Kidney Disease

　　1. Immune response: Deposition of circulating immune complexes; formation of immune complexes in situ.

　　2. Inflammatory response: Monocytes/macrophages, neutrophils, eosinophils, platelets, inflammatory mediators, etc., invade the kidneys. Ultimately, it leads to damage to the molecular barrier and charge barrier of the glomerular filtration membrane, an increase in the permeability of the glomerular filtration membrane to plasma proteins (mainly albumin), an increase in protein content in urine, and the formation of large amounts of proteinuria when it exceeds the reabsorption amount of the distal tubule.

　　3. Large amounts of proteinuria: When the molecular barrier and charge barrier, especially the charge barrier, of the glomerular filtration membrane are damaged, the permeability of the glomerular filtration membrane to plasma proteins (mainly albumin) increases, resulting in an increase in protein content in urine. When it exceeds the reabsorption amount of the distal tubule, it forms large amounts of proteinuria.

　　4. Changes in plasma proteins: Large amounts of albumin are lost in urine, promoting compensatory synthesis of albumin in the liver. When the increased synthesis of liver albumin is not enough to overcome the loss, hypoalbuminemia occurs. In addition, due to edema of the gastrointestinal mucosa, reduced food intake, insufficient protein intake, malabsorption, or loss can also be the cause of hypoalbuminemia.

　　5. Edema: Hypoalbuminemia leads to a decrease in plasma colloid osmotic pressure, causing water to enter the tissue spaces from the vascular lumen, which is the main cause of edema.

　　6. Hyperlipidemia: Increased concentration of LDL, VLDL, and lipoprotein(a) in serum, along with hypercholesterolemia and/or hypertriglyceridemia, often coexists with hypoalbuminemia. Its pathogenesis is related to the increased synthesis of lipoproteins by the liver and the weakened degradation of lipoproteins.

　　Nephropathy is a syndrome characterized by increased permeability of the glomerular basement membrane, which can be caused by various etiologies. Its clinical features include large amounts of proteinuria, hypoalbuminemia, hypercholesterolemia, and general edema. Nephropathy is prone to the following complications:

　　Infection:

　　Due to the large loss of immunoglobulins in urine, plasma proteins decrease, affecting antibody formation. The use of adrenal cortical hormones and cytotoxic drugs reduces the patient's overall resistance, making them highly susceptible to infections such as skin infections, primary peritonitis, respiratory tract infections, urinary tract infections, and even sepsis.

　　Coronary heart disease:

　　Patients with kidney disease often have hyperlipidemia and a hypercoagulable state of blood, so they are prone to coronary heart disease. Some reports indicate that the incidence of myocardial infarction in kidney disease patients is 8 times higher than that in normal people.

　　Thrombosis:

　　Patients with kidney disease are prone to thrombosis, especially membranous nephropathy with an incidence rate of 25% to 40%. The causes of thrombosis include edema, decreased patient activity, venous stasis, hyperlipidemia, increased blood viscosity due to blood concentration, elevated levels of fibrinogen and factors v, VII, VIII, X, and the blood tends to be hypercoagulable due to the use of adrenal cortical hormones.

　　Acute renal failure:

　　Patients with kidney disease often have large amounts of proteinuria, hypoproteinemia, and hyperlipidemia, and their bodies are often in a state of low blood volume and high coagulability. Vomiting, diarrhea, the use of antihypertensive drugs and diuretics, and excessive diuresis can all cause a sudden decrease in renal blood perfusion, leading to a decrease in glomerular filtration rate and causing acute renal failure. In addition, factors such as interstitial edema in kidney disease, protein concentration forming casts blocking the renal tubules, and other factors can also induce acute renal failure.

　　Electrolyte and metabolic disorders:

　　Recurrent use of diuretics or long-term unreasonable salt restriction can lead to secondary hyponatremia in kidney disease patients; the use of adrenal cortical hormones and large amounts of diuretics can cause excessive urination, and if potassium is not supplemented in time, hypokalemia may occur easily.

　　1. Edema: Edema of varying degrees, often the first symptom of nephrotic syndrome, often insidious onset, and severe cases often have serous cavity effusion.

　　2. Urination is less frequent, often less than 400ml/day, and even anuria.

　　3. Before onset, there is often a history of upper respiratory tract infection, skin infection, and other infections.

　　4. Common symptoms include fatigue, anorexia, pallor, and listlessness.

　　5. Blood pressure is mostly normal, with a few having hypertension.

　　The kidneys have a strong compensatory function. In the early stage or when the kidney lesions are not severe, most patients do not feel anything, even if some patients have discomfort such as low back pain, edema, poor appetite, etc., they usually attribute it to fatigue, sub-health, and rarely associate it with kidney problems. By the time symptoms such as hypertension and anemia appear and medical treatment is sought, the renal function has basically been lost, and it has developed to the middle stage or uremia stage. Therefore, regular physical examination is particularly important.

　　Adults should have a routine urine test and renal function test once a year. If the routine urine test shows proteinuria, elevated blood creatinine levels, and other abnormalities, it should be taken seriously and further examination by a specialist should be sought. High-risk populations for chronic kidney disease, such as the elderly over 60, family members of chronic kidney disease patients, patients with metabolic diseases such as diabetes, gout, hyperuricemia, hypertension, systemic lupus erythematosus, hepatitis, tumors, systemic infection, urinary tract stones, urinary tract infection, and urinary tract obstruction, those with a history of acute renal failure, and those with reduced renal units (unilateral or partial nephrectomy), should all have a urine routine test, renal function test, and renal B-ultrasound examination every six months to one year, regardless of whether there are symptoms.

　　Two, participate in aerobic exercise, exercise moderately, and do more physical activities and sweat in the sun, which can help eliminate excessive acidic substances in the body, thus preventing the occurrence of this disease.

　　Three, maintain a good mood, do not have excessive psychological pressure. Excessive pressure can lead to the deposition of acidic substances, affecting the normal progression of metabolism. Appropriate adjustment of mood and personal stress can maintain a weak alkaline body and thus prevent the occurrence of this disease.

　　Four, keep a regular life, people with irregular lifestyles, such as staying up all night to sing karaoke, play Mahjong, not going home at night, and irregular living, will worsen acidification of the body. Easy to get diabetes. It is necessary to develop good living habits to maintain a weak alkaline body and keep this disease away from you.

　　1. Collect and send urine samples for testing in a timely and correct manner: Urinalysis is a convenient, sensitive, and accurate indicator for diagnosis and judgment of the condition and efficacy, and it must be paid attention to.

　　2. For patients with edema and acute nephritis, accurately record the 24-hour intake and output each day. Edema patients should weigh themselves once a week, and abdominal hydrostatic patients should increase weighing once a week, and measuring abdominal circumference once a week.

　　3. For patients with hypertension, blood pressure should be measured regularly.

　　4. Handle specific issues according to symptoms, observe the early signs of renal function damage, and take protective measures for renal function to prevent the progression and恶化 of the disease.

　　Control the dietary structure, avoid excessive intake of acidic substances, and prevent the aggravation of acidic体质. The acid-base balance of diet is an important link in the treatment of this disease and the prevention of complications. In terms of diet, it is necessary to eat more foods rich in plant organic active bases, eat less meat, and eat more vegetables. Camel grass is rich in plant organic active bases, which can quickly eliminate acid toxins in the body, clarify urine acid toxins, and truly protect the kidneys. Stay away from smoking and drinking. Smoking and drinking are typical acidic foods. Unrestrained smoking and drinking can easily lead to acidification of the human body, making it possible for this disease to take advantage. Do not eat contaminated foods such as contaminated water, crops, poultry, fish, and eggs. Eat some green organic foods and prevent diseases from entering the body through the mouth. Patients with nephritis should abstain from sexual activity, even after recovery, for half a year to one year. If you are not clear about the specific situation, be sure to consult a doctor in a timely manner and follow the doctor's advice.

　　1. Treatment of Hypoalbuminemia

　　(1) Diet Therapy: Nephrotic syndrome patients are usually in negative nitrogen balance. If they can consume a high-protein diet, they may convert to positive nitrogen balance. However, consuming high protein by nephrotic syndrome patients can lead to increased urine protein, aggravating glomerular damage, without an increase in plasma albumin levels. Therefore, it is recommended to consume 1g of protein per kilogram per day, plus the amount of protein lost in urine each day. For every 1g of protein consumed, 138kJ (33kcal) of non-protein calories must be consumed simultaneously. The supplied protein should be high-quality protein, such as milk, eggs, fish, and meat.

　　(2)Intravenous infusion of albumin: since the albumin infused intravenously is lost through urine from the kidney within 1-2 days and is expensive. In addition, large-scale intravenous use of albumin has side effects such as immunosuppression, hepatitis C, triggering heart failure, delaying remission, and increasing recurrence rate, so strict indications should be strictly controlled when using intravenous albumin: ①Severe general edema, in patients who cannot achieve diuretic effects with intravenous injection of Furosemide, after intravenous infusion of albumin, followed by intravenous infusion of Furosemide (120mg of Furosemide added to 100-250ml of glucose solution, slowly infused for 1 hour), it is often possible for those who were previously ineffective to Furosemide to still achieve good diuretic effects. ②Clinical manifestations of plasma volume deficiency after diuretic with Furosemide. ③Acute renal failure caused by interstitial edema.

　　2. Treatment of edema

　　(1)Sodium-restricted diet:

　　Edema itself suggests an excess of sodium in the body, so it is of great importance to limit salt intake in patients with nephrotic syndrome. The daily salt intake of a normal person is 10g (containing 3.9g of sodium), but due to the tasteless diet after sodium restriction, the appetite is poor, which affects the intake of protein and calories. Therefore, the sodium-restricted diet should be moderate so that the patient can tolerate it without affecting their appetite, and the salt content of a low-sodium diet is 3-5g/d. Chronic patients, due to long-term sodium restriction, may lead to intracellular sodium deficiency, which should be paid attention to.

　　(2)Application of diuretics:

　　Diuretics can be divided according to different action sites:

　　①Loop diuretics: the main mechanism of action is to inhibit the reabsorption of chloride and sodium in the thick ascending limb of the loop of Henle, such as Furosemide (Lasix) and Bumetanide (Bumetanide) are the most powerful diuretics. The dose is 20-120mg/d for Furosemide, and 1-5mg/d for Bumetanide.

　　②Thiazide diuretics: mainly act on the thick ascending limb of the loop of Henle (cortical region) and the anterior segment of the distal tubule, by inhibiting the reabsorption of sodium and chloride, and increasing potassium excretion to achieve diuretic effects. The usual dose of hydrochlorothiazide is 75-100mg/d.

　　③Sodium-reabsorbing potassium diuretics: mainly act on the distal tubules and collecting ducts, and are aldosterone antagonists. The usual dose of Spironolactone is 60-120mg/d, the effect of using such drugs alone is poor, so they are often used in combination with potassium-wasting diuretics.

　　④Osmotic diuretics: can be freely filtered through the glomerulus without being reabsorbed by the renal tubules, thereby increasing the osmotic concentration of the renal tubules and preventing the reabsorption of water and sodium by the proximal and distal tubules, thereby achieving diuretic effects. The usual dose of low-molecular-weight dextran is 500ml/2-3d, mannitol 250ml/d, and caution should be exercised in patients with renal function damage.

　　The preferred diuretic for nephrotic syndrome patients is Furosemide, but the dosage varies greatly among individuals; intravenous administration is more effective, the method is: add 100mg of Furosemide to 100ml of glucose solution or 100ml of mannitol, and slowly drip for 1 hour; Furosemide is a potassium-wasting diuretic, so it is often used in combination with Spironolactone. After long-term application (7-10 days) of Furosemide, the diuretic effect decreases, and sometimes the dosage needs to be increased, and it is best to change to intermittent administration, that is, to stop the drug for 3 days before using it again. It is recommended that diuretics with different action sites be used in combination and alternately for patients with severe edema.

　　3. Treatment of hypercoagulable state

　　Patients with nephrotic syndrome are in a hypercoagulable state due to changes in coagulation factors, especially when plasma albumin is below 20-25g/L, there is a possibility of venous thrombosis. Currently, the commonly used anticoagulant drugs in clinical practice include:

　　(1) Heparin: Mainly activates the anticoagulant activity of antithrombin III (ATⅢ). The usual dose is 50-75mg/d intravenous infusion, so that the activity unit of ATⅢ is above 90%. Some literature reports that heparin can reduce proteinuria in nephrotic syndrome and improve renal function, but the mechanism of action is not clear. It is noteworthy that heparin (MW 65600) can cause platelet aggregation. Currently, there is a low molecular weight heparin for subcutaneous injection, once a day.

　　(2) Urokinase (UK): Directly activates plasminogen, leading to fibrinolysis. The usual dose is 20,000-80,000 U/d, start with a low dose, and can

　　It is administered intravenously with heparin. Monitor the euglobulin lysis time to keep it between 90-120 minutes. The main side effects of UK are allergy and bleeding.

　　(3) Warfarin: Inhibits the synthesis of vitamin K-dependent factors II, VII, IX, and X in liver cells, the usual dose is 2.5mg/d, taken orally, and monitor the prothrombin time to keep it at 50%-70% of normal people.

　　(4) Dipyridamole: A platelet antagonist, the usual dose is 100-200mg/d. The anticoagulation time for venous anticoagulation in general hypercoagulable state is 2-8 weeks, and then changed to warfarin or dipyridamole oral administration.

　　4. Treatment of hyperlipidemia

　　Patients with nephrotic syndrome, especially those with frequent recurrence, have a long duration of hyperlipidemia. Even after the nephrotic syndrome is relieved, hyperlipidemia still persists. In recent years, it has been recognized that hyperlipidemia affects the progression of kidney disease. Some drugs used to treat nephrotic syndrome, such as adrenal cortical hormones and diuretics, can worsen hyperlipidemia, so it is currently recommended to use lipid-lowering drugs for hyperlipidemia in nephrotic syndrome.

　　The lipid-lowering drugs that can be used include: ①Fibric acid derivatives (fibric acids): Fenofibrate, taken three times a day, 100mg each time, Gemfibrozil, taken twice a day, 600mg each time; this drug has a stronger effect on lowering blood triglycerides than on lowering cholesterol. This medicine occasionally causes gastrointestinal discomfort and an increase in serum transaminases. ②Hmg-CoA reductase inhibitors: Lovastatin (Mei Jiangzhi), 20mg bid, Simvastatin (Shu Jiangzhi), 5mg bid; these drugs mainly reduce intracellular Ch, lower plasma LDL-Ch concentration, and reduce the production of VLDL and LDL by liver cells. ③Angiotensin-converting enzyme inhibitors (ACEI): The main effects include lowering the concentration of Ch and TG in plasma; increasing the level of HDL in plasma, and its main lipoprotein ApoA-Ⅰ and ApoA-Ⅱ also increase, which can accelerate the clearance of Ch in peripheral tissues; reduce the infiltration of LDL into the arterial intima, and protect the arterial wall.

　　5. Treatment of Acute Renal Failure

　　The treatment methods for nephrotic syndrome complicated with acute renal failure vary due to different etiologies. For those caused by hemodynamic factors, the main treatment principles include: rational use of diuretics, adrenal cortical hormones, correcting hypovolemia, and dialysis therapy. Hemodialysis not only controls azotemia and maintains electrolyte acid-base balance but also can quickly remove water retention in the body. Acute renal failure caused by interstitial edema can recover renal function quickly after the above treatment.

　　When using diuretics, attention should be paid to:

　　①Timely use of diuretics:

　　In patients with nephrotic syndrome and severe hypoalbuminemia, the use of high-dose diuretics without supplementing plasma protein will exacerbate hypoalbuminemia and hypovolemia, and further worsen renal failure. Therefore, diuretics should be administered after supplementing plasma albumin (10-50g human albumin administered intravenously per day). However, if plasma albumin is supplemented excessively without timely diuretic therapy, it may lead to pulmonary edema.

　　②Appropriate use of diuretics:

　　Due to the relative hypovolemia and tendency of hypotension in patients with nephrotic syndrome, it is advisable to use diuretics with a daily urine output of 2000-2500ml or a daily weight loss of about 1kg.

　　③In patients with increased plasma renin levels, the use of diuretics after the blood volume decreases can further increase the plasma renin level. Diuretic therapy is not only ineffective but also exacerbates the condition. Such patients can only benefit from diuretic therapy after correcting hypoalbuminemia and hypovolemia.

　　Nephrotic syndrome complicated with acute renal failure is generally reversible. Most patients recover renal function gradually with increased urine output under treatment. A few patients may experience acute renal failure multiple times during the course of the disease, which can also be recovered. The prognosis is related to the etiology of acute renal failure. Generally, rapid progressive glomerulonephritis and renal vein thrombosis have poor prognosis, while those associated solely with nephrotic syndrome have a better prognosis.