1.

Cardiovascular changes
Between 50% and 65% of deaths that occur during ESRD result from cardiovascular
complication. The most common clinical manifestation is hypertension (which may also be
the because of renal failure). Hypertension is produced through the following:
Mechanism of volume overload
Stimulation of the renin-angiotensin system
Sympathetically mediated vasoconstriction; for example, increased level of dopamine
-hydroxylase
Absence of prostaglandin
Any of the many systemic complications of prolonged high blood pressure may be found.
The effects of volume overload on the heart as seen, including left ventricular
hypertrophy and heart failure. Heart failure may also result from anemia, vascular access,
complication of coronary artery disease, electrolyte imbalance, acidosis, myocardial
calcification, and thiamine depletion. Dysrhythmias may be caused by hyperkalemia,
acidosis, hypomagnesaemia, and decreased coronary perfusion.
Atherosclerosis is accelerated because of abnormal carbohydrate and lipid metabolism,
impaired fibrinolysis (which leads to the development of micro emboli), and
hyperparathyroidism. Arterial classifications have been identified. Other sides include the
abdominal aorta, feet, pelvis, hands, and wrist. These vascular calcifications also occur
within the heart, particularly at the mitral valve.
2. Respiratory changes
Some of the respiratory effects, such as pulmonary edema, can be attributed to fluid
overload. Pleuritis is a frequent finding, especially when pericarditis develops. A
characteristic condition called uremic lung is a type of pneumonitis condition that
response well to fluid removal. Metabolic acidosis causes a compensatory increase in
respiratory rate as the lungs work to eliminate excess hydrogen ions.
3. Musculoskeletal changes
The musculoskeletal system is affected early in the disease process, and up to 90% clients
with ESRD experience renal osteodystriphy. The condition develops insidiously and takes
several forms: osteomalacia, osteitis fibrosa, osteoporosis, and osteoclerosis. The etiologic
mechanism involves the kidney bone-parathyroid and calcium-phosphate-vitamin d
connections. As the GFR decreases, phosphate excretion decreases and calcium elimination
increases. Abnormal levels of calcium and phosphatase stimulate the release of parathyroid
hormone, which mobilizes calcium from the bones and facilitates phosphate excretion.
As the renal failure progresses, the kidney no longer converts vitamin D to its active from, 1,
25-dihydroxy-chocelcalciferol. The lack of the substance interferes with calcium absorption
from the intestine and paradoxically facilities phosphate retention. Thus mineralization of the
bone with calcium and phosphate is impaired. Demineralization of the bone frees more
calcium and phosphorus into the blood. As the disease progresses, the parathyroid gland may
become unresponsive to the normal feedback system and continue to produce parathyroid
hormone, accelerating renal osteodystrophy. Partial Para thyroidectomy is the treatment of

choice when hypercalcemia and high plasma levels of parathyroid hormone cannot be
controlled with medication,
In addition the bone demineralization, this progress leads to deposition of calcium in
subcutaneous, vascular, and visceral tissues throughout the body. In advanced stages, joint
paint is severe. The client may also report diffuse and generalized bone and muscle pain.
Bone deformities and frequent fractures are common. In children, bones fail to calcify,
causing growth retardation. Tissue calcifications may be lethal if they develop in vital tissues,
such as cerebral, coronary, or pulmonary vessels.
Some clients complain of muscle cramps. These may result of osmolar changes in the body
fluids or sometimes form hypocalcaemia.