PATHOPHYSIOLOGY

Hypertension is one of the leading causes of CKD due to the deleterious effects that
increased BP has on kidney vasculature. Long-term, uncontrolled, high BP leads to high
intraglomerular pressure, impairing glomerular filtration. Damage to the glomeruli lead to
an increase in protein filtration, resulting in abnormally increased amounts of protein in
the urine (microalbuminuria or proteinuria). Microalbuminuria is the presentation of small
amounts of albumin in the urine and is often the first sign of CKD. Proteinuria (protein-
to-creatinine ratio 200 mg/g) develops as CKD progresses, and is associated with a
poor prognosis for both kidney disease and CVD.

As discussed previously, the relationship between CKD and HTN is cyclic, as CKD can
contribute to or cause HTN. Elevated BP leads to damage of blood vessels within the
kidney, as well as throughout the body. This damage impairs the kidney's ability to filter
fluid and waste from the blood, leading to an increase of fluid volume in the bloodthus
causing an increase in BP.

Further loss of kidney function will lead to impaired insulin action, failure to convert
inactive forms of calcium, failure to produce erythropoetin, and increased production of
lipds which results to impaired blood glucose level, decreased calcium absorption,
anemia and advance atherosclerosis which increases the risk of the patient for
developing or building up of plaque in your coronary arteries -- a condition called
atherosclerosis -- that leads to blockages. The arteries, which start out smooth and
elastic, become narrow and rigid, restricting blood flow to the heart. The heart becomes
starved of oxygen and the vital nutrients it needs to pump properly.

In this case, a blood clot may totally block the blood supply to the heart muscle,
causing heart attack manifesting hypovolemia, hypotension, cold skin, weak pulse,
mental confusion, and anxiety due to lack of oxygen supply to the myocardium that
leads to cardiogenic shock which causes arrythmia.

Cardiogenic shock is the shock caused by inadequate cardiac function, as in myocardial

infarction or mechanical obstruction of the heart;

However, there are common mechanisms for disease progression. Pathologic features
include fibrosis, loss of renal cells, and infiltration of renal tissue by monocytes and
macrophages. Proteinuria, hypoxia, and extensive angiotensin II production all
contribute to the pathophysiology. In an attempt to maintain GFR, the glomerular
hyperfiltration; this results in endothelial injury. Proteinuria results from increased
glomerular permeability and increased capillary pressure. Hypoxia also contributes to
disease progression. Angiotensin II increases glomerular hypertension, which further
damages the kidney.