Serum cystatin C - a superior marker of rapidly reduced glomerular filtration after uninephrectomy in kidney donors compared to creatinine

Herget–Rosenthal, Stefan; Pietruck, Frank; Volbracht, Lothar; Philipp, Thomas; Kribben, Andreas

doi:10.5414/cnp64041

Cited by 96 publications

(65 citation statements)

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“…In the subgroup analyzed in this report, CIN occurred in 16.1 to 24.8% of patients using more sensitive creatinine and cystatin C definitions of CIN. The higher incidence rates of CIN using cystatin C are consistent with the observations that cystatin C is more sensitive than creatinine to acute changes in GFR (9,10). Furthermore the higher incidence of CIN obtained using these definitions provides more statistical power to explore the association with long-term AE rates as well as differences between treatment groups.…”

Section: Discussionsupporting

confidence: 80%

Contrast-Induced Nephropathy and Long-Term Adverse Events

Solomon

Mehran

Natarajan

et al. 2009

Clinical Journal of the American Society of Nephrology

264

163

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Background and objectives:The relationship of contrast-induced nephropathy (CIN) to long-term adverse events (AEs) is controversial. Although an association with AEs has been previously reported, it is unclear whether CIN is causally related to these AEs.Design, setting, participants, & measurements: We obtained long-term (>1 yr) follow-up on 294 patients who participated in a randomized, double-blind comparison of two prevention strategies for CIN (iopamidol versus iodixanol). A difference in the incidence of AEs between patients who had developed CIN and those who had not was performed using a 2 test and Poisson regression analysis. A similar statistical approach was used for the differences in AEs between those who received iopamidol or iodixanol. Multiple definitions of CIN were used to strengthen and validate the results and conclusions.Results: The rate of long-term AEs was higher in individuals with CIN (all definitions of CIN). After adjustment for baseline comorbidities and risk factors, the adjusted incidence rate ratio for AEs was twice as high in those with CIN. Randomization to iopamidol reduced both the incidence of CIN and AEs.Conclusions: The parallel decrease in the incidence of CIN and AEs in one arm of this randomized trial supports a causal role for CIN.

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Section: Discussionsupporting

confidence: 80%

Contrast-Induced Nephropathy and Long-Term Adverse Events

Solomon

Mehran

Natarajan

et al. 2009

Clinical Journal of the American Society of Nephrology

264

163

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“…Cystatin C is therefore used as a marker of glomerular filtration [16]. In addition, it has been suggested that s-cystatin C might be an earlier and more rapid indicator of change in GFR than s-creatinine [17]. In the present study no change in s-cystatin C over time was found in any of the treatment groups.…”

Section: Discussioncontrasting

confidence: 47%

Reversible elevations of serum creatinine levels but no effect on glomerular filtration during treatment with the direct thrombin inhibitor AZD0837

Schützer

Svensson

Zetterstrand

et al. 2010

Eur J Clin Pharmacol

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. Reversible elevations of serum creatinine levels but no effect on glomerular filtration during treatment with the direct thrombin inhibitor AZD0837. European Journal of Clinical Pharmacology, Springer Verlag, 2010, 66 (9), pp.903-910. <10.1007/s00228-010-0849-7>. F o r P e e r R e v i e w Reversible elevations of serum creatinine but no effect on glomerular filtration during treatment with the direct thrombin inhibitor AZD0837 was to evaluate whether the increase in s-creatinine is due to a decrease in renal glomerular filtration rate (GFR) or inhibition of tubular secretion of creatinine.Methods: Thirty healthy subjects aged 60-71 years were included in an open-label, randomised, placebo-controlled, two-way crossover study (D1250C00033) with AZD0837 450 mg extended-release formulation once daily for 8 days. Cimetidine was co-administered on Days 6-8 during both treatment periods. Blood and urine samples were collected for assessment of s-creatinine, s-cystatin C, endogenous creatinine clearance (CrCl) and urinary markers of renal damage. GFR was measured by the plasma clearance of iohexol.Results: A 6% increase in mean s-creatinine, but no increase in s-cystatin C, was observed during treatment with AZD0837. Co-administration of cimetidine resulted in a 21% increase in screatinine. A significant decrease in CrCl was found during AZD0837 treatment compared with placebo (-5.73 ml/min; 95% CI -11.3 to -0.12). No significant difference in GFR (-1.6 ml/min/1.73 m 2 ; 90% CI -3.7 to 0.5) was seen during treatment with AZD0837 versus placebo.No changes in renal damage markers were found during the treatment periods.Conclusions: An increase in s-creatinine, a decrease in CrCl, but no decrease in GFR, were found during treatment with AZD0837. Findings suggest that inhibition of renal tubular secretion of creatinine is the likely cause of the observed increase in s-creatinine.Word count = 249 words

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“…26,27 Normal contralateral renal function may have masked injury observed in our study. However, if the clamped kidney had sustained severe injury and decreased clearance, we would expect functional changes similar to those seen in donor nephrectomy studies in which serum cystatin C increased 37% and creatinine increased 19% at 24 hours, and both increased 52%-62% at 72 hours.…”

Section: Discussionmentioning

confidence: 62%

“…However, if the clamped kidney had sustained severe injury and decreased clearance, we would expect functional changes similar to those seen in donor nephrectomy studies in which serum cystatin C increased 37% and creatinine increased 19% at 24 hours, and both increased 52%-62% at 72 hours. 26 Increased creatinine without a concomitant decrease in clearance could indicate a transient defect of tubule creatinine secretion in our cohort. 28,29 In prior reports, the extent of structural damage during human AKI of diverse causes has appeared to be less than that seen in animal models during severe reduction of renal function.…”

Section: Discussionmentioning

confidence: 77%

Tolerance of the Human Kidney to Isolated Controlled Ischemia

Parekh¹,

Weinberg²,

Ercole

et al. 2013

Journal of the American Society of Nephrology

184

149

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Tolerance of the human kidney to ischemia is controversial. Here, we prospectively studied the renal response to clamp ischemia and reperfusion in humans, including changes in putative biomarkers of AKI. We performed renal biopsies before, during, and after surgically induced renal clamp ischemia in 40 patients undergoing partial nephrectomy. Ischemia duration was .30 minutes in 82.5% of patients. There was a mild, transient increase in serum creatinine, but serum cystatin C remained stable. Renal functional changes did not correlate with ischemia duration. Renal structural changes were much less severe than observed in animal models that used similar durations of ischemia. Other biomarkers were only mildly elevated and did not correlate with renal function or ischemia duration. In summary, these data suggest that human kidneys can safely tolerate 30-60 minutes of controlled clamp ischemia with only mild structural changes and no acute functional loss.

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Serum cystatin C - a superior marker of rapidly reduced glomerular filtration after uninephrectomy in kidney donors compared to creatinine

Cited by 96 publications

References 0 publications

Contrast-Induced Nephropathy and Long-Term Adverse Events

Contrast-Induced Nephropathy and Long-Term Adverse Events

Reversible elevations of serum creatinine levels but no effect on glomerular filtration during treatment with the direct thrombin inhibitor AZD0837

Tolerance of the Human Kidney to Isolated Controlled Ischemia

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