Common side effects include: low blood pressure, cough, hyperkalemia, headache, dizziness, fatigue, nausea, and kidney impairment. The main adverse effects of<unk>  inhibition can be understood from their pharmacological action. The other reported adverse effects are liver problems and effects on the fetus. Kidney problems may occur with all<unk> s that directly follows from their mechanism of action. Patients starting on an<unk>  usually have a modest reduction in glomerular filtration rate (GFR). However, the decrease may be significant in conditions of pre-existing decreased renal perfusions, such as renal artery stenosis, heart failure, polycystic kidney disease, or volume depletion. In these patients, the maintenance of GFR depends on angiotensin-II-dependent efferent vasomotor tone. Therefore, renal function should be closely monitored over the first few days after initiation of treatment with<unk>  in patients with decreased renal perfusion. A moderate reduction in renal function, no greater than 30% rise in serum creatinine, that is stabilized after a week of treatment is deemed acceptable as part of the therapeutic effect, providing the residual renal function is sufficient. Reduced GFR is especially a problem if the patient is concomitantly taking an NSAID and a diuretic. When the three drugs are taken together, the risk of developing renal failure is significantly increased. High blood potassium is another possible complication of treatment with an<unk>  due to its effect on aldosterone. Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the excretion of potassium,<unk> s can cause retention of potassium. Some people, however, can continue to lose potassium while on an<unk> . Hyperkalemia may decrease the velocity of impulse conduction in the nerves and muscles, including cardiac tissues. This leads to cardiac dysfunction and neuromuscular consequences, such as muscle weakness, paresthesia, nausea, diarrhea, and others. Close monitoring of potassium levels is required in patients receiving treatment with<unk> s who are at risk of hyperkalemia. Another possible adverse effect specific for<unk> s, but not for other RAAS blockers, is an increase in bradykinin level. A persistent dry cough is a relatively common adverse effect believed to be associated with the increases in bradykinin levels produced by<unk> s, although the role of bradykinin in producing these symptoms has been disputed. Many cases of cough in people on<unk> s may not be from the medication itself, however. People who experience this cough are often switched to angiotensin II receptor antagonists. Some (0.7%) develop angioedema due to increased bradykinin levels. A genetic predisposition may exist. A severe rare allergic reaction can affect the bowel wall and secondarily cause abdominal pain. Blood Hematologic effects, such as neutropenia, agranulocytosis and other blood dyscrasias, have occurred during therapy with<unk> s, especially in people with additional risk factors. Pregnancy In pregnant women,<unk> s taken during all the trimesters have been reported to cause congenital malformations, stillbirths, and neonatal deaths. Commonly reported fetal abnormalities include hypotension, renal dysplasia, anuria/oliguria, oligohydramnios, intrauterine growth retardation, pulmonary hypoplasia, patent ductus arteriosus, and incomplete ossification of the skull. Overall, about half of newborns exposed to<unk> s are adversely affected, leading to birth defects.<unk> s are ADEC pregnancy category D and should be avoided in women who are likely to become pregnant. In the U.S.,<unk> s must be labeled with a boxed warning concerning the risk of birth defects when taken during the second and third trimester. Their use in the first trimester is also associated with a risk of major congenital malformations, particularly affecting the cardiovascular and central nervous systems.
ACE inhibitor
Calcium channel blocker
Beta blocker
Angiotensin II receptor blocker
Lipase inhibitors
Antiplatelet drug
SGLT2 inhibitor
Potassium binder