Chronic Kidney Disease - Coursework Example

Name University Course Tutor Date Chronic Kidney Disease Introduction Chronic Kidney Disease is a glomerulonephritis syndrome that is increasingly causing morbidity and mortality worldwide (Chen et al. 2010; Hippisley-Cox & Coupland 2010). Understanding its epidemiology, pathogenesis and pathophysiology is important to assist in identifying interventions for risk reduction and management of the condition. Moreover, it is important to understand risk factors and other health conditions that are associated with the disease in order to draw an overall health care plan. This paper presents the research on the epidemiology, pathogenesis, and pathophysiology of chronic kidney disease. Chronic Kidney Disease (CKD), also referred to as albuminuria, is the progressive and ultimate loss of kidney function over a period of time-months to years (Levey et al. 2010). The kidney is the major excretory organ in the human body with the role of eliminating metabolic wastes and excess water from the blood. Loss of kidney function occurs when there is an accumulation of metabolic waste, water and other toxic substances in the body. The severity of the CKD occurs in five stages depending on the level of accumulation. In discussing the epidemiology, this research will focus with the incident, distribution, related factors and possible control of chronic kidney disease. Next, the pathogenesis will enable to understand the developmental process of the disease and the series of structural or functional alteration in the chronic kidney condition. The pathogenesis brings out the relationship between causative factors and clinical signs of the disease. Finally, the pathophysiology gives a detailed account of the alterations of the physiological processes enabled by the kidney as a result of disease. Epidemiology Chronic Kidney Disease (CKD) has the highest prevalence in the developed nations of the world and rising prevalence in the developing countries (Atkins 2005). CKD is a significant cause of morbidity and mortality in the world (Hippisley-Cox & Coupland 2010). Chronic kidney disease is classified as a glomerular disorder and mainly occurs when the glomerular filtration rate (GFR) is below 30 to 50 percent of the normal. Nevertheless, there are many other causes of CKD and these ranges from immunologic, metabolic, hereditary, and vascular from conditions such as hypertension and ischemia which may also depend on the location (Levey et al. 2010; Tomino 2010). Diabetes Mellitus and CKD Ohta, et al. (2010) studied the prevalence of CKD in Japanese patients with diabetes. The aim of the study was to compare the prevalence of CKD between patients with type I and type II diabetes. The decreased estimated glomerular filtration rate (eGFR) was compared between the two diabetic groups. Findings revealed that the prevalence of decreased eGFR was higher in type 2 diabetic patients as compared to type 1 on the percentage ratio of 25.2 versus 7.9. The research concluded that type II diabetic patients are twice as likely as type I diabetic patients to get CDK and also because of an age-dependent decreased eGFR. Diabetes mellitus usually manifest three major syndromes: first, non-nephritic or asymptomatic proteinuria in 50% type I and II diabetes mellitus; second, nephritic syndrome which occurs in approximately 20 years later; and third, chronic damage and loss of nephrons. The chronic damage and loss of nephrons is most responsible for CKD which can result to end stage kidney disease in 4 to 5 years (Ohta et al., 2010). Prevalence of CKD and risk factors in America According to the Centers for Disease Control and Prevention (CDC) (2007), an estimate of 16.8 percent of U.S adults at age 20 and older was affected with CKD between 1999 and 2004. Currently, between 1.9 and 2.3 million people of the Canadian population are affected with CKD. The CDC (2007) reports that cardiovascular disease; diabetes, obesity, and hypertension are the risk factors for CKD in the America. The prevalence rate has increased by 15.9 percent when compared to the 1988-1994 data of the same (CDC 2007). The data further shows that persons with cardiovascular disease (28.2%) or diabetes (40.2%) had a greater CKD prevalence as compared to those without the conditions (15.4% and 15.4% respectively). 24.6% of people with hypertension also had CKD as opposed to 12.5% who did not have the condition. CKD prevalence is also calculated on the basis of demographic characteristics such as sex, race, age group, ethnicity, and level of education. Findings reveal that 16.8 % of adults above age 20 had CKD. 5.7% had stage 1 CKD, 5.4% at stage 2, 5.4% at stage 3, and 0.4% at stages 4 and 5. With placement in age groups, all stages of CKD were most prevalent in persons over 60 years of age at 39.4%. 40-59 years were 12.6%, while 20-39 years were 8.5%. By education level, the CKD stages were more prevalent among persons with low education level-less than high school education at 22.1% as compared to those with high school education at 15.7%. The data further shows that CKD prevalence is higher among non-Hispanic blacks, at 19.9%, while at 18.7% Mexican Americans, while at 16.1% among the non-Hispanic whites. Most Mexican Americans (10.2%) had stage 1 CKD, as compared to 9.4% non-Hispanic blacks and only 4.2% non-Hispanic whites on the same disease stage. Prevalence of CKD and risk factors in Australia In Australia, CKD is caused by many risk factors. Males at 50 years and above are at the highest risk (Atkins 2005). Moreover, Diabetes mellitus is a leading cause for CKD stage 2 in the country, and also conditions like hypertension, overweight, smoking, and obesity. Other risk factors include the family history of renal diseases and the ethnicity. Ethnic groups of the Aborigine or the Torres Strait Islander are shown to be at higher risk for CKD. At least 18% of Australian adults have at least one of the CKD indicators. Atkins (2005) investigates the AUSDIAB data from 1999 to 2000, which evaluates the prevalence of diabetes, metabolic risk factors and other renal disease indicators in the broader Australian community, in which CKD is now a burden. The findings show that an estimate of 7.2% adults at 25 years and above has diabetes, 16.1% has impaired glucose metabolism, 60% are overweight or obese, 61% has high cholesterol levels, and 29% has high blood pressure. Prevalence of CKD in Europe The U.K estimates show that at least 8.8 percent of Great Britain and Northern Ireland populations have symptomatic CKD. Hippisley-Cox & Coupland (2010) investigate a method to predict the risk of CKD in men and women in England and the Wales. The observations made were that CKD at the moderate to severe stage was influenced by age, deprivation, ethnicity, smoking, systolic blood pressure, diabetes, cardiovascular disease, use of NSAIDs, peripheral vascular disease, and the family history of renal disease. Pathogenesis of Chronic Kidney Diseases Pathogenesis describes the relationship between causative factors and clinical signs of the CKD (CDC 2007). Clinical symptoms mostly appear in the 4 and 5 stages when there are evident disturbances in electrolyte or water balance, or metabolic derangements. Chronic kidney disease (CKD) is a syndrome of glomerulonephritis. Glomerulonephritis (GM) is classified into five major syndromes depending on the manifestation and disease progression. These are asymptomatic proteinuria and or haematuria, acute nephritis syndrome, rapidly progressive glomerulonephritis, nephritic syndrome, and chronic glomerulonephritis or chronic kidney disease. Chronic glomerulonephritis or CKD is a progressive disease to which the cause is mostly unknown but linked to causes such as systemic disease mostly diabetes mellitus and systemic lupus erythematosus (SLE). Glomerular disorders and tissue changes In glomerulonephritis, increased cells manifest the form of proliferation of connective tissue or infiltration of the inflammatory white cells (Vasavada & Agarwal, 2003). The basement membrane thickens and hardens-usually sclerosis in diabetes mellitus cases, and deposition of protein in immune complexes. The glomerular membrane is damaged and manifests altered membrane permeability as well as loss of glomerular tufts. CKD is slow but irreversible resulting to end-stage renal disease (ESRD) (Spasovski et al. 2009). ESRD requires maintenance or dialysis for survival. Causes of progress of CKD include chronic glomerulonephritis (GMN). The toxicity levels become high and there is traumatic loss of the nephrons (Vasavada & Agarwal, 2003). In CKD the nephrons can enlarge in size and increase in function in order to compensate for the lost function. One kidney alone can take over all kidney function, and hence 50% of loss of nephrons results to 50% reduction in the GFR. Nevertheless, the impaired function may not be noticed until there is 75-80 percentage loss of nephrons. The alteration to nephrons and increased flow mostly leads to further loss and damage. Progressive decrease of GFR leads to stage-5 of CKD as evidenced by renal insufficiency or chronic renal failure. The stage is also referred to as End Stage Kidney Disease (ESKD). Stage 5 is the end or established chronic kidney failure stage and the major stage of fatality (Spasovski et al. 2009). Primary disorders such as post streptococcal glomerulonephritis and IgA nephropathy are common causes to CKD. Most of the immune-mediated disorders such as circulating antigen-antibody complexes that are deposited; antibodies to antigens deposited in the glomerular, tubular antigens, autoantibody to Glomerulonephritis, and cell-mediated responses are among the causative factors. Hereditary diseases such as Alport’s syndrome in which there is defect of type IV collagen, are associated with CKD. Diabetes mellitus and chronic damage and loss of nephrons Patients with diabetes mellitus experience insulin deficiency and altered metabolism. Other manifestations include the thickening of the glomerular basement membrane and connective tissue matrix and hardening. Hemodynamic effects occur in the form of glomerular hypertrophy and increased GFR. This eventually results to diabetic nephropathy or diabetic glomerulosclerosis. The condition progress to CKD through gradual loss of the nephrons until the remaining volume cannot carry out the normal renal function. General CKD pathogenesis The CKD evolution features interstitial fibrosis as well as tubular atrophy (Vasavada & Agarwal 2003). The changes are enhanced by interactions between the infiltrating cells and the resident tissue components. Studies that involve animal models and human observations reveal that the infiltrating macrophages play a central role in both the initiation and progression of renal scarring (Eardley et al. 2008). Irrespective of the underlying cause, the process of renal scarring represents a common pathway for injury development and progression to the established stage of kidney failure (Eardley et al. 2008). Eardley et al. (2008) conducted a study to investigate the relationship between the interstitial capillary density and interstitial macrophages of which were measured in situ. The findings revealed that there was a significant correlation among 54 of the patients with less than 20% chronic damage regarding their urinary albumin to creatinine ratio. Conversely, 56 patients with over 20% chronic damage showed no correlation between urinary levels and macrophages although there were significant inverse correlations between capillary density and macrophages and chronic damage. The study concluded that proteinuria and urinary levels are significant for macrophage recruitment in the early disease. In the process of renal scarring, alternate pathways that relate to progressive tissue ischemia which is secondary to obliteration of the interstitial capillary layer predominate. Clinical observations reveal that despite the beneficial role of hyperfiltration and hypertrophy of the residual nephrons in CKD, the features hypothesize a major cause for progressive kidney dysfunction (Vasavada & Agarwal 2003). Kidney dysfunction is believed to occur as a result of increased pressure in the glomerular capillary which leads to damage on the capillaries causing sclerosis on the focal and segmental surfaces of the glomerular (Eardley et al. 2008). Pathophysiology of Chronic Kidney Disease Pathophysiology describes the alterations of the physiological processes enabled by the kidney as a result of disease (Spasovski et al. 2009). The kidney carries an excretory physiological function of filtering wastes from the blood. Normally, an estimate of one million nephrons is present in each of the kidneys and this contributes to the total glomerular filtration rate (GFR) (Spasovski et al. 2009). When renal injury occurs and regardless of the etiology, the kidney still has an innate ability to sustain the GFR even though a progressive destruction of nephrons is taking place. The kidney does this through mechanisms such as hyperfiltration and compensatory hypertrophy using the available healthy nephrons (Eardley et al. 2008). Therefore the nephrons adaptability allows for sustained normal clearance of the plasma solutes. However, when substances such as creatinine and urea increase to significant levels in the plasma, it shows that the GFR has decreased to beyond 50% and the renal reserve is exhausted (Spasovski et al. 2009). Consequently, the plasma creatinine value doubles and this is why the value is used to detect a 50% loss of the nephrons mass function. The progressive decrease of GFR is classified under 5 stages that are agreed upon internationally, and as adapted from the International Kidney Foundation (Gansevoort & Jong 2009). The description of the stage is based on the measurement GFR ml/min/1.73m2. Stage 1 Stage 1 of chronic kidney disease occurs when the GFR is measured at least 90 mL/min/1.73m2 or increased GFR by 75% (Gansevoort & Jong 2009). At this stage, there is evidence of kidney damage without decreased GFR and is usually asymptomatic. Nevertheless, hypertension is common at this stage. Stage 2 Stage 2 is mild kidney damage and occurs at a GFR of between 60-89 mL/min/1.73m2 (Gansevoort & Jong 2009). The stage is asymptomatic and although the plasma, urine creatinine, and urea levels are rising, it’s at subtle or nearly normal ranges. Hypertension is also common at this stage and evidence of damage can be determined from the urine. Other tale tells signs include increasing parathyroid hormone as well as early bone disease. The kidney plays a role in controlling hormones that help to maintain normal pressure levels of the blood. Therefore, failure of kidney function is a risk to high blood pressure. The kidney function loss may also become progressive. Usually, the diagnosis of stages 1 and 2 of CKD requires the presence of kidney damage for at least three months. Pathological abnormalities of the kidney such as scarring can be detected with imaging tests (Gansevoort & Jong, 2009). Additionally, urine composition abnormalities can be detected. These can be in the form of haematuria or proteinuria which refers to presence of proteins in urine. Stage 3 The patient is said to be at stage 3 of CKD when the GFR has dropped to 30-59 mL/min/1.73m2, and is also described as moderate kidney damage (Gansevoort & Jong 2009). This stage may be asymptomatic even with the 30% GFR although mild symptoms are common. Hypertension and kidney damage signs, and sometimes signs showing possibility of other organ dysfunction are manifested. The patient experiences mild azotaemia, referring to increased levels of creatinine and urine. The stage is also characterized by loss of erythropoietin leading to anemia. Poor functioning of the kidneys is a risk to iron-deficiency anemia, which is responsible for the feelings of weakness and fatigue (Vasavada & Agarwal, 2003).Metabolic acidosis also begins and the concentrating ability of nephrons results to polyuria, and nocturia. Eventually, this leads to sodium loss and dehydration. Stage 4 At stage 4 of CKD, the GFR is at 15-29 mL/min/1.73m2, and the stage features severely reduced GFR. The GFR is between 10-25 percent (Gansevoort & Jong 2009). Hypertension and sodium and water retention are highly manifested. Metabolic acidosis is also experienced including a negative nitrogen balance and loss of serum proteins and muscle mass. Triglycerides levels increase often as dyslipidemia, hyperinsulinemia, and insulin resistance. Increased insulin levels and lowered thyroid hormone levels are experienced. Bone is affected through hyparkalemia, hyperphosphatemia, and hypocalcemia (high phosphate and low calcium levels) when the GFR decreases to 25%. There is low vitamin D synthesis, low calcium absorption from the gut, and high calcium reabsorption from the bone. Lytic bone disease is common at this stage, and also anaemia as a result of decreased erythropoiten. Another manifestation of stage 4 of CKD is oliguria and fluid overload. The load delivered to the remaining nephrons is too high making it difficult for nephrons to reabsorb, concentrate, or excrete. According to Vasavada & Agarwal (2003), a positive sodium balance is a major attributive factor to hypertension physiology in cases of CKD. CKD progression makes it complicated for the kidneys to maintain their normal functions (Vasavada & Agarwal, 2003). Functional changes occur when it becomes difficult for the kidneys to filter metabolic wastes from the blood and sustain normal electrolyte levels and remove excess body fluids. The possibility of alteration of blood coagulation is high. CKD patients are prone frequent infections and even risk of malignancy. Stage 5/End-Stage Kidney Disease A patient is at stage 5 of CKD when the GFR is measured at less than 10% usually less than 15 mL/min/1.73m2 (Gansevoort & Jong 2009). The stage is characterized by major disturbances of fluid and electrolytes resulting to experiences such as metabolic acidosis, and increased plasma phosphate levels which are life-threatening. As the function of the kidney declines, waste products build up in the blood. Accumulation of the waste products generates symptoms such as nausea, pruritis, anorexia, vomiting, diarrhea, fatigue and weakness (Eddi et al. 2010). Major disorders of most body systems are experienced as well as neurologic syndromes such as sleeplessness, hiccups, and restless legs. At stage 2 of end stage kidney disease, clotting factors alter risking the patient to blood coagulation, and platelets impair causing a risk of bleeding. The stage is also characterized by chronic inflammation and immune depression (Eddi et al. 2010). Cardiovascular disorders are also most likely to occur because of hypertension and dyslipidaemia. Heart failure is likely to occur because of calcium deposition and atherosclerosis. Consequently, heart failure leads to pulmonary edema and the patient also experiences gut problems like gastroenteritis and bleeding ulcers. At stage 3, the level of sex and thyroid hormones reduce. The patient’s skin yellows and becomes frosted with uremic residue (Eddi et al. 2010). The patient is also susceptible to itching and other infection. At this stage, there is need to control the food and water intake and salts such as phosphates of potassium and sodium as well as supplement vitamin D, and erythropoietin should be managed (Vasavada & Agarwal 2003). The patient is treated with dialysis or renal transplant. However, after the first week of untreated ESKD, the patient experiences acidotic coma with deep and rapid respiration. In the last day, the arterial pressure falls rapidly and death ensues at pH 6.8 (Eddi et al. 2010). Conclusion The research has investigated the epidemiology, pathogenesis, and pathophysiology of chronic kidney disease. Chronic kidney disease is currently a non-communicable disease with increasing prevalence in the world. The importance of researching on the condition is that it is a major cause of morbidity and mortality in developed and now developing nations. Approximately 16.8 percent of Americans, 8.8 percent of U.K, and 18 percent of Australians suffer from CKD. Systemic, hereditary, immunologic, and vascular conditions among others are underlying causes to CKD. CKD describes the failure of the kidney to appropriately conduct its role of water-electrolyte balance and filtration of metabolic wastes from the blood. CKD occurs in five stages of which stage 1 to 3 is asymptomatic, while 4 and 5 shows that the kidney’s function is or has diminished. The kidney’s function fails in a progressive manner as a result of scarring of renal tissues because of a compensatory hyperfiltration process in disease onset. Proper medical care, diet, and lifestyle, can help to reduce the progression of CKD to stage 5 which renders the patient to continuous dialysis and major cause of fatality in CKD patients. References: Atkins, R. 2005. ‘Global perspectives of renal failure: The epidemiology of chronic kidney disease,’ Kidney International, vol. 67, pp. 14-18 Centers for Disease Control and Prevention/CDC. 2007. Prevalence of Chronic Kidney Disease and associated factors: United States, 1999-2004. CDC, vol. 56(8), pp. 161-165. Retrieved online at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5608a2.htm on September 7, 2011. Chen, N., HSU, C., Yamagata, K., & Langham, R. 2010. Challenging chronic kidney disease: Experience from chronic kidney disease prevention programs in Shanghai, Japan, Taiwan and Australia,’ Nephrology, vol.15, pp. 31-36 Eardley, K., Kubal, C., Zehnder, D., Quinkler, M., Lepenies, J., Savage, C., Howie, A., Kaur, K., Cooper, M., Adu, D., & Cockwell, P. 2008. ‘The role of capillary density, macrophage infiltration and interstitial scarring in the pathogenesis of human chronic kidney disease,’ Kidney International, 74, 495-504. Eddi, R., Malik, M., Shakov, R., Baddoura, W., Chandran, C., & Debari, V. 2010. ‘Chronic kidney disease as a risk factor for Clostridium difficile infection,’ Nephrology, vol.15, pp. 471-475 Gansevoort, R., & Jong, P. 2009. ‘The case of using albuminuria in staging chronic kidney disease,’ Journal of American Society of Nephrology, vol. 20, pp. 465-468, Retrieved September 21, 2011 from http://jasn.asnjournals.org/content/20/3/465.full.pdf Hippisley-Cox, J., & Coupland, C. 2010. ‘Predicting the risk of chronic kidney disease in men and women in England and Wales: Prospective derivation and external validation of QKidney Scores,’ BMC Family Practice, vol. 11(49), 1-13 Levey, A., Astor, B., Stevens, L., & Coresh, J. 2010. ‘Chronic kidney disease, diabetes, and hypertension: What’s in a name?’ Kidney International, vol. 78, pp. 19-22 Ohta, M., Babazono, T., Uchigatat, Y., & Iwamotot, Y. 2010. ‘Comparison of the prevalence of chronic kidney disease in Japanese patients with type 1 and type 2 diabetes,’ Diabetic Medicine, vol. 27, pp. 1017-1023 Spasovski, G., Massy, Z., & Vanholder, R. 2009. ‘Phosphate metabolism in chronic kidney disease: From pathophysiology to clinical management,’ Seminars in Dialysis, vol.22 (4), pp. 357-362 Tomino, Y. 2010. ‘Immunoglobulin A nephropathy and chronic kidney disease,’ Nephrology, vol. 15, pp. 23-26 Vasavada, N., & Agarwal, R. 2003. ‘Role of excess volume in the pathophysiology of hypertension in chronic kidney disease,’ Kidney International, vol. 64, 1772-1779 Read More