Common kidney diseases can be divided into two categories, namely glomerular diseases and tubulointerstitial diseases. Glomerular diseases are characterized by obvious proteinuria (often > 1.5g/24h) and hematuria (microscopic or gross hematuria). If there is a large amount of proteinuria (> 3.5g/24h) or glomerular hematuria (abnormal red blood cells in urine), it can definitely be a glomerular disease. Renal tubular and interstitial diseases are characterized by mild proteinuria (
According to the above classification, the second step of clinical diagnosis should be to determine which syndrome it belongs to. Glomerular diseases can be divided into the following syndromes:
1. Acute glomerulonephritis syndrome has a sudden onset, including hematuria, proteinuria, tubular urine, edema and hypertension.
2. Acute glomerulonephritis syndrome has an acute onset and rapid development, and oliguria or even anuria will soon appear; Hematuria, proteinuria, tubular urine; There may be edema, and high blood pressure is often mild. At first it was similar to severe acute nephritis, but it continued to develop rapidly, often accompanied by anemia and hypoproteinemia. Renal function deteriorated rapidly, and uremia appeared within weeks to months.
3. Asymptomatic proteinuria and/or hematuria without edema, hypertension, azotemia and other clinical manifestations, mainly manifested as mild to moderate proteinuria (often
4. Nephrotic syndrome with massive proteinuria (>; 3.5g/24h) and hypoproteinemia < 30g/L, (3 g/D 1), which may lead to obvious edema and increased blood cholesterol and other lipids.
5. Chronic glomerulonephritis syndrome mostly has long-term hypertension, edema and abnormal urine routine examination, proteinuria, tubular urine and a small amount of red blood cells and white blood cells: renal function is slightly damaged, and it progresses slowly without stopping. Finally, both kidneys shrink symmetrically, and renal failure may occur in the late stage.
After determining what kind of syndrome glomerular disease belongs to, the next step is to think about which basic disease causes the syndrome. We must rule out the possibility of glomerular damage (secondary glomerular disease) caused by systemic diseases in order to diagnose primary glomerular disease. Common secondary glomerular damage includes: systemic lupus erythematosus, vasculitis syndrome, allergic purpura, diabetic nephropathy, amyloidosis, infective endocarditis, hepatitis, pregnancy-induced hypertension syndrome, abnormal proteinemia, hereditary nephritis and so on.
Typical interstitial nephritis is characterized by mild proteinuria, albuminuria and occasional albuminuria. Renal tubular dysfunction is more serious and prominent than glomerulus. Renal tubular dysfunction is characterized by renal concentration dysfunction, renal sodium loss, potassium retention or loss, and hyperchlorinated acidosis. Radionuclide renal dynamic imaging showed asymmetry of bilateral renal function damage. The kidney may have asymmetric scar formation and calyx deformation, and in some cases, unilateral renal atrophy may occur. Most patients have their own special basic diseases. The common basic diseases of chronic interstitial nephritis are: chronic pyelonephritis, reflux nephropathy, renal nipple necrosis, painkiller nephropathy, heavy metal poisoning, uric acid nephropathy, hypercalcemia nephropathy, hypokalemia nephropathy and so on.
It is quite common to misdiagnose chronic interstitial nephritis as chronic nephritis in clinic. Differential diagnosis in this respect is very important. Many chronic interstitial nephritis can be treated, and its renal function deteriorates more slowly than chronic nephritis.
Key points of differential diagnosis: ① Chronic glomerulonephritis often has edema, hypertension and other medical history and manifestations; Chronic interstitial nephritis is often absent, and it is often diagnosed and treated because of other diseases or unexpected findings in routine physical examination; ② The former often has a lot of proteinuria (often >); 1.5g/24h), there are many types of cast or abnormal red blood cells in urine sediment, the latter has only mild proteinuria, mostly ~+,and the 24-hour urine protein quantification is often.
Second, we should know that CKD is a lifelong disease, and its treatment is different from traditional acute diseases. This is manifested in the following aspects: 1 and CKD's treatment goal is not to cure, but to restore the normal life and rehabilitation of patients; 2. Drug therapy is often not the core of CKD prevention and treatment, but the adjustment of patients' lifestyle is the key to CKD prevention and treatment, so CKD is also called lifestyle disease; 3. Medical staff can't play a leading role in the treatment of chronic kidney disease. Medical staff are only professional tutors for patients. The role of medical staff is not only to diagnose and prescribe drugs for patients, but more importantly, to teach patients appropriate knowledge and guide them to master corresponding skills to change their lifestyles, such as low-salt diet and reasonable dietary intake. Patients are not passively treated by medical staff, but actively participate in various treatment decisions; 4. Many times, the prevention and treatment of CKD is carried out by patients themselves, so the self-management of patients is the key to the success or failure of disease prevention and treatment. Unlike acute diseases, the curative effect depends more on the treatment of medical staff. The self-management of patients plays a vital role in the treatment of chronic kidney disease. Patients and their families need to master appropriate knowledge, and those who know are fearless. However, our existing medical system fails to provide patients with sufficient and appropriate information, nor does it allow patients to actively participate in the decision-making of disease treatment.
Secondary prevention refers to timely treatment of CKD patients, delaying the deterioration of renal function and preventing uremia.
The common clinical manifestations of patients with chronic kidney disease are proteinuria, edema and hypertension, and with the progressive decline of renal function, digestive tract symptoms such as anemia, calcium and phosphorus metabolism disorder, malnutrition, metabolic acidosis and nausea and vomiting gradually appear. Drug therapy for chronic kidney disease is also aimed at these manifestations. Drugs commonly used in clinic to treat kidney diseases are:
Immunosuppressants: Glucocorticoid (prednisone) and cytotoxic drugs (cyclophosphamide) are the most commonly used drugs to treat various primary or secondary glomerulonephritis. Glucocorticoid can inhibit immune and inflammatory reactions in many ways, affect the permeability of glomerular basement membrane, and play its role in eliminating urinary protein. The principle of hormone therapy is that the initial dose should be sufficient, the reduction should be slow and the maintenance time should be long. Other immunosuppressants, such as cyclosporine, xiaoxi, leflunomide and tripterygium wilfordii polyglycoside, can also be used for patients who can't use hormones, or patients who can't respond to hormone and cytotoxic drugs. Immunosuppressants often have great side effects and need to be closely monitored under the guidance of experts.
Lowering blood pressure: angiotensin converting enzyme inhibitors and angiotensin Ⅱ receptor antagonists can block the renin-angiotensin-aldosterone system. In addition to lowering blood pressure, they also have a unique renal protective effect, which can reduce proteinuria in patients with chronic renal diseases with normal or abnormal blood pressure and delay the progress of renal damage. It should be noted that patients with dehydration, moderate and severe renal insufficiency or bilateral renal artery stenosis should not choose these two drugs. Other commonly used antihypertensive drugs, including calcium channel blockers, diuretics, beta blockers and alpha blockers, are also widely used in chronic kidney disease.
Diuretics: Diuretics are mainly used for diuresis, detumescence and treatment of hypertension.
Nutritional preparation: Compound a- keto acid tablet, trade name Kaitong, is a compound preparation, which contains 4 calcium keto amino acids, 1 calcium hydroxy amino acid and 5 essential amino acids. Because nitrogen is reused in the body, urea production is inhibited and protein metabolism is improved. Clinically, as a low-protein diet, it can prevent and treat the damage caused by protein's metabolic disorder caused by chronic renal insufficiency, and delay the progress of kidney diseases.
Improve anemia: erythropoietin and iron are commonly used.
Phosphorus binder: Calcium carbonate is used to correct hypocalcemia and hyperphosphatemia in patients with chronic renal insufficiency and calcium and phosphorus metabolism disorder. Other phosphorus binders include calcium acetate, aluminum hydroxide gel, lanthanum carbonate, Renalgel, etc. Which has a similar function to calcium carbonate.
Active vitamin D3: Calcitriol is the main active component of vitamin D, which is normally produced in the kidney and can promote the absorption of calcium in the small intestine and renal tubules, thus correcting hypocalcemia and inhibiting hyperparathyroidism caused by chronic renal insufficiency.
Drugs for clearing gastrointestinal toxins: including medicinal activated carbon and some drugs to promote defecation.
Regulator of acid-base balance: sodium bicarbonate, also known as baking soda, is mainly used to correct metabolic acidosis in patients with chronic renal insufficiency.
It is worth noting that research shows that CKD is a lifestyle disease. On the one hand, factors closely related to lifestyle play an increasingly important role in the diseases that lead to CKD, among which kidney damage caused by diabetes and hypertension is the main cause of CKD in many countries. As we all know, the occurrence and development of diabetes and hypertension are closely related to lifestyle. On the other hand, lifestyle is an important reason for the progress of kidney diseases (no matter what the primary disease is), and it is also a common pathway for many kidney diseases. We know that the factors affecting the progress of chronic kidney disease can be divided into three categories. The first category is immutable factors: such as age, gender, race and genes. The second category is the controllable factors that affect the prognosis and CKD process, including blood pressure, proteinuria and metabolic factors (hyperglycemia, abnormal lipid metabolism, hyperuricemia, smoking, alcoholism, etc. ), and most of these factors are closely related to lifestyle. The third category is the primary diseases that cause kidney diseases.
A lot of evidence shows that the progress of CKD is related to systemic hypertension, and the deterioration of renal function is accelerated with the increase of blood pressure. Controlling blood pressure can effectively slow down the deterioration of renal function, especially for CKD patients with proteinuria. Therefore, in clinic, it is suggested that the target blood pressure should be controlled at 130/80 mmHg for patients with daily proteinuria less than 1g, and at 125/75 mmHg for patients with daily proteinuria greater than1g.. Hypertension is mostly related to lifestyle. Too much salt intake, too little exercise, mental stress and overwork will all lead to high blood pressure. Practice shows that simply controlling salt intake, increasing exercise and quitting smoking can effectively reduce blood pressure. It is suggested that for CKD patients, the daily salt intake should not exceed 6 grams. It is worth noting that salt is often hidden in various foods, and ordinary fresh food has about 3 grams of salt even without salt. Therefore, we suggest that patients should not add more than 3 grams of salt, including salt, soy sauce, chicken essence and so on.
It is not difficult to understand that CKD is closely related to our lifestyle, and the effective control of CKD is not a simple drug control. It should be said that drugs only play an auxiliary role in most CKD treatments, and it is more important to change our lifestyle and do a good job in self-management of diseases. For any CKD patient, once diagnosed, we suggest learning the following courses, including ① the basic knowledge of chronic kidney disease ② how to effectively prevent renal function deterioration? ③ Lifestyle and Chronic Kidney Disease ④ Complications and their management ⑤ Common drugs, examination and outpatient follow-up ⑤ Self-management and rehabilitation ⑤ Reasonable diet for patients with chronic kidney disease. Eight options of renal replacement therapy. Patients can learn about disease-related knowledge and prevention through websites (China Chronic Kidney Disease Network), newspapers and magazines, health education lectures and other channels.
Tertiary prevention refers to taking early treatment measures for patients with decreased renal function or even dialysis to prevent some serious complications of uremia, such as acute left heart failure, hyperkalemia, uremic encephalopathy, serious infection and bleeding. Because these complications often threaten the life of patients and are often the main cause of death. Among them, the prevention and treatment of cardiovascular complications is particularly important, which is the most important cause of death.
How to face the change of renal function?
Clinically, some patients often feel that they have paid great attention to protecting renal function, but after reexamination, they found that serum creatinine and urea nitrogen continued to rise, even to the point where dialysis was needed. What should I do at this time? In addition to timely referral to nephrologists, there are several issues worthy of attention:
There are errors in the examination of 1, serum creatinine and urea nitrogen, especially in different laboratories and even in the same hospital, so don't panic if there is little change (for example, from 170 umol/L to 180 umol/L), sometimes it is probably the error of detection. The 24-hour creatinine clearance rate also has a great error, and these values are only for clinical reference.
2. The blood urea value is greatly influenced by protein intake, and the protein intake of excessive blood urea may increase, otherwise it will increase, which does not mean the quality of renal function. Similarly, many drugs that excrete toxins from the intestine (rhubarb is often one of the main components) can reduce serum creatinine and urea nitrogen in a short time, which does not necessarily mean the improvement of renal function, but increases the excretion of ingested things from the intestine. After a long time, we should be alert to the possibility of malnutrition and decreased renal function.
3. The role of ACEI or ARB drugs, especially ACEI drugs, can increase serum creatinine, which can often be recovered after drug withdrawal. Now, it is generally understood that although ACEI can increase serum creatinine in the short term, it can still protect renal function in the long term, but we usually don't take this risk. When serum creatinine rises after taking the medicine, we will stop using these drugs.
4. Salt intake changes too much in a short time, because controlling salt can effectively lower blood pressure. When blood pressure drops, the use of antihypertensive drugs should be reduced in time, otherwise hypotension will easily occur and kidney damage will be aggravated. Climate will also play a role. In this case, renal function changes can be recovered if found in time and blood pressure is normal.
5. There are complications, such as colds and gastrointestinal inflammation. On the one hand, the occurrence of complications promotes the metabolism of the body, produces inflammatory reactions, and damages renal function. On the other hand, it is related to renal damage caused by drug treatment complications. In addition, complications may affect the patient's diet, resulting in a decrease in volume and blood pressure, resulting in insufficient blood supply to the kidneys.
6. Many factors may aggravate the condition of CKD, and these inducing factors must be eliminated. (1) dehydration and hypotension lead to insufficient blood flow and decreased renal perfusion, leading to renal ischemia and hypoxia; (2) using nephrotoxic drugs, such as nephrotoxic antibiotics, contrast agents and prostaglandin synthesis inhibitors; (3) Obstruction inside and outside the kidney, such as urate crystals in the kidney, urinary calculi, prostatic hyperplasia and hypertrophy, edema caused by severe nephrotic syndrome pressing renal tubules, diabetic renal papillary necrosis, etc. (4) Infection, bacterial infection toxin can directly damage renal tubules, and water-electrolyte disorder or circulatory failure caused by infection can aggravate the damage to kidneys; (5) Severe hypertension causes renal arteriole spasm, especially afferent arteriole spasm, and renal blood flow is reduced, or hypertension causes heart failure and renal blood flow is reduced, or renal ischemia is caused by rapid blood pressure drop when treating hypertension; (6) Water-electrolyte disorder; (7) High protein diet and massive proteinuria; (8) Severe hyperparathyroidism and metastatic calcification; (9) High decomposition state in vivo; (10) heart failure, etc. If the above factors can be found and controlled in time, renal function can often be reversed, which should be paid attention to clinically.