Final answer:
Patients with chronic kidney disease experience arterial stiffness primarily due to an increase in nitrogenous waste products (C).
Step-by-step explanation:
Arterial stiffness in chronic kidney disease (CKD) is primarily attributed to the accumulation of nitrogenous waste products. The kidneys play a crucial role in filtering and eliminating waste from the bloodstream, including urea and creatinine. In CKD, impaired renal function leads to a buildup of these nitrogenous waste products in the body.
Urea, a byproduct of protein metabolism, undergoes various processes that contribute to arterial stiffness. One significant mechanism is the formation of advanced glycation end products (AGEs). These compounds result from the reaction of urea with proteins in the arterial walls, causing cross-linking of collagen and elastin fibers. This process leads to decreased arterial elasticity and increased stiffness.
Additionally, the elevation of uremic toxins in the bloodstream contributes to endothelial dysfunction and oxidative stress, further exacerbating arterial stiffness. The clinical implications of this process include an increased pulse wave velocity and arterial stiffness index in individuals with advanced CKD.
In summary, the increase in nitrogenous waste products, particularly urea, is a key factor in the development of arterial stiffness in patients with chronic kidney disease (Option C). Understanding this relationship is essential for healthcare providers in managing and preventing vascular complications in CKD patients.