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Overview

Kidney disease is a common disease that if progresses, can lead to uremia. Chronic kidney disease alongside cardiovascular and cerebrovascular diseases, cancer and diabetes has become an increasing threat to human health. In China, primary glomerulonephritis is the main cause of more than half of patients with kidney disease, with secondary nephropathy, lupus nephritis and diabetic nephropathy not far behind. Furthermore, there is a larger proportion of patients with CKD that have cardiovascular or cerebrovascular disease compared to the general population. Finally, to add, the most common concomitant diseases of CKD are mineral and bone abnormalities, anemia, hypertension, hyperlipidemia, hypoalbuminemia, and hyperuricemia.

1. Risk

The main causes of chronic kidney disease are primary glomerulonephritis, hypertensive renal arteriosclerosis, diabetic nephropathy, secondary glomerulonephritis, tubulointerstitial lesions (chronic pyelonephritis, chronic uric acid nephropathy, obstructive nephropathy, Drug-induced nephropathy, ischemic nephropathy, hereditary nephropathy (polycystic kidney disease, hereditary nephritis).
The main risk factors of CKD are age, family history of CKD, diabetes, hypertension, obesity-metabolic syndrome, high protein diet, hyperlipidemia, hyperuricemia, autoimmune diseases, urinary tract infections, hepatitis virus infection, urinary calculi, urethral obstruction, urinary or systemic tumors, history of application of nephrotoxic drugs, cardiovascular disease, anemia, smoking.

2. Clinical manifestations

Patients in the early stages of chronic kidney disease may only have mild symptoms such as fatigue, backache, nocturia or in some cases no symptoms at all. However, a small number of patients may experience a loss of appetite, metabolic acidosis and mild anemia. As the disease progresses, the symptoms mentioned above are more obvious and would be more significant as the patient reaches renal failure. There are occasional cases of hypertension, heart failure, severe hyperkalemia, central nervous system disorders and an acid-base balance disorder alongside renal failure. This can be life threatening. Finally, some patients may present with skin symptoms such as hyperpigmentation, calcium deposition, itching, difficulty in sweating and ulceration.

Investigations and Diagnosis

ReLIA’s Biomarker Guide

1. Neutrophil gelatinase-associated lipocalin (NGAL)

Blood and Urine NGAL concentrations increase rapidly in acute renal injury (from causes such as cardiac surgery, kidney transplantation, renal ischemia, nephrotoxicity). Levels are most significant in 2 hours as compared to 24-72 hours for serum creatinine and urinary enzymes. Thus, NGAL can be used in the early diagnosis of AKI.
2 hour urinary NGAL levels are a strong predictor of AKI (reference value<150 ng/mL). NGAL. Furthermore, 2hour urinary NGAL levels have a higher sensitivity and specificity than serum NGAL. NGAL levels can also reflect the severity of kidney damage. An increase of 100 ng/mL in urinary NGAL is indicative of delayed renal recovery time by 20%. Finally, NGAL can be used to assess the prognosis of acute kidney injury,

2. Beta-2 microglobulin (β2-MG)

Under normal conditions, 99.9% of human beta-2 microglobulin is reabsorbed and broken down in the epithelial cells of the proximal tubules. Increased levels of β2-MG are indicative of renal tubular damage or an increase in filtration load. β2-MG concentrations in blood nad urine significantly increase in patients who have just had renal transplants. If it increases further it suggests transplant rejection. Finally, urine β2-MG levels help differentiate upper and lower urinary tract infections (UTI); urine β2-MG levels increase in upper UTI’s, but don’t change in lower UTI’s

3. Cystatin-C (Cys-C)

Cystatin-C is a protein that is expressed in all nucleated cells. It is produced at a constant rate and stays present regardless of age, sex, body weight, inflammation and other interfering factors., It can be freely filtered from the glomerulus and is reabsorbed and broken down in the epithelial cells of the proximal tubules. Furthermore, Cys-C is not secreted in the lumen. Therefore, impairment in renal function/GFR can leads to increases in blood Cys-C levels (> 10 times that of normal patients). If tubular cells are damaged, the amount of Cys-C that is reabsorbed and broken down substantially decreases, leading to an increase in urine Cys-C levels (>100 times that of normal patients).