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Lab Tests for Detecting Kidney Fibrosis

2012-11-21 08:23

Cysstain C

Cysstain C (Cys C) acts as a new endogenous marker as detecting kidney function. Compared with BUN (blood urea nitrogen), serum creatinine and creatinine clearance rate etc Cys C is much more favorable in lab tests. This kind of substance has a high sensitivity to evaluate one’s kidney function.


The major function of glomeruli is filter, so glomerular filtration declines once kidney fibrosis begins. β2-microglobulin runs freely from glomeruli, while is reabsorbed in proximal renal tubule. One’s kidney function affects concentration ofβ2-microglobulin in blood. It is one sensitive index indicating the kidney impairment in the very early stage.

High-sensitivity C-reactive protein (CRP) is the most sensitive as well as valuable index indicating inflammation. Its increase gives a clue to the occurrence of inflammation, and has widely used to detect and monitor infectious diseases in clinic. Most of the kidney disease patients have chronic inflammatory response so the detection of CRP means a lot to those patients.

Urinary N-acetyl-B-D-glucosaminidase (NAG)

Urinary N-acetyl-B-D-glucosaminidase couldn’t pass through glomeruli. This substance comes from kidneys and won’t be affected by NAG in blood.

NAG becomes a sensitive index for kidney damages because:

The change of NAG in urine appears early than any other indexes.

The elevated NAG becomes earlier than mAlb in patients with diabetic nephropathy. NAG is used to monitor hypertensive nephropathy and rejection after kidney transplant.

Urine Y glutamine transferase (GGT)

The increase of GGT in urine can be seen in patients with acute nephritis, nephritic syndrome, acute renal ischemia and acute renal failure.

In patients with SLE, their GGT in urine often is often regarded as one indicator of kidney impairment. If not, then there’s no kidney damages develop. In lupus patients, more than 70% of them have elevated GGT.

HA, LN, PCIII and C-1V

HA, LN, PCIII and C-1V are all the major ingredients of extracellular matrix. Large quantities of ECM synthesis and accumulation lays the foundation of kidney fibrosis.

The hyperplasia for PCIII leads to change of renal structure. Consequently, glomerulosclerosis and interstitial fibrosis develop.

If you are interested in other substances, like LN, C-1V and HA, please contact us. We’d like to offer detailed information for you anytime.

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