Anemi Common Systemic Consequence Of Chronic Kidney Disease ( Ckd )

Anemia is a disorder of the blood. It occurs when your body does not produce enough erythrocytes or red blood cells (RBCs). Without the erythrocytes oxygen can not be adequately delivered to the tissues and organs throughout the body. This will cause you to become weak and tired. A person may also experience headaches, skin pallor, and faintness. Your body may attempt to compensate for these symptoms by speeding up the heart rate and respiratory rate. This is the body’s attempt to return oxygen levels to normal(Thibodeau and Patton, 2005).

Destruction of Ed’s red blood cells has caused damage to his kidneys. How is the kidney involved in blood cell production?

Calcitriol moves to the nucleus of these cells and boost the role of proteins that carry calcium from inside the small intestine to the blood. Calcitonin does the opposite of the parathyroid hormone and vitamin D. While the parathyroid gland and vitamin D raise the calcium levels, calcitonin decreases it. Calcitonin is a hormone secreted by the C cell of the thyroid gland that lowers blood calcium levels by inhibiting bone resorption. (Lingohr-Smith, 2011).

Nutrition Monitoring and Evaluation: Monitor phosphorus lab values as well as keeping a check on her medication log and knowing when she comes off of Renvela, phosphate blocker.

Also known as normocytic anemia. This is the most frequent type of anemia most often happening to males over 85 years old. It is a common problem that occurs to men and women over 85 years old. Symptoms include and are caused by: a reduced production of normal-sized red blood cells even though presence of hemoglobin in the red blood cells is within the standard range; an increased production of HbS as is seen in sickle cell diseases; greater destruction and loss of red blood cells; an increase in plasma volume that is not compensated by anything else; a B2 (riboflavin) deficiency; and a B6 (pyridoxine) deficiency. (Brill & Baumgardner 2000).

1. Anemia, pp. 989. Anemia is a areduction in the total number of erythrocytes in the circulating blood or a decrease in the quality or quantity of hemoglobin. Anemias commonly result from (1) impaired erythrocyte production, (2) blood loss (acute or chronic), (3)increase erythrocyte destruction, or (4) a combination of these three. sThe fundamental physiologic manifestation of anemia is a reduced oxygen-carrying capacity of the blood resulting in tissue hypoxia.

Mutation of the CFH gene causes a disruption of the activation pathway in the body, therefore it begins to attack cells in the body specifically on the kidney or liver (Bu, Borsa, Gianluigi, & Smith, 2012). The attack on the kidney can lead to thrombotic microangiopathy (TMA), small vessel clots. Platelets will help minimize any leaking of vessels done by the attack of the disrupted activation pathway but after several clots form oxygen is cut off from certain parts of the kidney. When the kidney no longer receives oxygen, those parts begin to die off leading to thrombocytopenia, anemia and renal failure. When the kidney begins to fail, erythropoietin levels decrease. EPO binds to a receptor in the bone marrow to inhibit erythropoiesis. Therefore, RBC production in the bone marrow decreases when EPO levels decrease. (Bu, Borsa, Gianluigi, & Smith, 2012)

There are numerous factors that contribute to the development of this horrible disease, but the most important factor is vitamin D deficiency. When the minerals in osteoid crystallize, they require adequate concentration of calcium and phosphate. When the concentration is not at the correct level, ossification does not proceed normally (Huether & McCance, 2008). Vitamin D regulates the absorption of calcium from the intestine. When there is a lack of vitamin D, the concentration of calcium begins to fall (Huether & McCance, 2008). The body begins to regulate this calcium drop by increases the amount of PTH synthesis and secretion (Huether & McCance, 2008). An increase of PTH causes a clearance of phosphate and without the correct levels of phosphate mineralization of the bones cannot proceed in the correct manor (Huether & McCance, 2008). The abnormality of bone growth can occur in spongy and compact bone (Mayo

In order to deal with pain, many health care providers suggest taking over-the-counter medication like aspirin. High blood pressure is one of the most common symptoms in patients with PKD. Many patients have to make lifestyle changes and take various medications to lower blood pressure. Some lifestyle changes that may need to take place include a strict diet or an increase in exercise. About 50 percent of people with PKD experience kidney failure by the age of 60, and 70 percent will have kidney failure by age 70 (National Kidney Foundation, 2016). Although there is no way to reverse kidney failure, there are ways to prolong the life of the kidneys. Patients either need to receive dialysis or receive a kidney transplant. There are two types of dialysis. The first is hemodialysis. This is where a machine is used to filter toxins from the blood. The second is peritoneal dialysis. This is where the lining of the abdomen is used to filter blood from inside the body. A kidney transplant is when the unhealthy kidney is removed from the patient’s body and a healthy one is put in. The healthy kidney typically comes from a family member to reduce the risk of rejection (National Institute of Diabetes and Digestive and Kidney

Chronic kidney disease (CKD) affects 13% of the population, and it can lead to an increased risk of cardiovascular disease since it is associated with the precipitation of PO4 and Ca. The deposition of PO4 and Ca can consequently lead to the calcification and stiffening of vascular smooth muscle cells of arteries which increases cardiovascular morbidity and mortality. Increased levels of serum magnesium (Mg) are associated with slower development of CVD since Mg helps to upregulate factors that inhibit calcification and downregulate factors that promote calcification. In previous trials, Mg supplementation has been shown to reduce the development and progression of vascular calcification in end-stage renal disease. Studies have also shown

Another 87 residents would seek consult for this indication of < 15 ml/min/1.73m2. This proves that more education is needed for internal medicine residents. Residents were given two clinical vignettes on complications of CKD, anemia and bone mineral disorder of CKD stage III (GFR 30-59mL/min/1.72m2). Appoximately 134 residents (28.0%) would refer to the nephrologists for management of CKD, 134 residents (28.0%)and for bone mineral disorder by 215 residents (44.9%)(Babos, et al., 2009). Approximately half 281 (58.8%) of the residents would consider referral for a patient with a GFR of 15-30mL/min/1.73m2. Another 87 residents (18.2%) would consult a nephrologists for this indication at a GFR <15mL/min/1.73m2.

Severe renal insufficiency because result for bone demineralization of bone by increase of phosphate and decrease of calcium , cause of loss of vitamin D

Chronic kidney disease (CKD) is an irreversible condition that progresses causing kidney dysfunction and then to kidney failure. It is classified by a GFR of &lt;60mL/min for longer than 3 months. There are five stages of CKD: Stage 1 has kidney damage but has a GFR ≥ 90. Stage 2 has mild damage and a GFR of 60-89. Stage 3 has moderate damage and a GFR of 30-59. Stage 4 has severe damage and a GFR of 15-29. Stage 5 is also known as end stage renal disease (ESRD), this is kidney failure with a GFR of ≤ 15 and theses patients are typically on dialysis or in need of an immediate transplant. The leading cause of CKD is diabetes. Hypertension is also a major cause. Since most DM patients have HTN,

Chronic Kidney Disease (CKD) is among the leading causes of mortality throughout the world, and its prevalence and the health care costs resulting from it are considerable and increasing. CKD commonly is silent and asymptomatic until its late stages. Accordingly, CKD is diagnosed prior to symptomatic stage of kidney failure, resulting in delays in proper interventions and the emergence of adverse consequences in the CKD patients

A very narrow range of 9-11 mg per dl of calcium in blood is maintained by a negative feedback hormonal loop (Formation 2013). The thyroid gland secretes parathyroid hormone (PTH) in response to low calcium in the blood detected by the g-protein coupled receptor. PTH activates bone digesting Osteoclasts, which move along a bone surface, breaking down the matrix and in turn release Ca2+ and HPO42-. Calcium salts are converted into soluble forms by the hydrochloric acid secreted by the ruffle border of the Osteoclast. Bones can become so de mineralised that they develop large holes when blood calcium levels are too low for an extended period of time (Marieb & Hoehn 2010). Extracellular calcium levels between 9-11ng or higher results in the binding of calcium to the receptor inhibiting the secretion of PTH. Without the bodies capacity to detect changes in ECF calcium concentration, voltage gated ion channels can become unstable and result in hyperactivity of muscle and nerve cells (Humoral Regualtion 2013). According to the Harvard health publication: Calcium beyond the bones, fundamental processes such as growth may be underdeveloped or calcium may be deposited in soft tissues such as the heart and lungs when there is excess or inadequate levels of calcium (Calcium 2010). Most calcium deposits are benign however