Chronic kidney disease: caused by kidney blood vessels

2021-05-06 03:31 PM

Even in healthy people with no latent hypertension or diabetes, renal plasma volume and glomerular filtration rate (GFR) will decrease by 40-50% by age 80

Many types of blood vessel damage can cause kidney anaemia and kidney tissue death. The most common lesions are (1) Atherosclerosis of the large arteries of the kidney, with progressive hardening of the capillaries causing constriction; (2) fibromyalgia hyperplasia in one or more large arteries, causing blockage of blood vessels; and (3) renal sclerosis, resulting from hardening of the small arteries, arterioles, and glomeruli.

Atherosclerotic damage or hyperplasia of the major arteries usually affects only one kidney and therefore merely reduces the function of one kidney. Hypertension usually occurs when an artery in one kidney is squeezed while an artery in the other kidney is normal, a condition similar to Goldblatt's experiments on two kidneys.

Benign kidney sclerosis, the most common form of kidney disease, is found in at least 70% of forensic examinations of people who die at age 60. This type of vascular damage occurs in the small intercostal arteries and the radial arterioles of the kidney.

This is believed to begin the process of plasma drainage through vascular endothelial cells. This extravasation causes fibrin to be deposited into the medial layer between blood vessels, followed by thickening of the vessel wall which ultimately leads to vasoconstriction, and in some cases can lead to occlusion. circuit completely. Because there are no branches connecting the kidney's small blood vessels, blocking one of the results in the destruction of a corresponding number of nephrons to be supplied with the blood. Thus, part of the kidney parenchyma is replaced by fibrous tissue. When fibrosis occurs in the glomeruli, that damage is called glomerular fibrosis.

Renal fibrosis and glomerular fibrosis to some extent typically occur in people after 40 years of age, leading to a 10% reduction in functional nephrons over 10 years starting at age 40. Glomerular loss and nephron function are reflected by a gradual decrease in both blood flow to the kidney and GFR.

Figure. Effect of age on the number of functional glomeruli

Even in healthy people with no latent hypertension or diabetes, renal plasma volume and glomerular filtration rate (GFR) will decrease by 40-50% by age 80.

The frequency and severity of fibrosis of the kidney and glomerular fibrosis are greatly increased if accompanied by hypertension or diabetes. In fact, diabetes and high blood pressure are the two most important causes of end-stage chronic kidney disease, as discussed earlier. Thus, benign renal fibrosis associated with severe hypertension can lead to the rapid progression of malignant nephrotic fibrosis. The histological features characteristic of malignant nephrotic fibrosis includes a large amount of fibrin deposited in the arterioles and the vascular thickening process, with severe anaemia in the affected nephrons. In addition, although no reason has been found, the incidence of renal fibrosis and glomerulonephritis in blacks is higher than in whites of the same age and same degree of hypertension or diabetes. Disconnect the road.



Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Air in and out of the lungs: pressure causes the movement of air

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Nephron: The functional unit of the kidney

Prothrombin activation: initiates blood clotting

Estimated renal plasma flow: PAH clearance

Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

Graphical analysis of high-volume heart failure

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Red blood cells: differentiation and synthesis

Ammonia buffering system: excretes excess H + and creates new HCO3

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Reduced sodium chloride, dilates arterioles, increases Renin release.

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Origin of lymphocytes: the body's resistance to infection

Pathophysiology of fever

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

The endocrine regulates tubular reabsorption

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Self-regulation of glomerular filtration rate and renal blood flow

Physiological anatomy of the kidneys and urinary system

The kidneys excrete sodium and fluid: feedback regulates body fluids and arterial pressure