Renal Bone Disease: 200 Hours Dialysis Training

I will never look at an AV fistula the same again.

Not after this 6 months training.

I was looking at my own arm thinking, yeah, I think I would certainly qualify for an AV fistula. That's how it was when starting work too, you look at veins and see how beautiful they are and how easy it would be to cannulate them. Only doctors and vampires would understand.

So we were in ICU during the nephrology grand rounds and there was a patient who had had a parathyroidectomy.

So it's a good time to read up on renal bone disease.

Management of Renal Bone Disease Disease
Dr. Sunita Bavanandan Dept of Nephrology Hospital Kuala Lumpur

Mineral Bone Disease in Renal Failure
•Synonyms
–Renal osteodystrophy
–CKD-mineral bone disease (CKD-MBD)
•Common complication of renal failure

•Mineral bone disturbance:
–Low serum calcium
–High serum phosphate
–Parathyroid hormone
–Alkaline phosphatase

Types of Renal Bone Disease
1.High bone turn-over disease
–Secondary hyperparathyroidism
2.Low bone turn-over disease
–Adynamic bone disease
–Osteomalacia including aluminium bone disease
3.Mixed bone disease

Secondary hyperparathyroidism
•Most common form of renal bone disease
•Synonyms
–Osteitis fibrosa
–Hyperparathyroid bone disease
•Characterised by elevated PTH level

Pathogenesis
•Hypocalcaemia
–Low levels of active Vitamin D
–Kidneys are required for activation of Vitamin D
•Hyperphosphataemia
–Reduced renal clearance
•High iPTH (secondary hyperparathyroidism)
–Hypocalcaemia
–Hyperphosphataemia

Vitamin D
•Vitamin D (cholecalciferol) is inactive
•Needs to be converted to 1,25 DHCC
–DHCC = dihydroxycholecalciferol
•2 step activation
–Liver adds 25-hydroxy
–Liver adds 25-hydroxy
–Kidney adds 1-hydroxy
•Active Vitamin D (1,25DHCC)
–increases serum calcium and phosphate absorption from intestines
–calcifies bones
–suppresses PTH secretion

Pathogenesis of secondary hyperparathryodisim
•PTH regulates calcium homeostasis
•PTH increase stimulated by
–hypocalcaemia
–hyperphosphataemia
•PTH increases serum calcium
–increasing efflux of calcium from bones & increase GI & renal absorption

Features of RBD
Type      PTH      SAP      Calcium
SHPT     ↑           ↑           ↓
THPT     ↑↑         ↑↑         ↑
ABD       ↓↔       ↔         ↑      
SAP = serum alkaline phosphatase
SHPT = secondary hyperparathyroidism,
THPT = tertiary hyperparathyroidism
ABD = adynamic/aluminium bone disease

Features of tertiary hyperparathyroidism
•Hyperplastic parathryoid glands autonomous
•Non-suppressible by Vitamin D analogues
•Hypercalcaemia
•Very high alkaline phosphate level

CONSEQUENCES OF
Lab abnormalities
Bone abnormalities
Vascular calcification
CVD
Fractures
Mortality

Consequences of CKD -MBD
1.Bone disease
–Proximal muscle weakness
–Bone erosions, bone pain
–Fractures
–Marrow Fibrosis
–Erythropoietin resistance

Consequences of CKD-MBD
2.Systemic complications
–Vascular calcification, Calciphylaxis
–Soft tissue calcification
–Cardiovascular disease
–Increased mortality

At slide 16/50 suddenly can't copy and paste. Will read up and maybe continue later.

Tetiba boleh pulak copy paste slide 27/50...

                                                  2009           2003 NKF KDOQI  KDIGO
Calcium (mmol/l)                     2.1-2.37      2.1-2.37                   Normal range
Phosphate (mmol/l)                  1.13-1.78    1.13-1.78                 Toward normal range

range CaP product (mmol2/l2) <  4.54     < 4.54
Intact PTH (pg/mL)                  150 -300  150 -300                     2-9x ULN

Conversion for iPTH 1pmol/l = 9.5pg/ml
Corrected Calcium = Serum calcium + (40-serum albumin)x0.02
CaP product = Correct calcium x Phosphate

Baby pulak dah bangun...to be continued