Evaluation of kidney disease using e-GFR compared to measured creatinine clearance.

Measurement of renal function is required for diagnosis and stratification of kidney disease. GFR is considered as the best overall measure of kidney function for diagnosis and treatment of patients with CKD. Measuring GFR is time consuming and hence eGFR is calculated using equations with endogenous markers like SCr. Therefore, it is of interest to examine the accuracy of creatinine based estimates (CrCl and CG formula) of GFR among patients. Thus, 60 in-patients (30 men and 30 women) at the GVP hospital and 40 controls were enrolled in the study. SCr and 24 hrs urine creatinine are estimated using blood sample and same day 24-hr urine collection. SCr is estimated using the Kinetic Jaffe's method in Auto analyzer for serum and urine. eGFR is calculated using the CG formula for the SCr value. We evaluated the correlation between measured CrCl derived from 24-hr urine collection and calculated/predicted CrCl using the CG equations. A positive correlation was observed between measured GFR and e-GFR in case and control groups.

Black and White Adults With CKD Hospitalized With Acute Kidney Injury: Findings From the Chronic Renal Insufficiency Cohort (CRIC) Study.

RATIONALE & OBJECTIVE: Few studies have investigated racial disparities in acute kidney injury (AKI), in contrast to the extensive literature on racial differences in the risk of kidney failure. We sought to study potential differences in risk in the setting of chronic kidney disease (CKD). STUDY DESIGN: Prospective cohort study. SETTING & PARTICIPANTS: We studied 2,720 self-identified Black or White participants with CKD enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study from July 1, 2013, to December 31, 2017. EXPOSURE: Self-reported race (Black vs White). OUTCOME: Hospitalized AKI (≥50% increase from nadir to peak serum creatinine). ANALYTICAL APPROACH: Cox regression models adjusting for demographics (age and sex), prehospitalization clinical risk factors (diabetes, blood pressure, cardiovascular disease, estimated glomerular filtration rate, proteinuria, receipt of angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers), and socioeconomic status (insurance status and education level). In a subset of participants with genotype data, we adjusted for apolipoprotein L1 gene (APOL1) high-risk status and sickle cell trait. RESULTS: Black participants (n = 1,266) were younger but had a higher burden of prehospitalization clinical risk factors. The incidence rate of first AKI hospitalization among Black participants was 6.3 (95% CI, 5.5-7.2) per 100 person-years versus 5.3 (95% CI, 4.6-6.1) per 100 person-years among White participants. In an unadjusted Cox regression model, Black participants were at a modestly increased risk of incident AKI (HR, 1.22 [95% CI, 1.01-1.48]) compared with White participants. However, this risk was attenuated and no longer significant after adjusting for prehospitalization clinical risk factors (adjusted HR, 1.02 [95% CI, 0.83-1.25]). There were only 11 AKI hospitalizations among individuals with high-risk APOL1 risk status and 14 AKI hospitalizations among individuals with sickle cell trait. LIMITATIONS: Participants were limited to research volunteers and potentially not fully representative of all CKD patients. CONCLUSIONS: In this multicenter prospective cohort of CKD patients, racial disparities in AKI incidence were modest and were explained by differences in prehospitalization clinical risk factors.

Capmatinib-Induced Pseudo-Acute Kidney Injury: A Case Report.

We present a case of pseudo-acute kidney injury (AKI) following capmatinib therapy in an 84-year-old man with combined non-small cell (adenocarcinoma) and small cell lung cancer with MET exon 14-skipping mutation. His past medical history was significant for chronic kidney disease stage 3 with a baseline serum creatinine (Scr) of 1.6mg/dL rising to 2.44mg/dL (estimated glomerular filtration rate [GFR] 24mL/min/1.73m2) while on capmatinib. Scr improved to 1.84mg/dL with the cessation of capmatinib but rose again to 2.22mg/dL upon resumption of therapy. Further investigation with cystatin C and renal iothalamate clearance showed that despite fluctuation in Scr levels, there was not much variation in GFR calculated using these methods. Urinalysis and urinary protein-creatinine ratio were unremarkable. Treatment with capmatinib was continued at reduced dose and a third instance of rise in Scr was observed, followed by a spontaneous return to baseline. Thus, MET inhibitor therapy can result in an asymptomatic rise in Scr, and it must be distinguished from AKI with more accurate non-creatinine-based methods to evaluate GFR. This could spare such patients from invasive diagnostic tests, such as a kidney biopsy, and premature cessation of prognostically important cancer therapies.

Association Between Deceased Donor Acute Kidney Injury Assessed Using Baseline Serum Creatinine Back-Estimation and Graft Survival: Results From the French National CRISTAL Registry.

RATIONALE & OBJECTIVE: Deceased donor acute kidney injury (AKI) frequently leads to kidney discards, but its impact on long-term graft survival in kidney transplant recipients remains unclear. We investigated the association between deceased donor AKI assessed using back-estimation of baseline serum creatinine (Scr) and graft survival. STUDY DESIGN: Observational cohort study. SETTING & PARTICIPANTS: Adult patients represented within the French CRISTAL registry who received a single kidney allograft from brain-dead deceased donors between January 2006 and December 2017. EXPOSURE: A back-estimated Scr baseline value was derived for an assumed glomerular filtration rate at 75mL/min/1.73m2, using the MDRD Study equation. A refined classification system for donor AKI was implemented as follows: no AKI, undetermined AKI/chronic kidney disease (CKD), recovery from AKI, and ongoing AKI. OUTCOME: Death-censored graft survival. ANALYTICAL APPROACH: Multivariable Cox models using a robust variance estimator for paired kidneys from the same donor. RESULTS: We classified 26,786 recipients as follows: no AKI (n=19,276); undetermined AKI/CKD (n=1,745); recovery from AKI (n=2,392); and ongoing AKI (n=3,373). We observed 4,458 kidney graft losses during a median follow-up period of 5.7 years. Compared with no AKI, ongoing AKI was associated with an increased risk of graft failure (hazard ratio [HR], 1.24 [95% CI, 1.13-1.35]). The HRs for graft failure in the undetermined AKI/CKD and recovery from AKI groups (1.22 [95% CI, 1.07-1.38] and 1.18 [95% CI, 1.06-1.31], respectively) were similar to those observed in the ongoing AKI group. The adverse effect of deceased donor AKI was no longer evident when relying either on the admission or the lowest Scr throughout the procurement procedure as baseline Scr. LIMITATIONS: No measurement of urine output in donors. CONCLUSIONS: Deceased donor ongoing AKI, undetermined AKI/CKD, and recovery from AKI according to back-estimated baseline Scr are associated with decreased graft survival. The definition of baseline Scr as the first value measured on admission would have led to a misclassification bias and erroneous estimates.

Predictive value of kidney injury markers for early DGF in kidney transplant recipients / 器官移植

Objective To evaluate the predictive values of serum neutrophil gelatinase-associated lipocalin (NGAL), urine NGAL, serum cystatin C (Cys-C) and serum creatinine (Scr) for early delayed graft function (DGF) in kidney transplant recipients. Methods Clinical data, blood and urine samples of 159 kidney transplant recipients were collected. All recipients were divided into the DGF group (n=42) and immediate graft function (IGF) group (n=117) according to the incidence of DGF. Clinical data of all recipients were analyzed. The changes of serum NGAL, urine NGAL, Cys-C and Scr levels were statistically compared between two groups. The predictive values of different markers for early DGF were assessed. Results Among 159 kidney transplant recipients, DGF occurred in 42 cases with an incidence rate of 26.4%. There were statistically significant differences in donor age, cold ischemia time of donor kidney and complement-dependent cytoxicity (CDC) between the two groups(all P < 0.05). Within postoperative 2 weeks, the serum NGAL levels in the DGF group were higher than those in the IGF group (all P < 0.05). The Cys-C, Scr and urine NGAL levels in the DGF group were higher compared with those in the IGF group within 3 weeks after kidney transplantation(all P < 0.001). Serum NGAL, urine NGAL, Cys-C and Scr levels had certain predictive values for early DGF in kidney transplant recipients. Cys-C yielded the highest predictive value with a cut-off value of 4.73 mg/L, sensitivity of 0.833, specificity of 0.812 and area under the curve (AUC) of 0.895. Conclusions Cys-C has higher predictive value for early DGF in kidney transplant recipients compared with serum NGAL, urine NGAL and Scr.

Serum creatinine as a predictor of mortality in patients readmitted to the intensive care unit after cardiac surgery: a retrospective cohort study in China.

BACKGROUND: Patients readmitted to the intensive care unit (ICU) after cardiac surgery have a high mortality rate. The relationship between renal function and in-hospital mortality in readmitted patients has not been well demonstrated. METHODS: We retrospectively evaluated cardiac surgery patients who were readmitted to the ICU at least once. Data on serum creatinine levels before surgery and on the day of ICU readmission were collected. The estimated glomerular filtration rate (eGFR) was calculated according to the creatinine-based Chronic Kidney Disease-Epidemiology Collaboration equation. We used logistic regression models and restricted cubic spline curves with four knots (5%, 35%, 65%, 95%) to investigate the relationship between renal function indicators and mortality. RESULTS: Of the 184 patients evaluated, 30 patients died during hospitalization, yielding a mortality rate of 16.30%. Cardiac dysfunction (n=84, 45.65%) and respiration disorder (n=51, 27.72%) were the most common reasons for ICU readmission. Creatinine [odds ratio (OR): 1.14, 95% confidence interval (CI): 1.07-1.25] and eGFR (OR: 0.95, 95% CI: 0.93-0.98) were independently associated with in-hospital mortality after adjusting for various confounders. Both creatinine level and eGFR had a linear association with in-hospital mortality (P for non-linearity ˃0.05). CONCLUSION: Renal function is significantly associated with the in-hospital mortality of patients readmitted to the ICU after cardiac surgery, as evidenced by the independent correlation of both creatinine and eGFR with in-hospital mortality.

Real-Time Prediction of Acute Kidney Injury in Hospitalized Adults: Implementation and Proof of Concept.

RATIONALE & OBJECTIVE: Acute kidney injury (AKI) is diagnosed based on changes in serum creatinine concentration, a late marker of this syndrome. Algorithms that predict elevated risk for AKI are of great interest, but no studies have incorporated such an algorithm into the electronic health record to assist with clinical care. We describe the experience of implementing such an algorithm. STUDY DESIGN: Prospective observational cohort study. SETTING & PARTICIPANTS: 2,856 hospitalized adults in a single urban tertiary-care hospital with an algorithm-predicted risk for AKI in the next 24 hours>15%. Alerts were also used to target a convenience sample of 100 patients for measurement of 16 urine and 6 blood biomarkers. EXPOSURE: Clinical characteristics at the time of pre-AKI alert. OUTCOME: AKI within 24 hours of pre-AKI alert (AKI24). ANALYTICAL APPROACH: Descriptive statistics and univariable associations. RESULTS: At enrollment, mean predicted probability of AKI24 was 19.1%; 18.9% of patients went on to develop AKI24. Outcomes were generally poor among this population, with 29% inpatient mortality among those who developed AKI24 and 14% among those who did not (P<0.001). Systolic blood pressure<100mm Hg (28% of patients with AKI24 vs 18% without), heart rate>100 beats/min (32% of patients with AKI24 vs 24% without), and oxygen saturation<92% (15% of patients with AKI24 vs 6% without) were all more common among those who developed AKI24. Of all biomarkers measured, only hyaline casts on urine microscopy (72% of patients with AKI24 vs 25% without) and fractional excretion of urea nitrogen (20% [IQR, 12%-36%] among patients with AKI24 vs 34% [IQR, 25%-44%] without) differed between those who did and did not develop AKI24. LIMITATIONS: Single-center study, reliance on serum creatinine level for AKI diagnosis, small number of patients undergoing biomarker evaluation. CONCLUSIONS: A real-time AKI risk model was successfully integrated into the EHR.

AKI-A Relevant Safety End Point?

Acute kidney injury (AKI) is a common outcome evaluated in clinical studies, often as a safety end point in a variety of cardiovascular, kidney disease, and other clinical trials. AKI end points that include modest increases in serum creatinine levels from baseline may not associate with patient-centered outcomes such as initiation of dialysis, sustained decline in kidney function, or death. Surprisingly, data from several randomized controlled trials have suggested that in certain settings, the development of AKI may be associated with favorable outcomes. AKI safety end points that are nonspecific and may not associate with patient-centered outcomes could result in beneficial therapies being inappropriately withheld or never developed for commercial use. We review several issues related to commonly used AKI definitions and suggest that future work in AKI use more patient-centered AKI end points such as major adverse kidney events at 30 days or other later time points.

Timing of Recovery From Moderate to Severe AKI and the Risk for Future Loss of Kidney Function.

RATIONALE & OBJECTIVE: The extent of recovery of kidney function following acute kidney injury (AKI) is known to be associated with future chronic kidney disease. Less is known about how the timing of recovery affects the rate of future loss of kidney function. STUDY DESIGN: We performed a retrospective cohort study examining the independent association between the timing of recovery from moderate to severe AKI and future loss of kidney function. SETTING & PARTICIPANTS: 47,903 adult US veterans with stage 2 or 3 AKI who recovered to within 120% of baseline creatinine level within 90 days of peak injury. EXPOSURE: The timing of recovery of kidney function from peak inpatient serum creatinine level grouped into 1 to 4, 5 to 10, 11 to 30, and 31 to 90 days. OUTCOME: A sustained 40% decline in estimated glomerular filtration rate below that calculated from the last serum creatinine level available during the 90-day recovery period or kidney failure (2 outpatient estimated glomerular filtration rates<15mL/min/1.73m2, dialysis procedures > 90 days apart, kidney transplantation, or registry within the US Renal Data System). ANALYTICAL APPROACH: Time to the primary outcome was examined using multivariable Cox proportional hazards regression. RESULTS: Among 47,903 patients, 29,316 (61%), 10,360 (22%), 4,520 (9%), and 3,707 (8%) recovered within 1 to 4, 5 to 10, 11 to 30, and 31 to 90 days, respectively. With a median follow-up of 42 months, unadjusted incidence rates for the kidney outcome were 2.01, 3.55, 3.86, and 3.68 events/100 person-years, respectively. Compared with 1 to 4 days, recovery within 5 to 10, 11 to 30, and 31 to 90 days was associated with increased rates of the primary outcome: adjusted HRs were 1.33 (95% CI, 1.24-1.43), 1.41 (95% CI, 1.28-1.54), and 1.58 (95% CI, 1.43-1.75), respectively. LIMITATIONS: Predominately male population, residual confounding, and inability to make causal inferences because of the retrospective observational study design. CONCLUSIONS: The timing of recovery provides an added dimension to AKI phenotyping and prognostic information regarding the future occurrence of loss of kidney function. Studies to identify effective interventions on the timing of recovery from AKI are warranted.

Peripheral Artery Disease: Its Adverse Consequences With and Without CKD.

RATIONALE & OBJECTIVES: Chronic kidney disease (CKD) is a potent risk factor for macrovascular disease and death. Peripheral artery disease (PAD) is more common in patients with CKD and is associated with lower-limb complications and mortality. We sought to compare the prevalence of PAD in and outside the setting of kidney disease and examine how PAD affects the risk for adverse health outcomes, specifically lower-limb complications, cardiovascular events, and survival. STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: 453,573 adult residents of Manitoba with at least 1 serum creatinine measurement between 2007 and 2014. EXPOSURE: PAD defined by hospital discharge diagnosis codes and medical claims. OUTCOMES: All-cause mortality, cardiovascular events, and lower-limb complications, including foot ulcers and nontraumatic amputations. ANALYTICAL APPROACH: Survival analysis using Cox proportional hazards models. RESULTS: The prevalence of PAD in our study population was 4.5%, and patients with PAD were older, were more likely to be male, and had a higher burden of comorbid conditions, including diabetes and CKD. PAD was associated with higher risks for all-cause mortality, cardiovascular events, and lower-limb complications in patients with estimated glomerular filtration rate (eGFR) ≥ 60mL/min/1.73m2, those with CKD GFR categories 3 to 5 (G3-G5), and those treated by dialysis (CKD G5D). Although HRs for PAD were lower in the CKD population, event rates were higher as compared with those with eGFR≥60mL/min/1.73m2. In particular, compared with patients with eGFR≥60mL/min/1.73m2 and without PAD, patients with CKD G5D had 10- and 12-fold higher risks for lower-limb complications, respectively (adjusted HRs of 10.36 [95% CI, 8.83-12.16] and 12.02 [95% CI, 9.58-15.08] for those without and with PAD, respectively), and an event rate of 75/1,000 patient-years. LIMITATIONS: Potential undercounting of PAD and complications using administrative codes and the limited ability to examine quality-of-care indicators for PAD. CONCLUSIONS: PAD is more common in patients with CKD G3-G5 and G5D compared with those with eGFR≥60mL/min/1.73m2 and frequently leads to lower-limb complications. Medical interventions and care pathways specifically designed to slow or prevent the development of lower-limb complications in this population are urgently needed.

Postcontrast Acute Kidney Injury in Pediatric Patients: A Cohort Study.

RATIONAL & OBJECTIVE: The risks of iodinated contrast material administered to pediatric patients are not well defined. The purpose of this study was to examine the rates of postcontrast acute kidney injury (AKI), dialysis therapy, and death following administration of intravenous contrast material to pediatric patients. STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: Pediatric (aged <18 years) patients who underwent either contrast-enhanced (contrast group) or unenhanced (noncontrast group) computed tomography (CT) at our institution from December 2001 to January 2016. EXPOSURE: Intravenous iodinated contrast material. OUTCOMES: Postcontrast AKI based on serum creatinine-defined KDIGO criteria, dialysis therapy, and death. ANALYTICAL APPROACH: Risks for AKI, dialysis therapy, and death were compared between contrast and noncontrast group patients using a propensity score analysis incorporating clinical covariates related to contrast exposure. RESULTS: 2,201 pediatric patients (1,773 contrast and 428 noncontrast) were identified. Rates of AKI and dialysis therapy in the contrast group were 3.3% (59/1,773) and 0.1% (2/1,773), respectively. Following propensity score adjustment, no differences in risk for AKI (stage 1 AKI: OR, 0.75 [95% CI, 0.32-1.78], P=0.5; stage 2: OR, 2.00 [95% CI, 0.18-21.9], P=0.6; stage 3: OR, 0.50 [95% CI, 0.05-5.48], P=0.6), dialysis therapy (OR, 1.00 [95% CI, 0.06-15.9], P=0.9), or death (OR, 1.50 [95% CI, 0.53-4.22], P=0.4) were observed between the contrast and noncontrast groups. All patients with post-CT stage 3 AKI diagnosed also had contrast-independent potential causes of AKI. LIMITATIONS: The study's small sample size and low rates of postcontrast AKI, dialysis therapy, and death limited the ability to detect an effect of contrast administration on these outcomes. Unmeasured residual confounders may limit the validity of our results. Few patients had decreased kidney function at the time of CT. CONCLUSIONS: Rates of postcontrast AKI, dialysis therapy, and death following contrast-enhanced CT were very low in this pediatric cohort. Although not detectably different, an effect of contrast on these outcomes could not be ruled out.

Management of Acute Kidney Injury: Core Curriculum 2018.

Acute kidney injury (AKI) is a heterogeneous disorder that is common in hospitalized patients and associated with short- and long-term morbidity and mortality. When AKI is present, prompt workup of the underlying cause should be pursued, with specific attention to reversible causes. Measures to prevent AKI include optimization of volume status and avoidance of nephrotoxic medications. Crystalloids are preferred over colloids for most patients, and hydroxyethyl starches should be avoided. Volume overload in the setting of AKI is associated with adverse outcomes, so attention should be paid to overall fluid balance. Currently there are no targeted pharmacotherapies approved for the treatment of AKI. The optimal timing of renal replacement therapy in critically ill patients with AKI is unclear, but is an area of active investigation. Recent studies suggest that AKI is not a "self-limited" process, but is strongly linked to increased risk for chronic kidney disease, subsequent AKI, and future mortality.

Study on the relationship between anti-inflammatory cytokine IL-35 and delayed renal graft function / 器官移植

Objective To investigate the relationship between the interleukin (IL)-35 and the recovery of renal graft function. Methods Clinical data of 45 recipients receiving renal transplantation from donation after cardiac death (DCD) were retrospectively analyzed. According to the presence of delayed graft function (DGF) after renal transplantation, all recipients were divided into the immediate graft function (IGF) group (n=32) and DGF group (n=13). The serum creatinine (Scr) level and estimated glomerular filtration rate (eGFR) in the recipients were statistically compared between two groups at 1, 2, 3, 7, 14, 28 d and 3, 6 and 12 months after renal transplantation. The IL-35 levels in the serum and urine samples of the recipients were statistically compared between two groups at 1, 2, 3, 7, 14, 28 d following renal transplantation. Results In the DGF group, the renal function was restored slowly. Compared with the IGF group, the Scr level was significantly higher, whereas the eGFR was considerably lower in the DGF group at postoperative 7 d (both P<0.05). At 1 year after surgery, there was no significant difference in the Scr level between two groups. Compared with the IGF group, the eGFR in the DGF group was significantly lower at postoperative 1 year (P<0.05). At 1, 2, 3, 7, 14 d after operation, the serum levels of IL-35 in the DGF group were evidently lower than those in the IGF group (all P<0.05). Compared with the IGF group, the serum level of IL-35 in the DGF group was significantly increased at postoperative 28 d (P<0.05). At postoperative 1, 2, 3, 7 d, the IL-35 levels in the urine samples in the DGF group were significantly lower than those in the IGF group (all P<0.05). At postoperative 14 and 28 d, the IL-35 levels in the urine samples did not significantly differ between two groups (both P>0.05). Conclusions The low levels of IL-35 in the serum and urine of recipients after renal transplantation are associated with the incidence of DGF to certain extent, prompting that excessively weak systemic and local anti-inflammatory responses early after renal transplantation and uncontrolled excessive inflammatory response are probably the pivotal causes of DGF.

Analysis of early clinical efficacy of renal transplantation from extended criteria donor of the donation after cardiac death / 器官移植

Objective To compare the early clinical efficacy of renal transplantation between extended criteria donor (ECD) and standard criteria donor (SCD). Methods Clinical data of 85 recipients undergoing renal transplantation from donation after cardiac death (DCD) were retrospectively analyzed. According to the types of donors, all recipients were divided into the ECD group (n=31) and SCD group (n=54). The level of serum creatinine (Scr), incidence of early complications and clinical prognosis within 3 months after renal transplantation were compared between 2 groups. Results No statistical significance was observed in the levels of Scr within 1 month after renal transplantation between the ECD group and SCD group (all P>0.05). At postoperative 60 and 90 d, the level of Scr in the ECD group was (189±97) and (175± 69) μmol/L respectively, significantly higher than (142±49) and (135±41) μmol/L in the SCD group (P=0.005 and 0.002). In the ECD group and SCD group, the incidence of acute rejection (AR) was 6% and 15%, the incidence of delayed graft function (DGF) was 23% and 19%, the incidence of pulmonary infection was 10% and 6%, the incidence of other early complications was 32% and 15%, respectively, no statistical significance was identified (all P>0.05). In the ECD group and SCD group, the survival rate of the recipient was 97% and 94%, the survival rate of the renal was 84% and 91%, no statistical significance was identified (all P>0.05). Conclusions Compared with the SCD, renal transplantation from ECD can achieve equivalent early clinical efficacy. In the present condition of serious deficiency of donor kidney, the application of ECD can enlarge the supply of the donor kidney.

Performance of Serum Creatinine and Kidney Injury Biomarkers for Diagnosing Histologic Acute Tubular Injury.

BACKGROUND: The diagnosis of acute kidney injury (AKI), which is currently defined as an increase in serum creatinine (Scr) concentration, provides little information on the condition's actual cause. To improve phenotyping of AKI, many urinary biomarkers of tubular injury are being investigated. Because AKI cases are not frequently biopsied, the diagnostic accuracy of concentrations of Scr and urinary biomarkers for histologic acute tubular injury is unknown. STUDY DESIGN: Cross-sectional analysis from multicenter prospective cohort. SETTINGS & PARTICIPANTS: Hospitalized deceased kidney donors on whom kidney biopsies were performed at the time of organ procurement for histologic evaluation. PREDICTORS: (1) AKI diagnosed by change in Scr concentration during donor hospitalization and (2) concentrations of urinary biomarkers (neutrophil gelatinase-associated lipocalin [NGAL], liver-type fatty acid-binding protein [L-FABP], interleukin 18 [IL-18], and kidney injury molecule 1 [KIM-1]) measured at organ procurement. OUTCOME: Histologic acute tubular injury. RESULTS: Of 581 donors, 98 (17%) had mild acute tubular injury and 57 (10%) had severe acute tubular injury. Overall, Scr-based AKI had poor diagnostic performance for identifying histologic acute tubular injury and 49% of donors with severe acute tubular injury did not have AKI. The area under the receiver operating characteristic curve (AUROC) of change in Scr concentration for diagnosing severe acute tubular injury was 0.58 (95% CI, 0.49-0.67) and for any acute tubular injury was 0.52 (95% CI, 0.45-0.58). Compared with Scr concentration, NGAL concentration demonstrated higher AUROC for diagnosing both severe acute tubular injury (0.67; 95% CI, 0.60-0.74; P=0.03) and any acute tubular injury (0.60; 95% CI, 0.55-0.66; P=0.005). In donors who did not have Scr-based AKI, NGAL concentrations were higher with increasing severities of acute tubular injury (subclinical AKI). However, compared with Scr concentration, AUROCs for acute tubular injury diagnosis were not significantly higher for urinary L-FABP, IL-18, or KIM-1. LIMITATIONS: The spectrum of AKI cause in deceased donors may be different from that of a general hospitalized population. CONCLUSIONS: Concentrations of Scr and kidney injury biomarkers (L-FABP, IL-18, and KIM-1) lack accuracy for diagnosing acute tubular injury in hospitalized deceased donors. Although urinary NGAL concentration had slightly higher discrimination for acute tubular injury than did Scr concentration, its overall AUROC was still modest.

Changes of glomerular filtration rate in type 2 diabetic patients with normal serum creatinine and serum cystatin C / 中国糖尿病杂志

Objective To investigate the changesof glomerular filtration rate(eGFR)in type 2 diabetic patients with normal serum creatinine(Scr)and serum cystatin C(Cys-C). Methods A total of 166 patients with type 2 diabetes mellitus admitted into our hospital from January 2014 to September 2015 were enrolled in this study and divided into three groups according to the level of Scr and Cys-C:T2DM patients with normal Scr and Cys-C (normal group,n =109),T2DM patients with normal Scr and high level of Cys-C (high Cys-C group,n=40),and T2DM patients with high levels of Scr and Cys-C (high Scr Cys-C group,n=17). Normal group were further divided into two subgroups according to the level of eGFR:eGFR≥90 ml/(min·1.73 m2 )subgroup and eGFR<90 ml/(min·1.73 m2 )subgroup.Clinical characteristics and laboratory datawere collected in all subjects. eGFR were measured by 99mTc-DTPA nephro-dynamic imaging. Results The average value of eGFR were significantly different in normal group(82.68±13.45)ml/(min·1.73 m2 ),high Cys-C group(67.93 ±14.01)ml/(min·1.73 m2 )and high Scr,Cys-C group (50.54±15.10)ml/(min·1.73 m2 ). In normal group,the proportion of patients with eGFR equal or greater than 90 ml/(min·1.73 m2 )was 26.6%,patients with eGFR ranged from 60 to 89 ml/(min·1.73 m2 )was 72.5%,patients with eGFR ranged from 30 to 59 ml/(min·1.73 m2 )was 0.9%. After follow-up for three months,in normal group,the proportion of patients with CKD stage1 was 4.6%,patients with CKD stage 2 was 34.9%,and patients with CKD stage 3 was 0.9%.Multivariate logistic regressionanalysis in normal group showed that female,older age,higher TC,lower LVEF were risk factors for eGFR decline (P <0.05). Conclusion In T2DM patients with normal Scr and Cys-C, 73.4% of them had mild to moderate eGFR decline,and 40.4%entered CKD stage in this study.eGFR should be evaluated especially in T2DM patients with risk factors including female,older age,higher TC and lower LVEF.

Improving the measurement of longitudinal change in renal function: automated detection of changes in laboratory creatinine assay.

INTRODUCTION: Renal function is reported using the estimates of glomerular filtration rate (eGFR). However, eGFR values are recorded without reference to the particular serum creatinine (SCr) assays used to derive them, and newer assays were introduced at different time points across the laboratories in the United Kingdom. These changes may cause systematic bias in eGFR reported in routinely collected data, even though laboratory-reported eGFR values have a correction factor applied. DESIGN: An algorithm to detect changes in SCr that in turn affect eGFR calculation method was developed. It compares the mapping of SCr values on to eGFR values across a time series of paired eGFR and SCr measurements. SETTING: Routinely collected primary care data from 20,000 people with the richest renal function data from the quality improvement in chronic kidney disease trial. RESULTS: The algorithm identified a change in eGFR calculation method in 114 (90%) of the 127 included practices. This change was identified in 4736 (23.7%) patient time series analysed. This change in calibration method was found to cause a significant step change in the reported eGFR values, producing a systematic bias. The eGFR values could not be recalibrated by applying the Modification of Diet in Renal Disease equation to the laboratory reported SCr values. CONCLUSIONS: This algorithm can identify laboratory changes in eGFR calculation methods and changes in SCr assay. Failure to account for these changes may misconstrue renal function changes over time. Researchers using routine eGFR data should account for these effects.