Identify and briefly explain the structural and functional changes that occur in the kidneys as Chronic Renal Failure develops and explain why Rocaltrol and Epoetin are used in the management of chronic renal failure and they moderate this renal dysfunction
I: Identification, structural and functional causes of Chronic Renal Failure
- Introduction and identification
Chronic renal failure arises out of the existence of kidney disease and results in the progressive loss of function of the kidney. It graduates over a period of time, during which there is a loss of functioning kidney nephrons, accompanied by progressive deterioration of glomerular filtration, tubular reabsorptive capacity and endocrine functioning of the kidneys (Porth & Matfin, 2009).
The normal prostate glands size is around 4cm in diameter (Jenkins, 2013). It is a ‘doughnut’ shaped organ located inferior to the urinary bladder. Malfunctioning in it can contribute to alterations in urinary flow rates and can lead to acute urinary retention causing chronic renal failure.
The disease could be identified by a number of adverse health outcomes. There could be a loss in appetite, swelling in the face, body & abdomen and a sense of laxity. The laboratory identifier is an increase in the urea and creatinine levels as well as increase in the potassium level in the blood. There also takes place a reduction in the Glomerular Filtration Rate (GFR) and when the normal GFR of more than 90 ml of body fluid per minute is breached, it could result in chronic renal failure.
- 2. Structural Causes
The singularly important structural cause could be congenital one which results in the mal-development of kidney. There could also be abnormalities in the development of kidneys themselves and a classic example of this could be found in patients suffering from horse-shoe kidney. It is possible to have abnormalities in the texture of the renal parenchyma, presence of visible cysts and existence of hydronephrosis. While ultrasound scanning is the most used method to find out renal abnormalities, yet it needs to be kept in mind that such anomalies may not always show up for the reason that the renal anomalies can co-exist with other anomalies ( Stoll, 1996).
- Functional causes
The metabolic cause could be due to the prevalence of diabetes which can trigger chronic renal failure. When the patient is characterised by Glomerular Nephritides, there takes place an inflammation in the either of or both the kidneys. A systemic cause of chronic renal failure could be traced to the prevalence of hypertension. Scholarly research also indicates that chronic renal failure is associated with a high incidence of nutrition vitamin D insufficiency which gets reflected in the decreased levels of 25-hydroxyvitamin D (Andress, 2006). There could also be a reduced supply of blood to the kidneys.
II Prescription of Rolcaltrol and Epoetin
The role of vit 3 has been expanding in that it is prescribed now-a-days not only for maintenance of bone health but also in influencing many human physiological processes. Vitamin D receptor (VDR) is now not only known to be found in many cells, but also influence the proper functioning of various physiologic systems as the cardiovascular, muscle, central nervous systems, pancreas etc ( Norman, 2008). However, it needs to be noted that medications should be prescribed only after assessing the current renal functions of the patients (Liles, 2011).
Subject to such precautionary actions, Rolcaltrol is prescribed to make up vit D 3 deficiency. When no vit D 3 synthesis takes place in the system, it results in renal asteo-dystrophy. In order to arrest this Rolcaltrol is given. Rolcaltrol is also known to prevent hypercalcimia. Typical dosage is 0.25 μg po once a day or 1 to 4 μg two times a week.
Anemia has to be treated to keep the Hb between 11 and 12 G/dL. Since it gradually responds to recombinant human erythropoietin, it is given normally between 50 to 150 units/kg sc one to three times a week. It works by improving the red cell production.
The medication in themselves do not moderate chronic renal dysfunction. The treatment for chronic renal failure may need a multi-disciplinary approach and hence no generalization can be made.
Andress, D. L. (January 01, 2006). Vitamin D in chronic kidney disease: a systemic role for selective vitamin D receptor activation. Kidney International, 69, 1, 33-43.
Jenkins, G. W., & Tortora, G. J. (2013). Anatomy and physiology: From science to life. Hoboken, N.J.: Chichester: Wiley; John Wiley [distributor].
Liles, A. M. (January 01, 2011). Medication considerations for patients with chronic kidney disease who are not yet on dialysis. Nephrology Nursing Journal: Journal of the American Nephrology Nurses’ Association, 38, 3.
Norman, A. W. (January 01, 2008). From vitamin D to hormone D: fundamentals of the vitamin D endocrine system essential for good health. The American Journal of Clinical Nutrition, 88, 2.
Porth, C.M. & Matfin, G., (2009): Pathophysicology Concept of altered Mental Status (8th Ed): Philadelphia, PA, Lippincott Williams & Wilkins
Stoll, C., Alembik, Y., Dott, B., & Roth, M. P. (December 01, 1996). Evaluation of prenatal diagnosis of congenital gastro-intestinal atresias. European Journal of Epidemiology, 12, 6, 611-616.
Ulerich, L. (January 01, 2010). Vitamin D in chronic kidney disease–new insights. Nephrology Nursing Journal: Journal of the American Nephrology Nurses’ Association, 37, 4.)