Chronic Kidney Disease for Recent Literature and Publication

Question: Discuss about theChronic Kidney Disease for Recent Literature and Publication. Answer: Introduction The present paper will critically discuss CKD with reference to a case study of a patient, Glenda, who has the condition. The stages of CKD, the pathophysiology of CKD, management strategies and health promotion strategies will be analyzed. This is in a bid to demonstrate an understanding of patient-centered care and application of policy and principles of management of chronic kidney disease. The approaches of care in Glendas case will be critiqued on basis of appropriateness and any recommendations or alternatives posed with support from recent literature and publication; an evidence-based approach. Case description Glenda is a 56-year-old aboriginal woman from Tiwi islands. She presented to the local health center with complaints of facial pruritus, anorexia, nausea, and lethargy. She appeared confused. Her vitals were normal except for an elevated blood pressure of 159/97 mmHg. Her urine analysis was positive for protein. Glenda has a past medical history of similar complaints. She also presented with generalized edema, joint pain and stiffness, and lethargy in 2010. Her vitals had been erratic with a fever of 38.80 C, a pulse rate of 98 bpm, an elevated respiratory rate of 22 and a hypertension of 180/100 mmHg. Her urinalysis showed rust-colored urine that was positive for blood and protein. This was two weeks after a sore throat. She was then diagnosed with post-streptococcal glomerulonephritis and treated. Her social history involved her binge drinking fortnightly four or more drinks. She also smoked an average of 20 cigarettes per day. She had some estimated forty smoking pack years. She c laimed to exercise by frequently walking around the island. Her nursing discharge suggested monthly follow-up with measurements of blood pressure and urinalysis. During the current presentation, lab investigations were done. They showed an elevated urea of 45mmol/l, elevated serum creatinine of 1132 umol/L, decreased creatinine clearance of 8.2 ml/min, decreased serum sodium levels at 128 mEq/L, elevated serum potassium levels at 6 mEq/L, reduced bicarbonate levels at 11.5 mEq/L, an increased anion gap at 20, reduced calcium at 1.98mg/dL, elevated phosphate at 5.4 mg/dL and a reduced PH of 6.1. This interprets to a uremia, hyponatremia, hyperkalemia, hypocalcemia and a hyperphosphatemia with an anion gap metabolic acidosis. The presentation fits a picture of deranged renal function. CKD was established and she was started on hemodialysis on account of uremia and metabolic acidosis. She, however, opted for peritoneal dialysis in order to move back to her rural island and enjoy life and culture. Chronic Kidney Disease CKD according to Queensland Health (2015), is glomerular filtration rate (GFR) less than 60ml/min/1.73m2 with or without evidence of kidney damage for more than three months or evidence of kidney damage including albuminuria, hematuria not of urological origin, pathologic or anatomic kidney changes with or without deranged GFR for more than three months. It is estimated that one in eight Australians has indicators of CKD making it a very common condition (Kidney Health Australia, 2015). Of these, 10% do not know they have the condition as one can lose up to 90% of kidney function without any signs or symptoms (Kidney Health Australia, 2015). It is one of the major cardiovascular risk factors as it increases mortality due to cardiovascular causes (Levey Coresh, 2012). For this reason, early detection and management are important. Risk factors There are eight major risk factors for CKD progression and cardiovascular risk (Kidney Health Australia, 2015). Risk stratification and health promotion to prevent progression of CKD and cardiovascular events are targeted at the risk factors that are modifiable. The risk factors include diabetes mellitus, hypertension, established cardiovascular disease, family history of kidney failure, obesity with BMI of more than 30kg/m2, smoking, 60 years or older and Aboriginal or Torres Strait Islander origin (Kidney Health Australia, 2015; Levey, Astor, Stevens, Coresh, 2010; Razmaria, 2016; Murphree Thelen, 2010). Glenda has three of the eight risks in that she has hypertension, is a smoker with forty pack years and is an aboriginal from Tiwi islands. According to the Australian absolute cardiovascular risk assessment tool, Glenda has a high risk of developing cardiovascular disease in the next five years. Pathogenesis The pathogenesis of CKD starts with a renal insult. In Glendas case, this was post-streptococcal glomerulonephritis. The mechanisms of injury in her case was as a result of a sore throat she had in 2010. The body produces antibodies against streptococcal proteins as it tries to clear the sore throat. These antibodies, however, cross-react with basement membrane proteins in the kidney causing glomerular damage (Colledge, Walker, Ralston, 2013). At first, the glomerular membrane becomes leaky, losing the capacity for selective permeability hence large molecules like albumin pass through giving the patient proteinuria. The damage to glomerular components can affect vascular components giving rise to hematuria. Further damage starts leading to nephron loss reducing the excretory capacity of the kidney hence the progressive reduction in GFR. The kidney, however, has a large capacity for compensation and the remaining nephrons hypertrophy and hyper filtrate as they try to maintain the GFR within the normal range (Barrett, Barman, Boitano, 2017; Marieb Hoehn, 2013). This has been postulated to have an impact on the progression of kidney damage as the kidneys are overworking. One can lose up to 90% kidney function before symptoms appear (Kidney Health Australia, 2015). When the symptoms set it, they are related to renal function and represent the complications of CKD (Johnson Bonner, 2012). Inability to excrete waste is the main one leading to uremia. Glenda has uremia as manifested by facial pruritus (Colledge, Walker, Ralston, 2013). The kidney has important roles in maintaining metabolic homeostasis. When deranged, the kidney cannot buffer leading to metabolic acidosis. Glendas metabolic acidosis is anion gap positive metabolic acidosis due to increase in anions like phosphates. There are mineral derangements with calcium loss as calcium is replaced with phosphate leading to hyperphosphatemia (Murphree Thelen, 2010). Anemia is a complication as the kidney is an important synthesizing organ for erythropoietin. This is apparent in Glendas case as her hematocrit is on the lower side, an indication of anemia. Sodium and water handling is affected in CKD with sodium retention and fluid overload (Murphree Thelen, 2010). This is a major cause of ed ema in CKD. There is the development of renal bone disease due to derangements in bone turnover and secondary hyperparathyroidism (Murphree Thelen, 2010). Hypertension is both a cause and complication of CKD (Kidney Health Australia, 2015). Early detection and screening Due to the chronicity of CKD, eventual decline into end-stage renal failure and high cardiovascular risk, early detection and management of CKD is paramount (Razmaria, 2016). Screening for CKD is done to those who have any of the eight risk factors for developing CKD. Screening involves regular measurement of GFR and albuminuria with appropriate urinalysis, blood pressure monitoring, and blood sugar monitoring. If there are factors showing an increased risk, monitoring should be done every 1 to 2 years (Queensland Health, 2015). Staging and discussion CKD progresses through five stages as kidney function deteriorates to kidney failure. These stages form a continuum. The new staging recommendations take into consideration the GFR and the urine albumin-creatinine ratio (Kidney Health Australia, 2015). The management of CKD is heavily influenced by these stages hence a clear staging system should be used (Bauer, Melamed, Hostetter, 2008). Calculation of GFR is one of the variables that can affect this. Two methods exist; Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula and Modification of Diet in Renal Disease (MDRD) formula. The CKD-EPI formula is recommended (OCallaghan, Shine Lasserson, 2011). From these calculations, Glendas estimated GFR and need for dialysis put her at stage 5 of CKD. Stage one of CKD is when GFR is less than or equal to 90ml/min/1.73m2 in at least two urinalysis tests for more than three months (Kidney Health Australia, 2015). Stage 2 is when GFR is between 60 to 89 ml/min/1.73m2 in at least two urinalysis tests for more than three months. However, for these two stages, the GFR can be normal and CKD is only diagnosed if there is a sign of renal damage for example albuminuria, hematuria not of urological origin, pathologic or anatomic kidney changes (Kidney Health Australia, 2015). This is because the estimation of GFR can give low numbers for otherwise healthy individuals. Urine albumin-creatinine ratio (ACR) should be done to stratify the patient in categories of low, moderate or high risk of progressive renal impairment (Kidney Health Australia, 2015; Glassock, 2010) Management goals at these stages are aimed at slowing progression of kidney damage and cardiovascular risk management (Castner, 2010). This stage can be treated in the primary care setting but the bigger issue is assessing cardiovascular risk. CKD is a large risk for mortality from cardiovascular causes and a patient is more likely to die from cardiovascular causes than kidney failure (Johnson Bonner, 2012). Pointers of progressive kidney disease may include hematuria, rapidly worsening renal function, albuminuria, family history of renal failure and hypertension (Castner, 2010). Long-term monitoring of renal function, blood pressure, and proteinuria is indicated. Avoidance of nephrotoxic drugs is also an important nursing consideration. Lowering of cardiovascular risk starts with reducing the blood pressure. Angiotensin-converting enzyme (ACE) inhibitors and Angiotensin receptor blockers (ARBS) are the first line therapy for BP reduction in CKD and renal protection (Queensland Health, 2015). They decrease the risk of end-stage kidney disease by up to 40 %. Lifestyle modifications should be implemented including smoking cessation, appropriate nutrition change for example low sodium and low-calorie diet, weight reduction, reducing alcohol intake and increasing physical activity (Kidney Health Australia, 2015). Glycemic control is another measure. Lipid-lowering drugs can be used to further lessen the risk. Glenda should have been advised on these modifications early. She has three of the eight risk factors making these modifications crucial to her care. Stage three is divided into two subgroups; 3a and 3b. Stage 3a is when GFR is between 45 to 59 ml/min/1.73m2 in and 3b between 30 to 44 ml/ min/1.73m2, in at least two urinalysis tests for more than three months (Kidney Health Australia, 2015). This separation accurately stratifies risk assessment as 3a CKD present a low to moderate risk while 3b represents an already moderate to high risk of progression and cardiovascular events (Wyatt, 2016). Management of CKD at this stage involves monitoring and slowing kidney damage, cardiovascular risk, avoidance of nephrotoxic drugs and fluid overload, adjusting medication to fit kidney function, identification of complications of CKD and prompt referral to a nephrologist (Kidney Health Australia, 2015). As renal function worsens so do the complications. Treatment of these complications reduces the risk of progression and slows kidney damage. It is still paramount to continue cardiovascular risk reduction as for earlier stages (Welch, Johnson, Zimmerman, Russell, Perkins, Decker, 2015). These are the final stages of CKD as one slips into the end-stage renal disease. Stage 4 of CKD is when GFR is 15-29 ml/min/1.73m2 in at least two urinalysis tests for more than three months. Stage 5 is when GFR is less than 15 ml/min/1.73m2 in at least two urinalysis tests for more than three months or a requirement for dialysis (Kidney Health Australia, 2015). Glenda is at stage 5 of CKD owing to her need for dialysis. The absolute indication for her dialysis was uremia and metabolic acidosis with hyperkalemia (Rivara, Chen, Nair, Cobb, Himmelfarb, Mehrotra, 2017). Glenda should continue her peritoneal dialysis as outcomes are observed. If the condition worsens hemodialysis should be restarted as options of renal transplantation are sought. Management at this stage should be monitored by a renal specialist. The goals of care include monitoring for complications and cardiovascular events, preparation for informed decision making on the approach regarding end-stage renal failure (Ki dney Health Australia, 2015). They eventually would need dialysis or renal transplant. Conclusion In conclusion, CKD is a chronic illness that progresses through five stages each with a number of management strategies and goals. Early detection through screening is important in managing and slowing the progress of the disease. 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