Cystatin C

Last updated
CST3
Crystal structure of human cystatin C monomer.png
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases CST3 , ARMD11, HEL-S-2, cystatin C
External IDs OMIM: 604312 MGI: 102519 HomoloGene: 78 GeneCards: CST3
Orthologs
SpeciesHumanMouse
Entrez

1471

13010

Ensembl

ENSG00000101439

ENSMUSG00000027447

UniProt

P01034

P21460

RefSeq (mRNA)

NM_001288614
NM_000099

NM_009976

RefSeq (protein)

NP_000090
NP_001275543

NP_034106

Location (UCSC) Chr 20: 23.63 – 23.64 Mb Chr 2: 148.71 – 148.72 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Cystatin C or cystatin 3 (formerly gamma trace, post-gamma-globulin, or neuroendocrine basic polypeptide), [5] a protein encoded by the CST3 gene, is mainly used as a biomarker of kidney function. Recently, it has been studied for its role in predicting new-onset or deteriorating cardiovascular disease. It also seems to play a role in brain disorders involving amyloid (a specific type of protein deposition), such as Alzheimer's disease. In humans, all cells with a nucleus (cell core containing the DNA) produce cystatin C as a chain of 120 amino acids. It is found in virtually all tissues and body fluids. It is a potent inhibitor of lysosomal proteinases (enzymes from a special subunit of the cell that break down proteins) and probably one of the most important extracellular inhibitors of cysteine proteases (it prevents the breakdown of proteins outside the cell by a specific type of protein degrading enzymes). Cystatin C belongs to the type 2 cystatin gene family.

Role in medicine

Kidney function

Glomerular filtration rate (GFR), a marker of kidney health, is most accurately measured by injecting compounds such as inulin, radioisotopes such as 51chromium-EDTA, 125I-iothalamate, 99mTc-DTPA or radiocontrast agents such as iohexol, but these techniques are complicated, costly, time-consuming and have potential side-effects. [6] [7] Creatinine is the most widely used biomarker of kidney function. It is inaccurate at detecting mild renal impairment, and levels can vary with muscle mass but not with protein intake. Urea levels might change with protein intake. [8] Formulas such as the Cockcroft and Gault formula and the MDRD formula (see Renal function) try to adjust for these variables.

Cystatin C has a low molecular weight (approximately 13.3 kilodaltons), and it is removed from the bloodstream by glomerular filtration in the kidneys. If kidney function and glomerular filtration rate decline, the blood levels of cystatin C rise. Cross-sectional studies (based on a single point in time) suggest that serum levels of cystatin C are a more precise test of kidney function (as represented by the glomerular filtration rate, GFR) than serum creatinine levels. [7] [9] Longitudinal studies (following cystatin C over time) are sparse, but some show promising results. [10] [11] [12] Although studies are somewhat divergent, most studies find that cystatin C levels are less dependent on age, gender, ethnicity, diet, and muscle mass compared to creatinine, [13] [14] and that cystatin C is equal or superior to the other available biomarkers in a range of different patient populations, including diabetic patients, in chronic kidney disease (CKD), and after kidney transplant. [15] It has been suggested that cystatin C might predict the risk of developing CKD, thereby signaling a state of 'preclinical' kidney dysfunction. [16] Additionally, the age-related rise in serum cystatin C is a powerful predictor of adverse age-related health outcomes, including all-cause mortality, death from cardiovascular disease, multimorbidity, and declining physical and cognitive function. [17] The UK's National Institute for Health and Care Excellence (NICE) guideline for the assessment and management of CKD in adults concluded that using serum cystatin C to estimate GFR is more specific for important disease outcomes than use of serum creatinine, and may reduce overdiagnosis in patients with a borderline diagnosis, reducing unnecessary appointments, patient worries, the overall burden of CKD in the population. [18]

Studies have also investigated cystatin C as a marker of kidney function in the adjustment of medication dosages. [19] [20]

Cystatin C levels have been reported to be altered in patients with cancer, [21] [22] [23] (even subtle) thyroid dysfunction [24] [25] [26] and glucocorticoid therapy in some [27] [28] but not all [29] situations. Other reports have found that levels are influenced by cigarette smoking and levels of C-reactive protein. [30] However, inflammation does not cause an increase in the production of cystatin C, since elective surgical procedures, producing a strong inflammatory response in patients, do not change the plasma concentration of cystatin C.[ medical citation needed ] Levels seem to be increased in HIV infection, which might or might not reflect actual renal dysfunction. [31] [32] [33] The role of cystatin C to monitor GFR during pregnancy remains controversial. [34] [35] Like creatinine, the elimination of cystatin C via routes other than the kidney increase with worsening GFR. [36]

Death and cardiovascular disease

Kidney dysfunction increases the risk of death and cardiovascular disease. [37] [38] Several studies have found that increased levels of cystatin C are associated with the risk of death, several types of cardiovascular disease (including myocardial infarction, stroke, heart failure, peripheral arterial disease and metabolic syndrome) and healthy aging.[ citation needed ][ clarification needed ] Some studies have found cystatin C to be better in this regard than serum creatinine or creatinine-based GFR equations. [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] Because the association of cystatin C with long term outcomes has appeared stronger than what could be expected for GFR, it has been hypothesized that cystatin C might also be linked to mortality in a way independent of kidney function. [51] In keeping with its housekeeping gene properties, it has been suggested that cystatin C might be influenced by the basal metabolic rate. [52]

Proposed shrunken pore syndrome

The glomerular sieving coefficients for 10–30 kDa plasma proteins in the human kidney are relatively high with coefficients between 0.9 and 0.07.[ medical citation needed ] [53] These relatively high sieving coefficients, combined with the high production of ultrafiltrate in health, means that proteins less than or equal to 30 kDa in plasma normally are mainly cleared by the kidneys and at least 85% of the clearance of cystatin C occurs in the kidney.[ medical citation needed ] [54] If the pores of the glomerular membrane shrink, the filtration of bigger molecules, e.g. cystatin C, will decrease, whereas the filtration of small molecules, like water and creatinine, will be less affected. In this case, cystatin C-based estimates of GFR, eGFRcystatin C, will be lower than creatinine-based estimates eGFRcreatinine, so that a hypothesized condition, named shrunken pore syndrome, is identified by a low eGFRcystatin C/eGFRcreatinine-ratio.[ medical citation needed ] [55] This syndrome is associated with a very strong increase in mortality. [56]

Neurologic disorders

Mutations in the cystatin 3 gene are responsible for the Icelandic type of hereditary cerebral amyloid angiopathy, a condition predisposing to intracerebral haemorrhage, stroke and dementia. [57] [58] The condition is inherited in a dominant fashion. The monomeric cystatin C forms dimers and oligomers by domain swapping [59] and the structures of both the dimers [60] and oligomers [61] have been determined.

Since cystatin 3 also binds amyloid β and reduces its aggregation and deposition, it is a potential target in Alzheimer's disease. [62] [63] Although not all studies have confirmed this, the overall evidence is in favor of a role for CST3 as a susceptibility gene for Alzheimer's disease. [64] Cystatin C levels have been reported to be higher in subjects with Alzheimer's disease. [65]

The role of cystatin C in multiple sclerosis and other demyelinating diseases (characterized by a loss of the myelin nerve sheath) remains controversial. [66]

Other roles

Cystatin C levels are decreased in atherosclerotic (so-called 'hardening' of the arteries) and aneurysmal (saccular bulging) lesions of the aorta. [67] [68] [69] [70] Genetic and prognostic studies also suggest a role for cystatin C. [71] [72] Breakdown of parts of the vessel wall in these conditions is thought to result from an imbalance between proteinases (cysteine proteases and matrix metalloproteinases, increased) and their inhibitors (such as cystatin C, decreased).

A few studies have looked at the role of cystatin C or the CST3 gene in age-related macular degeneration. [73] [74] Cystatin C has also been investigated as a prognostic marker in several forms of cancer. [75] [76] Its role in pre-eclampsia remains to be confirmed. [77] [78] [79] [80]

Laboratory measurement

Cystatin C can be measured in a random sample of serum (the fluid in blood from which the red blood cells and clotting factors have been removed) using immunoassays such as nephelometry or particle-enhanced turbidimetry. [81] It is a more expensive test than serum creatinine (around $2 or $3, compared to $0.02 to $0.15), which can be measured with a Jaffe reaction. [82] [83] [84]

Reference values differ in many populations and with sex and age. Across different studies, the mean reference interval (as defined by the 5th and 95th percentile) was between 0.52 and 0.98 mg/L. For women, the average reference interval is 0.52 to 0.90 mg/L with a mean of 0.71 mg/L. For men, the average reference interval is 0.56 to 0.98 mg/L with a mean of 0.77 mg/L. [81] The normal values decrease until the first year of life, remaining relatively stable before they increase again, especially beyond age 50. [85] [86] [87] Creatinine levels increase until puberty and differ according to gender from then on, making their interpretation problematic for pediatric patients. [86] [88]

In a large study from the United States National Health and Nutrition Examination Survey, the reference interval (as defined by the 1st and 99th percentile) was between 0.57 and 1.12 mg/L. This interval was 0.55 - 1.18 for women and 0.60 - 1.11 for men. Non-Hispanic blacks and Mexican Americans had lower normal cystatin C levels. [85] Other studies have found that in patients with an impaired renal function, women have lower and blacks have higher cystatin C levels for the same GFR. [89] For example, the cut-off values of cystatin C for CKD for a 60-year-old white women would be 1.12 mg/L and 1.27 mg/L in a black man (a 13% increase). For serum creatinine values adjusted with the MDRD equation, these values would be 0.95 mg/dL to 1.46 mg/dL (a 54% increase). [90]

Based on a threshold level of 1.09 mg/L (the 99th percentile in a population of 20- to 39-year-olds without hypertension, diabetes, microalbuminuria or macroalbuminuria or higher than stage 3 chronic kidney disease), the prevalence of increased levels of cystatin C in the United States was 9.6% in subjects of normal weight, increasing in overweight and obese individuals. [91] In Americans aged 60 and 80 and older, serum cystatin is increased in 41% and more than 50%. [85]

Molecular biology

The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and the kininogens. The type 2 cystatin proteins are a class of cysteine proteinase inhibitors found in a variety of human fluids and secretions, where they appear to provide protective functions. The cystatin locus on the short arm of chromosome 20 contains the majority of the type 2 cystatin genes and pseudogenes.

The CST3 gene is located in the cystatin locus and comprises 3 exons (coding regions, as opposed to introns, non-coding regions within a gene), spanning 4.3 kilo-base pairs. It encodes the most abundant extracellular inhibitor of cysteine proteases. It is found in high concentrations in biological fluids and is expressed in virtually all organs of the body (CST3 is a housekeeping gene). The highest levels are found in semen, followed by breastmilk, tears and saliva. The hydrophobic leader sequence indicates that the protein is normally secreted. There are three polymorphisms in the promoter region of the gene, resulting in two common variants. [92] Several single nucleotide polymorphisms have been associated with altered cystatin C levels. [93]

Cystatin C is a non-glycosylated, basic protein (isoelectric point at pH 9.3). The crystal structure of cystatin C is characterized by a short alpha helix and a long alpha helix which lies across a large antiparallel, five-stranded beta sheet. Like other type 2 cystatins, it has two disulfide bonds. Around 50% of the molecules carry a hydroxylated proline. Cystatin C forms dimers (molecule pairs) by exchanging subdomains; in the paired state, each half is made up of the long alpha helix and one beta strand of one partner, and four beta strands of the other partner. [94]

History

Cystatin C was first described as 'gamma-trace' in 1961 as a trace protein together with other ones (such as beta-trace) in the cerebrospinal fluid and in the urine of people with kidney failure. [95] Grubb and Löfberg first reported its amino acid sequence. [95] They noticed it was increased in patients with advanced kidney failure. [96] It was first proposed as a measure of glomerular filtration rate by Grubb and coworkers in 1985. [97] [98]

Use of serum creatinine and cystatin C was found very effective in accurately reflecting the GFR in a study reported in the July 5, 2012 issue of the New England Journal of Medicine. [99]

Related Research Articles

<span class="mw-page-title-main">Creatinine</span> Breakdown product of creatine phosphate

Creatinine is a breakdown product of creatine phosphate from muscle and protein metabolism. It is released at a constant rate by the body.

<span class="mw-page-title-main">Kidney failure</span> Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, hyperkalaemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.

<span class="mw-page-title-main">Inulin</span> Natural plant polysaccharides

Inulins are a group of naturally occurring polysaccharides produced by many types of plants, industrially most often extracted from chicory. The inulins belong to a class of dietary fibers known as fructans. Inulin is used by some plants as a means of storing energy and is typically found in roots or rhizomes. Most plants that synthesize and store inulin do not store other forms of carbohydrate such as starch. In the United States in 2018, the Food and Drug Administration approved inulin as a dietary fiber ingredient used to improve the nutritional value of manufactured food products. Using inulin to measure kidney function is the "gold standard" for comparison with other means of estimating glomerular filtration rate.

<span class="mw-page-title-main">Uremia</span> Type of kidney disease, urea in the blood

Uremia is the term for high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would be normally excreted in the urine. Uremic syndrome can be defined as the terminal clinical manifestation of kidney failure. It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. The former denotation will be used for the rest of the article.

<span class="mw-page-title-main">Glomerular filtration rate</span> Renal function test

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<span class="mw-page-title-main">Assessment of kidney function</span> Ways of assessing the function of the kidneys

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<span class="mw-page-title-main">Acute kidney injury</span> Medical condition

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<span class="mw-page-title-main">Chronic kidney disease</span> Medical condition

Chronic kidney disease (CKD) is a type of kidney disease in which a gradual loss of kidney function occurs over a period of months to years. Initially generally no symptoms are seen, but later symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications can relate to hormonal dysfunction of the kidneys and include high blood pressure, bone disease, and anemia. Additionally CKD patients have markedly increased cardiovascular complications with increased risks of death and hospitalization.

<span class="mw-page-title-main">Podocyte</span> Type of kidney cell

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<span class="mw-page-title-main">Loop diuretic</span> Diuretics that act along the loop of Henle in the kidneys

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<span class="mw-page-title-main">Diabetic nephropathy</span> Chronic loss of kidney function

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Contrast-induced nephropathy (CIN) is a purported form of kidney damage in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury.

In medicine, the urea-to-creatinine ratio (UCR), known in the United States as BUN-to-creatinine ratio, is the ratio of the blood levels of urea (BUN) (mmol/L) and creatinine (Cr) (μmol/L). BUN only reflects the nitrogen content of urea and urea measurement reflects the whole of the molecule, urea is just over twice BUN. In the United States, both quantities are given in mg/dL The ratio may be used to determine the cause of acute kidney injury or dehydration.

Renal angina is a clinical methodology to risk stratify patients for the development of persistent and severe acute kidney injury (AKI). The composite of risk factors and early signs of injury for AKI, renal angina is used as a clinical adjunct to help optimize the use of novel AKI biomarker testing. The term angina from Latin and from the Greek ankhone ("strangling") are utilized in the context of AKI to denote the development of injury and the choking off of kidney function. Unlike angina pectoris, commonly caused due to ischemia of the heart muscle secondary to coronary artery occlusion or vasospasm, renal angina carries no obvious physical symptomatology. Renal angina was derived as a conceptual framework to identify evolving AKI. Like acute coronary syndrome which precedes or is a sign of a heart attack, renal angina is used as a herald sign for a kidney attack. Detection of renal angina is performed by calculating the renal angina index.

A renal diet is a diet aimed at keeping levels of fluids, electrolytes, and minerals balanced in the body in individuals with chronic kidney disease or who are on dialysis. Dietary changes may include the restriction of fluid intake, protein, and electrolytes including sodium, phosphorus, and potassium. Calories may also be supplemented if the individual is losing weight undesirably.

<span class="mw-page-title-main">Andrew S. Levey</span> American nephrologist (born 1950)

Andrew S. Levey is an American nephrologist who transformed chronic kidney disease (CKD) clinical practice, research, and public health by developing equations to estimate glomerular filtration rate (GFR), and leading the global standardization of CKD definition and staging.

In pharmacology, augmented renal clearance (ARC) is a phenomenon where certain critically ill patients may display increased clearance of a medication through the kidneys. In many cases, it is observed as a measured creatinine clearance above that which is expected given the patient's age, gender, and other factors. The phenomenon is most commonly observed in patients with neurologic damage, sepsis, major trauma, or burns.

<span class="mw-page-title-main">Shrunken pore syndrome</span> Type of kidney disorder

Shrunken pore syndrome (SPS) is a kidney disorder described in 2015 in which the pores in the glomerular filtration barrier are hypothesized to have shrunken so that the glomerular filtration rate (GFR) of 5–30 kDa proteins, for example cystatin C, is selectively reduced compared to that of small molecules such as water and creatinine. The syndrome is associated with premature death. SPS has been identified in children.

Kidney ischemia is a disease with a high morbidity and mortality rate. Blood vessels shrink and undergo apoptosis which results in poor blood flow in the kidneys. More complications happen when failure of the kidney functions result in toxicity in various parts of the body which may cause septic shock, hypovolemia, and a need for surgery. What causes kidney ischemia is not entirely known, but several pathophysiology relating to this disease have been elucidated. Possible causes of kidney ischemia include the activation of IL-17C and hypoxia due to surgery or transplant. Several signs and symptoms include injury to the microvascular endothelium, apoptosis of kidney cells due to overstress in the endoplasmic reticulum, dysfunctions of the mitochondria, autophagy, inflammation of the kidneys, and maladaptive repair.

Anders Grubb is a Swedish chemist, physician, and academic. He is currently a Senior Professor of Clinical Chemistry at Lund University.

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