Patients with Chronic Kidney Disease
Patients with Chronic Kidney Disease
Pathophysdiology
The following paper is interested in the effects of hyperglycemia on geriatric diabetics patients with chronic kidney disease, In doing so, it reflects three distinct disease entities. They are hyperglycemia, which serves as the dominant variable; geriatric diabetes and chronic kidney failure. Consequently, the pathophysiology of these three entities will be addressed separately.
Hyperglycemia
When hyperglycemia occurs, it represents a medical emergency. However, the extent to which blood sugar is elevated can be directly related to underlying disease conditions. These may include kidney failure, infections and systemic disease. While disease processes may be obvious, this does not necessarily indicate that they are impacting blood sugar, and generating the hyperglycemia observed, rather, impaired fasting glucose (IFG) as well as impaired glucose tolerance (IGT) may also be involved. People who have extensive β-cell destruction with no residual insulin secretion need insulin to live and can experience hyperglycemia more frequently than other persons affected by diabetes. This metabolic abnormality can continue to develop and progress into serious complications, regress, or remain same. As such, hyperglycemia indicates the level at which an underlying metabolic process and its treatment impact diabetes process (American Diabetes Association 2013).
Gerich (2013) conducted a literature review of clinical trials with diabetics, including geriatrics. The researcher contends that hyperglyceia occurs in every person diagnosed with diabetes, because this is the physiological dysfunction that defines the disease. It is further argued that diabetes progresses due pancreatic β- deficiency. This researcher advances that insulin dysfunction and high blood sugar development are interrelated. At first, deterioration of glucose homeostasis occurs, followed by a depletion of postprandial glycemic control. These physiological changes lead to morning hyperglycemia, ultimately progressing to become nocturnal hyperglycemia. When glucose does not performs its normal function a prediabetic stage, is established. However, years (FPG) levels elapse before elevated fasting plasma glucose can show up in someone’s blood sample. It appears as 2-hour postprandial plasma glucose (PPG) of 140 to 199 mg/dL. This can be determined after a 75 g oral glucose tolerance test is administered. Postprandial hyperglycemia level is an essential criterion in obtaining optimal glycemic levels (Gerich, 2013).
Diabetes mellitus
Insulin regulates glucose synthesis in the body. The process begins in the blood and moves into cells for further breakdown. These include those of the liver, adipose tissue and muscle. Consequently, insulin deficiency/insensitivity within cellular receptors significantly contributes to development of hyperglycemia and subsequently diabetes glyconeogenisis, stimulating glucose transportation and absorption into muscle tissue and cells. Ultimately, the storage of glucose as glycogen is enhanced when insulin is released into the blood through beta cells located in the islets of langerhans (Sattar, Mizuno, Ray & Ford, 2010).
In the pathophysiology of hyperglycemia the role of Insulin sufficiency cannot be over emphasized. When cells do not respond adequately to the circulating insulin hyperglycemia is the end product. Metabolic ketoacidosis (DKA) could eventually develop which creates osmotic irregularities within cells. This occurs as a result of nonabsorption of glucose and glucose storage in the liver and muscles. Ultimately, inadequate protein synthesis and other metabolic derangements will be present. Further, as glucose concentrations continue to be elevated, the kidney threshold reaches a maximum reabsorption level and gluocuria occurs. This is a consequence of hyperglycemia, resulting in an increase in osmotic pressure. Reabsorption of water by the kidneys is then reduced and polyuria may occur. Electrolytes and any other essential elements are lost, resulting in a depleted blood volume. This reduction is the replaced through osmosis, as from body fluid stored in cells and compartments. This results in the dehydration and thirst, which are common hallmarks of diabetics. In geriatric patients with chronic renal failure, these indicators, or side effects, can be significantly more severe. Hyperglycemia which is actively progressing towards Diabetic ketoacidosis (DKA) is a medical emergency, especially in geriatric patients, over the age of 60, because kidney function is depleted as the result of natural tissue reduction and cell changes that occur as part of the aging process (Sattar et. al, 2010).
Chronic Renal Failure
Studies reveal that the rates of chronic renal failure among elderly diabetic patients are increasing, though the degree to which these rates are increasing varies across the globe. One population study, Prevalence of Chronic Kidney Disease and Its Related Risk Factors in Elderly of Southern Iran was conducted by a group of researchers from within that country, considers this issue in detail. With respect to pathophysiology related to this issue, the study determined that proteinuria, hypotension, diabetes and body mass index were all essential contributing factors to chronic kidney disease among the elderly in the population of interest. Further the study defined the 0pathopysiological manifestations of the condition, including: anemia, which can be defined as low blood hemoglobin below 10 g/dL, hyperphosphatemia, hyperglycemia, high blood sugar levels, metabolic acidosis and hyperparathyroidism. Hyperglycemia, in geriatric diabetics patients with chronic renal/kidney failure, indicates an increased risk of severe dehydration, as a result of nonabsorption of fluid by the kidney and increased urination. Bodies of elderly people contain less adipose tissue due to the aging proccess and the pathophysiology of hyperglycemia allows cells to use up alternative glucose resources stored in adipose tissue and body mass is lost at a faster rate and more extensively (Malekmakan, Khajehdehi, Pakfetrat, 2013).
Diagnosis
The diagnosis of hyperglycemia is typically subsequent to the diagnosis of diabetes and to some degree related to chronic renal failure in diabetics of any age group. It encompasses a random blood glucose, which shows a high glucose level in the blood. This, followed by a fasting blood sugar test, indicates a medical issue. The normal range for people 59 and under is between 80 and 120 mg/dL (4 and 7 mmol/L), assuming no other underlying medical conditions are present. However, among geriatric patients, ages 60 years and over, the normal random blood sugar range is between 100 and 140 mg/dL (6 and 8 mmol/L), assuming no other underlying medical conditions are present. An AIC test may also be ordered, which evaluates the patient’s blood sugar level for the past three to four months. An AIC level above 7 is considered hyperglycemia. Among the elderly, with chronic conditions such as kidney disease and diabetes , AIC levels are anticipated to be higher (Gerich, 2013).
Treatment
Treatment of hyperglycemia in a geriatric diabetic patients with chronic kidney failure focuses on reducing high blood sugar levels. Scientists argue that hyperglycemia is a pathophysiology of diabetes mellitus. Therefore, in developing a treatment approach for it, a diabetes mellitus intervention is also created. However, geriatric diabetics with chronic kidney failure require far more than blood sugar control management. Peritoneal dialysis to a great extent determines the specific treatment approach. Non dialysis geriatric diabetic patients initially may receive intra venous fluid to rehydrate the elderly patient
. If the patient is not on peritoneal dialysis oral antidiabetic agents are used in controlling blood sugar levels. These include glipize 10mg daily or B.D according to the extent, which blood sugar needs to be controlled. Dialysis patient are usually administered insulin. However chronic renal failure is associated with insulin resistance. As such, the insulin of choice is given to fast long-acting insulin analogues. Sulfonylureas are contraindicated drugs in chronic kidney failure Self care education is essential l in preventing the serious effects of hyperglycemia on kidney. Absorptions difficulties could lead to water retention. Blood sugar control is emphasized and taking prescribed medications that postpone complications of diabetes (Neto & Gomes, 2013).
References:
American Diabetes Association (2013). Diagnosis and Classification of Diabetes Mellitus
Diabetes Care. 36(1) S67-S74
Gerich, J. (2013). Pathogenesis and management of postprandial hyperglycemia: role of incretin-
based therapies. International Journal of General Medicine. 6: 877–895
Neto, P., & Gomes, V(2013). Management of hyperglycemia in patients
with chronic kidney disease. JNEPHROL, 26(4): 629- 635
Malekmakan L. Khajehdehi, P., & Pakfetrat.M. ( 2013). Prevalence of Chronic Kidney Disease
and Its Related Risk Factors in Elderly of Southern Iran: A Population-Based Study. ISRN
Nephrology 2013 (2013), Article ID 427230, 6 pagesN
Sattar, N. Mizuno., Ray, K. Ford ,I . ( 2010). Statins and risk of incident diabetes: a collaborative
meta-analysis of randomized statin trials. The Lancet 375 (9716): 735–42
