11. What is the pathophysiological basis of renal changes in long-standing hypertension?(350-400 words)Long-term hypertension leads to irreversible changes to the vasculature of the kidneys.Prolonged, increased pressure on the walls of vessels causes increased load, which, inturn, leads to an increase in wall tension. This raises the wall tensile stress (Yang et al.,2014, p. 10). To normalise the wall tensile stress, changes to the vessel wall occurs. Thesechanges can be seen as thickening and hardening of the wall itself, known asarteriosclerosis, as well as a narrowing of the vessel lumen due to vasoconstriction(Minesh, 2020). Increased systemic pressure is also transmitted through to theglomerulus by the afferent arteriole, which controls intraglomerular pressure. Theafferent and efferent arterioles are sheathed in smooth muscle cells. As the afferentarteriole meets the glomerulus, these cells act as a band, tightening or relaxing inresponse to systemic pressure exerted on the afferent arteriole wall (Yang et al., 2014, p.10). Therefore, increased systemic pressure results in constriction of the band leading todecreased blood flow through the glomerulus. In patients with chronic kidney disease,this auto regulatory response may become impaired. Impairment of this function allowsthe translation of increased systemic pressure into the glomeruli and causes damage tothe renal microvasculature (Griffin, 2017, p. 692). The result is decreased filtrateformation. The nephrons take this decrease in blood flow to be a sign of dehydration andstimulate the Renin- Angiotensin – Aldosterone systems to decrease excretion of sodiumand, through osmosis, retain water or extracellular volume (Ku et al., 2019). If blood flowthrough the nephrons is inhibited enough and for a prolonged amount of time, damageto the nephrons occurs and becomes permanent (Minesh, 2020). These nephrons are nolonger able to process blood and fulfil their function. In early stages of kidney disease,healthy nephrons will compensate for the damaged nephrons. This is often anasymptomatic stage and patients in early stages of renal failure are most often diagnosedthrough unresponsive hypertension and proteins in the urine (Judd & Calhoun, 2015). Asmore nephrons become damaged, the kidneys are unable to continue to compensate and2completely filter the blood. This is marked by a decreased in glomerular filtration rate,and an increase in urinary sediment, particularly albumin. This is end stage renal diseaseor ESRD (Rodríguez-Ortiz et al., 2018, p. 1) (Hanratty et al., 2011, p. 2609).2. Based on the clinical picture and laboratory investigations provided, what stage ofchronic kidney disease this patient is in and what will be the main management approachat this stage? (100-150 words)Based on the laboratory results and patient history, this patient is now in end stage renaldisease. This is characterised by anaemia. The kidneys are no longer able to produceenough erythropoietin, which stimulates red blood cell production in the bone marrow(Babitt & Lin, 2012, p. 1633). It also results in nausea and vomiting, loss of appetite andthe resulting weight loss. Nausea and vomiting in kidney failure is usually attributed tothe build-up of toxins, specifically uraemia, in the blood. It is also a common side effect ofdialysis, usually due to the dramatic decreased in fluid volume (Asgari et al., 2016, p. 54).This patient will be managed with dialysis and other medications to address thehypertension such as ACE (angiotensin converting enzyme) inhibitors and diuretics. ACEinhibitors, which are the current best practice for these patients, are used to attempt toreverse the role the Renin- Angiotensin- Aldosterone system plays in the reabsorption offluid through the nephrons, which perpetuates the cyclic effect between hypertensionand chronic kidney disease (Phan et al., 2014). Dialysis would be used to clean the bloodin place of the kidneys; this patient would most likely need to be on dialysis multiple timesa week (Tedla et al., 2011).3ReferencesAsgari, M. R., Asghari, F., Ghods, A. A., Ghorbani, R., Hoshmand Motlagh, N., & Rahaei,F. (2016). Incidence and severity of nausea and vomiting in a group of maintenancehemodialysis patients. Journal of Renal Injury Prevention, 6(1), 49–55.https://doi.org/10.15171/jrip.2017.09Babitt, J. L., & Lin, H. Y. (2012). Mechanisms of Anemia in CKD. Journal of the AmericanSociety of Nephrology, 23(10), 1631–1634.https://doi.org/10.1681/asn.2011111078Griffin, K. A. (2017). Hypertensive Kidney Injury and the Progression of Chronic KidneyDisease. Hypertension, 70(4), 687–694.https://doi.org/10.1161/HYPERTENSIONAHA.117.08314Hanratty, R., Chonchol, M., Havranek, E. P., Powers, J. D., Dickinson, L. M., Ho, P. M.,Magid, D. J., & Steiner, J. F. (2011). Relationship between Blood Pressure andIncident Chronic Kidney Disease in Hypertensive Patients. Clinical Journal of theAmerican Society of Nephrology, 6(11), 2605–2611.https://doi.org/10.2215/cjn.02240311Judd, E., & Calhoun, D. (2015). Management of Hypertension in CKD: Beyond theGuidelines. Advances In Chronic Kidney Disease, 22(2), 116-122.https://doi.org/10.1053/j.ackd.2014.12.0014Ku, E., Lee, B., Wei, J., & Weir, M. (2019). Hypertension in CKD: Core Curriculum2019. American Journal Of Kidney Diseases, 74(1), 120-131.https://doi.org/10.1053/j.ajkd.2018.12.044Minesh, K. (2020, January 27). What Is Renal Hypertension? WebMD.https://www.webmd.com/hypertension-high-blood-pressure/guide/what-is-renalhypertension#1Phan, O., Burnier, M., & Wuerzner, G. (2014, December). Hypertension in Chronic KidneyDisease – Role of Arterial Calcification and Impact on Treatment. US NationalLibrary of Medicine National Institutes of Health.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6159424/Rodríguez-Ortiz, M. E., Pontillo, C., Rodríguez, M., Zürbig, P., Mischak, H., & Ortiz, A.(2018). Publisher Correction: Novel Urinary Biomarkers For Improved PredictionOf Progressive eGFR Loss In Early Chronic Kidney Disease Stages And In High RiskIndividuals Without Chronic Kidney Disease. Scientific Reports, 8(1), 1.https://doi.org/10.1038/s41598-018-36919-7Tedla, F., Brar, A., Browne, R., & Brown, C. (2011). Hypertension in Chronic KidneyDisease: Navigating the Evidence. International Journal Of Hypertension, 2011, 1-9. https://doi.org/10.4061/2011/1324055Yang, J., Cho, K., Kim, J., Kim, S., Kim, C., You, G., Lee, J., Choi, S., Lee, S., Kim, H., Heo, J.,Cha, T., & Lee, J. (2014). Wall shear stress in hypertensive patients is associatedwith carotid vascular deformation assessed by speckle tracking strain imaging.Clinical Hypertension, 20(1), 10. https://doi.org/10.1186/2056-5909-20-10pathophysiological basis of renal changes
