Assessment of Serum Cystatin C as a Marker of Kidney Function in Children
The purpose of this study is to assess serum cystatin C as a marker of kidney function (glomerular filtration rate, GFR) in children aged 2-14. The individual production rate and possible extra renal elimination of cystatin C based on body composition data is included to develop new algorithms to estimate GFR.
Furthermore, day-to-day variation on serum cystatin C is investigated.
Today, children's kidney function (glomerular filtration rate, GFR) can be monitored by two methods:
1. indirectly by serum creatinine, or
2. directly by injection of a radioactive substance followed by several blood samples.
The first method is inaccurate with many drawbacks, whereas the latter is precise but time-consuming and unpleasant for the child. Therefore, there is a need for a new method for investigating GFR in children.
Serum cystatin C is a small protein that is produced with a constant rate in all nucleated cells in the body. It meets many of the characteristics of an ideal marker of GFR because of the way it is excreted in the kidneys. However, earlier studies have not proven serum cystatin C to be convincingly better than serum creatinine. Why? If there is considerable extra renal elimination, serum cystatin C alone isn't enough to estimate GFR. Therefore, the individual production rate and possible extra renal elimination of cystatin C are included in this study. To assess these factors, the children are submitted to bioelectrical impedance spectroscopy (BIS) to estimate their body composition, including body cell mass as cystatin C is produced in all nucleated cells. To validate the BIS data, dual energy x-ray absorptiometry (DEXA) will be conducted on 100 of the included children.
Based on serum cystatin C and the individual, age-corrected extra renal elimination rate of cystatin C, new algorithms to calculate GFR can be developed.
Furthermore, day-to-day variation in serum cystatin C and BIS data, which is expected to be low, is investigated in 100 of the included children.
1. Day-to-day variation on serum cystatin C is low.
2. Serum cystatin C raises parallel to falling GFR with time, which means that serum cystatin C can be used to monitor changes in kidney function in each patient.
3. Based on body composition, regression analysis and serum cystatin C values, GFR can be estimated in children aged 2-14.
4. GFR calculated as stated above is a more precise measurement of kidney function and changes in kidney function than GFR estimated from serum creatinine.
5. Data of body composition estimated by BIS do not deviate from data estimated by DEXA
6. Day-to-day variation in data for body composition measured by BIS is low.
The project includes 200 children aged 2-14 who are referred for routine examination of GFR in two Departments of Nuclear Medicine.
Observational Model: Case-Only, Time Perspective: Prospective
Department of Nuclear Medicine, University Hospital Aarhus, Skejby
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00300066
- Information obtained from ClinicalTrials.gov on July 15, 2010
The purpose of this study is to determine if LY2382770 is safe and effective at protecting kidney function in patients with kidney disease due to diabetes.
Autosomal dominant polycystic kidney disease (PKD) is the most common inherited kidney disease, affecting more than 400,000 people in the U.S. and 5 million people worldwide. PKD is the 4t...
A non-invasive urinary test that detects kidney injuries in liver transplant (LT) candidates would be useful for monitoring of kidney damage. Particularly, the ability to predict irreversi...
FGF-23 is a newly described protein that is an important regulator of phosphorus in the body. This protein increases in people with kidney disease and people who need dialysis have very h...
The causes of deterioration of transplanted kidney function are poorly understood. The purpose of this study is to determine the disease processes that cause transplanted kidney dysfunctio...
Few studies have prospectively evaluated the progression of chronic kidney disease (CKD) in children and adolescents, as well as factors associated with progression.
Drug-induced kidney disease is a frequent cause of renal dysfunction; however, there are no standards to identify and characterize the spectrum of these disorders. We convened a panel of international...
Proteomics has long been considered an ideal platform, and urine an ideal source for biomarker discovery in human autoimmune kidney diseases. A number of studies have examined the urine proteome to id...
Chronic kidney disease (CKD) is a worldwide public health problem which is at high increased risk of cardiovascular disease (CVD) and renal failure. Deterioration of kidney function causes an increase...
Medical and Biotech [MESH] Definitions
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
A complication of kidney diseases characterized by cell death involving KIDNEY PAPILLA in the KIDNEY MEDULLA. Damages to this area may hinder the kidney to concentrate urine resulting in POLYURIA. Sloughed off necrotic tissue may block KIDNEY PELVIS or URETER. Necrosis of multiple renal papillae can lead to KIDNEY FAILURE.
An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.