Provide an in depth discussion on the pathophysiology of Chronic Kidney Disease as it occurs over time. Include signs and symptoms, diagnostic studies and the underlying pathophysiologic process causing the signs and symptoms.
Chronic kidney disease (CKD) is a chronic illness characterized by a steady loss in kidney function over a given period in an individual’s life. Diabetes, hypertension, and polycystic kidney disease are common causes of this condition and can lead to other life-threatening complications. The pathophysiology of chronic kidney disease (CKD) is set in motion in two stages of damage. Firstly, the underlying etiology is affected by a series of mechanisms that irritate specific glomerulonephritis, renal tubes, and the overall immune complex deposition (Kasper et al., 2018). Secondly, the hyperfiltration of viable nephrons occurs, resulting in a significant decrease in renal mass, which then further exacerbates the deterioration of kidney function.
Symptoms of CKD include hypertension, hyperphosphatemia, and metabolic acidosis. Diagnosis is typically based on specialized examinations that aim to evaluate the level of serum creatinine and any history of kidney disease. Screening is often used during diagnosis. Individuals with obesity, a history of high blood pressure, and hypertension are screened for CKD since they represent demography that stands a higher risk of developing the condition. The projected GFR (Egfr) is calculated and compared to the ratio of albumin-to-creatine (ACR) from the urine specimen provided (Arici, 2014, p. 22).
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The medical practitioner would then have to determine the glomerular filtration rate (GFR) by assessing the level of serum creatinine in the urine sample. Similarly, kidney ultrasonography is also employed to diagnose the presence of CKD. The ultrasound probes any uncontrolled alterations in glomerular sclerosis, interstitial swelling, or tubular atrophy. Furthermore, an intricate underlying pathophysiological process causes the signs and symptoms mentioned above. Hypertension in persons with CKD stems from an increase in fluid surplus and vasoactive hormones, which dramatically increase acute health risks and sudden death. Hyperphosphatemia is caused by an insufficient phosphate elimination mechanism, which ultimately results in the calcification of blood vessels. Metabolic acidosis is the result of a diminished capacity of proximal tubule cells to produce sufficient ammonia.