1. Do you have to use antihypertensive drugs when you suffer from kidney disease? There are some patients suffering from kidney disease often ask: how they are taking antihypertensive drugs, and I do not have to take it? The reason is simple, because your blood pressure is not high. Renal hypertension has a certain mechanism in its development, and only by understanding the mechanism of its development can we explain how to apply antihypertensive drugs. General renal hypertension is due to elevated blood pressure caused by renal parenchymal lesions and renal artery lesions, which is called renal hypertension in symptomatic hypertension. Its pathogenesis and pathological features: First, the pathological features of renal parenchymal disease are manifested as glomerular vitelliform degeneration, mesangial and connective tissue proliferation, tubular atrophy, and narrowing of renal fine arterioles, resulting in both substantial damage and insufficient blood supply to the kidneys. Secondly, the middle layer of the renal artery wall is proliferating with mucinous muscle fibers, forming most of the small aneurysms, making the inner wall of the small renal arteries protrude in a bead-like manner, resulting in segmental stenosis of the renal arteries. Thirdly, it is non-specific aortitis, which causes insufficient perfusion of renal blood flow. Volume-dependent hypertension: approximately 90% of renal parenchymal hypertension is due to sodium and water retention and blood volume expansion. When renal parenchymal lesions cause the kidneys to lose the ability to excrete the appropriate (not excessive) amount of water and salt contained in the diet, this causes water and sodium retention in the body, which in turn causes excessive blood volume causing hypertension. This mechanism occurs whenever mild renal insufficiency is present. Plasma renin and angiotensin II (AII) levels are usually low in these patients. Their hypertension can be lowered by restricting water and salt intake or by removing excess water and salt from the body through dialysis. Renin-dependent hypertension: renal artery stenosis and 10% of renal essential hypertension are due to elevated renin-angiotensin-aldosterone. Diuresis and dehydration not only can not control this kind of hypertension, but also often due to diuresis and dehydration after the decline in renal blood flow leads to increased renin secretion, resulting in higher blood pressure. The application of the angiotensin antagonist saralasin can lead to a dramatic decrease in this type of hypertension, indicating that the renin-angiotensin system plays a major role in the pathogenesis of this type of hypertension. Non-pharmacological treatment: This includes the promotion of a healthy lifestyle and the elimination of behaviors and habits that are detrimental to mental and physical health, in order to achieve a reduction in the risk of hypertension and other cardiovascular diseases. Adjustment of lifestyle habits, smoking cessation, moderation of alcohol consumption, correct treatment of environmental stress, and maintaining a normal state of mind. For patients undergoing dialysis for end-stage renal failure, the first step is to adjust water and salt intake to achieve ideal dry weight. Pay attention to low sodium and low fat. Low sodium can not only effectively control sodium and water retention, but also increase the antihypertensive effect of ACEI and calcium channel blocker (CCB). If you belong to the volume-dependent hypertension, then through the above introduction of non-pharmacological treatment methods can be very good control of blood pressure. 2.Why are ACEIs preferred for antihypertensive drugs? Antihypertensive drugs to block the renin-angiotensin system (RAS) as the preferred method. Currently, there are two major classes of RAS-blocking drugs used in clinical practice: ACEI and Ang II receptor antagonists. The principle of medication should be to avoid renal damaging drugs, start at a low dose, and use a combination of drugs. ACEI can block the generation of angiotensin II, reduce aldosterone synthesis, from reducing vascular resistance and blood volume to reduce systemic blood pressure; in addition, ACEI can also act on the renal tissues of the local RAS system, dilate the glomerular outflow and inlet arterioles, and dilate the glomerular outflow arterioles is stronger than the inlet arterioles, to improve the high transmembrane pressure in the glomerulus, high filtration and high perfusion phenomenon, to delay the process of renal damage; to improve the kidney, and to improve the renal function. It can improve the high transmembrane pressure, high filtration and high perfusion phenomenon in the glomerulus, slow down the process of renal damage; improve the permeability of the glomerular filtration membrane to albumin, and reduce the urinary protein; reduce the accumulation of glomerular extracellular matrix, and alleviate the glomerulosclerosis. At present, it is believed that ACEI has the most certain effect of protecting the kidney among antihypertensive drugs, and the commonly used ACEIs are captopril, enalapril, benazepril, ramipril, fosinopril and so on. Based on the above mechanism, so it is recommended that ACEI antihypertensive drugs as the first choice of therapeutic drugs. 3.Can I take ACEI antihypertensive drugs orally all the time? The use of ACEI should start with a small dose and gradually increase the dosage to control the blood pressure in a satisfactory range. (1)It is generally believed that serum creatinine (Scr) 265μmol/L or less can be used safely, if the increase of Scr after using the drug is not more than 50%, and can be recovered within 2 weeks without stopping the drug, then it is a normal reaction; if the increase of Scr is more than 50% or the absolute value of Scr is more than l33μmol/L, and the drug has not been decreased for 2 weeks, then it is an abnormal reaction, and the drug should be discontinued. (2)Among them, benazepril has strong permeability to renal tissues, and metabolites are partially excreted through bile, and the dosage needs to be reduced only when creatinine clearance (Ccr) is <30 ml/min; while fosinopril has the largest proportion of bile excretion of all ACE1 drugs, and the dosage does not need to be adjusted even if renal function decreases. (3) Elderly patients may have renal artery atherosclerosis, ACEI antihypertensive will be particularly sensitive. The use of ACEI in patients with bilateral renal artery stenosis and isolated renal artery stenosis may lead to acute renal failure and should be contraindicated. (4) Patients with end-stage renal disease (ESRD) have more side effects of ACEI, such as hyperkalemia, neutropenia, allergic reactions, chronic cough, renal impairment, etc. ACEI and EPO may affect the efficacy of EPO, and it is recommended to increase the dose of EPO. Therefore, ACEI antihypertensive drugs are not all-powerful, and not once and for all, master the above characteristics, for the use of medication is beneficial. 4, ACEI antihypertensive drugs and ARB antihypertensive drugs the same? ACEI can block the generation of angiotensin II, reduce aldosterone synthesis, from reducing vascular resistance and blood volume to reduce systemic blood pressure. Angiotensin II receptor antagonist (ARB) class: it has a highly selective blockade of ATl and increase AT2 effect; from the mechanism of action, the two action targets are not the same, but the purpose of the action is the same.ARB class is applicable to and prohibited by the same objects as ACEI. Different from ACEI, ARB class hyperkalemia and low incidence of cough, does not reduce renal blood flow, its efficacy is not affected by ACE gene polymorphisms; can inhibit the non-ACE catalyzed Ang Ⅱ a variety of effects, part of the can also reduce blood uric acid (such as chlorthalidomide). 5.Can patients with kidney disease use diuretics? Diuretics are one of the most valuable anti-hypertensive drugs. Among them, potassium-excreting diuretics include high-efficiency labeled diuretics represented by furosemide and intermediate-acting thiazide diuretics represented by hydrochlorothiazide, which are suitable for patients with sodium retention in renal disease, high potassium, and high residual renal function, and therefore there is a tendency to hypokalemia, hyperuricemia, and hyperglycemia. The aldosterone receptor blocker represented by antithymotrypsin is a potassium-preserving diuretic, which inhibits the action of aldosterone to diuretics and also lowers blood pressure, and reduces the damage of aldosterone to the cardiovascular system, because of its potassium-preserving effect, it is used with caution in patients with renal insufficiency. Indopamine, with diuretic and calcium antagonism, especially for mild to moderate hypertension. It has a long-lasting effect, lowers blood pressure smoothly, and does not cause disorders of sugar, lipid and uric acid metabolism. From the above characteristics, different patients should be based on different characteristics to choose different classes of diuretics. 6, why some people eat Lovoxil blood pressure is very good, and I eat Lovoxil but can not control blood pressure? Lovoxil (amlodipine benzenesulfonate) belongs to the calcium antagonist (CCB) class of drugs, which is mainly through the expansion of peripheral resistance vessels and lower blood pressure, because calcium antagonists can reduce glomerular capillary pressure, reduce the deposition of macromolecules in the glomerular mesangial area, inhibit the proliferation of mesangial cells and stroma to reduce the development of glomerulosclerosis, so as to have a renoprotective effect. The main categories include non-dihydropyridines and dihydropyridines, dihydropyridines are mainly nifedipine, felodipine, amlodipine, etc. At present, it is recommended to use long-acting or extended-release preparations, and its short-acting preparations can cause large fluctuations in blood pressure, as well as disorders of glucose and lipid metabolism, and aggravation of proteinuria, which are no longer recommended for use. However, for some hemodialysis patients with obvious water and sodium retention and high blood pressure, with large fluctuations in blood pressure, it is recommended to change to short-acting antihypertensive drugs to control immediate blood pressure and combined with dialysis dehydration antihypertensive treatment. Therefore, blood pressure treatment is not the same for everyone, and antihypertensive drugs should be applied according to their respective characteristics. 7.What are the advantages of using receptor blockers for antihypertensive treatment in patients with renal disease? β-blockers can block the sympathetic nerve antihypertensive effect, the representative drugs are atenolol, metoprolol, but need to pay attention to the side effects of bradycardia, conduction block, and bronchial asthma, use with caution. a1 receptor blocker can selectively block the a1 receptor of the postsynaptic membrane of the vascular smooth muscle, so as to make the vasodilatation, resulting in the decrease of peripheral vascular resistance and the decrease of the volume of the return blood to lower blood pressure, and it has little impact on the heart rate, and it also doesn't affect the renal blood flow and glomerular filtration, and it also has no influence on the renal blood flow. It has little effect on heart rate and does not affect renal blood flow or glomerular filtration rate. Representative drugs are prazosin, terazosin and uradil, etc. α, β-blocker is a new type of antihypertensive drugs, has the ability to promote the release of nitric oxide from the endothelial cells of the glomerular capillaries, resulting in intracellular ATP outflow, thus making the glomerular microvessels relax and dilate, and improve microcirculation. For example, atenolol (Arotinolol) and carvedilol (Carvedilol), combined with calcium antagonists, not only show effective antihypertensive effects, but also effectively alleviate the further decline of renal function and the occurrence of cardiovascular complications. In addition, most of the α- and β-blockers have high protein binding rates, and dialysis patients do not need to adjust the dose or mode of administration. However, because carvedilol's blockade of β1 and β2 receptors is non-selective. Side effects on glucose metabolism and respiratory diseases should be noted. 8. Is it okay to use one antihypertensive drug for dialysis patients? The main cause of elevated blood pressure in hemodialysis patients is that about 90% of renal substantial hypertension is due to sodium and water retention and blood volume expansion. Secondly, renal artery stenosis and 10% of renal hypertension are due to elevated renin-angiotensin-aldosterone. Instead of controlling this type of hypertension, diuresis and dehydration often lead to an increase in renin secretion due to the decrease in renal blood flow after diuresis and dehydration, resulting in an increase in blood pressure. The application of the angiotensin antagonist saralasin can cause this type of hypertension to fall dramatically, indicating that the renin-angiotensin system plays a major role in the pathogenesis of W2S hypertension. Therefore, antihypertensive therapy is recommended in combination: antihypertensive drugs are usually started at a low dose, and if the blood pressure fails to reach the target, the dose of the drug should be increased according to the patient's tolerance. If the first drug is ineffective, a rational combination of drugs should be chosen, usually a small dose of a second antihypertensive drug, rather than increasing the dose of the first drug. Combination of drugs are: ACEI + diuretics; diuretics + beta blockers; beta blockers + calcium channel blockers; ACEI + calcium channel blockers; ACEI + ARB can synergize to lower blood pressure and reduce the occurrence of side effects. For hypertensive patients, antihypertensive drugs are never far from their hands, but in winter, the sphygmomanometer should also be never far from their hands. Especially for patients with unstable blood pressure, it is recommended to measure blood pressure 2 to 3 times a day to observe the change of their blood pressure in the morning, midday and evening to avoid cardiovascular and cerebrovascular accidents due to the sudden rise of blood pressure. There are many measures that can be used to regulate blood pressure in life, such as diet, emotion and so on, which have a great influence on the condition of hypertension. 9. Why some patients with renal anemia do not need to use erythropoietin? Renal anemia refers to anemia caused by various factors, such as insufficient production of erythropoietin (Epo) in the kidney or some toxins in uremic plasma interfering with the production and metabolism of erythrocytes, and it is a common complication of chronic renal insufficiency to the end stage. The degree of anemia is often related to the degree of renal decompensation. Renal anemia is a concomitant symptom of chronic kidney disease, and is often associated with renal anemia when the patient's kidneys are severely damaged and the blood creatinine value is greater than 308 μmol/L. What factors may cause renal anemia in patients with kidney disease? When renal function starts to be impaired, the total amount of erythropoietin produced by the kidneys will not be enough to meet the needs of the body, which becomes one of the main causes of renal anemia. In addition, chronic renal insufficiency, uremia patients, the body accumulates a large number of metabolic toxins, reducing the survival time of red blood cells; chronic kidney disease patients control protein intake for a long time, while the urine protein is constantly lost from the patient's body; chronic kidney disease patients tend to hemorrhage; all these situations may lead to chronic kidney disease patients to develop renal anemia. For the above causes, most patients need to use erythropoietin to treat renal anemia, but for polycystic kidney patients, their own lack of erythropoietin, so do not need additional supplementation. In addition, some patients do not need to use erythropoietin when their hemoglobin reaches 12g/l or even 13g/l or more. Therefore, in the clinical work, the treatment program of different patients need to be constantly adjusted. 10. Why is iron sucrose used regularly in renal anemia in dialysis patients? Anemia in dialysis patients is caused by insufficient production of erythropoietin (Epo) in the kidney or some toxin substances in uremic plasma interfering with the production and metabolism of red blood cells. However, in the course of treatment, patients with essential amino acid deficiencies should be given essential amino acid therapy, and those with vitamin B6, vitamin B12, folic acid, and ascorbic acid deficiencies can be supplemented appropriately. However, patients with chronic blood loss during dialysis treatment should be supplemented with iron. Iron, as a raw material for the formation of hemoglobin generation, needs to be tested regularly, and a large number of clinical trials as well as domestic and international literature report that intravenous iron supplementation therapy is used as the first choice. Common intravenous iron agents include iron dextrose and iron sucrose, etc. While iron dextrose is prone to allergic reactions, iron sucrose is safer and more effective than iron dextrose, so it is more widely used in clinical practice. The molecular weight of iron sucrose is between 34,000-54,000 Da, which is a large molecule, so it can be administered during the dialysis process. Generally, after supplementing sufficient amount of iron once, ferritin is within the normal range, you can not need to use iron temporarily, but generally need to check once every three months to maintain sufficient amount of iron to ensure hemoglobin stability. 11, why supplement calcium carbonate and active vitamin D? Chronic renal failure patients early blood phosphorus filtration is impaired, urinary phosphorus excretion is reduced, blood phosphorus retention, due to calcium and phosphorus metabolism, resulting in a decrease in blood calcium, due to both caused by parathyroid hyperplasia, increased secretion of PTH, PTH action on the bones to release Ca2+ to restore the level of calcium in the blood, resulting in a large amount of calcium loss in the bone, which leads to the emergence of osteoporosis. When renal failure further develops, the compensatory function fails, high blood phosphorus, low blood calcium persists, PTH also big secretion, continue to mobilize bone calcium release, so the vicious circle, finally lead to fibrous osteitis, the formation of severe renal bone disease. Therefore, early should take calcium carbonate can supplement blood calcium, inhibit parathyroid hyperplasia, reduce its mobilization of bone calcium release, while inhibiting blood phosphorus elevation, reduce parathyroid hyperplasia. In renal failure, phosphorus increases significantly in cortical tubular cells, and has the effect of severely inhibiting the synthesis of 1,25(OH)2D3. 1,25(OH)2D3 has the effect of promoting bone salt deposition and intestinal calcium absorption, when it is synthesized, coupled with the decrease in persistent hypocalcemia and the loss of protein-bound vitamin D in dialysis patients can lead to impaired bone salt deposition and cause osteochondritis dissecans, and at the same time, intestinal calcium absorption is reduced, then the secondary disease is caused by the decrease in calcium absorption. At the same time, decreased intestinal calcium absorption and decreased blood calcium can lead to fibrous osteitis secondary to hyperparathyroidism. Therefore, timely supplementation of active vitamin D can promote intestinal calcium absorption, increase blood calcium production, prevent parathyroid hyperplasia, reduce bone calcium loss and delay the progress of renal bone disease. 12.Is it better to use low molecular heparin calcium or heparin sodium in dialysis? Heparin sodium is an anticoagulant, which has effects on many parts of the coagulation process and can prolong the clotting time and prothrombin time. It has a rapid anticoagulant effect both in vivo and in vitro. It acts mainly on fibrin formation and also reduces platelet aggregation. It can be used for the prevention and treatment of thromboembolic diseases, can prevent the formation and expansion of thrombus, and at the same time as an extracorporeal anticoagulant in extracorporeal circulation, so it is currently used as a commonly used drug in dialysis. Adverse reactions: ① overdose can cause spontaneous bleeding, ② heparin-induced thrombocytopenia; ③ occasional allergic reactions such as asthma, rhinitis, urticaria, conjunctivitis, fever, etc.; ④ long-term application can occasionally produce temporary alopecia, osteoporosis and spontaneous fracture, etc.; ⑤ intramuscular injection can cause local hematoma. Low molecular heparin calcium injection: prevention of thromboembolic disease, especially prevention of thromboembolic disease in general surgery or orthopedic surgery. Prevention of clot formation in hemodialysis in hemodialysis, administered by intravascular injection; adverse reactions: occasional thrombocytopenia, thrombosis, signs of hemorrhage, skin necrosis and hematoma at the site of injection, allergic reactions, increased aminotransferases; pay attention to monitoring platelet count. On hemodialysis, adjust dose when anticoagulant factor Xa activity is less than 0.4 IU/mL or more than 1.2 IU/mL. Use with caution in the presence of hepatic or renal insufficiency, organic lesions prone to bleeding, history of choroidal retinal vasculopathy, and after brain or spinal cord surgery. Contraindications: contraindicated in patients with a history of any heparin-induced thrombocytopenia, bleeding tendencies and symptoms associated with coagulation disorders, organic injuries prone to bleeding, acute bacterial endocarditis. Therefore, it is most appropriate to grasp the characteristics, indications, and contraindications of the above two drugs, and choose the appropriate drug based on the patient's own characteristics to achieve the goal of smooth dialysis without bleeding.