How high blood pressure affects the kidneys
The approximately one million nephrons in each kidney act as functional units. They consist of the renal corpuscles and the tubule system attached to them. The renal corpuscles in turn consist of a fine vascular cluster – the glomerulum – and a Bowman capsule surrounding it. The Bowman capsule consists of two layers. The inner layer is formed by specialized cells, the so-called podocytes, and is directly adjacent to the glomerular capillaries. A further layer separates the Bowman capsule from the outside. Between these two layers is a cavity called the capsule space. The vessel walls of the capillary and the podocytes adjacent to them together form the blood-urine barrier. This barrier is comparable in its function to a filter that prevents the passage of cells and large proteins. Driven by blood pressure, a cell- and largely protein-free primary urine is filtered out of the blood through the blood-urine barrier into the capsule space.
Except for a lower protein content, it corresponds mainly to blood plasma. Approximately 180 l of primary urine is produced daily. During the passage through the tubular system, water and the nutrients contained in it are removed, so that ultimately about 1.5 l of final urine is produced and excreted.
Continuous blood flow is crucial for urine production and the associated excretion of toxic and metabolic products. For this reason, the kidneys pass at rest about 20% of the blood pumped through the circulation per minute. After the gastrointestinal tract, they are thus the organs that are best perfused at rest.
By dilating and constricting the blood vessels to and from, the kidney can regulate the pressure in the glomerular capillaries and thus ensure constant filtration. However, this autoregulation only works in the range of systolic blood pressure between 80 mmHg and 180 mmHg. If the blood pressure is too low, the filtration stops, but if it exceeds the autoregulation range, the filtration and also the amount of urine produced is increased, which can lead to a loss of water and nutrients.
If the blood flow to the kidneys decreases, they release renin, which triggers a signal cascade that leads to an increase in blood pressure. Through this mechanism, the cause of arterial hypertension may be in the kidney itself. The cause of such secondary hypertension is, for example, reduced renal blood flow due to a narrowing (stenosis) in the supplying renal arteries. As a result, the kidney releases more renin to improve its perfusion. This form of hypertension usually does not respond adequately to drug therapy, since lowering blood pressure reduces renal perfusion and again leads to increased renin secretion. The therapy of such a therapy-resistant form of hypertension consists of correcting the constriction and restoring an unimpeded blood flow in the kidney.
However, the kidney is much more often the cause of arterial hypertension. Sustained elevated blood pressure beyond systolic 140 mmHg damages the vascular system – including the renal arteries and glomerular vessels.
Arterial hypertension also promotes the development of arteriosclerosis. If arteriosclerotic plaques form in the renal artery leading from the aorta, renal artery stenosis and undersupply of the kidney may occur. In response to the reduced perfusion, the kidney releases more renin and thus increases the circulation. The result is a self-reinforcing vicious circle.
Over time, high blood pressure thus impairs kidney function. As a sign of the barrier disorder, the blood protein albumin, which is normally too large to pass the blood-urine barrier, increasingly passes into the urine. A so-called microalbuminuria develops. With progressive damage to the glomerula, ever larger amounts of albumin enter the urine (macroalbuminuria). Externally, this becomes noticeable by foaming of the urine. If the protein content in the blood drops sharply due to the loss of protein, edema can occur because the amount of blood proteins can no longer bind the water sufficiently in the vascular system.
Long-term hypertension leads to pathological remodelling processes that increasingly constrict the vessels in the kidney. The reduced supply and inflammatory processes lead to a progressive loss of glomerula and atrophy of the tubule system. With the loss of functional tissue, the filtration rate and renal function decreases continuously.
However, renal insufficiency usually develops only slowly and can be delayed or even prevented by effective blood pressure control. However, if these processes continue unhindered, a shrunken kidney and terminal renal failure threaten to result in an almost complete loss of kidney function.
The kidney interacts in a complex way with systemic blood pressure. On the one hand, it can contribute to the development of arterial hypertension; on the other hand, high blood pressure leads to its damage in the long term. For this reason regular blood pressure checks are essential and should be part of every physical examination. They can not only provide indications of existing functional limitations of the kidney, but can also prevent the development of renal insufficiency by treating high blood pressure at an early stage.
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