Cystatin C: current step and future prospects

La cystatine C est une protéine de bas poids moléculaire présentée comme un marqueur alternatif de la créatinine pour l’évaluation de la fonction rénale, en particulier dans les populations où la relation de la créatinine à la masse musculaire rend ce paramètre particulièrement inopérant. Cet article tente de synthétiser les connaissances actuelles sur la physiologie de la cystatine C et son utilisation comme marqueur de filtration glomérulaire, seule ou au sein de formules d’évaluation du débit de filtration glomérulaire. De plus, il présente les données récentes pouvant augurer d’autres types d’applications, en particulier en cardiologie, en cancérologie et en pharmacologie clinique.Cystatin C is a low molecular weight-protein, which may replace creatinine for the evaluation of renal function, particularly in the clinical settings where the relationship between creatinine production and muscular mass impairs the clinical performance of creatinine. This paper intends to summarize the current knowledge about the physiology of cystatin C and about its use as a renal marker, alone or within formulas developed to estimate the glomerular filtration rate. Moreover, this paper reviews the recent data about potential other applications of cystatin C, especially in cardiology, in oncology and in clinical pharmacology

Discrepant post-filter ionized calcium concentrations by 2 common gas analyzers in continuous renal replacement therapy using regional citrate anticoagulation: another piece of the puzzle

International audienc

Creatinine: past and present.

Serum creatinine is certainly one of the most prescribed biological parameters. In this review article, we remind some historical data regarding creatinine. Different methodologies to measure creatinine in blood and urine are deeply described. We also discuss the physiological reason for its use as a glomerular filtration rate marker. However, analytical and physiological limitations are described and discussed. Creatinine clearance usefulness is finally largely discussed

Analytical study of three cystatin C assays and their impact on cystatin C-based GFR-prediction equations.

BACKGROUND: Cystatin C-based equations are used to estimate GFR. However, three cystatin C immunoassays are on the market. Difference in cystatin C assays could have strong consequences on the accuracy and precision of cystatin C-based equations. We have performed an analytical study of these three assays and studied potential differences between assays on the precision of cystatin C-based equations. METHODS: We have studied imprecision, recovery, linearity and interferences of the three immunoassays (nephelometric assay from Siemens and turbidimetric assays from Dako and Gentian). The impact of differences in cystatin C assays has been studied for the equations published by Levey (Siemens assay) and Grubb (Dako assay). RESULTS: Analytical performance of the Dako assay is slightly less high. For cystatin C values below 2.5 mg/L, no statistical difference is found between results given by the Dako and the Gentian assays. So, both assays can be used in the Grubb equation. Cystatin C results are different with the Siemens assay. The Levey equation, built with the Siemens assay, can only be used with cystatin C values measured with this assay. Using the Dako or Gentian assay results in the Levey equation can lead to differences in estimating GFR up to 6 mL/min/1.73 m2. Differences can reach 9.5 mL/min/1.73 m2 if the Siemens assay is used in the Grubb equation. CONCLUSION: The Siemens and Gentian assays seem analytically more valid than the Dako assay for cystatin C determination. Differences in cystatin C assays can lead to significant differences in cystatin C-based equations. However, these differences seem less important than the differences observed with creatinine and creatinine-based equations

Elevated Serum Ferritin Is Associated with Reduced Survival in Amyotrophic Lateral Sclerosis

<div><h3>Background</h3><p>Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder caused by the loss of motor neurons. Its etiology remains unknown, but several hypothesis have been raised to explain motor neuron death, including oxidative stress. Dysregulation of cellular iron metabolism can lead to increased oxidative stress, and existing data argue for a role of iron metabolism in ALS pathophysiology.</p> <h3>Methods</h3><p>We performed a retrospective analysis of iron metabolism (IM) variables (serum levels of iron, transferrin, ferritin, and TSC for Transferrin Saturation Coefficient) in a cohort of 694 ALS patients and 297 healthy controls.</p> <h3>Results</h3><p>Serum ferritin levels and TSC were higher, whereas serum transferrin levels were lower in ALS patients than controls. In addition, patients with a high level serum ferritin had a shorter survival time compared to those with low level serum ferritin (618 days versus 921 days for men subgroup; p = .007). Site of onset and ALS-FRS score were not associated with IM variables.</p> <h3>Conclusion</h3><p>This study suggests that ALS patients may have increased iron storage, as measured by increased serum ferritin and TSC. Elevated serum ferritin may also have a deleterious impact on survival in ALS.</p> </div

Does the long term interdisciplinary follow up of stone-formers reduce the rate of urological intervention in recurrences?

Certains patients lithiasiques sont hautement récidivants, malgré les progrès considérables en urologie et une prise en charge des facteurs de risque. Nous avons fait l’hypothèse qu’une prise en charge interdisciplinaire au long court dédiée au diagnostic du processus lithogène, à l’analyse des causes de récidive, et à la détermination d'objectifs chiffrés de prévention, réduirait le nombre de gestes chirurgicaux pour récidive lithiasique et améliorerait ainsi la qualité de vie des patients

How useful is an oral calcium load test for diagnosing recurrent calcium stone formers?

peer reviewedHypercalciuria is the main risk factor for recurrent calcium urolithiasis. The goal of our study is to determinate how useful an oral calcium load test is for stone formers to classify different forms of hypercalciuria in pathogenetic categories defined as renal or absorptive according to the current knowledge. Between June 2013 and February 2016, a prospective study was carried out on 117 documented recurrent hypercalciuric stone formers undergoing an oral calcium load test modified from the original description by Pak. After 2 days of calcium-restricted diet, urine and blood were analyzed at baseline and 120 min after receiving orally 1 g of calcium. Total and ionized calcium, parathyroid hormone from serum and urine calcium and creatinine were assessed in order to divide patients in three groups as previously described: resorptive, absorptive, and renal hypercalciuria. This allowed the identification of 19, 39, 34 and 33 patients with normocalcemic primary hyperparathyroidism (NPHPT), renal hypercalciuria aka renal calcium leak (RCL), absorptive hypercalciuria (AH) and unidentified cause, respectively. Patients with NPHPT (who required parathyroidectomy) experienced a lower PTH decrease (41.41 ± 12.82 vs. 54.06 ± 13.84% p  0.37 mmol/mmol), without hyperparathyroidism. AH was diagnosed by the presence of ΔUCa/Cr > 0.60 mmol/mmol between baseline and 120 min without any other anomaly. For all remaining patients, results were inconclusive due to the lack of sufficient increase in serum calcium or because the cause of lithogenesis could not be clearly identified. The oral calcium load test is useful in nearly 80% of patients by identifying the different forms of hypercalciuria causing urolithiasis and by guiding treatment, including parathyroid surgery