Chronic kidney disease

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal function over a period of months or years in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia. In this condition, the GFR falls below 10% of the normal rate.

Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis.

The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing a reduced appetite.

Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate (rate at which the kidneys filter blood) and as a result a decreased capability of the kidneys to excrete waste products.

Symptoms of chronic kidney disease:
Stage 1 and 2
*Asymptomatic, hypertension

Stage 3 and 4
*Anemia – loss of energy,
*Decreasing appetite; poor nutrition
*Abnormalities in Calcium, Phosphorus metabolism
*Sodium, water, potassium, and acid base abnormalities

Stage 5
*All the above – accentuated; eventually overt uremia

The prevalence of chronic kidney disease amongst people with other co-morbidities such as diabetes, hypertension, and coronary heart disease will be considerably higher than 4.9%.

Conditions associated with a high risk of silent development of parenchymal kidney disease:
• Hypertension, diabetes mellitus, heart failure
• Atherosclerotic coronary, cerebral, or peripheral vascular disease
Chronic kidney disease

What is hypertensive heart disease?

Hypertension can lead to hypertensive heart disease, which is a condition that represents an important underlying mechanism for the occurrence of blood pressure-related CVD morbidity and mortality.

Hypertensive heart disease encompasses anatomical changes and altered physiology of heart muscle, coronary arteries, and great vessels.

Hypertensive heart disease is a constellation of abnormalities that includes left ventricular hypertrophy (LVH), systolic and diastolic dysfunction, and their clinical manifestations including arrhythmias and symptomatic heart failure.

Hypertensive heart disease results from chronic high blood pressure. Hypertension can be defined as blood pressure as a systolic blood pressure higher than 120 mm Hg or a diastolic pressure more than 80mm Hg. The risk of cardiovascular mortality doubles for every 20mmHg systolic and 10mmHg diastolic pressure increase over a baseline blood pressure of 115/75.

Clinically, hypertensive heart disease is characterized by the presence of left ventricular hypertrophy (LVH) in the absence of a cause other than arterial hypertension.

Hypertensive individuals with hypertensive heart disease are more prone to myocardial infarction, congestive heart failure, stroke, and sudden death then persons with hypertension alone.

The main risk factor for hypertensive heart disease is high blood pressure. The risk increases if the person overweight, not exercise enough, smoking, eating food high in fat and cholesterol.

Types of hypertensive heart disease:
*Narrowing of the arteries
*Thickening and enlargement of the heart
What is hypertensive heart disease?

Left ventricular hypertrophy

Left ventricular hypertrophy is both a major maladaptive response to chronic pressure overload and an important risk factor in patients with hypertension. The development of left ventricular hypertrophy is highly correlated with systolic hypertension.

Left ventricular hypertrophy can be defined by the increased left ventricular mass; with myocardial cell hypertrophy and an increase in collagen within myocardium. At the cellular level, the cardiomyocytes expand in thickness and length, but with little or no increase in the number of cells, to compensate for the increased hemodynamic stress on the ventricular wall.

It is a marker for and contributes to coronary events, stroke, heart failure, peripheral arterial disease, and cardiovascular mortality in patients with hypertension

Complications of left ventricular hypertrophy include atrial fibrillation, diastolic heart failure, systolic heart failure, and sudden death.

Age, race, gender and body size can influence cardiac mass; this might occur through cardiac load. Hypertensive left ventricular hypertrophy is a risk factor for high insulin level and insulin resistance.
Left ventricular hypertrophy

Renovascular disease

Renovascular disease especially when it is due to atherosclerosis, is a relatively common cause of difficult-to-control hypertension and/or ischemic nephropathy.

Renovascular disease is an independent risk factor for left ventricular hypertrophy, perhaps reflecting the adverse effects of chronic activation of the rennin-angiotensin system.

Renovascular disease is the most frequent correctable cause of secondary hypertension, its prevalence varies according to the clinical circumstances, being relatively uncommon in patents with mild hypertension but quite common (incidence 20% to 45%) in patients with severe or refractory hypertension.

Several recognized clinical situations that show the presence of renovascular disease are:
*Accelerated hypertension at any age
*Episodes of flash pulmonary edema with normal ventricular function
*Acute unexplained rise in serum creatinine after an angiotensin-converting enzyme inhibitor
*Elevated serum creatinine in patients with severe or refractory hypertension
*Asymmetrical renal size
*Moderate to severe hypertension in a patient with diffuse atherosclerotic disease

Two clinical subgroups comprise the majority of patients with renovascular hypertension:  fibromuscular dysplasia and atherosclerotic disease. Fibromuscular dysplasia of the renal arteries accounts less than 10% of all renovascular hypertension and occurs mainly in younger women.
Renovascular disease

Hypertensive heart disease

Hypertension is a powerful predictor of cardiovascular mortality and death from all causes. It is a major risk factor for the development of systolic heart failure as well as heart failure in the setting of preserved left ventricular function.

Hypertensive heart disease can be defined as the response of the heart to the afterload imposed on the left ventricle by the progressively increasing arterial pressure and total peripheral resistance.

Severe hypertension may directly damage arterioles and cause atherosclerosis. High blood pressure is also a risk for stroke.

The risk of cardiovascular events is increased two or three times in men and women with hypertension. It is estimated that 14% deaths from coronary heart disease in men and 12% of deaths from coronary heart disease in women are due to hypertension.

Hypertensive heart disease is characterized by increased left ventricular mass leading to left ventricular hypertrophy in the absence of aortic stenosis or hypertrophic cardiomyopathy. Other manifestations include diastolic dysfunction and microvascular changes that cause coronary blood flow abnormalities.

Left ventricular hypertrophy increases the rletaove risk for amrtlaity by twofold in subjects with coronary artery disease and by four fold in those with normal epicardial coronary arteries.

In the development of hypertensive heart disease, myocyte hypertrophy is also associated with apoptosis, collagen deposition, a ventricular fibrosis, with as impairment of coronary hemodynamics as well, thus profoundly influencing functional properties of the left ventricle.
Hypertensive heart disease

Pulmonary insufficiency

In pulmonary insufficiency, blood ejected into the pulmonary artery during systole flows back into the right ventricle during diastole, causing a fluid overload in the ventricle and ventricular hypertrophy; it may ultimately result in right-sided heart failure.

Pulmonic insufficiency is frequently very difficult to appreciate on physical exam, particularly if the pulmonary pressures are normal.

In the fetus, severe pulmonary inefficiency causes hydrops and death.

Alternately, pulmonary insufficiency may be well-tolerated functional disturbance until late adulthood or come to medical attention because of a dilated main pulmonary artery detected on a routine chest x-ray.

The causes of pulmonary insufficiency may be the result of a rare congenital lesion or the stretching of the valvular ring by long lasting pulmonary hypertension. Rarely, prolonged use of a pressure-monitor catheter in the pulmonary artery will lead to this disorder.
Pulmonary insufficiency

Pulmonary venous hypertension

Pulmonary hypertension may occur from blockage of the left atrium by a myxoma or thrombus.

Congenital and acquired heart lesions can cause pulmonary venous hypertension.

Congenital causes include hypoplastic left heart syndrome, aortic coartation, interrupted aortic arch, anomalous origin of a coronary artery, valvular aortic stenosis, cor triartrium, total anomalous pulmonary connection below the diaphragm and pulmonary vein stenosis or atresia.

Pulmonary venous hypertension necessitates a passive rise in pulmonary systolic pressure to maintain a driving force across the vasculature.

Volume overloaded cause shear force injury to the vascular endothelium, which leads to vascular remodeling and luminal narrowing.

Pulmonary venous hypertension may be identified on radiographs, pulmonary angiogram or nuclear medicine perfusion scans.

Pulmonary venous hypertension is considered mild with wedge pressures of 10 to 13 mm Hg, moderate with equalization of upper and lower lobe blood flow and wedge pressures of 14 to 16 mm Hg.
Pulmonary venous hypertension