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Foundations of Renal Nursing

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Added on  2020-01-28

Foundations of Renal Nursing

   Added on 2020-01-28

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Foundations of Renal Nursing 1Foundations of Renal NursingStudent’s Name:Instructor’s Name:Date:
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Foundations of Renal Nursing 2Table of contents Assignment 1 1.1Chronic kidney disease and acute kidney injury...............................(3)1.11 End stage renal disease (ESRD) - CKD and associated vascular calcification (CVD)...........................................................................(3)-Etiology.................................................... ....... (5)-Pathogenesis...................................................... (5)2.1 Acute kidney Injury....................................................... (7)-Etiology and Epidemiology.................................... (8)-Pathophysiology...................................................(9)-Neurohormonal pathogenesis.................................. (10)-Diagnosis......................................................... (11)-Triggers of AKI (Sepsis-induced AKI)....................... (11) -Early diagnosis and management of sepsis-induced AKI....(11)Assignment 22.1 Poster Presentation2.11 Renal biopsy: purpose, procedure, indications, and contraindicationsAssignment 33.1 Case Study..................................................................... (12)References ........................................................................................ (20)
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Foundations of Renal Nursing 3Chronic kidney disease and acute kidney injuryAssignment 1:Part A:Chronic kidney disease (CKD) is one of the major health concerns in the world [1]. In the UnitedStates, the occurrence of CKD is most prevalent and thus the associated illnesses and number ofcases of CKD are much high [1]. Also, the number of recorded cases of renal failure induced byCKD is one of the most commonly encountered [1]. In most cases, a predominant number of thepatients affected are of the geriatric category [1]. These patients are terminally affected by CKDand are diagnosed mostly in the end stages of renal disease or failure [1]. In such cases, themanagement of the disease is mostly either dialysis or transplantation of the kidney [1]. In mostcases of CKD, there is an association of declined levels of glomerular filtration rate or GFR [1].In the following section, we discuss one of the major illnesses associated with CKD [1]. We shallalso look at one of the primary causes of acute kidney injury (AKI) and enumerate the commonsymptoms of AKI in clinical presentation settings [1].1.11 End stage renal disease (ESRD) - CKD and associated vascular calcification (CVD):CKD is a condition that involves pathological anomalies in the structure or the functioning of thekidney when present for longer than three months and attribute noticeable health implications[2]. There can be several instances of abnormality in the structure and function of the kidney butwithout any health implications [2]. Therefore, CKD is a diagnosis that involves implications onhealth [2]. In most CKDs, there is a decline in the metabolic functions and even in endocrine orexcretory systems [3]. There can be incidences of acute kidney injury in most types of CKD [3].With the onset of AKI in CKD patients, the process of kidney failure is accelerated [3]. With
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Foundations of Renal Nursing 4most types of CKD, there is an associated risk of cardiovascular disease incidence [3].Irrespective of race, gender, or etiology of patients, there are three main types of associateddiseases with CKD [3]. The first is an incidence of drug toxicity [3]. The risk of interactions ofdrug is commonplace in CKD and the pharmokinetic data of drug excreted in the kidney requireadjustment of dosages for patients with drug intolerance and drug toxicity [3]. The second is theincidence of endocrine and metabolic disorders and abnormalities [3]. With the decline in thelevel of GFR, there is development of several conditions such as anemia, bone and mineraldisorders, acidosis etc which are all induced by complications in the endocrine system [3]. Thethird is the most common which is the risk of cardiovascular disease in CKD [3]. The reductionin the GFR is found to be an important precursor for the development of CVD and mortalityassociated with it [3]. Kidney failure and acute kidney injury are also resultants of the incidenceof reduction in GFR [2, 3]. Although research has not established definitively that the CKD is amarker or a causative factor of CVD, the incidence of CVD morbidity and mortality has a clearassociation with CKD [4]. The most common CKD is the end stage renal disease (ESRD) and it is associated with CVD andcoronary artery calcification [4].The incidence of CVD involves the Framingham risk factorsthat are listed as its causative factors [4]. Of these, the first and the most prevalent causativefactor is diabetes, which is a co-morbid condition of ESRD [4]. The second factor ishypertension and it is a frequently co-morbid incidence in ESRD [4]. The common reasons in thepathophysiology of CKD with CVD include arterial calcification and extensive medialcalcification [4]. These are additionally responsible for cardiovascular mortality in CKD [4]. Etiology: Framingham risk factors are commonly attributed with the incidence of CKDand cardiovascular mortality [4]. However, scientists have found that the Framingham
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Foundations of Renal Nursing 5risk factors do not suffice for the complete understanding of CVD and co-morbidity withCKD [4]. In patients with ESRD, irrespective of their age, calcification in the coronaryartery is much common [4]. The incidence of coronary artery calcification has rapidprogression in almost all cases [4]. With the presence of ESRD, the calcification is higher[4]. Medial thickness of calcification is much greater in ESRD patients as compared tonon-ESRD patients [4]. Research has demonstrated that one of the probable reasons forincrease in cardiovascular mortality in ESRD patients is the incidence of large vesseldisease [4]. Additionally, scientists have found that there is an elevation in the levels ofmyocardial oxygen demand, afterload in the vascular system, subendocardial ischemia,pulse pressure, pulse wave velocity etc [4]. The increase in these factors is included in theelastic arteries of the carotid and aorta along with the femoral arteries [4]. Studies haveillustrated that there is an increase in excessive atherosclerosis in patients with ESRD [4].In patients with ESRD, the likelihood of atherosclerotic lesions being more heavilycalcified is higher [4]. Calciphylaxis is a common occurrence exclusively in patients withESRD [4]. Calcific uremic arteriolopathy is a disorder in which there are medialcalcification sites leading to skin necrosis ultimately [4].Pathogenesis: Scientists have not completely understood the pathogenesis of vascularcalcification in CKD [4]. The occurrence of this disease is almost similar to the generalpopulation in patients with CKD as well [4]. It has several causative factors to which thegeneration of vascular calcification may be attributed [4]. Studies have found that thereare both traditional and uremic-specific risk factors for vascular calcification in patientswith CKD [4]. The role of these causative risk factors is yet to be determined in research[4]. Primarily, the non-traditional factors include hyperphosphatemia, hypercalcimia,
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Foundations of Renal Nursing 6elevated homocysteine levels, oxidized LDLs, elevated C-reactive proteins etc [4]. Theduration for which dialysis is carried out along with the data of disorders of mineralmetabolism provide enough insight on the occurrence of vascular calcification of CKD[4]. In most patients with CKD, there is a direct correlation between disorders of themineral metabolism and vascular calcification [4]. The disorders of mineral metabolismwould include abnormal levels of calcium and phosphorous in serum [4]. It most cases ofCKD, patients with a progression in the disease tend to develop pathological elevation inparathyroid hormone (PTH) [4]. At the initial stages of disease onset, the patientstypically have hypocalcemia [4]. However, these patients will develop hypercalcimiawhen administered with vitamin D or calcium [4]. Studies have demonstrated that in rats,when CKD is induced in vitro or naturally occurring in vivo, they tend to develop medialcalcification [4]. However, they do not develop atherogenic or intimal calcification [4].The management for such calcification generally includes the administration ofphosphate binders [4]. However, studies have found that in rat models, there is areduction in the calcification of the aortic vasculature when administered with non-calcium containing phosphate binders [4]. In the rat models that were administered withcalcium containing phosphate binders there was the occurrence of hypercalcimia [4].Research has found that in these models, there is an occurrence of altered mineralhomeostasis or hyperparathyroid bine disease of the secondary type [4]. These findings inliterature indicate that there is an important role for the excess intake of calcium in thepathogenesis of vascular calcification in patients with CKD [4]. Altered mineralmetabolism also results from the intake of calcium when the rats are treated with less-calcimic drugs [4]. In the pathology of medial vascular calcification, these factors play a
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