Secondary Hyperparathyroidism: Pathophysiology and Treatment
Secondary Hyperparathyroidism: Pathophysiology and Treatment
Secondary hyperparathyroidism is a frequently encountered problem in the management of patients with chronic kidney disease (CKD). Its pathophysiology is mainly due to hyperphosphatemia and vitamin D deficiency and resistance. This condition has a high impact on the mortality and morbidity of dialysis patients. Early diagnosis of secondary hyperparathyroidism is crucial in the management of patients with CKD. The treatment remains a challenge for patients and their clinicians. It should include a combination of dietary phosphorus restriction, phosphate binders, vitamin D analogues, and calcimimetics.
The prevalence of chronic kidney disease (CKD) in the United States has increased from 10% during 1988 to 1994 to around 13% during 1999 to 2004. This goes in pair with an increasing prevalence of diabetes mellitus and hypertension. Current classification of CKD is based on the presence of parenchymal damage for stages I and II and a decrease in glomerular filtration rate (GFR) regardless of parenchymal damage for stages III and higher ( Table 1 ). CKD stage III is the most common CKD stage, with a rate reaching 30% in patients older than 70 years of age. This high number of CKD patients represents a challenge for both nephrologists and primary care physicians, especially when dealing with blood pressure, anemia, volume status, and, most importantly, the combination of secondary hyperparathyroidism and mineral bone disease. This article reviews the mechanisms and causes of secondary hyperparathyroidism and provides a stepped approach for its management.
Abstract and Background
Abstract
Secondary hyperparathyroidism is a frequently encountered problem in the management of patients with chronic kidney disease (CKD). Its pathophysiology is mainly due to hyperphosphatemia and vitamin D deficiency and resistance. This condition has a high impact on the mortality and morbidity of dialysis patients. Early diagnosis of secondary hyperparathyroidism is crucial in the management of patients with CKD. The treatment remains a challenge for patients and their clinicians. It should include a combination of dietary phosphorus restriction, phosphate binders, vitamin D analogues, and calcimimetics.
Background
The prevalence of chronic kidney disease (CKD) in the United States has increased from 10% during 1988 to 1994 to around 13% during 1999 to 2004. This goes in pair with an increasing prevalence of diabetes mellitus and hypertension. Current classification of CKD is based on the presence of parenchymal damage for stages I and II and a decrease in glomerular filtration rate (GFR) regardless of parenchymal damage for stages III and higher ( Table 1 ). CKD stage III is the most common CKD stage, with a rate reaching 30% in patients older than 70 years of age. This high number of CKD patients represents a challenge for both nephrologists and primary care physicians, especially when dealing with blood pressure, anemia, volume status, and, most importantly, the combination of secondary hyperparathyroidism and mineral bone disease. This article reviews the mechanisms and causes of secondary hyperparathyroidism and provides a stepped approach for its management.
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