97 •3883 patients on HD •Placebo or Cinacalcet •Death +CV events No benefit in cinacalcet on death Higher risk of GI side effects but lower risk parathyroid surgery Difficult study – high crossover and drop out
- 48. Calcimimetics – overviewof effects No effect on mortality Less Parathyroid surgery More hypocalcaemia More Nausea
- 49. EVOLVE Study –Cinacalcet impact on fractures EVOLVE INVESTIGATORS NEJM.2012.367;2482-97 •3883 patients on HD •Placebo or Cinacalcet •Death +CV events •No impact on fracture
- 51.
- 52. How would youmanage? • Increase alfacalcidol dose • Switch alfacalcidol to paracalcitol • Add cinacalcet to alfacalcidol • Parathyroidectomy • Do nothing – leave alone
- 53. Less Parathyroid surgery Parathyroidectomy– risks exchanging high turnover bone disease for adynamic bone disease
- 54. HT/Osteitis Fibrosa LT:ABD MIXED Osteoporosis VLPL
- 55.
- 56. DOPPS PTH andOutcomes Tentori et al, 2015
- 57. How would youManage VLPL? • Stop calcium Supplementation • Stop Vitamin D supplementation • Reduce Dialysate calcium Supplementation • None of the Above • All of the above
- 58. How would youManage VLPL? • Stop calcium Supplementation • Stop Vitamin D supplementation • Reduce Dialysate calcium Supplementation • None of the Above • All of the above
- 59. CKD-MBD: General managementtips • Adynamic Bone Disease with low PTH: • stop calcium binders and vitamin D supplements. • High turnover Bone Disease (with PTH >9 times normal): • ensure native vitamin D levels normal. Control phosphate. Increase calcitriol/alfacalcidol as much as calcium/phosphate allow. • High turnover Bone Disease (with PTH >9 times normal) with hypercalcaemia: low calcium dialysate, non-calcium binders, switch to cinacalcet, consider parathyroidectomy • Always ensure magnesium levels and vitamin D3 levels maintained
- 60. What KDIGO saysabout PTH in dialysis • In patients with CKD5D we suggest maintaining iPTH levels between 2 –9 times upper limit of normal(2C). • In patients with CKD5D and elevated or rising iPTH, we suggest calcitriol, vitamin D analogues, calcimimetics or a combination to lower PTH (2B). • In patients with hypercalcaemia recommend stopping or reducing calcitriol or vitamin D sterols (1B). • In patients with hyperphosphataemia, recommend stopping or reducing calcitriol or vitamin D sterols (2D).
- 61. Ca,Pi, Mg, ALP ALP,PTH VitaminD 25D 1,25D ……..????? CKD-MBD
- 62. Ca,Pi, Mg, ALP ALP,PTH VitaminD 25D 1,25D FGF23 CKD-MBD
- 63. FGF23 and CKD lotholevelsof CKD patients have been ein thevery early stagesof CKD and to KD progresses [36]. In a rodent CKD vels in plasma, urine, and kidney were se in parallel [36], but the relationship elsin CKD patientsremainsto bedeter- ore, almost all modelsof CKD, includ- avebeen createdbyrenal tissueablation, tis, nephrotoxin, diabetic nephropathy, e kidney damage, are characterized by wnregulation of Klotho mRNA and pro- ey and by low plasma or urine-soluble ]. Plasma soluble Klotho levels are also early stagesof CKD [58].Pavik et al.[63] dingthatsolubleKlothoand1,25(OH)2D nd FGF23 levels increase in the early nd that PTH levelsincreasein themore Akimoto et al. [64] haverecently shown Klotho levels of CKD patients, rather Klotholevels,arelinked totheir number phrons.Sakan et al.[65] recentlyreport- renal α-Klotho levelsweresignificantly um FGF23 levels were significantly ele- d intermediate CKD, serum P levelsre- he normal range. Despite falling renal heincreasein FGF23 enhanced urinary d serum 1,25(OH)2D levelsin early and D, though not in advanced CKD. In ad- ubleKlotho levelsfell significantly over overlapping distinct mechanisms of initiation and pro- gression [68, 69].Vascular calcification isadynamicpro- Fig. 5. Timeprofileof changesinplasmaFGF23,Klotho,activevi- taminD,andphosphatelevelsasCKDprogresses. Thedecreasein Klothoproteininthebloodisanearlyevent inCKDandisprogres- sivelyreducedalongwiththedeclineof renal function.LowKlotho partiallyinducesFGF23resistance,causinganinitial compensatory increasein blood FGF23tomaintain Phomeostasis. Theincrease inFGF23decreasesactivevitaminDlevelsandisfollowedbyeleva- tion of PTH. Hyperphosphatemia is relatively late event in ad- vancedCKD[reprintedwithpermissionfrom 60]. Colorversionavailableonline
- 64.
- 65. FGF23 and CKD havebeenfound to predict mortality not only among di- alysispatientsbut amongpredialysisCKD patientsaswell [22]. tial to facilitate thebinding of FG The potential role of soluble Klo in vivo remainsunknown at this Fig. 2. Plasma FGF23 levels in thefour CKD stage groups. Boxes represent the interquartile range with the upper and lower edges representing the75th and 25th percentiles, respectively. Thereisa statistically significant linear increase in plasma FGF23 levels acrossthefour CKD groupsdivided by eGFR[reprinted with per- mission from 21]. Fig. 3. Klotho family showing theth themammalian genome. Homologo mainsareconserved. Solubleformso byalternativesplicingof itstranscrip of thetransmembraneformbyβ-secr Colorversionavailableonline
- 66. FGF23 and CKDMortality Figure 2. FGF23 is an independent risk factor for mortality in CKD stages 2–4 The cumulative incidence of death of CKD stage 2–4 patients increases significantly with ascending quartiles of baseline FGF23 levels in unadjusted analyses (plot) and after full multivariable adjustment (hazard ratios and 95% confidence intervals in the inset). 86 Wolf Page 20 $watermark-text$watermark-tex Wolf, 2012
- 67.
- 68. FGF23 & CKD-MVD Jimboand Shimosawa, 2014
- 69.
- 70. HT/Osteitis Fibrosa LT:ABD MIXED ………???? CKD-MBD
- 71. HT/Osteitis Fibrosa LT:ABD MIXED Osteoporosis CKD-MBD
- 72. Kalwansky S etal. Osteoporosis Int (2003) 14: 570–576 Significant co-prevalence of osteoporosis and CKD in the elderly Increasing osteoporosis with declining kidney function Age eGFR<35mls/min 20-29 0% 30-39 0% 40-49 0% 50-59 0% 60-69 7.3% 70-79 21.3% 80+ 53.9%
- 73. Healthcare database 679114adults, Ontario, Canada Naylor Kl et al. Kidney International (2014) 86, 810–818 Fractures are more common in CKD
- 74. RANK-RANKL-OPG regulate Osteoclasticactivity Lewiecki, E. M. (2011) Nat. Rev. Rheumatol. Maturation of preosteoclasts dependent on RANKL and OPG activity
- 75. Improving bone density Targetingbone resorption Salam S, Eastell RE, Khwaja A, AJKD 2014 Bisphosphonate Denosumab
- 76. How would youmanage osteoporosis and low impact fractures in a Patient CKD3 • Bisphosphosphonates • Denosumab • Bone biopsy • Do nothing as risk of adynamic bone disease with anti-osteoporosis medication
- 77. The problem withbisphosphonates in CKD • Clearance by kidney • 50% of dose deposits in skeleton and may be there for 10 years! • Exacerbate adynamic bone disease (may require bone biopsy) • Atypical fractures • FSGS
- 78. How would youmanage osteoporosis and low impact fractures in a Patient with CKD4-5 • Bisphosphosphonates • Denosumab • Bone biopsy • Do nothing as risk of adynamic bone disease with anti-osteoporosis medication
- 79. Approach to fragilityfracture in CKD Salam S, Eastell RE, Khwaja A AJKD 2014 ABD
- 80. Fractures – itsnot just about bone Bone Strength Falls Postural hypotension, autonomic dysfunction, drugs FRACTURES Soft Tissue padding Fraility Lifestyle Nutrition Exercise
- 82. HT/Osteitis Fibrosa LT:ABD MIXED Osteoporosis
- 83. Ca,Pi, Mg, ALP ALP,PTH VitaminD 25D 1,25D FGF23
- 84. CKD-MBD 2017 Professor MeguidEl Nahas Global Kidney Academy Sheffield, UK