THE HEART AND THE KIDNEYS

PHOTO BY STEPHEN FADEM

The heart has four chambers. The right side of the heart receives blood from the body into the right atrium. It then travels through the tricuspid valve to the right ventricle, a powerful muscle that pumps the blood through the pulmonary valve into the lungs. Here, carbon dioxide is exchanged for oxygen. The blood returns to the heart through pulmonary veins and enters the left atrium. From the left atrium, the blood is pumped through the mitral valve to the left ventricle. The left ventricle is another powerful muscle. It then pumps blood through the aortic valve into the aorta. The aorta carries the blood to the renal arteries. These arteries divide until they become arterioles. The blood then enters the glomerular filters discussed in an earlier post.

The heart must work constantly for the kidneys to be able to do their job. The heart is nourished through the coronary arteries. As we age, hardening and plaques form in these coronary arteries and can cause serious heart disease. Coronary artery disease is strongly associated with both hypertension and diabetes; it is independently worsened with kidney disease.

Kidney disease is associated with hypertension. Hypertension may not only be a cause of kidney disease but almost always accompanies it. The elevated pressures inside blood vessels damage their walls, causing damage and narrowing, and reducing their production of nitric oxide. Nitric oxide plays a key role in the blood vessel relaxation mechanisms.

There are five heart conditions most commonly associated with chronic kidney disease

1.     Atherosclerosis – hardening of the arteries. This is characterized by the slow buildup of an atheromatous deposit over several years. Macrophages are immune cells that phagocytize (eat) foreign particles. Cholesterol-containing lipoprotein is devoured by macrophages that subsequently die from their overindulgence of cholesterol and accumulate calcium. As the calcium hardens, plaque buildup occludes the blood vessel, leading to angina. The plaque may eventually rupture causing an acute myocardial infarction. This is known as a heart attack in simple terms. It can often lead to permanent heart damage and can be fatal. Statin and aspirin therapy have been helpful in reducing cardiac events once they occur. 

2.     Left ventricular hypertrophy – Chronic hypertension leads to the loss of nitric oxide, making it impossible for the muscle cells of the blood vessel wall to contract. When they remain in the contracted state they increase the resistance inside blood vessels and the pressure. Hypertension results in the loss of elastin and deposit of a material known as hyaline. These, along with impaired nitric oxide formation cause the blood vessels to become narrowed. The higher pressure forces the heart to work harder. This causes a defect in both the filling and the pumping of blood. The muscles of the heart enlarge, outstripping their blood supply. Eventually, they become fibrotic or scarred.

3.     Vascular calcification – Defects in acid-base metabolism result in a loss of calcium from bone. Along with elevated serum phosphorus, signals inside the vascular smooth muscle cell transcribe the DNA of the cell to make bone-like material. This makes the blood vessel walls stiff, leading to the same conditions as hypertension. 

4.     Calcified heart valves – The increased calcium that leaks from the bone must find a spot in which to deposit. The heart valves thus become victims of this excess calcium deposition and become stiff and narrowed. This reduces the functioning of the heart valves, making them leak, interfering with the heart’s dynamics.

5.     Rhythm disturbances – The increased scar tissue in the heart leads to conduction abnormalities that reduce the ability of contraction signals conducted from the pacemaker of the heart, the sinus node, to properly propagate throughout the heart. Alternate sites take over. In the atrial chambers, this may manifest as atrial fibrillation. In the ventricle, it can become a fatal arrhythmia.