Limitations of Creatinine in Quantifying the Severity of Cyclosporine-Induced Chronic Nephropathy

Tomlanovich, Stephen J.; Golbetz, Helen; Perlroth, Mark G.; Stinson, Edward B.; Myers, Bryan D.

doi:10.1016/s0272-6386(86)80107-x

Cited by 141 publications

(67 citation statements)

References 18 publications

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“…In addition, creatinine can be very inappropriate in these patients as they often have important co-morbidities and are treated with steroids, which have a negative effect on muscle mass (150); furthermore, cyclosporine can also influence tubular creatinine secretion (151). In this context, several groups have tried to establish whether CysC could be a more sensitive marker than creatinine for the early detection of deterioration in GFR in renal transplant patients.…”

Section: Utility Of Cysc In Transplantationmentioning

confidence: 99%

Cystatin C: current position and future prospects

Séronie-Vivien

Delanaye

Piéroni³

et al. 2008

Clinical Chemistry and Laboratory Medicine

164

145

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Cystatin C is a low-molecular-weight protein which has been proposed as a marker of renal function that could replace creatinine. Indeed, the concentration of cystatin C is mainly determined by glomerular filtration and is particularly of interest in clinical settings where the relationship between creatinine production and muscle mass impairs the clinical performance of creatinine. Since the last decade, numerous studies have evaluated its potential use in measuring renal function in various populations. More recently, other potential developments for its clinical use have emerged. This review summarises current knowledge about the physiology of cystatin C and about its use as a renal marker, either alone or in equations developed to estimate the glomerular filtration rate. This paper also reviews recent data about the other applications of cystatin C, particularly in cardiology, oncology and clinical pharmacology. Clin Chem Lab Med 2008;46:1664-86.

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Section: Utility Of Cysc In Transplantationmentioning

confidence: 99%

Cystatin C: current position and future prospects

Séronie-Vivien

Delanaye

Piéroni³

et al. 2008

Clinical Chemistry and Laboratory Medicine

164

145

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“…Furthermore, creatinine level may not reflect the degree of renal damage and may be affected by other factors such as body weight, race, age, sex, total body water volume, drugs, muscle metabolism, and protein intake. [1][2][3] This drawback is unfortunate because acute kidney injury may occur in 7% to 10% hospitalized patients. 4 Other biomarkers have been evaluated for early detection of acute kidney injury such as neutrophil gelatinase-associated lipocalin (NGAL), an ion transporting agent that was identified using functional genomics and proteomics technology.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Qurashi

Ghamdi²,

Jaradat³

et al. 2014

Exp Clin Transplant

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Objectives: To investigate the predictive value of urinary neutrophil gelatinase-associated lipocalin in the occurrence of delayed graft function after kidney transplant. Materials and Methods: In this prospective cohort study of 67 consecutive patients who received a living-related (40 patients [61%]) or deceased-donor kidney transplant (27 patients [39%]), urinary neutrophil gelatinase-associated lipocalin was determined in the first 100 mL perfusate of the donor kidney and in urine at 6 hours after transplant. Patients were followed (11 ± 7 mo) for changes in estimated glomerular filtration rate and delayed graft function. Results: The mean urinary neutrophil gelatinaseassociated lipocalin level at 6 hours after transplant was significantly higher after deceased-donor (781 ± 452 ng/mL) than living-donor transplant (229 ± 223 ng/mL; P ≤ 0.001). The decrease in estimated glomerular filtration rate from 6 to 12 months after transplant was positively correlated with the urinary neutrophil gelatinase-associated lipocalin levels in the perfusate in living-donor transplant. A significant correlation was noted between the occurrence of delayed graft function and the urinary neutrophil gelatinase-associated lipocalin level at 6 hours after living-donor transplant. In the deceased-donor group, the occurrence of delayed graft function was correlated with urinary neutrophil gelatinase-associated lipocalin levels in the perfusate. In deceased-donor kidney transplant, the mean urinary neutrophil gelatinase-associated lipocalin level in the perfusion fluid was significantly greater from donors who had terminal serum creatinine > 150 μmol/L, and urinary neutrophil gelatinase-associated lipocalin level at 6 hours after transplant was significantly greater in transplants with longer cold ischemia time and donors who had hypertension. Conclusions: Urinary neutrophil gelatinase-associated lipocalin levels in the donor kidney perfusate and 6 hours after transplant may be a useful predictor of delayed graft function and decreased graft function from 6 to 12 months after transplant.

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“…Neither test can accurately diagnose the type of renal injury. As every nephrologist knows, serum creatinine is a poor marker of early CKD because the serum concentration is greatly influenced by changes in muscle mass and tubular secretion (2). Hence, the normal reference interval must be relatively wide, and use of serum creatinine alone to follow disease progression is fraught with difficulty.…”

mentioning

confidence: 99%

“…Testing a therapy for CKD using a clinical end point takes a long time, and intermediate surrogate end points that can be evaluated in a shorter time frame are needed. Furthermore, significant renal disease (e.g., fibrosis) can exist with minimal or no change in creatinine because of renal reserve, enhanced tubular secretion of creatinine, or other factors (2,3). Sensitive markers of early injury, especially those that correlate with early fibrosis and progression, are desperately needed.…”

mentioning

confidence: 99%

Discovery of Protein Biomarkers for Renal Diseases

Hewitt¹,

Dear²,

Star³

2004

Journal of the American Society of Nephrology

271

150

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Abstract. Animal models and human studies have been useful in dissecting the molecular mechanisms of renal disease and finding new disease targets; however, translation of these findings to new clinical therapeutics remains challenging. Difficulties with detecting early disease, measuring drug effectiveness, and the daunting cost of clinical trials hampers the development of new therapeutics for renal diseases. Many existing laboratory tests were discovered because of inspired recognition that a particular protein might prove useful in clinical practice. New unbiased genomic and proteomic techniques identify many constituents present in biologic samples and thus may greatly accelerate biomarker research. This review focuses on the steps needed to develop new biomarkers that are useful in laboratory and clinical investigations, with particular focus on new proteomic screening technologies. New biomarkers will speed the laboratory and clinical development of new treatments for renal diseases through mechanistic insights, diagnoses that are more refined, early detection, and enhanced proof of concept testing.

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Limitations of Creatinine in Quantifying the Severity of Cyclosporine-Induced Chronic Nephropathy

Cited by 141 publications

References 18 publications

Cystatin C: current position and future prospects

Cystatin C: current position and future prospects

Untitled

Discovery of Protein Biomarkers for Renal Diseases

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