How is uremia formed?

After many people have kidney disease, they become uremia indistinctly. It is even unclear when the kidney started to be “injured”. Uremia is not a single-onset disease, it is the end stage of the development of chronic kidney disease, that is, the state of kidney failure. So where does chronic kidney disease come from? Chronic kidney disease is mainly divided into two categories, one is primary kidney disease, and the other is secondary kidney disease. 1. Primary nephropathy Primary nephropathy refers to a disease that originates inside the kidney, such as glomerulitis, pyelonephritis, occult nephritis, and kidney stones. If it does not recover after more than 3 months, and the relevant examination indicators are always abnormal, or the effective glomerular filtration rate is less than 60%, it can be regarded as “chronic kidney disease”. 2. Secondary kidney disease is caused by other diseases. The secondary kidney disease, such as high blood pressure, is like pressing a mountain on the kidney. It is likely to cause excessive blood vessel pressure, protein leakage, and structural effects on the filter. The destruction eventually leads to hardening of the kidneys. Another example is diabetic nephropathy, which has become the second leading cause of uremia. Excess blood sugar will produce a large amount of glycosylation end products, which are deposited in the kidneys, block the renal tubules and blood vessels, cause various inflammatory reactions or microvascular lesions, and eventually “stretch” the glomeruli. In addition, gout, lupus erythematosus, and hyperlipidemia are all high-risk factors. If it cannot be cured or contained effectively, it can easily develop into uremia.

There are three types of nephritis, you can’t carelessly, be careful that the kidney will never get better

Everyone knows that the kidney is one of our most important organs. Once inflamed, it may damage kidney function and cause problems with the body’s metabolic system. However, there are three types of kidney inflammation, each of which has a different cause and damage to kidney function. For example, pyelonephritis, you don’t have to be too panic and feel that you will definitely have kidney failure. The kidney is a very complex organ, which looks like a big pea, but the structure inside is very finely divided, so when a lesion occurs, it will have different effects and reactions; but the main function of the kidney is to metabolize waste in the body, you can imagine Cheng is the same as the recycling plant and sewage treatment plant in the body, there are many units, but the whole has a common function. The blood entrained with waste will first be filtered through the glomerulus, which can be thought of as the “sediment” of the sewage treatment plant. The glomerulus will retain the macromolecular substances that can be recycled, such as most of the water and protein. After filtering the blood, another round of treatment is performed in the renal tubules to discharge small molecules such as urea and uric acid. The electrolyte depends on whether the body needs it. Too much is discharged and too little is left. Toxic substances are also metabolized here. After these filtrations, urine is finally left to be excreted. At this time, it will be stored in the kidney calyx and renal pelvis in the center of the kidney, which is also the source of the urinary tract system, and then the urine will follow the ureter, bladder, and urethra The channel is drained, which is why urinary tract infections can cause pyelonephritis. In short, pyelonephritis is an inflammation of the “reservoir”. Basically, 90% of pyelonephritis comes from urinary tract infections, that is, infection from the urethra and bladder all the way to the renal pelvis. The doctor said that girls are more prone to urinary tract infections and are more likely to cause pyelonephritis, because the rate of hospitalization for pyelonephritis is slightly higher than that of boys, about 1.1 to 1.5 times. Another reason may be that bacteria in the blood flow to the kidneys to cause infections or infections through the lymph fluid, but in general, pyelonephritis is caused by bacterial infections. The doctor said: “Bacteria have a very strong multiplying ability. 100 bacteria will become 10,000 in 30 minutes”, so it is very important to sterilize the first time. Pyelonephritis will initially have symptoms of dysuria and urinary urination. Later, it will cause backache and fever, and urine will become thicker due to increased white blood cells. The doctor said that if there is no natural fever after 1 to 3 days of treatment, hospitalization should be considered, but if the white blood cells in the blood exceed 10,000, if there is a fever, they must be hospitalized; generally, the acute phase requires about 10 to 14 days of antibiotic treatment If there is hospitalization, the hospitalization is limited to 7 days. Although acute pyelonephritis does not need to be too scared and will not damage kidney function, if it is not treated, it may also be caused by bacteria invading the blood, and septicemia, shock and even death. Even if it is a fluke, it does not immediately cause death, and it evolves into chronic pyelonephritis. The kidney will gradually shrink because the pelvis has been in an inflamed state. As mentioned above, the glomerulus is the part of the kidney that filters large molecules, so if the glomerulus is inflamed, it cannot filter proteins, and even the blood cell protein such as red blood cells cannot be retained, so it will cause proteinuria and hematuria. Because there is no way to filter the water, it will also cause edema and high blood pressure in the extremities, but the acute symptoms come and go quickly. At present, most glomerulonephritis does not know the cause, which is called primary glomerulonephritis. Other common causes, such as autoimmune diseases, or immune reactions caused by viruses or bacteria attack the glomerulonephritis. Wait, but in simple terms, glomerulonephritis can be said to be a reaction caused by immune diseases. Common tonsillitis, upper respiratory tract infections, pneumonia, and otitis media may cause acute glomerulonephritis in infants, young children, and adolescents. Hepatitis B and C may cause acute glomerulonephritis in adults. Acute glomerulonephritis does not actually cause much damage to renal function, but chronic glomerulonephritis is the number one cause of renal failure in statistics. Chronic glomerulonephritis is mostly caused by the deposition of immunoglobulin IgA in the kidney, and immune diseases such as rheumatoid arthritis and lupus erythematosus may induce the deposition of immunoglobulin. Most steroids are now used to delay the progress of kidney disease. Other supplementary drugs and dietary treatments are tailored according to the physical condition of each person. As mentioned earlier, the renal tubule is the part of the kidney that is responsible for filtering small molecules and most toxic substances.

Reminder: There is a problem with the kidneys, there will be these abnormal signals when urinating, this self-check manual is collected

Hello everyone, I am a nephrologist. I think I should be able to insert a few words about kidney health and abnormal urination. As the title says, what abnormalities do people with kidneys have when urinating? I can only say too much, because there are many types of kidney disease, it may be a disease of nephrology, or it may be a disease of urology. It is possible that a kidney disease has multiple manifestations, and it is possible that multiple kidney diseases have the same manifestation. Since the subject does not specifically describe how the kidney is not good, so here today I will comprehensively talk to you about my views. What role does the kidney play in the formation of urine? This mainly depends on the glomerular filtration function and the glomerular reabsorption and secretion function! ●The glomerular filtration function ① Everyone’s understanding of urine must not simply be understood as “simple water composition”. In fact, urine contains water and various metabolic wastes in the body. Our glomerular filtration function is the main way of excretion of human metabolites. Some nitrogen-containing wastes such as urea and creatinine can be filtered by the glomerulus, and some organic acids such as hippuric acid and benzene Formic acid and various amines can be partially filtered by the glomeruli. ② From a microscopic point of view, our kidney is actually composed of millions of glomeruli, and the glomerulus is composed of many small arteries to form a spherical shape. When the average arterial pressure of our body fluctuates in the range of 80-160mmhg, the self-regulating mechanism of kidney blood flow in our body is at its best. On the one hand, it can ensure that the glomerular filtration rate can still run steadily when the body changes in hemodynamics, so that the metabolic waste in the body can be discharged, on the other hand, it also ensures the balance of body fluids. ●The reabsorption function of renal tubules involves the formation of original urine. Everyone, please note that our daily urine filtered by the glomerulus can actually reach 180L, and this raw urine cannot be excreted temporarily. Because it contains water, glucose, amino acids and other substances that our body still needs, these raw urine will be reabsorbed into the blood by the renal tubules and collecting tubes. Therefore, the resulting urine is about 1.5L a day, which is also a normal urine output range for a day. What kind of kidney disease (bad kidney) will be abnormal when urinating? ●Urinary tract infections ① When it comes to urinary tract infections, professional explanations are infectious diseases caused by the growth and reproduction of various pathogenic microorganisms in the urinary tract. Let’s say the popular point is that the urinary tract infection and inflammation. Clinically, it can be divided into upper urinary tract infection and lower urinary tract infection, and the most common upper urinary tract infection is “pyelonephritis”, which is plainly a kidney problem. ②If it is pyelonephritis, what abnormalities will occur during urination? Here I tell you that the most common are frequent urination, urgency, and painful urination. I always want to relieve urination. Every time there is not much urination, it may be just a few drops. After urination, there is burning and pain in the urethra. So this pyelonephritis (poor kidney) can occur when urinating these abnormalities. ●Acute renal failure ① This is actually a comprehensive concept. We generally call it acute kidney injury. It refers to the clinical appearance of a sudden decrease in kidney function caused by various causes in a short time (a few hours to a few days). Syndrome. There are many causes, such as special drugs, poisons, infections, burns, insufficient capacity, and urinary obstruction. However, please note that no matter what kind of cause you cause, everyone can see that the kidney is damaged. ② What are the abnormalities of acute renal failure in terms of urination alone? The most common are oliguria, anuria, and dark urine. In the opening chapter, I talked to you that urine is formed by the metabolism of the kidneys. Now, if the kidneys have problems, it will inevitably lead to “urine production obstacles.” As the so-called kidneys have problems, how can you metabolize urine, so this type of urination may be reduced urinary tract or anuria (oliguria is less than 400ml in 24 hours, less urine is less than 100ml in 24 hours ). ● IgA nephropathy specific pathogenesis of the disease I will not repeat them here, it is a kind of kidney disease. The root cause is “IgA-based immune complex deposition” in the mesangial area of ​​our kidneys and hyperplasia of the mesangium of the glomeruli. To put it bluntly, it means that this mesangial area does not have these inexplicable things under normal circumstances. Now that this abnormal situation occurs, it will inevitably lead to

From a scientific perspective: the effect of obesity on IgA nephropathy, after reading, decide whether you want to lose weight

In primary glomerular disease, few people study the pathological role of obesity in the progression of glomerular disease. The purpose of this study was to investigate the effect of non-diabetic obesity on the clinicopathological manifestations of IgA nephropathy. Methods: 74 patients diagnosed with IgA nephropathy by renal biopsy were retrospectively assigned to two groups according to Japanese obesity standards: non-obese group (N group: n = 50), BMI & lt. n = 24), BMI≥25kg / m2. The clinical and pathological data at the time of renal biopsy were analyzed. In addition, after treatment with angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor antagonist (ARB), follow-up for 1 year to evaluate the therapeutic effect of proteinuria between the two groups. Results: Compared with the non-obese group, the obese group had significantly increased urinary protein excretion (P & lt.0.05). There was no significant difference in the incidence of hypertension and hyperlipidemia between the two groups. Under the light microscope, the glomerular volume of the obese group increased significantly (p & lt.0.0001); however, there was no difference in the severity of mesangial matrix increase and crescent formation between the two groups. Under the transmission electron microscope, the glomerular basement membrane (gbm) in the obese group was significantly thickened (p & lt.0.001). Of the 61 patients who were followed for 1 year, 15 patients were given acei or arb without steroids. The purpose of acei or arb treatment without steroids is to reduce proteinuria in obese patients, but this change in treatment has not achieved statistical significance. & lt.span = & quot. & quot. & gt. The glomerular volume of the obese group increased significantly (p & lt.0.0001); however, there was no difference in the severity of mesangial matrix increase and crescent body formation between the two groups. Under the transmission electron microscope, the glomerular basement membrane (gbm) in the obese group was significantly thickened (p & lt.0.001). Of the 61 patients who were followed for 1 year, 15 patients were given acei or arb without steroids. The purpose of acei or arb treatment without steroids is to reduce proteinuria in obese patients, but this change in treatment has not achieved statistical significance. Conclusion: For patients with IgA nephropathy, obesity will not only cause an increase in glomerular volume, but also lead to changes in the ultrastructure of the glomerular basement membrane (GBM). Both of these changes will increase proteinuria in patients.

What is IGA nephropathy?

IGA is immunoglobulin A, which can be divided into serotype and secretory type. The serotype IGA is a monomer, and the immune effect is relatively weak. Secretory IGA has two bodies and three bodies and is the main component of the body’s mucosal defense system. It is widely distributed in milk, saliva, and gastrointestinal tract, respiratory tract, and urogenital tract mucus secretions. It can inhibit the adhesion of microorganisms to the respiratory tract epithelium, slow down the propagation of viruses, has an important immune barrier, and has antibody activity against certain viruses, bacteria, and general antigens. It is the first line of defense to prevent pathogens from invading the body. IGA nephropathy is the most common primary glomerular disease, which refers to the deposition of IGA or IGA in the mesangial area, with or without other immunoglobulin deposition in the mesangial area Primary glomerulopathy. The clinical manifestations are recurrent gross hematuria or microscopic hematuria, which may be accompanied by proteinuria of varying degrees, and some patients may have severe hypertension or renal insufficiency.

Clinical suggestion of IgA nephropathy, under what circumstances should renal puncture be considered? Don’t resist

When clinical clues suggest IgA nephropathy, different countries and different scholars have different criteria for grasping the indications of renal biopsy. Foreign patients with asymptomatic hematuria generally do not advocate active renal puncture. Therefore, the international KDIGO guidelines recommend that patients with glomerular hematuria need to review and monitor blood pressure, proteinuria and renal function regularly, but some scholars believe that as long as There are no contraindications, and patients with clear glomerular hematuria should be mobilized for renal puncture because hematuria caused by certain etiologies (such as thin basement membrane nephropathy) does not require treatment at all. It is generally believed that for patients with clinically suggestive IgA nephropathy, renal biopsy is of greater significance in the following cases: 1. The 24-hour urine protein quantity is greater than 1 gram; 2. There is an increase in blood creatinine at the onset; 3. Hematuria is obviously accompanied by an increase in blood creatinine in a short period of time; 4. Hematuria is accompanied by hypertension; 5. Glomerulopathy suspected to be secondary to systemic diseases; 6. Suspected to be associated with other glomerular diseases. Some scholars believe that if the renal biopsy is performed according to the standard of 24-hour proteinuria greater than 1 gram, some patients who need active treatment may be missed. For example, some patients have a 24-hour urine protein of about 0.5 grams, but renal pathology shows that it has been moderate Degree (Lee classification) injury, advocated in units with more mature renal biopsy technology, as long as there is persistent proteinuria accompanied by microscopic hematuria, kidney biopsy can be considered.

Can chronic nephritis be cured? Doing these four things is the most important

Chronic nephritis, also known as chronic glomerulonephritis, can be caused by a variety of reasons. Strictly speaking, chronic nephritis cannot be cured. The course of chronic nephritis is very long, and the disease progresses slowly and continuously. Of course, if chronic nephritis is discovered early and scientifically treated, chronic nephritis can be completely controlled. Chronic nephritis is mainly characterized by proteinuria, hematuria, edema, and hypertension, and is often accompanied by impairment of renal function. However, if you allow the disease to progress unchecked, you can enter end-stage renal failure. Chronic nephritis can be divided into the following types according to the main lesions of most glomeruli: ① mesangial proliferative glomerulonephritis; ② focal-segmental glomerulosclerosis; ③ membranous nephropathy Glomerulonephritis; ⑤ hyperplastic sclerosing glomerulonephritis. Treatment methods can be divided into Chinese medicine treatment and Western medicine treatment. Western medicine treatment: Patients can be controlled with drugs such as antihypertensive drugs, diuretics, immunosuppressants, coagulation and platelet depolymerization drugs. However, long-term use of Western medicine will increase the burden on the kidneys to a certain extent, have certain side effects and patients will be dependent on the drug. Traditional Chinese medicine treatment: Chronic nephritis has various causes due to the disease, and the complications caused by it are also very many. There are often various pathological changes that are mixed with the real and the false. The treatment of traditional Chinese medicine is not only to cure the kidney, but also to combine the treatment of lung, spleen, liver, and evil. Chinese medicine treatment is not easy to relapse, but the treatment process takes a long time. How to treat patients with chronic nephritis? First, we must pay attention to the combination of work and rest, maintain a regular life, and avoid overwork to help the kidney function recover. Chronic nephritis patients should pay more attention to rest. If the condition permits, they should participate in outdoor activities such as walking, playing Tai Chi or practicing Qigong, etc., breathing fresh air to enhance blood circulation and improve physical fitness. The second is to ensure a good night’s sleep. Adequate sleep is the most basic of keeping in good health and can quickly eliminate fatigue. A lot of blood will flow to the kidneys, improving kidney function and helping the repair of nephrons. In addition, pay attention to hygiene, when patients with chronic nephritis have intestinal infections, oral infections or respiratory tract infections, it will aggravate hematuria and promote the leakage of urine protein, which will aggravate the condition. Therefore, close-fitting clothes should be changed frequently and washed in the sun, and the nails should be trimmed to keep the skin clean and bathed every two days. Finally, use drugs with caution. Most drugs are excreted through the kidneys. Antipyretic and analgesic drugs, as well as cold and Chinese medicines, will damage the kidneys. Chronic nephritis has a long course, generally from the first discovery of urinary abnormalities to the development of chronic renal failure, which can take 10 to 30 years or more. The prognosis is significantly different due to the types of pathological damage of chronic glomerulonephritis and whether there are complications. Accompanied by high blood pressure, large amounts of proteinuria and co-infection, insufficient blood volume, the use of nephrotoxic drugs, etc., can accelerate the development of chronic renal failure. Active treatment improves symptoms, protects residual nephrons, and helps delay the deterioration of renal function. The treatment of chronic nephritis can be said to be quite slow and complicated. Patients should seek medical treatment as soon as possible, actively cooperate with the doctor, master some treatment methods for chronic nephritis, and pay special attention to personal diet on weekdays.

Xiebeilu: What are the pathological grades of allergic purpura nephritis?

Allergic purpuric nephritis (henoch-schionleinpurpuranephritis, HSPN) is a clinically common secondary kidney disease, the main pathological change is necrotizing small vasculitis, which can involve the skin, gastrointestinal tract, joints and kidneys and other systems / organs. HSPN with severe nephritis often progresses to end-stage renal disease. Clinically, different types of HSPN patients should adopt individualized treatment strategies. & nbsp. At present, according to the guidelines of the Nephrology Group of the Pediatrics Branch of the Chinese Medical Association, the treatment plan is formulated according to the pathological grade or clinical classification. According to the clinical manifestations of HSPN, it is divided into hematuria, proteinuria, hematuria and proteinuria, acute nephritis, nephrotic syndrome, acute nephritis, and chronic nephritis. & nbsp. The pathological grading standards are: & nbsp. I, mild glomerular abnormalities. & nbsp. II, simple mesangial hyperplasia. & nbsp. III, mesangial hyperplasia with few glomerular crescents and / or nodules Segmental disease. & Nbsp.IV: The disease is the same as grade III, 50% ~ 75% of the glomeruli are accompanied by glomerular crescent formation and / or segmental disease. & Nbsp.V grade: The disease is the same as grade III , Most glomerular lesions. Grade VI: Membranoproliferative glomerulonephritis. & nbsp. Angiotensin-converting anzyme inhibitor (ACEI) or angiotensin II receptor antagonist (angiotensin II receptor blocker) is routinely used in children with pathological grade IIa or isolated microproteinuria or urinary occult blood (+) , ARB), can reduce proteinuria to improve hematuria, hypertension and edema, and also can reduce the permeability of the glomerular filtration membrane by inhibiting the renin-angiotensin system to protect kidney function. & nbsp. For children with pathological grade IIb, IIIa or non-nephrotic proteinuria and poor treatment effect and persistent proteinuria, glucocorticoid therapy can be used for half a year. Hormones have powerful anti-inflammatory effects, so they are currently the first-line basic medication for HSPN treatment. & nbsp. For children with pathological grade IIIb, IV or nephrotic proteinuria, nephrotic syndrome, and acute nephritis syndrome, the combination of hormones and other drugs is preferred. & nbsp. A cohort study of Chinese adult patients shows that reducing the patient ’s proteinuria to & lt.0.4g / d while controlling hypertension can improve kidney prognosis. Patients with mild to moderate HSPN may consider ACEI and / or ARB treatment. However, children with pathological grade V, VI, or progressive nephritis have severe clinical manifestations and rapid disease progression. The treatment is usually triple or quadruple therapy, which should receive glucocorticoids, immunosuppressants, warfarin, and dipyridamole. Combination therapy. & nbsp. At present, there is relatively little evidence-based medicine for the treatment of HSPN. In view of the relatively low incidence of HSPN, more large-scale, multi-center prospective research has yet to be carried out.

Can patients with proteinuria with chronic kidney disease eat seafood? The problem that bothered you has been solved

Persistent proteinuria is one of the main clinical features of chronic kidney disease. Proteinuria is usually caused by glomerular filtration membrane loss. The continued presence of proteinuria will eventually lead to glomerular sclerosis. For the treatment of proteinuria, not only rely on the treatment of drugs, but also strictly limit the intake of animal protein and plant protein to reduce the burden on the kidneys. Some patients believe that animal protein only includes pork, beef, lamb, duck, chicken and other meats, and often ignore seafood. Seafood is a high-protein, low-fat food. The protein content of fish, shrimp, and crabs can be as high as 15% -20%, and the protein content of shark fins, sea cucumbers, scallops, etc. is more than 70%. Therefore, patients with chronic kidney disease limit protein foods, including seafood. In addition, seafood contains many purines, such as mixed with beer, will cause hyperuricemia, hyperuricemia also has a negative impact on the kidneys. Hyperuricemia refers to physiological conditions at 37 ° C and a blood pH of 7.4. Serum uric acid content exceeds 416 μmol / L (7.0 mg / dl) in males and 357 μmol / L (6.0 mg / dl) in females. Uric acid is the product of purine metabolism in the body. The metabolism of purine in the human body mainly comes from the following two pathways: one is the exogenous pathway, mainly from food, accounting for 20% of the source of uric acid in the body, because the purine ingested in food is almost in the body Can be converted into uric acid, so high purine diet can cause increased blood uric acid. The second is the endogenous pathway, which accounts for about 80% of uric acid in the body, and is the main source of uric acid production in the body, including increased synthesis of purine and accelerated decomposition. The kidney is the main way to excrete uric acid, mainly through glomerular filtration and renal tubular transport metabolism. Increased blood uric acid for a long time can cause the formation of urate crystals and precipitates, which accumulate in the joint soft tissues and form “gout nodules”. Accumulation in the renal tubules and glomeruli will damage the glomerular vascular filtration membrane, causing renal insufficiency, leading to renal failure and uremia in severe cases. At the same time, hyperuricemia stimulates the blood vessel walls of the cardiovascular and cerebrovascular vessels, which can promote the occurrence of cardiovascular diseases. Finally, remind patients with kidney disease who need to limit protein intake, as well as various meats, to limit their intake.

Talk about the kidney membrane

The human body is a very magical structure, protected by layers. In the medical field, it is known that the kidney has a protective barrier, that is, the glomerular filtration membrane, and the middle layer is the basement membrane. Most nephritis is related to this. We talked about hematuria and proteinuria before, and there is a problem here, let’s talk about this membrane now! 1. The function of the kidney Traditional Chinese medicine talks about the main water of the kidney, and regulates the water channels to maintain the distribution and excretion of body fluid. In Western medicine, the kidney has the function of secreting urine, regulating water in the body, and expelling metabolites and poisons. Both Chinese and Western medicine are consistent. 2. Filtration Membrane & nbsp. & Nbsp. & Nbsp. When glomeruli filter water and toxins, they pass through three layers of filtration membranes. The membrane of the kidney is like a sieve. When the human blood passes by thousands of horses, it needs to pass through this barrier. The useful substances are left to be reabsorbed through the renal tubules, and harmful ingredients are filtered out and excreted from the body. (The picture comes from the upper kidney line) The first layer is composed of capillary endothelial cells. The second layer is the basement membrane of the glomeruli. The third layer is the epithelial cell layer of the glomeruli. Under normal circumstances, water, creatinine, urea and other “thin” toxins have relatively small molecular weights, so they can pass through the pores freely and pass through these three layers of filtration membranes. However, some “obese” substances, such as albumin, cannot pass through the filter membrane freely. Only when there is a problem with this barrier, the protein will leak out, so the protein can be seen in routine urine testing. This condition is an abnormal state, most of which are seen in various nephritis, such as lupus nephritis, purpuric nephritis, chronic glomerulonephritis and so on. The three-layer filtration membrane has the smallest pore size of the glomerular basement membrane and the strongest blocking effect on various substances. So how does the basement membrane change: 1. When the basement membrane thickens, collagen fibers proliferate, and there are some compounds loaded on the basement membrane, which destroys this membrane and affects permeability. 2. When the basement membrane becomes thinner, the permeability of the membrane increases, and red blood cells pass through the pore size, which can cause hereditary glomerular lesions. 3. When the basement membrane ruptures, it is more serious glomerular loss. The destruction of the membrane will cause various glomerular diseases, so it is important to protect this membrane. How to protect, simply say in daily life, regular work and rest, reasonable diet, physical fitness, avoid drug abuse, especially nephrotoxic drugs, regular medical examination, early detection and early treatment. 

What to do if there is low protein?

When low protein appears, is it necessary to have a high protein diet and protein supplement therapy? the answer is negative. 1. Simply supplementing the protein will not help the low protein. The basic reason for the low protein is that the protein leaks from the kidney in a large amount. If the protein is not leaked, the newly added protein will also be missed, so supplementing the protein alone will not help the hypoproteinemia. The cause of most glomerular filtration membrane damage is autoimmune damage, so many chronic kidney patients use hormones and immunosuppressants to suppress immunity and repair the damage. If the protein leakage is reduced or the leakage is stopped, the plasma protein quantity will naturally recover. In addition, the antihypertensive drugs of sartans and puli also have the effect of repairing damage and reducing proteinuria. 2. A large amount of proteinuria will further damage the kidneys. As mentioned earlier, the protein filtered from the glomeruli will be absorbed by the renal tubules. However, when the protein is filtered too much, it exceeds the ability of the renal tubules to absorb. The protein damages the renal tubules, and when damaged, it secretes cytokines which in turn further damage the glomeruli. Therefore, protein intake should be limited, and daily protein intake should be limited to 0.8g // Kg body weight. 3. Protein is added only in very serious cases. However, when the condition is particularly serious, plasma albumin <20g / L, the blood is in a hypercoagulable state, and edema is difficult to correct, an appropriate amount of albumin can be infused. The formation of proteinuria is because the gap on the glomerular basement membrane increases and the permeability increases, so that large protein can leak into the urine through the basement membrane to form proteinuria. At this time, if a large amount of high protein is eaten, the amount of protein leaking through the glomerular basement membrane per unit time will increase, and the waste generated by the human metabolism will increase, thereby increasing the burden on the kidney. For patients with kidney disease, excessive protein supplementation will not only make up for those lost, but will also accelerate the burden of the kidneys and accelerate the process of kidney function damage. Therefore, the usual diet should be: reduce the intake of non-quality protein such as: wheat starch, vermicelli, low-protein rice, low-protein noodles, etc. Proper intake of high-quality protein, such as: eggs, milk, lean meat, fish and shrimp, soy products, etc. As an important metabolic organ of the human body, the kidney's health is closely related to the daily diet. Therefore, it is important to choose a high-quality low-protein diet for patients with kidney disease. If you have any related problems such as kidney disease, you can directly write to Mo Feifan or leave a message online

Can kidney disease be prevented? Just keep doing this

Hematuria is the most likely symptom of patients with kidney disease. Hematuria often represents kidney disease and urinary disease. Today we talk about common glomerular disease with hematuria as the main symptom. 1. Glomerulonephritis hematuria after acute streptococcal infection is generally the first symptom of the disease. Almost all patients will have hematuria, and about 40% of patients have hematuria visible to the naked eye. 2. IgA nephropathy generally finds 40% -50% of patients with paroxysmal gross hematuria, which usually occurs within hours or 1-3 days after respiratory infection and gross hematuria, and occasionally occurs after gastrointestinal infection or after exercise After hematuria attack. And children will reach more than 80%. It is found that patients with persistent microscopic hematuria, that is, hematuria seen under the microscope account for 30% -50%. This kind of hematuria is often not obvious, but microscopic hematuria will always exist, accompanied by proteinuria, which can be seen in various generation. 3. Mesangial capillary glomerulonephritis, also called mesangial proliferative glomerulonephritis, 10% -20% of patients often present with episodes of hematuria after respiratory infection. 4. Mesangial proliferative glomerulonephritis has less gross hematuria, but there are many patients with microscopic hematuria, accounting for about 60% -70%. 5. Rapid Nephritis For patients with clinical manifestations of Rapid Nephritis Syndrome, if gross hematuria occurs, it may be accompanied by oliguria, anuria, and renal insufficiency, which requires vigilance. 6. Allergic purpura hematuria is relatively common, and at the same time as hematuria, there will be some changes on the skin and joints. 7. Primary systemic vasculitis and renal involvement almost all have hematuria, gross hematuria accounts for 1/3, proteinuria is relatively common, and some patients will also have nephrotic syndrome-like lesions. Some of these seven types of glomerular diseases, which are mainly hematuria, are not easily detected by the naked eye, and some are accompanied by other dangerous symptoms after hematuria. Therefore, this is also to tell you that when hematuria appears, it may not be noticeable to the naked eye, and often when our body is different, our kidneys have already been damaged. How can hematuria appear and be discovered in time? In fact, it is very simple and not strange, as long as you usually do a habit-physical examination. If you have any related problems such as kidney disease, you can directly send a letter to Dr. Mo Feifan

Always heard that diabetes affects the kidneys? Nephrology doctors come to analyze in depth for you

Hello everyone, I am a nephrologist, and my job is to deal with patients with kidney disease. I do n’t hide from everyone that in recent years, more and more people have suffered from uremia, but whether from an epidemiological perspective or from From the perspective of clinical experience, diabetes has basically become the main cause of uremia. This is especially true in Western countries. I think many people have heard of uremia, and even more, it is likened to “undead cancer”. Why can uremia be linked to diabetes? What is the causal relationship between the two? Today, I will come to the bottom for everyone. Let ’s take a look at what the epidemiology is. ● When it comes to diabetes, I think basically everyone has heard it more or less, because now it is a very common chronic species like high blood pressure. In fact, it has seriously threatened human health. According to the statistics of the International Diabetes Federation (IDF), the number of diabetic patients in the world has reached 366 million in 2011. Looking back, we look at the country. In the past 30 years, due to the rapid development of China ’s economy As a result of changes in lifestyles and an aging population, the prevalence of diabetes in China is also increasing rapidly. In 2012, the prevalence of diabetes in adults in China has risen to 11.6%, of which the prevalence of diabetes in men is 12.1% and the prevalence of women is 11% ● When it comes to diabetes, nature and kidneys are inseparable because of abnormal metabolism of diabetes It caused glomerular sclerosis. Note that this is one of the most common and serious chronic microvascular complications of diabetes. In Western countries, it has become the first disease that causes end-stage renal failure (uremia). In China, diabetic nephropathy is the second most common cause of end-stage renal disease after glomerular disease. Of course, this is still a few years ago, and its proportion has also increased year by year. Note that no matter from type 1 or type 2 diabetes, about 30% -40% of patients will develop into “diabetic nephropathy”. Once diabetic nephropathy patients have “proteinuria”, kidney function will be progressive over time Decreased to end-stage renal disease. What is the mechanism of diabetes caused kidney disease? ● For this pathogenesis, a large number of experts and scholars at home and abroad have tried to confirm through research to provide theoretical support for the treatment of diabetic nephropathy, but because the etiology of diabetic nephropathy is very complex, there is currently no uniform on this pathogenesis The conclusion is as follows: Abnormal glucose metabolism ▼ When researching the pathogenesis of diabetic nephropathy, the impact of the patient’s kidney on the “high blood sugar” is the focus of the study. Some people have tried to pass effective aldose reductase Looking for inhibitors, which can reduce the metabolism of the polyol pathway, thereby reducing or blocking the occurrence of diabetic nephropathy, here everyone may have some difficulties in understanding, I say the popular point is that I want to use this to find the root cause It really solves its treatment problems, but the impact of the production of aldose reductase inhibitors includes the following aspects: ▼ There is a clear correlation between the production rate of aldose reductase inhibitors and the blood glucose concentration of the body ▼ Metabolites The amount is determined by the contact time of protein and high concentration sugar The longer the half-life of white matter, the greater the accumulation of non-enzymatic glycates. When the blood sugar level in the body is high, the protein kinase C of the body is activated, which causes the contractility of the body’s blood vessels to change. ▼ Diabetes During the pathogenesis of kidney disease, excessive glucose load in the kidney tissue can induce abnormal expression of various growth factors. Its role involves changes in glomerular hemodynamics (I will analyze them separately below), extracellular matrix metabolism, cell proliferation and There are many aspects of cell hypertrophy. Note that cytokines are a type of soluble protein or glycoprotein that can specifically bind to target cell receptors, have high biological activity and a wide range of biological effects. They pass through autocrine, paracrine, and endocrine pathways. Play a role, regulate cell proliferation and differentiation, participate in various physiological activities of tissues and organs, and play an important role in various pathological injuries. Different cytokines also have different roles, in insulin, blood glucose levels, and glycosylation end products , Protein kinase C activity, changes in hemodynamics, vasoactive factors and other factors Mutual constraints and mutual adjustments constitute a complex cytokine network during the pathogenesis of diabetic nephropathy, especially transforming