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A silent killer in dialysis population


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Bone diseases are common accompaniments in the management of patients with chronic kidney disease. Bone diseases start showing up when the GFR ( Glomerular Filtration Rate) starts to fall below 50 ml/min. Common links in the pathogenesis of bone disease in CKD are defective filtration of phosphorus and deficient production of active vitamin D3 which leads to hypocalcaemia and hyperphosphatemia secondarily leading to hyperparathyroidism and bone diseases. The manifestations of bone diseases in CKD ( chronic kidney disease) can include a spectrum of diseases like classical hyperparathyroidism (Osteitis fibrosa cystica), osteomalacia, osteoporosis and recently recognised low bone turnover disease or adynamic bone disease.

Adynamic bone disease is characterised by reduced osteoblast and osteoclast number and low or absent bone formation rate as measured by tetracycline labelling (a method of studying bone formation rate in bone biopsy samples). The osteoid thickness is normal or reduced, distinguishing it from osteomalacia.

Associated laboratory findings may include an i-PTH less than 100 pg/ml (11 pmol/ L), low serum bone specific alkaline phosphatase and occasionally a slightly elevated serum ionised calcium level.

Vertebral and peripheral bone densities tend to be normal or low. The causes of adynamic bone histology are unknown, but persistently low PTH levels play a major causal role. Susceptible population include the elderly, women, diabetics and those of Caucasian race. It is more common in peritoneal dialysis patients and in those who use dialysate calcium more than 2.5 m Eq/ L. Aluminium toxicity is a rare cause of adynamic bone disease. Initially thought to be asymptomatic and not requiring treatment, adynamic bone disease is now known to be associated with a higher fracture rate, hypercalcemia and vascular and soft tissue calcification. The latter manifestation leads to increased incidence of cardiovascular events in CKD patients who are already in the risk of more cardiovascular deaths because of uremic atherosclerotic milieu and malnutrition.

The goal of managing this special group of patients is to maintain PTH in normal range for the stage of CKD. Strategies employed are use of low calcium dialysate, maintaining serum calcium in low normal range, serum phosphorus in high normal range, avoiding use of calcium based phosphorus binders and active vitamin D. Calcimimetics have no role in the management of adynamic bone diseases. New strategies include use of teriparatide, a synthetic form of PTH which is still in clinical trial settings.

Vinod Chandran MD, DM Nephrologist Badr Al Samaa Hospital, Ruwi

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