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Secondary Hyperparathyroidism in the Diabetic Patient with Chronic Kidney Disease

US Endocrinology, 2005;(1):39-42 DOI:


Diabetes and Chronic Kidney Disease
In the US, diabetic nephropathy accounts for the majority of chronic kidney disease (CKD). It contributes significantly to morbidity and mortality among the diabetic population1,2 and accounts for approximately 40% of patients with end-stage renal disease.3 The earliest manifestation of renal involvement in diabetes is the presence of microalbuminuria, as defined by urine albumin excretion of 30–300mg/day.4 Progression to overt proteinuria (urine albumin excretion greater than 300mg/day) and diabetic nephropathy occur more frequently in those with poor glycemic control, glomerular hyperfiltration, and hypertension.5

Not all kidney disease in diabetics is attributable to diabetic nephropathy. Despite an increasing population of diabetics in the population, advances in the care of the diabetic patient have reduced the incidence of overt progression to diabetic nephropathy.6,7 The natural history of diabetic nephropathy, which had previously been characterized by a decline in glomerular filtration rate (GFR) by approximately 10–15ml/min per year,8 can be reduced to a rate of decline of 3.7ml/min per year with antihypertensive therapy alone.9 In one series of type 1 diabetics in Sweden, the incidence of diabetic nephropathy after 20 years was found to decrease from 28% to 5.8%.10 However, a study by Kramer et al. found that 30% of diabetics with estimated GFR of <60ml/min had neither albuminuria nor retinopathy.11 This illustrates the important principle that diabetics continue to be susceptible to other types of renal disease and the manifestation of chronic kidney disease in this population may be due to causes other than diabetic nephropathy.

The management of chronic kidney disease, including diabetic nephropathy, consists not only of protecting residual renal function and instituting renal replacement therapy when necessary, but also in treating the myriad complications of kidney disease, including renal osteodystrophy.The impact of these complications on the health and survival of patients with chronic kidney disease is significant. Elevations in the serum phosphorus, the calcium-phosphorus product, and parathyroid hormone (PTH) levels are associated with vascular calcifications, an increase in cardiovascular morbidity and mortality, and an overall increase in the relative risk of death from all causes in the CKD population.12,13