Lipid Management Strategies in Patients With Chronic Kidney Disease

The National Kidney Foundation Kidney Disease Prognosis Quality Guidelines indicate that more than 90% of patients with chronic kidney disease (CKD) have elevated total cholesterol, 85% elevated low-density lipoprotein cholesterol (LDL-C), and 50% high-density lipoprotein cholesterol (HDL-C) decreased. LDL-C is the most important risk factor for atherosclerotic cardiovascular disease, and atherosclerotic cardiovascular disease is a common complication of CKD. Only 5% of CKD patients progress to end-stage renal disease, and eventually die. However, it is as high as 30% for cardiovascular diseases. Therefore, LDL-C is very harmful and should be taken seriously.

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Lipid metabolism disorders are common in CKD patients, but the lipid metabolism mechanisms are different in patients with different etiologies or different stages of CKD (such as nephritis, renal failure, dialysis, and diabetic nephropathy). Lipid metabolism disorders in CKD patients such as chronic nephritis and nephrotic syndrome are due to the leakage of a large amount of protein, which stimulates the liver to synthesize lipoproteins, resulting in hyperlipidemia. Patients with nephrotic syndrome will leak lipoproteins that protect the human body, such as high-density lipoproteins. Changes in the receptors of lipoproteins in such patients will also cause lipid metabolism disorders. Diabetic nephropathy is essentially vascular damage, which is very sensitive to lipid metabolism, and lipid metabolism disorder can occur itself, and lipid metabolism disorder will aggravate vascular damage. Therefore, lipid metabolism disorder in diabetic nephropathy will form a vicious circle.

Currently, the field of nephrology completely separates diabetic nephropathy from non-diabetic nephropathy. However, in the stage of renal insufficiency, this abnormal lipid metabolism is another pathophysiological mechanism. Patients with end-stage renal failure are commonly associated with hyperinsulinemia, which can stimulate abnormal lipid metabolism. Increased toxins in patients with uremia may also inhibit lipoproteins and cause lipid metabolism disorders, and changes in lipoprotein receptors will also have the same effect. During the dialysis phase, the heparin used during dialysis, especially the high glucose dialysate used by peritoneal dialysis patients, can stimulate lipid metabolism disorders. To sum up, the etiology and pathophysiological mechanism of abnormal lipid metabolism in different types of CKD patients are quite different, so they should be treated differently.

Abnormal lipid metabolism causes vascular damage, which has been proved in a large number of studies in the cardiovascular field, and abnormal lipid metabolism can also cause renal vascular damage. After a large amount of lipoprotein deposits in the kidney, it will stimulate local tissue hyperplasia and cause an inflammatory reaction. In addition, lipoproteins, especially low-density lipoprotein oxidation disorders, will also stimulate endothelial cells, causing inflammation in renal blood vessels, resulting in tissue fibrosis, arteriosclerosis, and eventually glomerulus sclerosis. After hyperlipidemia damages blood vessels and endothelial cells, chronic inflammatory reactions occur in the tissue and accelerate the progress of kidney disease. Clinically, hyperlipidemia should be actively controlled to slow down the development of kidney disease.

In the past, many nephrologists believed that abnormal lipid metabolism in CKD patients may be due to transient damage caused by long-term proteinuria. After the proteinuria is eliminated, the patient's lipoprotein levels will naturally return to normal. Therefore, we do not place a very high priority on lipid-lowering therapy in CKD patients. More and more studies have found that there is a very close relationship between abnormal lipid metabolism and kidney disease lesions, especially glomerulosclerosis, and strict lipid reduction is required for patients with kidney disease, especially those with hyperlipidemia.

Therefore, clinically, the appropriate lipid-lowering drug should be selected according to the patient's lipid metabolism as much as possible. For patients with severe hyperlipidemia or severe lipid metabolism abnormality, strong lipid-lowering drugs can be used; for patients with mild lipid metabolism, Moderate-intensity statins are recommended for patients with abnormalities, especially those who need long-term use. All in all, it is necessary to keep the patient's blood lipid level normal for a long time.

In clinical practice, CKD patients often use a variety of drugs, but most drugs are metabolized by the liver and kidney. For CKD patients who need long-term treatment, to reduce further kidney damage caused by the use of drugs, it is necessary to emphasize small doses, long-term persistence, and Safety first. Statins are the cornerstone of dyslipidemia drug therapy.

The Global Organization for Improving Kidney Disease Prognosis updated the lipid management guidelines for CKD patients (2016), referring to the current American Heart Association/American College of Cardiology (AHA/ACC) adult cholesterol management guidelines, abandoning the LDL-C target value and emphasizing the role of statins in CKD. Central position in the treatment of dyslipidemia. Based on the newly published research results in recent years, the Global Organization for Improving the Prognosis of Kidney Diseases has updated the 2013 guidelines, and the points worthy of attention are as follows:

1. Referring to the current AHA/ACC adult cholesterol management guidelines, the LDL-C target value was abandoned, and the core position of statins in the treatment of CKD dyslipidemia was emphasized.

2. Except for patients on long-term dialysis, it is recommended that all CKD patients aged ≥ 50 years receive statin therapy; it is recommended for patients with severe disease [CKD stage 3-5, glomerular filtration rate (eGFR) <60 ml/(min·1.73 ㎡)] Combined treatment with statin and ezetimibe.

3. For CKD patients aged 18-49 who have not received long-term dialysis treatment, statin therapy should only be used in the following four situations: (1) Diagnosed coronary heart disease. (2) Combined with diabetes. (3) Have a history of ischemic stroke. (4) Framingham's 10-year cardiovascular event risk ≥ 10%.

4. Due to decreased renal excretion function, multiple comorbidities, or the use of multiple drugs, CKD patients have a significantly increased risk of adverse reactions when using lipid-lowering drugs. Therefore, it is recommended for patients with eGFR<60 ml/(min·1.73㎡) Moderate-intensity statin therapy should be used, such as atorvastatin 20 mg, rosuvastatin 10 mg, simvastatin 40 mg, pravastatin 40 mg, fluvastatin 80 mg or pitavastatin 2 mg.

5. Patients with CKD should avoid the combination of fibrates and statins.

6. Ezetimibe alone is not recommended for lipid-lowering therapy.

7. Patients with CKD stage 1-2 and eGFR<60 ml/(min·1.73㎡) can refer to the blood lipid treatment strategy of the general population.

8. Before starting statin therapy, transaminase levels should be tested for all CKD patients. If there is no clinical evidence of liver damage and myopathy, routine testing of creatine kinase levels is not necessary.

9. Patients on long-term dialysis treatment should not start statin or statin combined with ezetimibe therapy, but those who have received the above-mentioned drug treatment before dialysis can continue to take the drug after starting dialysis.

10. All adult patients undergoing kidney transplantation should receive statin therapy.

AHA/ACC latest consensus: low-carb diet, high-fat diet can reduce triacylglycerol.

Hypertriglyceridemia is associated with abdominal obesity, insulin resistance, low high-density lipoprotein, high triglycerides, and hypertension. The traditional view is that hypertriglyceridemia is caused by a high-fat diet, excessive alcohol consumption, certain drugs, etc. The latest consensus of AHA/ACC breaks the traditional idea of reducing triacylglycerol with a low-fat diet and makes more people realize that only by eating fewer carbohydrates such as staple foods can the true reduction of triacylglycerol be achieved.