Hypertension affects which organs

Thus, evaluation of persons with suspected or established hypertension must include a meticulous search for evidence of target organ damage. Fortunately, treatment with all antihypertensive medications that results in significant BP reductions also reduces fatal and nonfatal hypertensive complications and significantly slows down the progression to organ failure. Because of the important role that adverse activation of the renin-angiotensin-aldosterone system plays in target organ damage, drugs that antagonize this system have provided consistent and compelling proof of organ protection in both primary and secondary prevention of adverse outcomes.

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Although there have been few reports on the treatment of heart failure due to diastolic dysfunction, ARBs reduce the frequency of hospitalization as well as preserving systolic function. Cardiac hypertrophy is caused by pressure load and often regresses through sustained antihypertensive treatment.

Epidemiological studies have revealed that cardiac hypertrophy is one of the independent factors that determine the prognosis of hypertensive patients. The mortality rate and incidence of cardiac events or heart failure due to coronary artery disease are high in patients with cardiac hypertrophy.

There are few clinical trials specifically designed to directly compare the cardiac hypertrophy-regressing effects among various antihypertensive drugs. A meta-analysis of large clinical trials has reported that RA system inhibitors and long-acting Ca channel blockers are the most effective drugs. Atrial fibrillation increases the incidence of, and mortality due to, cardiovascular events 2—5 times, because it markedly increases the risk of cardiogenic brain embolism.

Atrial fibrillation decreases with the regression of left ventricular hypertrophy by antihypertensive treatment. Recently, many large clinical studies have reported that the new onset of atrial fibrillation can be prevented by RA system inhibitors.

As the risk of cardiovascular accidents is high in patients with chronic kidney disease CKD , its early detection is extremely important. For this purpose, urinalysis and calculation of the estimated glomerular filtration rate eGFR should be performed in all hypertensive patients. Albuminuria is closely related to the progression of kidney damage and the occurrence of cardiovascular disease CVD , and its control is important for the simultaneous protection of the heart and kidneys.

Regarding lifestyle, smoking cessation, reduction of salt intake, maintenance of an appropriate body weight and restriction of protein intake according to renal function should be practiced. Exercise guidance should be given depending on renal function. An ACE inhibitor or ARB is the first choice, and the dose should be increased according to the level of urinary albumin excretion.

Combination therapy with several antihypertensive drugs is often required. For patients undergoing hemodialysis, antihypertensive drugs should be selected considering the drug metabolism, excretion route and dialyzability. Hypertension causes functional or structural changes to varying degrees in the kidney from an early stage. Renal dysfunction may also cause hypertension.

Hypertension and the kidney are closely related to each other, and a vicious circle is established as hypertension exacerbates renal dysfunction, and vice versa. Therefore, strict management of blood pressure as well as treatment of the primary disease is important.

In Japan, major causes of chronic dialysis are diabetic nephropathy, glomerulonephritis and nephrosclerosis. The number of patients undergoing chronic dialysis has steadily increased, and diabetic nephropathy and nephrosclerosis are primary causes of this increase. In contrast, the number of new patients who become dependent on dialysis due to chronic glomerular nephritis has begun to decrease.

Therefore, the early detection and treatment of renal damage are important. CKD has been shown to be a risk factor for CVD not only in the general population 11,12,,,,, but also in patients with heart failure, myocardial infarction, diabetes mellitus and hypertension, and in elderly people. The proposed mechanism may involve oxidative stress, inflammation and abnormal Ca-P metabolism, which are called non-classical risk factors. Microalbuminuria has been established as a risk factor for the development of overt nephropathy and death in diabetic patients, , but it has also recently been shown to be a strong predictive factor for the occurrence of CVD in hypertensive patients and the general population.

In diseases in which urinary albumin is not observed at an early stage hypertension, diabetes mellitus, etc. Epidemiological studies have shown that CKD patients are more prevalent than expected. In Japan, with aging of the population, patients with lifestyle-related diseases such as obesity, hypertension and diabetes mellitus are increasing. Thus, early detection, treatment and prevention of CKD are important. As type II diabetes occurs more frequently in hypertensive patients, kidney damage due to obesity or hypertension underlies the disease in some patients.

In patients with diabetic nephropathy, the survival rate is poor, and the mortality rate increases with the urinary albumin level and severity of renal dysfunction. Periodic monitoring of the urinary albumin level and GFR is necessary. Treatment for diabetic nephropathy involves the intensive management of multiple risk factors, and antihypertensive treatment is the same as that for CKD.

An inappropriate lifestyle is the major background factor for the present increase in CKD patients. Obesity and an excessive salt intake accelerate kidney damage by mechanisms dependent on and independent of blood pressure. Lifestyle modifications are the most basic and important factor in the treatment of CKD, in which maintaining an appropriate body weight, restricting salt intake and cessation of smoking are essential. There are reports that obesity is involved in the development of end-stage renal failure and proteinuria and that proteinuria is alleviated by weight reduction.

Restriction of salt and protein intake is important to control blood pressure and prevent the progression of renal dysfunction.

Restriction of protein intake has been shown to prevent the progression of renal insufficiency and reduce the relative risk of death. Exercise should be guided according to the renal function.

Vigorous exercise that would reduce the renal blood flow should be avoided in patients with renal insufficiency. The objective of antihypertensive treatment in CKD patients is to inhibit or prevent the progression of renal dysfunction and to prevent the occurrence or recurrence of CVD by reducing blood pressure Figure The three principles of blood-pressure-lowering treatment for CKD patients are: 1 achieving the target of blood pressure control, 2 suppressing the RA system and 3 reducing or, if possible, normalizing urinary albumin and protein excretion.

The higher the blood pressure, the higher the rate of decline in renal function; therefore, management of blood pressure is extremely important for inhibiting the decline in renal function.

Although RA system inhibitors reduce urinary albumin and protein excretion and have pressure-independent renoprotective actions, further renoprotection can be obtained by achieving a sufficient reduction in blood pressure. As they are particularly effective in patients with a high urinary protein level, ,, an ACE inhibitor or ARB should be administered, except in special cases such as those with contraindications.

Dissociation is observed between the blood-pressure-lowering doses and anti-proteinuric doses of RA system inhibitors. Added to this, a combination of an ACE inhibitor and an ARB has been suggested by meta-analysis to be more effective than either drug alone in reducing urinary albumin or protein excretion. Usually, RA system inhibitors produce gradual reductions in blood pressure, and they rarely cause a rapid decrease in blood pressure after administration.

If a rapid decline in blood pressure is observed, it may be caused by dehydration, extreme restriction of salt intake, excessive administration of a diuretic or renal artery stenosis. Measurement of home blood pressure is effective in detecting a rapid decline in blood pressure.

Advanced renal dysfunction was used to be considered a contraindication for ACE inhibitors, but their renoprotective effect is now known to be particularly notable in patients with reduced renal function.

Urinary protein not only indicates glomerular or vascular damage but is also considered to exacerbate the renal function. Indeed, decreases in urinary protein level have been reported to have a preventive effect against the progression of renal dysfunction regardless of blood pressure. For reducing urinary protein or albumin excretion, the administration of an ACE inhibitor or ARB along with strict blood pressure control is necessary, and the use of either drug at a high dose or the combination of both is also useful.

However, this decrease is a reflection of functional change rather than the progression of renal tissue damage, because the GFR returns to its previous level on discontinuing the drug. As a decrease in renal function usually becomes apparent within a few days after commencing administration, serum creatinine level should be measured before and 2 weeks 1 week if possible after the first administration.

If exacerbation of renal function is noted, its cause, such as bilateral renal artery stenosis, should be sought. An increase in the serum K level may also be observed, and its treatment comprises the concomitant use of a diuretic or administration of sodium bicarbonate.

The administration of NSAIDs should be avoided, because they exacerbate renal function and increase the serum K level. Added to this, as ACE inhibitors are excreted via the kidney, with some exceptions, their dose adjustment is necessary in patients with reduced renal function.

However, dose adjustment is mostly unnecessary for ARBs, which are excreted via the bile. In CKD patients, multiple drug combination therapy is necessary to achieve the target blood pressure. In addition, the hypotensive and antiproteinuric effects of RA system inhibitors are dependent on the body fluid volume. Therefore, management of the body fluid volume is extremely important. If the body fluid volume cannot be controlled sufficiently by salt restriction guidance, the hypotensive and antiproteinuric effects of RA system inhibitors are expected to be enhanced by the concomitant use of a diuretic.

A diuretic was used concomitantly in most patients in a clinical study that showed the renoprotective effect of RA system inhibitors. Attention to electrolyte abnormalities such as hypokalemia and dehydration is necessary in aggressive diuretic treatment.

Recently, aldosterone blockers have been reported to reduce urinary protein excretion, , but they should be administered with utmost caution to patients with renal dysfunction because of the risk of hyperkalemia. Evidence related to the renoprotective effect of long-acting Ca channel blockers is insufficient.

The usefulness of Ca channel blockers lies in their strong hypotensive effect, which is unaffected by disease type. Patients with renal dysfunction often exhibit grade II or III hypertension, and multiple drug combination therapy including a Ca channel blocker is often required to achieve the target of blood pressure control. Indeed, a combination of an ARB and a Ca channel blocker has been reported to have more favorable hypotensive and antialbuminuric effects than an increase in the dose of an ARB.

Ca channel blockers have diverse characteristics, and clinical studies reported that some Ca channel blockers showed antiproteinuric effects similar to those of ACE inhibitors. In addition, because of problems such as the timing of measurements, as blood pressure differs before and after dialysis, insufficient evidence has been obtained regarding blood pressure control in dialysis patients.

Recently, the usefulness of ABPM and home blood pressure has been suggested. An increase in pulse pressure is correlated with a poor outcome in dialysis patients, and the outcome is poorer as the diastolic pressure becomes lower at the same systolic pressure, and as systolic blood pressure becomes higher at the same diastolic pressure. As for the therapeutic approach, volume-dependent components of blood pressure should be controlled first.