Physiologically with chronic renal failure and the GFR

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Explain what happens physiologically with chronic renal failure and the GFR. Support with evidence. Include important labs that are monitored in the process.
Chronic renal failure can also be described as chronic kidney disease (CKD). According to McCance and Huether (2018), “chronic kidney disease (CKD) is the progressive loss of renal function associated with systemic diseases such as hypertension, diabetes mellitus, systemic lupus erythematosus, or intrinsic kidney disease, including acute kidney injury, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies, or vascular disorders.” CKD is directly related to the decline of the glomerular filtration rate (GFR). There are stages of CKD depending on the value of the GFR. There are many factors that can contribute to the development of CKD, however, the two main things that have been consistent to be main contributors are proteinuria and increased angiotensin II activity. McCance and Huether (2018) states that, “proteinuria contributes to tubulointerstitial injury by accumulating in the interstitial space and activating complement proteins and other mediators and cells, such as macrophages, that promote inflammation and progressive fibrosis.” Angiotensin II causes glomerular and systemic hypertension that directly impacts the nephrons, which are the main filters in your kidneys. It also increases glomerular capillary permeability, contributing to proteinuria. In addition, “Angiotensin II also may promote the activity of inflammatory cells and growth factors that participate in tubulointerstitial fibrosis and scarring” (McCance