Renal blood flow, characterized by excretory function, is about 20% of cardiac output, and the kidneys are frequently exposed to high concentrations of drugs through the processes of glomerular ultrafiltration and tubular concentration, and a wide range of drugs in the body can cause functional or organic renal damage. In a multicenter clinical study, the risk of kidney disease in patients taking long-term oral cyclooxygenase inhibitors was 2.1 times higher than in the general population. Symptoms of renal toxicity from cyclooxygenase inhibitors include edema, hypertension, elevated blood inosine, and elevated lipids. Both selective and non-selective NSAIDs can cause edema and hypertension. In severe cases cyclooxygenase inhibitor renal toxicity can lead to renal ischemia or failure, nephrotic syndrome, interstitial nephritis, renal papillary necrosis, and renal stones. Renal failure due to analgesic nephropathy manifests itself in 6% of all patients with renal failure, 16% of drug-induced acute renal failure and 3% of all acute renal failure, and 30% of end-stage renal failure. Comparatively, sulindac and bis-salicylate have fewer renal side effects than other cyclooxygenase inhibitors. Sulindac may be a safe alternative to other cyclooxygenase inhibitors in patients with mildly impaired renal function when renal blood flow and glomerular filtration rate are dependent on prostaglandin production. In the absence of clear risk factors present, cyclooxygenase inhibitors have fewer renal side effects. Cyclooxygenase inhibitors are more likely to cause renal damage in certain vulnerable populations or in the presence of risk factors such as pediatrics, the elderly, renal insufficiency, hypertension, cardiac insufficiency, cirrhosis, nephrotic syndrome, glomerulonephritis, combination of other renal-damaging medications and potassium-preserving diuretics, or when cyclooxygenase inhibitors are used in excessive dosages or in combination with multiple medications. In the presence of renal risk factors, the side effects of all cyclooxygenase inhibitors are similar, the superiority of sulforaphane and bis(salicylate) does not stand out, and all cyclooxygenase inhibitors should be avoided. The key to preventing cyclooxygenase inhibitor renal damage is to avoid the misuse of cyclooxygenase inhibitors, especially in patients with risk factors, try to use non-cyclooxygenase inhibitor analgesics, and when they have to be used, they should be used with less renal damage or selective cyclooxygenase-2 inhibitors, and appropriately reduce the dosage to avoid the use of combination drugs. Cyclooxygenase inhibitor renal damage is generally reversible, early detection and timely treatment, its prognosis is generally better. Renal function, urine routine and water electrolytes should be checked during treatment, and the drug should be stopped immediately once creatinine clearance decreases. Those with chronic renal failure should be treated with dialysis. Risk factors for cardiovascular damage with cyclooxygenase inhibitors Selective COX-2 inhibitors significantly reduce gastrointestinal side effects, and their use has been on the rise since they were introduced into clinical practice in the 1990s. However, cardiovascular events such as hypertension, coronary heart disease, and myocardial infarction have been of concern since 2002, when some patients were found to be suffering from hypertension, coronary heart disease, and myocardial infarction following the use of COX-2 inhibitors. 2004 adenomatous polyp prophylaxis clinical trial showed a 2-fold increase in the number of myocardial infarction and stroke events associated with the administration of Merck’s Vanlope (rofecoxib), which forced Merck to discontinue Vanlope on September 30, 2004, and Merck suffered a significant loss. Merck & Co. suffered significant losses. Large clinical trials have shown that cardiovascular and cerebrovascular events associated with selective COX-2 inhibitors are related to daily dose and duration of therapy. The use of selective COX-2 inhibitors at high doses and over long periods of time significantly increased the incidence of cardiovascular and cerebrovascular adverse events. It is currently believed that both conventional cyclooxygenase inhibitors and selective COX-2 inhibitors increase cardiovascular and cerebrovascular adverse events (e.g., thrombotic events, hypertension, MI, CHF, and severe coronary artery disease), and that the increase in cardiovascular and cerebrovascular adverse events is a class effect of cyclooxygenase inhibitors. Among the cyclooxygenase inhibitors, naproxen may have the lowest risk of causing cardiovascular events. The greater the inhibition of COX-1, the fewer the cardiovascular and cerebrovascular adverse events but the more the upper gastrointestinal tract adverse events; the greater the inhibition of COX-2, the fewer the upper gastrointestinal tract adverse events but the more the cardiovascular and cerebrovascular adverse events. Selective COX-2 inhibitors inhibit prostaglandins but not thromboxanes, thus leading to an imbalance between prothrombotic and antithrombotic effects and procoagulation. By decreasing the production of the dilating PGI2, selective COX-2 inhibitors tip the balance in favor of prothromboticism and may increase the incidence of thrombotic events in the cardiovascular system. The use of cyclooxygenase inhibitors can cause symptoms such as heart failure in some patients, particularly in those with a history of cardiovascular disease and impaired left ventricular function. In patients with cardiovascular risk factors such as ischemic heart disease or stroke, hypertension, hyperlipidemia, diabetes mellitus, or peripheral arterial disease, the use of NSAIDs should be avoided in patients with selective COX-2 inhibitors, even though the combination of selective COX-2 inhibitors and aspirin does not reduce the rate of cardiovascular and cerebrovascular adverse events, and naproxen may be one of the better choices. Caution is warranted in the use of ibuprofen because it weakens the antiplatelet effect of aspirin. Caution should be exercised in selecting drug therapy for patients with cardiovascular disease predisposing factors. Cyclooxygenase inhibitors can sometimes raise blood pressure in people with normal blood pressure and can antagonize many hypertensive medications resulting in poor blood pressure control, especially in the elderly who buy pain medications over the counter and have difficulty controlling their high blood pressure. Cyclooxygenase inhibitors affect the blood pressure-lowering effects of almost all hypertension medications, including diuretics (e.g., dihydroclonidine), beta-blockers (e.g., Betalucil), alpha-blockers (e.g., Doxaben), and vasoconverting enzyme inhibitors (e.g., captopril). The effects of cyclooxygenase inhibitors are variable and may be related to the type and dose of the drug, with non-selective cyclooxygenase inhibitors having the following order of severity of effect: piroxicam > anti-inflammatory pain > ibuprofen > diclofenac > naproxen > flurbiprofen > sulbutamic acid. In patients on antihypertensive therapy, sulindac is the most appropriate anti-inflammatory agent because, unlike other cyclooxygenase inhibitors, it rarely interacts with antihypertensive drugs. There is no evidence that celecoxib is associated with the development of hypertension, and rofecoxib significantly increases the risk of developing hypertension, which is twice as high in patients taking rofecoxib as in those taking celecoxib in patients with chronic kidney disease, liver disease, and congestive heart failure. The increase in blood pressure caused by the combination of cyclooxygenase inhibitors and vascular converting enzyme inhibitors is the most pronounced of all antihypertensive medications. For example, anti-inflammatory pain reduces the antihypertensive effect of enalapril by up to 45%, and patients with hypertension who are taking vascular converting enzyme inhibitors should be especially careful when using cyclooxygenase inhibitors. Combining cyclooxygenase inhibitors with calcium ion blockers is safe.