Ambulatory blood pressure monitoring can be especially useful for spotting night-time increased blood pressure. If this type of monitoring is not suitable for you, your doctor might offer to lend you a blood pressure machine so you can take your own readings throughout the day. This is called home blood pressure monitoring.
This is to check for other problems that high blood pressure can cause. Your doctor will also calculate your risk of having cardiovascular problems and explain this to you. Some experts recommend a lower target than this e. Your doctor will recommend the best target for you.
Your doctor will suggest lifestyle changes and medications to bring your blood pressure below this target. Taking the steps below can help to lower your blood pressure and reduce your risk of having a cardiovascular problem :. If you have high blood pressure and ADPKD, your doctor should discuss options for medication with you.
Medications to reduce blood pressure are known as antihypertensive drugs. However, some people are advised to take more than one. Your doctor will probably recommend an angiotensin-converting enzyme ACE inhibitor or angiotensin-II receptor blocker ARB , unless there is a reason you cannot take these. A common side effect of these medicines is that your blood pressure may become too low. This is called hypotension and can make you feel dizzy or tired. Some people get a persistent dry cough with ACE inhibitors.
Other side effects are less common — ask your doctor for more information to help you decide which medication might be best for you. Other medicines sometimes used to reduce blood pressure are calcium channel blockers and diuretics.
If your ACE inhibitor or ARB is not controlling your blood pressure sufficiently, your doctor may suggest adding one of these medications. If you have any side effects, talk to your doctor.
There are many medications to lower blood pressure, so work together with your doctor to find the right one for you. These medicines work by reducing the amount or action of a hormone in your body called angiotensin II.
This hormone can increase blood pressure. If your blood pressure is not well controlled, your doctor can recommend different or additional medications for you. Some people like to check their blood pressure themselves.
While you should not rely on this instead of having checks with your doctor, it can be helpful to put your mind at ease. Your kidney specialist or GP might suggest home monitoring, and some chemists offer free blood pressure checks.
To find your nearest chemist offering this service, go to bloodpressureuk. Alternatively, you could consider buying your own approved blood pressure monitor. ADPKD can increase blood pressure in two main ways: 1 by altering the lining of your blood vessels, and 2 by activating hormones that control blood pressure.
Narrower vessels mean the blood has less room to flow, increasing blood pressure. You could think of it like a motorway where a lane has been closed — the traffic becomes busier as it fights for space. In this study, MSNA was found to correlate closely with mean arterial pressure [ 27 ]. Hypertension is the most treatable associated feature of ADPKD, and the medical community has been increasingly proactive in enhancing patient and physician awareness about the importance of BP control.
Given the risk that hypertension confers for progression to renal failure in ADPKD and that cardiovascular causes are still the most common cause of death in this disorder, these are remarkable accomplishments.
As in the general hypertensive population, diet and lifestyle changes should be the first-line treatments for hypertensive ADPKD patients. Salt restriction may be of particular importance, since a positive correlation between urinary sodium excretion a surrogate marker of sodium intake and total kidney volume [but not the decline in estimated glomerular filtration rate eGFR ] was shown in participants in the CRISP cohort.
The discrepancy between the effect on cyst growth and kidney function may be due to the lag time between structural and functional changes in ADPKD and may become apparent with a longer follow-up [ 48 ]. In the absence of an adequate response to these lifestyle modifications, pharmacotherapy should be started.
The hypothetical benefits of high water intake to delay cyst growth by suppressing antidiuretic hormone ADH and cAMP pathway have been suggested by animal models and small size human studies [ 49 , 50 ]. The recommended use of ACE-I in ADPKD as a first-line antihypertensive therapy is based on the understanding of the pathophysiology of hypertension in this disease and also on limited evidence from clinical trials.
However, enalapril, but not amlodipine, had a consistent antiproteinuric effect [ 23 ]. A larger meta-analysis of eight clinical trials by Jafar et al.
A retrospective analysis of a longitudinal cohort of ADPKD patients comparing the renal outcomes of 33 patients 14 patients on a diuretic and 19 patients on an ACE inhibitor showed a similar BP control over a mean follow-up period of 5. However, the annual decline in creatinine clearance was significantly greater in the diuretic group 5. Additionally, urinary protein excretion was significantly increased in the diuretic, but not in the ACE-inhibitor, group [ 52 ].
Given that the hypertension in ADPKD is due to bilateral intrarenal ischemia, particular attention should be paid to the risk of acute renal failure after initiation of ACE-I. This complication is primarily seen in patients with underlying renal insufficiency, massive cystic disease, concomitant diuretic use or acute cyst hemorrhage. Finally, it should be noted that enalapril did not show any significant effect on the rate of kidney disease progression in 61 normotensive ADPKD patients who were enrolled in a placebo-controlled, randomized clinical trial over a 3-year follow-up period [ 55 ].
Whether normotensive ADPKD patients should be on any antihypertensive therapy is not clear at this time. To date, there is only one randomized trial comparing the effect of candesartan versus amlodipine in 49 hypertensive ADPKD patients [ 56 ]. Additionally, although ARB therapy prevents the action of angiotensin II in systemic and renal circulations by binding to the angiotensin II Type 1 receptor, angiotensin II levels increase with chronic ARB therapy and exogenous angiotensin II responses are also not totally suppressed [ 57 , 58 ].
The follow-up for both studies is 6—9 years. Decisions for dose titration and addition of new agents are based on home BP monitoring.
Another study of 28 hypertensive ADPKD patients randomized to atenolol or enalapril showed that patients randomized to atenolol needed additional agents more often than patients on enalapril.
However, the study did not show any difference between the two interventions on the rate of decline of kidney function or microalbuminuria [ 55 ]. As mentioned earlier, amlodipine a dihydropyridine calcium-channel blocker has been shown to be as effective as enalapril in controlling BP in ADPKD patients.
The authors concluded that the use of CCBs should be avoided as a first-line treatment in ADPKD unless treatment of resistant hypertension is needed [ 61 ]. The use of the target organ benefits of amlodipine may also differ from ACE-I, where improvement of LVH and reduction in urinary protein excretion are not as apparent.
Therefore, this class of agent is an effective line of antihypertensive therapy but should be used after other blockers of the RAAS have been implemented. The amount of urinary protein excretion was increased in the patients treated with diuretics, which was not present in the ACE inhibitor group. The preliminary data on the beneficial role of amiloride on reduction of cyst growth in MDCK cysts have not been replicated in human studies. The study was limited by not including patients with conserved renal function and a short follow-up duration 2.
If needed, hydrochlorothiazide, clonidine, spironolactone or a combination of agents were used as additional lines of treatment.
Throughout the 7 years of study, substantial BP separation was obtained, with mean BP of 90 and mmHg for the rigorous and standard BP control groups, respectively. Final results are expected in November All ADPKD females of child-bearing age should be educated about the chances of transmitting the disease to their offspring and also about the teratogenicity and maternal and fetal harms associated with the use of antihypertensive agents particularly inhibitors of the RAAS at the time of initiation of therapy.
These risks include oligohydramnios, skull hypoplasia, cardiovascular congenital defects, anuria, real failure and death for the fetus and maternal acute kidney injury particularly during the late stages of pregnancy. If possible, family planning should be started after stopping the blockers of the RAAS and introducing antihypertensive agents with the best pregnancy safety profiles Aldomet or Labetalol.
If oliguria occurs, attention should be directed toward support of BP and renal perfusion. Lactation and breastfeeding also constitute a contraindication to the use of ACE-Is since those agents may be excreted in the maternal milk. Because no human information is available on the use of ARBS during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant. The US Food and Drug Administration has approved several ACE-Is and ARBs for treatment of hypertension and multiple observational and randomized clinical trials have concluded on the safety and efficacy of these agents in children older than 6 years of age [ 65 ].
As an example, lisinopril and losartan can be used at respective doses of 0. The data for children younger than 6 years of age are scattered. A recently published report from the California poison control system on patients exposed to Lisinopril in a year-long study, showed a low rate of true hypotensive episodes 2. Hypertension is extremely common, a significant cardiovascular risk factor and a risk factor for progression to renal failure in ADPKD.
It is a treatable complication in PKD and may be due to a primary vasculopathy in this condition. Defects in primary cilium causing endothelial dysfunction and the activation of the RAAS are central pathophysiologic explanation for development of hypertension in ADPKD.
Treatment of hypertension effectively reduces cardiovascular mortality and may also slow down the progression of kidney disease. After implementing diet and lifestyle modification strategies and in the absence of contraindications, an ACE inhibitor should be the initial antihypertensive agent in this population.
Careful monitoring of renal function and serum potassium levels is indicated after institution of an ACE inhibitor. Their use may be particularly useful in hypertensive ADPKD patients with significant elevations in serum creatinine concentrations, concomitant cardiac disease and intolerance to both ACE inhibitors and ARBs.
Diuretics should only be considered in conjunction with inhibitors of the RAAS and under careful monitoring of serum creatinine, particularly in patients with advanced renal insufficiency where the risk of acute deterioration of kidney function on the combination therapy with a diuretic is higher. The results of ongoing randomized clinical trials such as HALT-PKD trials ending in will establish whether a more aggressive BP target is beneficial in this population.
Chapman is a consultant to Otsuka on Tolvaptan, and also a consultant to Pfizer and Sanofi. Google Scholar. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract.
Mechanisms and management of hypertension in autosomal dominant polycystic kidney disease. Department of Medicine.
Correspondence and offprint requests to: Arlene Chapman; E-mail: abchapm emory. Oxford Academic. Olubunmi Williams. Genes can also determine the likelihood of developing a disease. A genetic disease can happen if one or both parents pass abnormal genes to a child. This happens through something called dominant inheritance or recessive inheritance.
If one parent has the disease and passes an abnormal gene to the child, it is called dominant inheritance. The risk is the same for every child, regardless of how many children develop the disease. If both parents carry the abnormal gene, and both parents pass an abnormal gene to the child, it is called recessive inheritance. This form of the disease is passed from parent to child by dominant inheritance. In other words, only one copy of the abnormal gene is needed to cause the disease.
Symptoms usually begin between the ages of 30 and 40, but they can begin earlier, even in childhood. This form of the disease is passed from parent to child by recessive inheritance. Symptoms can begin in the earliest months of life, even in the womb. It tends to be very serious, progresses rapidly, and is often fatal in the first few months of life. It occurs in 1 out of 25, people. ACKD can happen in kidneys with long-term damage and severe scarring, so it is often associated with kidney failure and dialysis.
About 90 percent of people on dialysis for 5 years develop ACKD. People with ACKD usually seek help because they notice blood in their urine. This is because the cysts bleed into the urinary system, which discolors urine.
Should people with PKD have children? Individuals with PKD who are concerned about passing the disease to their children may want to consult a genetics counselor to help them with family planning. Many university medical centers have this service. Most of the women with PKD 80 percent have successful and uneventful pregnancies.
However, some women with PKD have an increased risk for serious complications for themselves and their babies. This includes women with PKD who also have:. Women who have PKD with high blood pressure develop pre-eclampsia or toxemia in 40 percent of pregnancies. This is a life-threatening disorder for both the mother and baby, and it can develop suddenly and without warning.
Therefore, all women with PKD, particularly those who also have high blood pressure, should be followed closely during their pregnancy by their doctor.
If you have more questions, you should speak to your doctor. You can also get more information from:. Skip to main content. Polycystic Kidney Disease. What is polycystic kidney disease? How common is PKD? What other organs besides the kidney are affected by PKD? What are the clues that someone has PKD?
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