1.What is diabetic nephropathy?
Diabetic nephropathy is one of the most common and serious complications of diabetes. It is an abnormal protein excretion and filtration caused by glomerular microangiopathy due to diabetes, and is clinically characterized by proteinuria, progressive renal impairment, hypertension, edema, and severe renal failure in advanced stages, and is one of the major causes of death in diabetic patients.
2.Does diabetic nephropathy occur in both type I and type II diabetes?
Both will. The proportion of diabetic nephropathy occurring in type I (IDDM) diabetes is higher, about 35%-50%, and the incidence of type II (NIDDM) is about 20%. However, because the incidence of type II patients in diabetic patients far exceeds that of type I, type II patients account for 70%-80% of diabetic kidney failure dialysis patients.
3.What are the clinical manifestations of diabetic nephropathy?
(1) Proteinuria: It can be the only manifestation in the early stage. During this period, proteinuria is intermittent and gradually develops into persistent, and urine microscopy can reveal leukocytes and tubular type.
(2) Edema: Patients with diabetic nephropathy usually do not have edema in the early stage, and a few patients may have mild edema after the decrease of plasma protein. When the 24-hour urine protein exceeds 3.5 grams, edema is obvious.
(3) Hypertension: Hypertension is seen in diabetic patients with long-term proteinuria, but it is not very serious. Hypertension can aggravate nephropathy.
(4) Anemia: Patients with diabetic nephropathy who have significant azotemia may have mild to moderate anemia. Anemia is a disorder of erythropoiesis.
(5) Abnormal renal function: The interval from the appearance of proteinuria to abnormal renal function varies greatly. If diabetes is well controlled, proteinuria can be present for many years without abnormal renal function. If the control is not good, renal insufficiency will gradually aggravate.
4.Diabetic nephropathy staging?
Currently, the internationally accepted staging of diabetic nephropathy is the 1987 Mogensen staging. mogensen divided type l diabetic nephropathy into 5 stages. morgensen staging criteria are as follows.
Stage I: l clinical manifestations without nephropathy (glomerular hyperfiltration phase). This stage is characterized by renal hypertrophy and increased glomerular filtration rate (GFR). Biochemical examination GFR > 150 ml/min and urinary microalbumin excretion rate (UAER) was normal. Pathological examination only showed an increase in glomerular volume and the triple high phenomenon of glomerular hyperperfusion, hyperhydrostatic pressure and hyperfiltration.
Stage II: Normal albuminuria stage. Patients in this stage also have no obvious clinical manifestations, and the duration of the disease is more than 5 years. microalbumin appears in the urine, and the microalbumin excretion rate (UAER) at rest is normal (<20 μg/min), but the UAER can be mildly increased during stress. gfr is normal or mildly increased. Pathological examination shows thickened gbm and increased thylakoid stroma.
Stage III: microalbuminuria stage. The clinical characteristics of this stage are persistent microalbuminuria, UAER between 20-200 μg/min, 24-hour urine microalbumin quantification between 30-300 mg, urinary routine protein is mostly negative; glomerular filtration rate is normal. Pathological examination revealed diffuse diabetic glomerulosclerosis.
Stage IV: clinical proteinuria stage. Urine routine protein is persistently positive, 24-hour urine protein quantification >0.5g, UAER >200μg/min, and glomerular filtration rate gradually decreases. Clinical symptoms of nephrotic syndrome, decreased creatinine clearance, and hypertension were present. Pathological examination revealed nodular diabetic glomerulosclerosis with partial glomerular desolation.
Stage V: End-stage renal failure. Glomerular filtration rate decreases further, GFR < 15 ml< span="">/min or dialysis has been performed, often with massive proteinuria. Chronic renal failure was clinically present. Pathological examination reveals nodular diabetic glomerulosclerosis in the context of a majority of glomerular desolation.
5.When to screen for diabetic nephropathy?
In type 1 diabetic patients, the first screening test for microalbuminuria was recommended 5 years after diagnosis, however, there are reports showing that microalbuminuria occurs in many patients within the first 5 years, especially those with poor glycemic and lipid control, obesity, and blood pressure at the high end of normal; type 1 diabetic patients, especially those with poor metabolic control and obese type 1 diabetic patients, should undergo microalbuminuria screening 1 year after the diagnosis of diabetes. The test for albuminuria should be performed 1 year after the diagnosis of diabetes.
Patients with type 2 diabetes need to be screened for diabetic nephropathy from the time of diagnosis, as it has been reported that about 7% already have microalbuminuria.
However, a positive test does not confirm the diagnosis of persistent microalbuminuria, which needs to be repeated within 3-6 months, and the diagnosis can be confirmed if two of the three tests are positive; after the first test, both type 1 and type 2 diabetic patients should be examined once a year thereafter.
6.What are the indicators of diabetic nephropathy screening test?
Urine albumin creatinine ratio (ACR), serum creatinine and glomerular filtration rate (eGFR).
7.Does diabetic patients have diabetic nephropathy once they have microalbuminuria?
Microalbuminuria is not only associated with diabetic nephropathy, but also with various other complications of diabetes, including hypertension, hyperlipidemia, atherosclerosis and cardiovascular disease. Therefore, the presence of microalbuminuria does not necessarily mean that diabetic nephropathy has occurred, and it is controversial whether its presence necessarily progresses to significant proteinuria and then chronic renal decline. In several large series of long-term observations, it was found that only 30%-45% of diabetic patients with microalbuminuria turned into clinically significant proteinuria in 10 years, and another 30% of microalbuminuria disappeared, which is more obvious in type 2 diabetes. This is more obvious in type 2 diabetes. Therefore, it should be examined several times and followed up continuously before it can be determined.
8.Does the presence of dominant proteinuria (24-hour urine protein quantification >0.5g) in diabetic patients mean that they have diabetic nephropathy?
There are three possibilities for diabetic patients to have dominant proteinuria: (1) diabetes mellitus complicated by diabetic nephropathy; (2) diabetes mellitus combined with non-diabetic nephropathy (NDRD); (3) diabetic nephropathy combined with NDRD. Therefore, it cannot be said that once a diabetic patient has dominant proteinuria, he or she has diabetic nephropathy. To clarify the cause of dominant proteinuria, only kidney biopsy puncture can be performed to clarify the diagnosis through renal pathology.
9.What clinical conditions should be considered when diabetes mellitus is combined with other kidney diseases?
Diabetic patients with proteinuria must carefully exclude other possible causes of proteinuria before diagnosing diabetic nephropathy, especially for type 2 diabetic patients who cannot clearly identify the time of onset. Diabetes mellitus combined with other nephropathies should be considered clinically in the following cases: (1) absence of diabetic retinopathy; (2) low or rapidly decreasing GFR; (3) rapidly increasing proteinuria or nephrotic syndrome; (4) intractable hypertension; (5) active manifestation of urinary sediment with predominantly aberrant red blood cells or with erythrocyte tubular pattern; (6) signs or symptoms of other systemic diseases; (7) GFR decrease of more than 30% within 2-3 months after the start of ACEI/ARB treatment, etc. Renal biopsy should be considered in the above cases to exclude other causes of glomerulopathy.
10.How should diabetic nephropathy be treated?
Active prevention and treatment of early diabetic nephropathy is because microalbuminuria, i.e. early diabetic nephropathy, is reversible, unlike massive albuminuria, i.e. clinical diabetic nephropathy.
Integrated treatment should be given after entering clinical diabetic nephropathy.
In the late stage, renal replacement therapy (hemodialysis, peritoneal dialysis and renal transplantation) is given.
11.The goal of controlling blood sugar in diabetic nephropathy?
Strictly control blood glucose, ideally the blood glucose at any moment should be controlled within the normal range, the target of blood glucose control is fasting blood glucose <6.0mmol/L, 2 hours after meal blood glucose <8.0mmol/L, glycosylated hemoglobin <7%.
12. Types of oral hypoglycemic drugs for patients with diabetic nephropathy.
The oral hypoglycemic drugs frequently used in clinical practice usually cover the following types.
First, sulfonylureas: usually the hypoglycemic process can effectively reduce the secretion of insulin;
Second, biguanides: usually used in extra-islet tissues to prevent the digestion of glucose by the intestinal wall and to prevent gluconeogenesis;
Third, alpha glucosidase inhibitors: usually used to inhibit alpha glucosidase activity in the upper part of the small intestine, reducing the digestion of oligosaccharides and monosaccharides;
Fourth, insulin sensitizers: in the past few years, thiazolidinedione derivatives have emerged to reflect the function of enhancing insulin sensitivity. The thiazolidinediones pioglitazone and rosiglitazone are able to reduce insulin resistance, and the latter uses binding to peroxisome proliferator-activated receptor 7 to improve islet β-cell action;
Fifth, non-sulfonylurea insulin stimulants: they can give insulin relief as soon as possible, greatly reduce postprandial blood glucose, and are consumed before eating, also known as mealtime glucose regulators. These drugs have a short functional time, rarely form hypoglycemia, and most use the gastrointestinal tract excretion, with kidney function victims can also be used.
13. Precautions when choosing sulfonylureas for patients with diabetic nephropathy.
Most sulfonylureas are metabolized by the liver and excreted from the kidneys, and are prone to accumulation when GFR<60 ml/min leading to intractable hypoglycemia, so they are prohibited when the liver and kidneys are incompetent, especially long-acting preparations (such as glibenclamide).
Gliquidone is mainly excreted via biliary tract, and is the only drug among sulfonylureas with low renal excretion rate (about 5%). It is safe to use when GFR<60 ml< span="">/min, but should be prohibited when GFR<30 ml/min.
In addition, patients with ischemic cardiomyopathy should avoid the use of glibenclamide, so as not to damage the ischemic pre-adaptation protection mechanism and aggravate myocardial ischemia.
14. Precautions when choosing α glucosidase inhibitors in patients with diabetic nephropathy.
Alpha glucosidase inhibitors are overwhelmingly not absorbed after oral administration, and only 2% are excreted by the kidneys, and can be used in patients with mild renal impairment, but are prohibited when the serum creatinine is ≥176.8 μmoL/L.
15, diabetic nephropathy patients choose thiazolidinediones precautions.
Thiazolidinediones are mainly excreted from the feces via the biliary tract, and a small amount is excreted from the urine as metabolites, so patients with renal failure do not need to adjust the dose for patients with diabetic nephropathy; but thiazolidinediones can also cause water and sodium retention, weight gain, increased risk of heart failure, so obvious edema, with heart disease and heart failure tendency, liver disease and renal failure patients should be used with caution.
16. Precautions when choosing non-sulfonylurea insulin secretagogues for patients with diabetic nephropathy.
Non-sulfonylurea insulin secretagogues, by binding to sulfonylurea receptors on the pancreatic beta-cell membrane, stimulate the pancreas to secrete insulin faster and more after meals, thus effectively controlling postprandial hyperglycemia. These drugs, including repaglinide and nateglinide, appear to stimulate first-phase insulin secretion. Glinides are primarily metabolized in the liver and their metabolites have no hypoglycemic effect and are mostly cleared with bile, with only about 8% of the dose excreted via the kidneys. Studies have shown that there is no significant difference in the half-life of nateglinide in moderate-to-severe renal insufficiency compared with the healthy population, especially for elderly and diabetic nephropathy patients, and should be used with caution in patients with hepatic insufficiency.
17, the choice of hypoglycemic drugs for patients with diabetic nephropathy.
Patients with diabetic nephropathy should select glucose-lowering drugs according to the level of renal function.
Glipizide, Reglanet-type insulin promoters, alpha-glucosidase inhibitors and other oral hypoglycemic drugs can be used for patients with mild to moderate renal insufficiency;
Thiazolidinediones (e.g., vindia) have renoprotective effects (lowering blood pressure, improving vascular endothelial function, inhibiting inflammatory response) independent of glucose lowering, in addition to improving insulin resistance and lowering blood glucose;
Early use of insulin in patients with diabetic nephropathy with renal insufficiency can effectively control blood glucose without liver and kidney damage;
Patients with diabetic nephropathy should not take metformin or hypoglycemia.
18.Why diabetic nephropathy patients should not take metformin or hypoglycemic drugs?
Metformin or hypoglycemia is rapidly absorbed after oral administration, and 90% of the drug is excreted from the urine in 24 hours. This drug can promote anaerobic enzymes and produce lactic acid. When diabetes is complicated by nephropathy, the excretion of lactic acid metabolites is impaired, acid accumulates in the body, which increases the burden on the kidneys and promotes the deterioration of kidney function, and it is easy to induce lactic acidosis to occur.
19, diabetic nephropathy patients in oral hypoglycemic drugs, should pay attention to what drugs have interactions with?
ACEI/ARB is the first-line drug for diabetic patients to lower blood pressure and proteinuria, which can improve the body’s sensitivity to insulin without affecting the metabolism of sugar and fat, and the dose of oral hypoglycemic drugs can be reduced appropriately when combined with them. When combined with moderate doses of aspirin, the hypoglycemic effect of oral hypoglycemic drugs is enhanced.
Non-selective β-blockers (e.g., insulin) can inhibit insulin secretion from the pancreas, reduce the body’s sensitivity to insulin and make glucose tolerance decline; they can also inhibit the decomposition of liver glycogen, affect lipid metabolism and aggravate hypoglycemic reactions caused by hypoglycemic drugs, which should be avoided in diabetic patients as much as possible, and if needed, the dosage of hypoglycemic drugs should be adjusted and blood glucose monitoring should be strengthened.
Itraconazole/Fluconazole increase the blood concentration of Reglanet, and should be avoided in combination. Thiazide diuretics can cause hypokalemia, and low potassium can reduce insulin secretion and decrease insulin sensitivity. Combining with sulfonylureas can cause severe hyperglycemia and hyperosmolar coma, so caution is needed when combining the two drugs.
20. Characteristics of insulin metabolism in patients with diabetic nephropathy.
The half-life of insulin in blood is very short (<5m i n), and insulin is eliminated in the liver by 60% to 80%, in the kidney by 10% to 20%, and in muscle and fat by 10% to 20%, and only less than 1% of insulin is excreted in the urine as a prototype. It was found that the clearance of insulin by the kidneys of patients with diabetic nephropathy is reduced by 30% to 40%.
21. Types of insulin in patients with diabetic nephropathy.
According to the different time of insulin action, it is divided into the following categories: rapid-acting insulin (menthol insulin, lysergic insulin), short-acting insulin, medium-acting insulin (N P H), long-acting insulin, extra-long-acting insulin (glargine insulin, dettol insulin) and premixed insulin.
22.How to choose insulin for patients with diabetic nephropathy?
Fast-acting insulin analogues: lysergic acid insulin (Ural) has an onset of action of 5-15 min, a peak effect of 1-1.5 h and lasts 2-4 h after subcutaneous injection; menthol insulin (Novalis) has an onset of action of 10-20 min, a maximum effect of 0.7-1.5 h and lasts 3-3.5 h. Compared with conventional insulin, fast-acting insulin analogues have a higher free insulin peak in the blood than human insulin. Compared with conventional insulin, the peak free insulin in blood is 2-3 times higher than that of human insulin, and the duration of action is also significantly shorter, which is unique in reducing the occurrence of hypoglycemia in diabetic nephropathy.
The solubility of glargine insulin is reduced in physiological body fluids, and after subcutaneous injection, local precipitation is formed and slowly decomposed and absorbed, and its long-lasting effect is achieved by subcutaneous slow-release technology, rather than by its own long metabolism time. The concentration of glargine insulin is relatively stable and without obvious peak in circulation, which can reduce the incidence of hypoglycemia and is more suitable for patients with end-stage renal disease than intermediate-acting insulin.
Deferox insulin can bind to plasma albumin and release slowly to target organs after dissociation, thus it is not suitable for use in patients with nephrotic syndrome.
For dialysis patients, due to the diversity of dialysis regimens and the many factors affecting blood glucose, a daily basal-mealtime insulin regimen is appropriate for insulin therapy.
Pre-mixed insulin is not recommended for use in diabetic abdominal dialysis patients because of the great variability of absorption between individuals and the small controllability of insulin metabolism.
23.What is the dosage of insulin for patients with diabetic nephropathy?
The dosage of insulin in patients with diabetic nephropathy can be determined according to the stage of chronic kidney disease (CKD).
Patients with CKD stage 1 to 2 should weigh the advantages and disadvantages, and any kind of oral hypoglycemic drug can be applied at this time;
In patients with CKD stage 3 to 5, some oral medications should be used with caution or reduced dosage, and insulin therapy should be initiated. Impaired renal function is accompanied by increased insulin resistance and decreased insulin clearance, and the net effect is a decrease in insulin requirement. There is no statistical difference in the amount of insulin reduction in patients with different types of diabetes, and a very small number of patients with type 2 diabetes have significantly reduced insulin dosage or even discontinued it without hyperglycemia when combined with severe renal dysfunction. The American College of Physicians recommends that insulin dosage be reduced by 25% if GFR falls to 10-15 ml/min and by 50% if GFR is <10 ml/min.
24.Patients with diabetes mellitus in CKD stage 3 to 5, considerations for glucose-lowering treatment.
Patients with CKD stage 3 to 5, glucose-lowering drugs should be treated with insulin, preferably with basal-mealtime insulin dosing regimen, mealtime insulin is preferable to rapid-acting insulin, blood glucose should be closely monitored, and the dose should be adjusted according to GFR level to avoid the occurrence of hypoglycemia as much as possible.
25.Why is hypoglycemia more likely to occur in diabetic nephropathy when treated with insulin?
Hypoglycemia is a common complication of insulin therapy. When diabetes combined with renal disease, especially uremia, patients often have gastrointestinal symptoms, poor appetite and low food intake; decreased renal inactivation of insulin and prolonged insulin half-life; gastric vegetative neuropathy, delayed gastric emptying and altered food digestion and absorption; reduced gluconeogenesis and glycogen storage in the kidney; there may be different degrees of anterior pituitary hypofunction, making insulin antagonist hormone levels are reduced, etc. Therefore, in patients with diabetes mellitus combined with CKD, attention should be paid to adjusting the dose of insulin regardless of the type, otherwise, hypoglycemia is likely to occur.
26.The goal of blood pressure lowering in patients with diabetic nephropathy?
Effective control of blood pressure is needed, and the blood pressure should be controlled below 140/90 mmHg in adults, and can be moderately relaxed in the elderly.
27.The choice of antihypertensive drugs for patients with diabetic nephropathy?
Angiotensin-converting enzyme inhibitors (ACEI) (including captopril, elapril, fosinopril, ramipril, perindopril, midazapril, etc.) and angiotensin II receptor antagonists (ARB) (including colesartan, valsartan, irbesartan, olmesartanate, etc.) are preferred and used early (when blood pressure is normal);
Calcium antagonists (CCB) can also be used as first-line drugs without adverse effects on glucose and lipid metabolism, and long-acting formulations or short-acting controlled-release agents are recommended;
β-blockers can aggravate metabolic disorders, mask hypoglycemic symptoms and aggravate peripheral vascular disease, so they should be used with caution and β1-blockers should be chosen when necessary;
Alpha-blockers have a definite antihypertensive effect, have no effect on glucose metabolism, and can improve lipid metabolism and reduce the difficulty of urination in patients with prostatic hyperplasia, but can cause postural hypotension, and should be used with caution in the elderly and with vegetative neuropathy;
Diuretics are not used as the first line of treatment. Thiazide diuretics have many dose-related side effects, such as elevated blood glucose, hypokalemia and hyperlipidemia, so the dose should be small.
28, ACEI/ARB drugs are antihypertensive drugs, why do doctors say that these drugs can reduce urine protein and delay the deterioration of renal function?
ACEI/ARB are strong antihypertensive drugs, which can dilate both glomerular inlet and outlet small arteries, but their dilating effect on the outlet small arteries is stronger than that on the inlet small arteries, which eventually leads to the reduction of glomerular capillary pressure and reduces the workload of renal units, thus reducing urine protein, and secondly, it can also reduce glomerular capillary venous pressure; increase the selective permeability of glomerular basement membrane, and reduce the filtration of glomerular protein. Decrease the filtration of glomerular protein; and reduce the ability of glomerular thylakoid cells to take up and remove macromolecules, which makes the progressive decline of renal function delayed.
29.What are the precautions in the use of ACEI/ARB drugs?
ACEI/ARB drugs are the first-line drugs for patients with diabetic nephropathy and should be used as early as possible, but in terms of their use, attention should be paid to
They are contraindicated in patients with upper renal artery stenosis and should be used with caution in non-dialysis patients with renal artery stenosis on one side or (and) blood creatinine greater than 265 μmol/L (3 mg/dl), as they may cause a further decrease in glomerular filtration rate and cause a dramatic deterioration in renal function, further impairing residual renal function.
Because these two classes of drugs can cause irritating dry cough, they should be used with caution in patients with inherent cough and asthma. Pharmacology indicates that ARBs hardly cause dry cough, but they are still found to cause dry cough during clinical use.
In addition, ACEI/ARB drugs can increase blood potassium, so patients with high potassium and chronic renal insufficiency should avoid using them together with potassium-protective diuretics, β-blockers and potassium supplements.
30.Why are CCB drugs also recommended as first-line drugs for the treatment of hypertension in diabetic nephropathy?
Although in theory and animal experiments, calcium channel blockers inhibit Ca flow across the cell membrane into pancreatic β-cells and affect insulin secretion, in clinical practice, small doses of this drug can lower blood pressure without affecting insulin secretion and glucose metabolism. Moreover, these calcium antagonists have no side effects on the central nervous system and cardiovascular system, and do not affect lipid metabolism. Because of its vasodilating effect, renal blood flow increases and sodium retention decreases, while it may favor the improvement of renal hemodynamics and urinary protein excretion in diabetic patients. Therefore, for most diabetic nephropathy hypertension or, the combination of ACEI/ARB and CCB can be preferred, of course, there are now a combination of these two types of drugs available.
31, dietary prescription for diabetic nephropathy patients?
Diet for diabetic nephropathy: It is important to ensure adequate calories and nutrition, but also to limit carbohydrates, fats and proteins.
Caloric supply must be sufficient to maintain normal physiological needs. The criterion of whether the calorie intake can meet the body’s needs is that the patient’s weight is not too high or too low and can be maintained steadily within the standard range for a long time. Carbohydrates account for 55%-60% of the caloric intake, fat accounts for 20%-25%, and protein accounts for 15%-20%.
Too much fat in the body can lead to atherosclerosis, so the intake of fat should be limited. It is best to use vegetable oils instead of animal fats, such as olive oil, peanut oil is richer in monounsaturated fatty acids, can also be used as a source of energy.
32.After suffering from diabetic nephropathy, the doctor said to reduce the intake of protein. What should I eat then?
After suffering from diabetic nephropathy, patients will be asked to reduce dietary protein. While the calories are reduced, the patient needs to eat additional foods that are high in calories but low in protein to replace them. The calorie deficit is partially replaced with carbohydrate-rich foods such as lotus root powder, almond cream, wheat starch, etc. (Starch is a product of flour, mung beans, sweet potatoes, etc. after their protein is extracted. About 20 grams of starch by food exchange has the same effect on blood sugar as 25 grams of raw flour.) These foods contain almost no vegetable protein, but are high in calories almost as much as in the same amount of flour. You can also add vegetable oils rich in monounsaturated fatty acids: olive oil, tea seed oil, for diabetics will not cause an increase in blood sugar and is conducive to lowering blood lipids.
33.Why should diabetic nephropathy patients have a low protein diet?
Clinical and experimental studies have observed that high protein diet can increase glomerular perfusion and pressure and aggravate the renal hemodynamic changes caused by diabetes, while low protein diet can slow down the process of renal function damage in diabetic patients.
34.To control blood sugar means to eat less carbohydrates, right?
Some people with diabetic nephropathy mistakenly believe that to control blood sugar, the less carbohydrates they eat, the better. In fact, carbohydrates provide the body with about 50% to 60% of dietary energy (equivalent to about 4-6 taels of raw food), if the food intake is not enough, the body will consume protein and fat to produce heat to maintain life requirements, the result will make diabetic nephropathy patients with ketoacidosis, increased levels of toxins, malnutrition, etc.. If caloric intake is too high then you need to control the total dietary calories, including dietary protein, fat and carbohydrates.
35.How to detect weight change after diabetic nephropathy in patients?
It is very important to maintain an appropriate weight. Wake up early in the morning on an empty stomach, empty urine and stool, wear very little clothing and weigh, if the weight does not change within 2-3 weeks, it means that the diet calories and consumption is basically the same.
36.What should I do to maintain my weight for normal and thin diabetic nephropathy patients?
For diabetic nephropathy patients with normal body type and thin, the intake of starch and vegetable oil should be increased appropriately when reducing dietary protein food to maintain the intake of calories with the same as their previous one, so that the blood sugar is well controlled.
37.For the obese diabetic nephropathy patients, how should they reduce their weight?
Obese diabetic nephropathy patients often need to lose weight, if you need to lose weight should ask a nutritionist to help you maintain a healthy condition slowly reduce weight. If you are gaining weight rapidly, please tell your doctor. Rapid weight gain with shortness of breath and increased blood pressure should be alert to the possibility of too much water in the body.
38.How much protein should diabetic nephropathy patients consume every day?
The recommended protein intake for patients with diabetic nephropathy in chronic kidney stage 1 to 3 is 0.75 g/standard kg body weight/day + the amount of protein lost in urine each day. For example, a patient who is 155 cm tall and has a 24-hour urine protein quantification of 2 grams, that is, 38 + 2 = 40 grams of protein per day;
The recommended protein intake for patients in chronic kidney stage 4 and 5 (not on dialysis) is 0.6 g/standard kg body weight/day + the amount of protein lost in urine per day, for example, a patient of 155 cm height with a 24-hour urine protein quantification of 2 g, i.e. 30 + 2 = 32 g of dietary protein per day. Of which 50% is high quality protein. Dietitians do not recommend dietary protein consistently below 30 grams per day in patients without medical aspects of nutritional support.
39. Why do doctors recommend diabetic nephropathy patients to take keto acid supplements?
In order to prevent malnutrition in patients with diabetic nephropathy, it is recommended that they be supplemented with keto acids when they are on a low protein diet. -Keto acids are amino acid precursors that can be converted to the corresponding amino acids in the body through transamination or amination. -Keto acid can reduce azotemia, improve metabolic acidosis; replenish the body’s lack of amino acids, improve protein metabolism; reduce insulin resistance, improve glucose metabolism; increase lipase activity, improve lipid metabolism; reduce blood phosphorus, increase blood calcium, reduce secondary hyperparathyroidism; reduce protein urine excretion, delay the progression of chronic kidney disease.
40.How to eat salt in diabetic nephropathy?
Low-salt diet is not only good for blood pressure control, but also good for early nephropathy control and reducing edema symptoms. It is best to control the amount of salt within 6 grams per day. If it is accompanied by edema, hypertension and heart failure, the salt intake should be lower. In addition. You should also eat less sodium-rich food, such as various kinds of pickled vegetables, shrimp, curd, soy products, etc.
41.Why do you advocate early dialysis for diabetic nephropathy patients?
Generally speaking, patients with diabetic nephropathy show symptoms of uremia earlier than those with non-diabetic nephropathy. In diabetic nephropathy, the serum creatinine (Scr) level often does not reflect the severity of the disease, and its water and sodium retention, anemia and systemic toxicity symptoms are more significant compared with non-diabetic end-stage renal failure. For this reason, patients with diabetic nephropathy renal failure should receive replacement therapy earlier than patients with non-diabetic renal failure.
42. Indications for dialysis in patients with diabetic nephropathy.
(1) Scr>440-528μmol/L, when there are serious complications such as the presence of severe metabolic acidosis, water and sodium retention, gastrointestinal reactions, heart failure, hyperkalemia, dialysis treatment should be started at about 440μmol/L Scr; if the general condition is acceptable and there are no serious complications, dialysis treatment should also be started at 528μmol/L Scr;
(2) Endogenous creatinine clearance (Ccr) <15 ml/min. For elderly and wasted patients, Ccr should prevail. In elderly diabetic patients with malnutrition and nephrotic syndrome, receiving dialysis treatment at Ccr15-20 ml/min can improve the prognosis.
43.What are the advantages and disadvantages of hemodialysis and peritoneal dialysis for patients with diabetic nephropathy?
Hemodialysis is good for blood glucose control and has good dialysis adequacy, but it is difficult to establish arteriovenous fistula and cardiovascular accidents are likely to occur during dialysis; peritoneal dialysis is often used as continuous ambulatory peritoneal dialysis (CAPD), which has the advantage of helping to protect residual renal function in the short term and can be performed in patients with cardiovascular accidents because anticoagulants are not necessary. However, the use of glucose as an osmotic solute makes it difficult to control the patient’s blood sugar level.
44.How should patients with diabetic nephropathy choose their dialysis method?
Peritoneal dialysis (PD) has less impact on the cardiovascular system and has a stronger effect on protecting residual renal function than hemodialysis (HD), but since most PD fluids use dextrose as the main osmotic agent, not only is the glucose content high, but after dialysis it can cause metabolic disorders (such as hyperglycemia, hyperinsulinemia, hyperlipidemia and obesity), and after the glucose in the dialysis fluid is absorbed, it can produce a large amount of of end-stage glycosylation products (AGEs) and lead to thickening of blood vessel walls, inducing tissue ischemia and other dysfunctions. Some studies have shown that the survival rate of PD patients with diabetic nephropathy under 55 years of age is comparable to that of PD patients with non-diabetic nephropathy; however, for older PD patients with diabetic nephropathy over 60 years of age, the survival rate decreases significantly. Therefore, clinically, younger patients with diabetic nephropathy tend to prefer PD, while older patients with diabetic nephropathy are mainly on HD. Of course, the choice of dialysis modality depends on the specific clinical condition of the patient.
45. Is kidney transplantation available for patients with end-stage diabetic nephropathy?
For patients with end-stage diabetic nephropathy, kidney transplantation is currently the most effective treatment, accounting for about 20% of kidney transplant patients in the United States. In recent years, the 5-year survival rate for cadaveric kidney transplantation is 79% and 91% for living kidney transplantation, while the 5-year survival rate for those on dialysis is only 43%. The survival rate of living kidneys, especially those from relatives, is significantly higher than that of cadaveric kidney transplants. However, the survival rate of transplanted kidneys in patients with diabetic nephropathy is still 10% lower than that of non-diabetic patients. Kidney transplantation alone does not prevent the reoccurrence of diabetic nephropathy or improve other diabetic comorbidities.
Combined pancreas-kidney transplantation has the potential to normalize glycosylated hemoglobin and creatinine levels and improve other diabetic comorbidities, so the patient’s quality of life is better than that of the kidney transplant recipient alone.
46. What is the prevention strategy for diabetic nephropathy?
Class I prevention: prevent the occurrence and development of normal protein-free urine to microalbuminuria.
Grade II prevention: prevent the development of microalbuminuria to clinical proteinuria.
Class III prevention: prevent the progression of clinical proteinuria to end-stage nephropathy.
47.What are the specific measures for prevention of diabetic nephropathy?
Strict control of hyperglycemia; strict control of hypertension; regulation of disorders of lipid metabolism; smoking cessation; low protein diet; weight reduction; reduction of insulin resistance, etc.