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Diabetic nephropathy

  Diabetic nephropathy is one of the most important comorbidities in diabetic patients. China's incidence also showed an upward trend, has become the second cause of end-stage renal disease, second only to a variety of glomerulonephritis. Because of its complex metabolic disorders, once the development of end-stage renal disease, kidney disease is often more difficult than the treatment of other, so timely prevention and treatment of delayed diabetic nephropathy is of great significance.

  Etiology and pathogenesis

  Diabetic nephropathy etiology and pathogenesis is unclear. It is thought that multi-factor participation, in a certain genetic background and part of the risk factors under the common role of disease.

  1. genetic factors

  The incidence of diabetic nephropathy in males was higher in women than in females, and studies in the United States found that diabetic nephropathy was more common in Africa and Mexicans than whites in the same living environment. Some families in the same race were predisposed to diabetic nephropathy. Suggesting that genetic factors exist. Type 1 diabetes in 40% to 50% of microalbuminuria, type 2 diabetes during the observation period, only 20% to 30% of diabetic nephropathy, suggesting that genetic factors may play an important role.

  2. Kidney hemodynamic abnormalities

  Early diabetic nephropathy can be observed in renal hemodynamic abnormalities, manifested as glomerular hyperperfusion and high filtration, renal blood flow and glomerular filtration rate (GFR) increased, and increased protein intake increased The degree of more significant.

  3. High blood sugar caused by metabolic abnormalities

  Hyperglycemia mainly through renal hemodynamic changes and metabolic abnormalities caused by renal damage, including metabolic abnormalities leading to kidney damage mechanisms include: ① renal tissue local glucose metabolism disorders, non-enzymatic glycation by glycosylation terminal Metabolites (AGES); (2) polyol pathway activation; (3) diacylglycerol-protein kinase c pathway activation; (4) glucosamine pathway metabolic abnormalities. In addition to the above mentioned metabolic abnormalities involved in early high filtration, more importantly, to promote the glomerular basement membrane (GBM) thickening and extracellular matrix accumulation.

  4. hypertension

  Almost any diabetic nephropathy is accompanied by hypertension in type 1 diabetic nephropathy hypertension and microalbuminuria occurred in parallel, while in type 2 is often before the onset of diabetic nephropathy. Blood pressure control and diabetic nephropathy are closely related.

  5. Vasoactive metabolic disorders

  The development of diabetic nephropathy may have a variety of vasoactive substances in the metabolic disorders. Including RAS, endothelin, prostaglandins and growth factors such as metabolic abnormalities.

  Clinical manifestations and disease staging

  Diabetic nephropathy is one of diabetic complications of systemic microangiopathy, so when the occurrence of diabetic nephropathy is often combined with other organs or systems of microangiopathy such as diabetic retinopathy and peripheral neuropathy. Type 1 diabetic patients with diabetic nephropathy in the onset of 10 to 15 years or so, and type 2 diabetic patients with diabetic nephropathy time is short, and older, and more associated with other underlying diseases.

  According to the course of diabetic nephropathy and pathophysiology of the evolution process, Mogensen has suggested that the diabetic nephropathy is divided into the following five issues:

  1. Glomerular hyperfiltration and renal hypertrophy

  This initial change is consistent with hyperglycemia and partial remission after glycemic control. There were no histopathological lesions in this period.

  2. normal albuminuria period

  GFR higher than normal levels. Renal pathological manifestations of GBM thickening, mesangial matrix increased, urinary albumin excretion rate after exercise (UAE) increased (> 20μg / min), rest returned to normal. If this period can be a good control of blood sugar, the patient can be long-term stability in the period.

  3. Early diabetic nephropathy, also known as "sustained microalbuminuria period"

  GFR began to decline to normal. Renal pathology showed glomerular nodular lesions and small arteriosclerosis. UAE continued to rise to 20 ~ 200μg / min to appear microalbuminuria. Current patients with high blood pressure. ACEI or ARB drug treatment, can reduce urinary albumin excretion, delay the progress of kidney disease.

  4. Clinical diabetic nephropathy

  Pathological typical K-W nodules. Persistent massive albuminuria (UAE> 200μg / min) or proteinuria more than 500mg / d, about 30% of patients with nephrotic syndrome, GFR continued to decline. This period is characterized by urinary protein does not decrease with the GFR decreased. Once the patient into the IV, the disease is often sexual development, if not actively controlled, GFR will drop by an average of 1ml / min per month.

  5. end-stage renal failure

  GFR <10 ml / min. The amount of urinary protein decreased due to glomerular sclerosis. Obvious symptoms of uremia, need dialysis.

  The above staging mainly based on type 1 diabetic nephropathy, type 2 diabetic nephropathy is not obvious.

  Proteinuria and diabetic nephropathy are closely related. Microalbuminuria not only means glomerular filtration barrier, but also that systemic vascular endothelial dysfunction and found that cardiovascular complications are closely related.

  Diabetic nephropathy nephrotic syndrome and general primary glomerular disease compared to the degree of edema often more obvious, and often accompanied by severe high blood pressure. Because of this disease glomerular capillary capillary pressure, coupled with glomerular filtration membrane protein barrier function seriously damaged, so some patients with end-stage renal failure can also have a large number of proteinuria.

  Diagnosis and differential diagnosis

  Diabetic patients with renal damage should be considered in diabetic nephropathy, the family has kidney disease, significant hypertension, insulin resistance, GFR was significantly higher or with severe hypertension in diabetic nephropathy occurred risk factors. Microalbuminuria is a marker for the diagnosis of diabetic nephropathy. Microalbuminuria UAE continued to increase 20 ~ 200μg / min, or urinary albumin 30 ~ 300mg / 24h or urinary albumin: urine creatinine of 30 ~ 300μg / mg.

  As microalbuminuria is the clinical diagnosis of early diabetic nephropathy in the main clues, the current American Diabetes Association suggested that for patients with type 1 diabetes, 5 years after the onset of urinary albumin will be screening; for type 2 diabetes in the Diabetes should be diagnosed at the same time check. But a positive test, can not be diagnosed as persistent microalbuminuria, need to review in 3 to 6 months, if 3 times in 2 positive, can be diagnosed; if negative, should be checked once a year.

  Microalbuminuria is also associated with a variety of other complications of diabetes, including hypertension, hyperlipidemia, atherosclerosis and cardiovascular disease. Therefore, microalbuminuria does not necessarily represent the occurrence of diabetic nephropathy, and its inevitable progress after the emergence of significant proteinuria and chronic renal failure is still controversial. In a few large series of long-term observation found that microalbuminuria in diabetic patients, 10 years, only 30% to 45% of clinically significant proteinuria, and another 30% of microalbuminuria disappeared, which in the Type 2 diabetes is more pronounced. So should be checked several times, continuous follow-up can be determined.

  Significant proteinuria (> 500mg / d) or nephrotic syndrome and so suggestive of renal lesions in type 1 diabetes, where proteinuria with diabetic retinopathy, especially after puberty patients, almost can be identified as diabetic nephropathy.

  Type 2 diabetes associated with proteinuria in diabetic patients, in the diagnosis of diabetic nephropathy must be carefully ruled out other causes of proteinuria, especially for the time of onset can not be clear in patients with type 2 diabetes. Clinical manifestations of the following conditions should be considered in diabetic patients with other renal diseases: ① obvious proteinuria but no diabetic retinopathy; ② acute renal injury; ③ nephritis hematuria, urinary sediment to deformed red blood cells or red blood cell tube type; ④ Without nephrotic syndrome with hypertension; ⑤ short-term proteinuria increased significantly. The occurrence of renal biopsy should be considered in addition to other causes of glomerulonephritis.


  Treatment of diabetic nephropathy varies according to different stages. Clinically for the following aspects:

  1. Control blood sugar

  Glycosylated hemoglobin (HbA1c) should be controlled at 7.0% or less. Strict control of blood glucose can partially improve the abnormal renal hemodynamics; at least in type 1 diabetes can delay the emergence of microalbuminuria; reduced microalbuminuria has been converted to significant clinical proteinuria.

  2. Control of blood pressure

  Diabetic nephropathy is not only common in hypertension, but also lead to the occurrence and development of diabetic nephropathy important factors. Angiotensin converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) are preferred for antihypertensive agents. These drugs have improved renal hemodynamics, reduce urinary protein excretion, inhibition of mesangial cells, fibroblasts and macrophages activity, improve the filtration membrane permeability and other pharmacological effects. Even if the body under normal blood pressure can also produce kidney protection, and does not depend on the improvement of hemodynamics after blood pressure. The main side effects of ACEI hyperkalemia, renal dysfunction and dry cough and so on. The target for blood pressure is blood pressure 130 / 80mmHg in patients with proteinuria. Beta-blockers and diuretics are not recommended for first-line use because of their potential glycolipid metabolic disorder unless combined with tachycardia or marked edema. The role of calcium channel blockers (CCBs) in renal protection in patients with diabetic nephropathy is unknown, but diltiazem appears to be superior to dihydropyridines, which are not recommended for diabetic nephropathy alone.

  3. Diet therapy

  High protein diet increased glomerular hyperperfusion, high filtration, so the idea of ​​the principle of quality protein. Protein intake should be high bioavailability of animal protein, early protein intake should be limited to 0.8g / (kg · d), has a large number of proteinuria and renal failure patients can be reduced to 0.6g / (Kg · d). In patients with advanced renal injury, should add α-keto acid. In addition, it was suggested to fish, chicken and other parts instead of red meat (such as beef, lamb, pork), and the addition of polyunsaturated fatty acids. There is also no need to unduly limit the intake of vegetable proteins such as soy protein.

  4. End-stage renal disease replacement therapy

  Into end-stage renal failure may renal replacement therapy, but its prognosis is worse than non-diabetic patients.

  Diabetic nephropathy patients with diabetic complications more common, uremia symptoms earlier, should be appropriate to relax the indications for renal replacement therapy. General endogenous creatinine clearance rate dropped to 10 ~ 15ml / min or with significant gastrointestinal symptoms, hypertension and heart failure can not be controlled to enter the maintenance of dialysis. Hemodialysis and peritoneal dialysis long-term survival rate is similar to the former for blood glucose control, dialysis adequacy is good, but the arteriovenous fistula difficult to establish, the process of dialysis prone to cardiovascular and cerebrovascular accident; the latter often use continuous ambulatory peritoneal dialysis CAPD), its advantage is conducive to the protection of residual renal function in the short term, because there is no need to use anticoagulants in patients with cardiovascular and cerebrovascular accident can be implemented, but glucose as infiltration solute the blood glucose levels difficult to control.

  5. Organ transplantation

  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 of cadaveric kidney transplantation was 79%, live kidney transplantation was 91%, while the 5-year survival rate of dialysis patients only 43%. The survival rate of living kidney, especially relatives, was significantly higher than that of cadaveric kidney transplantation. But the survival rate of diabetic nephropathy in patients with transplanted kidney is still 10% lower than non-diabetic patients. Simple kidney transplantation does not prevent the recurrence of diabetic nephropathy, can not improve other complications of diabetes.

  Combined pancreas and kidney transplantation may cause patients with glycated hemoglobin and serum creatinine levels returned to normal and improve the other complications of diabetes, so patients with better quality of life than simple kidney transplant.


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