Post-transplant hypertension is common in patients after renal transplantation, with prevalence rates ranging from approximately 50% to 80% in adults and 47% to 82% in children. If hypertension is not well controlled, it can lead to cardiovascular complications and shorten the survival of the transplanted kidney. Therefore, the management of post-transplant hypertension is one of the major challenges that kidney transplant patients need to face after surgery. Epidemiological studies of post-transplant hypertension Based on the results of available epidemiological studies, the risk factors for post-transplant hypertension are initially summarized as follows: pre-transplant hypertension, obesity, males, African-Americans, and renal source being elderly. Risk factors specific to transplantation include delayed recovery of renal function, use of calmodulin phosphatase inhibitors (CNIs) and glucocorticoids, recurrent exacerbations of the condition, acute rejection, and post-transplant proteinuria. Although it is generally recognized that hypertension adversely affects the post-transplant kidney, exactly whether hypertension accelerates the rate of graft renal failure is difficult to assess, as both hypertension and renal failure are mutually reinforcing. Diagnosis of post-transplant hypertension Major epidemiologic and clinical trials have used blood pressure data measured in hospitals to determine whether a patient has hypertension. However, these data do not actually fully reflect the changes in a patient’s blood pressure. Many patients suffer from white coat hypertension and occult hypertension, and hospital-measured blood pressure can be misleading in our diagnosis. A study was conducted to compare the results of ambulatory blood pressure monitoring (ABPM), home blood pressure monitoring (HBPM), and hospital blood pressure monitoring (CBP) in post-transplant patients. The results showed that the results of ambulatory blood pressure monitoring were superior to those of hospital blood pressure monitoring. Therefore, in order to better prevent the occurrence of cardiovascular and cerebrovascular events, patients should be more recommended to use the method of ambulatory blood pressure monitoring to monitor their blood pressure, which is an important guideline for the management of renal transplant patients. Pathophysiologic factors of post-transplant hypertension 1, Donor factors Post-transplant hypertension is likely to be related to the donor’s older age, suffering from hypertension, and poor renal quality, and also to the difference in the size of the transplanted recipient’s and donor’s kidneys, which can result in poor filtration of the renal units, leading to intraglomerular hypertonicity and even glomerular hypertrophy. 2.Recipient factors Post-transplant hypertension is also closely related to the recipient itself. Many patients suffer from hypertension for a long time before receiving transplantation, which will lead to their vascular sclerosis, thus accelerating the progress of post-transplant hypertension. Alternatively, recipients who are older, physically obese, suffer from obstructive sleep apnea syndrome, or have certain endocrine tumors (e.g., pheochromocytomas, adrenal adenomas) can also have an effect on post-transplant hypertension. The main cause of post-transplantation secondary hypertension is renal artery stenosis, with a prevalence of about 1% to 23%, mostly related to the anastomotic stenosis of the renal arteries after transplantation, rejection reaction, atherosclerosis and so on. Clinical manifestations may include hypertension, hypokalemia, secondary aldosteronism, decreased renal function, and decreased perfusion pressure of the transplanted kidney. Regarding the detection of renal artery stenosis, renal artery color Doppler is the first choice, and if it cannot be determined, CT or angiography can be continued. If medical treatment fails, percutaneous angioplasty is the treatment of choice. Primary aldosteronism is also a common cause of secondary hypertension. Severe hypertension with hypokalemia should be suspected first in patients presenting with severe hypertension, especially if they have been treated with ACEIs and ARBs. Primary aldosteronism and obstructive sleep apnea syndrome are an independent risk factor for pulmonary hypertension and should be taken seriously. Acute and chronic rejection, recurrent renal disease, and posttransplant hypertension Common causes of posttransplant hypertension include acute immune response, chronic graft injury (chronic rejection, interstitial fibrosis, and tubular atrophy), microvascular thrombosis, and recurrent renal disease. Acute rejection stimulates the patient’s renin-angiotensin system, releasing renin and vasoconstrictor substances, causing vasoconstriction and leading to hypertension. Chronic graft injury combined with hypertension is similar to chronic renal failure combined with hypertension and requires long-term treatment. Focal glomerulosclerosis is the type of relapsing disease most frequently reported to be associated with worsening hypertension. Immunosuppressive Drugs and Posttransplant Hypertension Drugs that suppress rejection after transplantation can also cause an increase in blood pressure, such as glucocorticoids and immunosuppressive drugs. Glucocorticoids cause sodium and water retention through their action on aldosterone, thereby increasing blood pressure. Cyclosporin A causes constriction of the renal vasculature, especially the small glomerular entry arteries, which increases renal vascular resistance, and also enhances vascular sensitivity to natriuresis and activation of sympathetic nerve activity, etc. All of these changes lead to an increase in blood pressure. Given that the risk of acute rejection is much greater than the risk of poor blood pressure control, we should control blood pressure in a safer way than adjusting the dose of immunosuppressive drugs. Pharmacologic strategy for post-transplant hypertension Regarding the goal of blood pressure control in post-transplant patients, maintaining as low a blood pressure as possible (<140/90 mmHg) is beneficial in prolonging the life of the transplanted kidney. Ideally, thiazide diuretics and medullary diuretics can be applied should maintain the ideal volume load of the patient, and the patient should be given a low dose of glucocorticoids to prevent immune damage. Antihypertensive drugs can be chosen from beta-blockers and calcium channel blockers (CCBs) as needed, whereas ACEIs and ARBs should be avoided in the early post-transplant period because they affect renal hemodynamics and potassium homeostasis. Non-pharmacological treatment is also very important and patients are advised to increase exercise, control weight, stop smoking and eat a low salt diet. A study comparing an experimental group on a sodium-restricted diet of 80-100 mmol/day with a control group on an unrestricted diet showed that after three months the blood pressure in the Na-restricted group was under some control compared to the control group, and the results were statistically significant. Pharmacologic Principles of Drugs for Post-Transplant Hypertension Treatment For the general population, conventional antihypertensive drugs do not burden their renal function and the risk of medical sequelae is much smaller. For kidney transplant patients, on the other hand, the pharmacokinetics of the drugs are somewhat altered, and the risk of using antihypertensive drugs is much greater. Antihypertensive drugs and food can interact with each other, grapefruit is one of our favorite fruits, but you can't eat grapefruit when taking antihypertensive drugs. Because grapefruit can calcium antagonist binding, enhance the effect of calcium antagonists, so that the blood concentration of the drug greatly increased. The most prominent is felodipine, bioavailability will be doubled, amlodipine and nifedipine and non-dihydropyridine CCB because of its own bioavailability is better, so it is less affected, only 20% to 30% increase. Cytochrome P450 (cytochromeP450 or CYP450, for short) is a multifunctional oxidoreductase among the pharmacological enzymes. The P450 enzyme system of antihypertensive drugs has both inducible and inhibitory properties, and many chemicals can induce or inhibit the P450 enzyme, thus affecting the therapeutic efficacy and adverse effects of drugs. Drugs that can induce P450 include rifampicin, phenobarbital, etc., which can cause shortening of the duration of action or therapeutic failure at normal therapeutic doses. Inhibitors of P450 include verapamil and diltiazem, which may result in prolonged duration of action and increased adverse effects. The interaction of verapamil and deltamethasone with cytochrome P450 can be applied clinically to reduce the dose of antihypertensive drugs. Antihypertensive drugs can be used in conjunction with other drugs, such as: discretionary addition of diuretics on the basis of the original antihypertensive drugs can enhance the effect of antihypertensive drugs. Antihypertensive drugs can be used in conjunction with antihypertensive drugs that accelerate the heart rate. We should systematically evaluate the various factors that affect the pharmacodynamics and pharmacokinetics of antihypertensive drugs and use them as the basis for further improving and adjusting the antihypertensive treatment program for renal transplant patients. Hypertension in pediatric post-transplant patients Hypertension is the most common traditional risk factor for cardiovascular events in children after renal transplantation, and comprehensive reports from all over the world have shown that the prevalence of hypertension in children after renal transplantation is about 47% to 80%, with a large proportion of them belonging to the categories of refractory hypertension and insidious hypertension. In children after renal transplantation, blood pressure is an independent risk factor affecting the duration of kidney survival after transplantation. Children and young adults have a high prevalence of cardiovascular disease after renal transplantation, and hypertension has been shown to cause structural changes in the heart and is an early marker of cardiovascular disease. It has been reported that the most common cardiac structural change in children after renal transplantation is left ventricular hypertrophy, with a prevalence of left ventricular hypertrophy of approximately 40% at 1 year after transplantation. Children after transplantation also have increased carotid artery intima-media thickness, which is an early sign of atherosclerosis. In a study in which investigators performed biannual carotid ultrasound and echocardiography in renal transplant recipients, it is important to note that at the last visit, blood pressure was well controlled in 82% of the patients, the prevalence of left ventricular hypertrophy was only 4.5%, and the carotid intima-media thickness did not worsen over time. We therefore speculate that the cessation of carotid intima-media thickness progression and the reduction of left ventricular hypertrophy may be related to good blood pressure control. Ideal blood pressure differs between children and adults, and renal transplanted children should be maintained as close as possible to the 90th percentile for their age, sex, and height, with ACEIs and ARBs preferred for antihypertensive medications if significant proteinuria is present.Long-term use of an ABMP is recommended for monitoring blood pressure to prevent fluctuations in blood pressure caused by refractory hypertension and nocturnal paroxysmal hypertension.The use of ABMPs is recommended for children and adolescents, as well as for adults and adults. In conclusion, there is enough evidence to prove the benefit of aggressive blood pressure control for the survival of transplanted kidneys in both adults and children. The next step, however, is to individually refine the goals of blood pressure reduction in kidney transplant patients. For secondary hypertension, such as that caused by aldosteronism and sleep apnea syndrome, more clinical trials are needed to determine optimal blood pressure control goals and treatments.