Changes

<big>'''Secondary hyperparathyroidism'''</big> can be either renal or nutritional in origin:

<big>'''Secondary hyperparathyroidism'''</big> is usually diffuse hyperplasia of the parathyroid glands and  can be either renal or nutritional in origin:

Secondary '''renal hyperparathyroidism''' is a complication of '''chronic renal failure'''. This is due to '''hyperphosphataemia developing as a result of impaired glomerular filtration rate'''. '''Reduced vitamin D''' synthesis is also thought to contribute to low serum calcium levels and subsequent stimulation of the parathyroid gland. Renal production of [[Calcium#Calcitriol|calcitriol]] is also reduced, exacerbating the resulting [[hypercalcaemia]].  

Secondary '''renal hyperparathyroidism''' is a complication of '''chronic renal failure'''. This is due to relative '''hyperphosphataemia developing as a result of impaired glomerular filtration rate'''. '''Reduced vitamin D''' synthesis or absorbtion is also thought to contribute to low serum calcium levels and subsequent stimulation of the parathyroid gland. Renal production of [[Calcium#Calcitriol|calcitriol]] (active Vitamin D3) is also reduced, exacerbating the resulting [[hypercalcaemia]].  

Secondary '''nutritional''' hyperparathyroidism is caused by excessive '''phosphorus intake''' causing a total or relative calcium deficiency by '''binding calcium in the gut and decreasing its absorption'''.  This category encompasses '''bran disease in horses and also [[Metabolic Bone Disease|metabolic bone disease]] in reptiles'''.

Secondary '''nutritional''' hyperparathyroidism is caused by excessive '''phosphorus intake''' causing a total or relative calcium deficiency by '''binding calcium in the gut and decreasing its absorption'''.  This category encompasses '''bran disease in horses and also [[Metabolic Bone Disease|metabolic bone disease]] in reptiles'''.