Essay on Physiology of Chronic Renal Failure and GFR

Chronic renal failure is also known as chronic kidney disease. It is the progressive loss of renal function associated with systemic health conditions like diabetes mellitus, hypertension, obstructive uropathies, and acute kidney injury. CKD is referenced to declining GFR, and kidney damage is indicated by a GFR less than 60ml/min/1.73m² for more than three months (McCance & Huether, 2019). eGFR is used to estimate the functioning of the kidneys. However, GFR may not be effective in identifying stage 1 and 2 CKD because it may be normal in such cases. Kidneys can adapt to the loss of nephron mass. Changes caused by increased levels of creatinine, potassium, and urea and changes in water and salt balance do not become superficial until renal function reduces to less than 25% after the depletion of renal reserves. Studies indicate that loss of nephron mass as kidney damage progresses results in the surviving nephrons sustaining normal functioning of the kidney (McCance & Huether, 2019). The nephrons can perform compensatory hypertrophy and hyperfunction in their rates of filtration, secretion, and reabsorption. They can also uphold adaptive modifications in the regulation of solutes and water in declining GFR.

The urine of individuals suffering from chronic kidney failure may have increased amounts of red blood cells and protein. However, the end products of excretion are similar to those from kidneys that function normally. Significant changes occur during the advanced stages of renal failure, where nephrons have reduced functioning (McCance & Huether, 2019). Severe injury results in an impaired proliferative reaction in epithelial cells, causing interstitial capillary loss and fibroblast proliferation. Glomerulosclerosis and tubulointerstitial also lead to end-stage kidney disease.

Factors that contribute to the development of chronic kidney disease are complex, and they involve the interaction of several cells, cytokines, and structural modifications. Factors that contribute to chronic kidney failure include prolonged obstruction of the urinary tract, inherited kidney disease, recurrent kidney infection, and interstitial nephritis (Romagnani et al., 2017). This condition can affect any part of the body. It can cause fluid retention whereby an individual can have swollen arms and legs. One can also develop anemia, heart disease, weak bones, reduced sex drive, damaged central nervous system, and pregnancy complications.

The symptoms of chronic kidney disease are described through uremia and azotemia. Azotemia is characterized by increased amounts of serum urea, serum creatinine, and other nitrogenous components associated with reduced kidney functioning (McCance & Huether, 2019). Uremia is related to the buildup of urea and other nitrogenous compounds and toxins. Toxins are brought about by the accumulation of end products of protein metabolism, changes in electrolytes and fluid, absorption of toxins from gut bacteria, and metabolic acidosis (Ammirati, 2020). CKD’s general symptoms include anorexia, hypertension, nausea, vomiting, diarrhea, loss of weight, edema, and cardiovascular disease.

People can prevent the development of CKD by following instructions on over-the-counter medications, maintaining a healthy weight, quitting smoking, and managing health conditions like diabetes with the help of a doctor (Ammirati, 2020). Smoking can damage kidneys and make the existing kidney disease worse. They can also undergo regular tests to test for the functioning of their kidneys.

References

Ammirati, A. L. (2020). Chronic kidney disease. Revista da Associação Médica Brasileira, 66, s03-s09. https://doi.org/10.1590/1806-9282.66.S1.3

McCance K., L., & Huether, S., (2019). Pathophysiology: The biological basis for disease in adults and children. (8th Edition). Mosby.

Romagnani, P., Remuzzi, G., Glassock, R., Levin, A., Jager, K. J., Tonelli, M., Massy, Z., Wanner, C., & Anders, H.-J. (2017). Chronic kidney disease. Nature Reviews Disease Primers, 3, 17088. https://doi.org/10.1038/nrdp.2017.88