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Diagnosis and treatment of chronic kidney disease

Glomerular filtration rate (GFR) is the best index for evaluating renal function, and can be calculated by measuring the renal clearance rate of internal and external filtration markers. Creatinine is a product of muscle metabolism and is influenced by GFR and muscle mass (age, sex, ethnicity, and body type).
Cystatin C is a low molecular protein that is influenced by age and sex, but is less affected by muscle mass and diet. Glucocorticoids, inflammation, smoking and hyperthyroidism increase cystatin C concentration. The combined use of cystatin C and creatinine improves the accuracy of eGFR assessment.
Urinary protein was consistently higher than normal, suggesting renal damage and increased glomerular permeability. Proteinuria is associated with an increased risk of ESKD and early death, and early reduction of albuminuria can delay progression of kidney disease.
Imaging examination
In patients with chronic kidney disease, the kidneys usually shrink and echo increases, helping to identify acute kidney injury. In addition, renal ultrasonography can also identify renal parenchymal diseases and hydronephrosis caused by obstructive diseases, as well as congenital or hereditary kidney diseases. Other image examinations, such as pixel scanning, CT and MRI, can assist in the diagnosis.
renal biopsy
Patients with suspected CKD can be diagnosed with a viable renal biopsy. In addition, renal biopsy is helpful to guide the treatment and determine the extent of the disease. The risk of kidney biopsy includes severe bleeding, unilateral nephrectomy, and even death.
CKD treatment

Anemia - usually positive pigmented anemia - is a common symptom of CKD, and its prevalence increases with the decline in GFR. Renal anemia is associated with adverse outcomes such as lower quality of life, increased risk of cognitive impairment, increased cardiovascular disease, hospital admissions, and mortality.
CKD mineral and bone abnormalities
Mineral and bone disorder is a common complication of CKD, as follows: calcium, phosphorus, parathyroid hormone (PTH) or vitamin D metabolism; bone turnover, mineralization, growth or abnormal bone strength; or bone calcification (including blood vessels and skin).
CKD pathological mechanism of mineral and bone abnormalities
There is no randomized controlled trial of whether alkaline therapy improves bone density in non dialysis dependent CKD patients; oral hemodialysis with sodium bicarbonate reduces the progression of secondary hyperparathyroidism in ESKD hemodialysis patients. Statins can effectively reduce total cholesterol, low-density lipoprotein cholesterol and proteinuria, but can not delay the progression of chronic kidney disease.
Cohort studies show that the risk of cancer in patients with ESKD dialysis is as high as 10%-80%, while kidney transplant recipients are at an increased risk of cancer by 1.9-9.9 times as much as the general population. The risk of cancer varies from place to place, and the risk of kidney cancer and thyroid cancer is particularly pronounced. Post transplant immunodeficiency and viral infections led to a dramatic increase in the incidence of cancer. No studies have shown an increased risk of breast or prostate cancer in ESKD patients.


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