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Chapter: Medical Physiology: Kidney Diseases and Diuretics

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Hypertension and Kidney Disease

As discussed earlier, hypertension can exacerbate injury to the glomeruli and blood vessels of the kidneys and is a major cause of end-stage renal disease.

Hypertension and Kidney Disease

As discussed earlier, hypertension can exacerbate injury to the glomeruli and blood vessels of the kidneys and is a major cause of end-stage renal disease. Conversely, abnormalities of kidney function can cause hypertension. Thus, the relation between hypertension and kidney disease can, in some instances, propagate a vicious circle: primary kidney damage leads to increased blood pressure, which in turn causes further damage to the kidneys, further increases in blood pressure, and so forth, until end-stage renal disease develops.

Not all types of kidney disease cause hypertension, because damage to certain portions of the kidney cause uremia without hypertension. Nevertheless, some types of renal damage are particularly prone to cause hyper-tension. A classification of kidney disease relative to hypertensive or nonhypertensive effects is the following.

Renal Lesions That Reduce the Ability of the Kidneys to Excrete Sodium and Water Promote Hypertension. Renal lesions thatdecrease the ability of the kidneys to excrete sodium and water almost invariably cause hypertension. There-fore, lesions that either decrease GFR or increasetubular reabsorption usually lead to hypertension ofvarying degrees. Some specific types of renal abnormal-ities that can cause hypertension are as follows:

   1.  Increased renal vascular resistance, which reducesrenal blood flow and GFR. An example is hypertension caused by renal artery stenosis.

 

   2.  Decreased glomerular capillary filtration coefficient, which reduces GFR. An example of this is chronic glomerulonephritis, which causes inflammation and thickening of the glomerular capillary membranes, thereby reducing the glomerular capillary filtration coefficient.

 

3.     Excessive tubular sodium reabsorption. An exampleis hypertension caused by excessive aldosterone secretion, which increases sodium reabsorption mainly in the cortical collecting tubules.

Once hypertension has developed, renal excretion of sodium and water returns to normal because the high arterial pressure causes pressure natriuresis and pres-sure diuresis, so that intake and output of sodium and water become balanced once again. Even when there are large increases in renal vascular resistance or decreases in the glomerular capillary coefficient, the GFR may still return to nearly normal levels after the arterial blood pressure rises. Likewise, when tubular reabsorption is increased, as occurs with excessive aldosterone secretion, the urinary excretion rate is ini-tially reduced but then returns to normal as arterial pressure rises. Thus, after hypertension develops, there may be no sign of impaired excretion of sodium and water other than the hypertension. Normal excretion of sodium and water at an elevated arterial pressure means that pressure natriure-sis and pressure diuresis have been reset to a higher arterial pressure.

Hypertension Caused by Patchy Renal Damage and Increased Renal Secretion of Renin. If one part of the kidney isischemic and the remainder is not ischemic, such as occurs when one renal artery is severely constricted, the ischemic renal tissue secretes large quantities of renin. This secretion leads to the formation of angiotensin II, which can cause hypertension. The most likely sequence of events in causing this hypertension, is (1) the ischemic kidney tissue itself excretes less than normal amounts of water and salt; (2) the renin secreted by the ischemic kidney, and subse-quent increased angiotensin II formation, affects the nonischemic kidney tissue, causing it also to retain salt and water; and (3) excess salt and water cause hyper-tension in the usual manner.

A similar type of hypertension can result when patchy areas of one or both kidneys become ischemic as a result of arteriosclerosis or vascular injury in specific portions of the kidneys. When this occurs, the ischemic nephrons excrete less salt and water but secrete greater amounts of renin, which causes increased angiotensin II formation. The high levels of angiotensin II then impair the ability of the surrounding otherwise normal nephrons to excrete sodium and water. As a result, hypertension develops, which restores the overall excretion of sodium and water by the kidney, so that balance between intake and output of salt and water is maintained, but at the expense of high blood pressure.

Kidney Diseases That Cause Loss of Entire Nephrons Lead to Renal Failure But May Not Cause Hypertension. Loss of largenumbers of whole nephrons, such as occurs with the loss of one kidney and part of another kidney, almost always leads to renal failure if the amount of kidney tissue lost is great enough. If the remaining nephrons are normal and the salt intake is not excessive, this condition might not cause clinically significant hypertension, because even a slight rise in blood pressure will raise the GFR and decrease tubular sodium reabsorption sufficiently to promote enough water and salt excretion in the urine, even with the few nephrons that remain intact. However, a patient with this type of abnormality may become severely hypertensive if additional stresses are imposed, such as eating a large amount of salt. In this case, the kidneys simply cannot clear adequate quanti-ties of salt with the small number of functioning nephrons that remain.


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