CINACALCET (SENSIPAR) Calcimimetic Agents in CKD | ESRD | Dialysis and Hemodialysis Patients
Patients with chronic kidney disease have special issues in regulating mineral metabolism.
The kidneys actively hold onto necessary minerals and excrete or get rid of minerals thought to be in excessive supply.
Some of these minerals necessary for cellular functions include sodium, potassium, calcium and phosphorous.
The kidneys play a unique role in calcium regulation due to the fact that healthy kidneys activate a form of Vitamin D. Vitamin D in turn facilitates absorption of Calcium from the intestines from the food or from bones.
Other important glands in this metabolic system are the parathyroids. These small glands in the neck secrete a hormone called PTH or parathyroid hormone that boosts the absorption of calcium from the intestine or bones if the body is deemed to have too little calcium.
Patients with abnormal, or scarred kidneys do not make sufficient active Vitamin D. Chronic kidney disease (CKD) patients or end stage renal disease (ESRD) patients
therefore may be deficient in calcium and have an elevated parathyroid level. This elevated PTH level is called secondary hyperparathyrodism.
There are several methods of helping to control mineral metabolism in ESRD and CKD patients. Some of these methods include diet, Vitamin D supplementation and drugs which help absorb excessive minerals from the intestine. A relatively new medication acts to help decrease parathyroid hormone production by making the parathyroid gland more sensitive to calcium. This new class of medication is called a calcimimetic because it mimics the effects of calcium on the parathyroid glands.
The articles reference below discuss calcimemetics in CKD and ESRD.
Schumock GT, et al
Center for Pharmacoeconomic Research, Department of Pharmacy Practice, and Department of Pharmacy Administration, University of Illinois at Chicago, Chicago, Ill.
Calcimimetic Agents in CKD ESRD Dialysis and Hemodialysis Patients
Am J Nephrol. 2010 Apr 30;31(6):482-489.
Borchhardt KA, Diarra D, Sulzbacher I, Benesch T, Haas M, Sunder-Plassmann G.
Division of Nephrology and Dialysis, Department of Medicine III, Medical University Vienna, Vienna, Austria.
J Nephrology. 2010 May 2. pii: 8E39C3E1-CF8D-4F2A-94D3-D72F4B99DFFC.
Guerra R, Auyanet I, Fernández EJ, Pérez MA, Bosch E, Ramírez A, Suria S, Checa MD.
Department of Nephrology, Hospital Insular de Gran Canaria, Las Palmas de Gran Canaria - Spain.
Journal of the American Society of Nephrology. 2009 Jul;20(7):1527-32.
Gattone VH 2nd, Chen NX, Sinders RM, Seifert MF, Duan D, Martin D, Henley C, Moe SM.
Department of Anatomy and Cell Biology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, Indiana 46202, USA. vgattone@iupui.edu
Comment in:
J Am Soc Nephrol. 2009 Jul;20(7):1421-5.
New Feature from Hemodialysis.com: Hemodialysis or Chronic Kidney Disease Abstract of the Week
Zasuwa G, Frinak S, Besarab A, Peterson E, Yee J.
Division of Nephrology and Hypertension, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Although monitoring of vascular accesses by physical examination is nearly as sensitive as surveillance measurements by vascular access pressure when performed by examiners, the frequency of examinations is limited by time.
We developed intravascular access pressure surveillance as a surrogate to physical examination. Using real-time data from hemodialysis machines, we derived intravascular access pressure ratios for each dialytic procedure. An automated, noninvasive surveillance algorithm that generated a "warning" list of patients at risk for thrombosis was formulated.
We hypothesized that this algorithm would reduce access thrombosis frequency. We designed a study comparing thrombosis rates during a baseline 6-month interval to three subsequent 6-month periods of active surveillance.
Referrals for interventions during this 18-month period were based on persistently abnormal elevated vascular access pressure ratio tests (VAPRT) >0.55.
Thrombosis rates declined progressively for arteriovenous grafts (AVG) during the intervention period compared with the baseline period.
Arteriovenous fistula (AVF) thrombosis rates decreased during postintervention months 13-18 during employment of the VAPRT.
We conclude that use of VAPRT can reduce thrombosis rates in vascular accesses, and the magnitude of the effect is larger and more consistent in arteriovenous grafts (AVGs) than autologous AVFs.
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