METHODS: Study subjects include patients with various levels of renal function recruited from the nephrology clinic and wards of a tertiary hospital. The blood samples collected were analyzed for serum cystatin C and creatinine levels by particle-enhanced turbidimetric immunoassay and kinetic alkaline picrate method, respectively. DNA was extracted using a commercially available kit. -Polymerase chain reaction results were confirmed by direct DNA Sanger sequencing.
RESULTS: The genotype percentage (G/G = 73%, G/A = 24.1%, and A/A = 2.9%) adhere to the Hardy-Weinberg equilibrium. The dominant allele found in our population was CST3 73G allele (85%). The regression lines' slope of serum cystatin C against creatinine and cystatin C-based eGFR against creatinine-based eGFR, between G and A allele groups, showed a statistically significant difference (z-score = 3.457, p < 0.001 and z-score = 2.158, p = 0.015, respectively). Patients with A allele had a lower serum cystatin C level when the values were extrapolated at a fixed serum creatinine value, suggesting the influence of genetic factor.
CONCLUSION: Presence of CST3 gene G73A polymorphism affects serum cystatin C levels.
Methods: We evaluated commonly used surrogate and imputed baseline creatinine values against a "reference" creatinine measured during follow-up in an adult clinical trial cohort. Known AKI incidence (Kidney Disease: Improving Global Outcomes [KDIGO] criteria) was compared with AKI incidence classified by (1) back-calculation using the Modification of Diet in Renal Disease (MDRD) equation with and without a Chinese ethnicity correction coefficient; (2) back-calculation using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation; (3) assigning glomerular filtration rate (GFR) from age and sex-standardized reference tables; and (4) lowest measured creatinine during admission. Back-calculated distributions were performed using GFRs of 75 and 100 ml/min.
Results: All equations using an assumed GFR of 75 ml/min underestimated AKI incidence by more than 50%. Back-calculation with CKD-EPI and GFR of 100 ml/min most accurately predicted AKI but misclassified all AKI stages and had low levels of agreement with true AKI diagnoses. Back-calculation using MDRD and assumed GFR of 100 ml/min, age and sex-reference GFR values adjusted for good health, and lowest creatinine during admission performed similarly, best predicting AKI incidence (area under the receiver operating characteristic curves [AUC ROCs] of 0.85, 0.87, and 0.85, respectively). MDRD back-calculation using a cohort mean GFR showed low total error (22%) and an AUC ROC of 0.85.
Conclusion: Current methods for estimating baseline creatinine are large sources of potential error in acute infection studies. Preferred alternatives include MDRD equation back-calculation with a population mean GFR, age- and sex-specific GFR values corrected for "good health," or lowest measured creatinine. Studies using surrogate baseline creatinine values should report specific methodology.
Results: Prior to total hip arthroplasty, 20% of all patients met the chronic renal dysfunction criterion of glomerular filtration rates <60ml/min/1.73m2 (glomerular filtration rate categories G3a-G5). Incidence rates of acute kidney injury and acute deterioration of kidney function after total hip arthroplasty were 0.49% and 6.9%, respectively. Multivariate regression analysis showed that diabetes mellitus and use of nonsteroidal anti-inflammatory drugs before total hip arthroplasty were significant risk factors for acute deterioration of kidney function. Advanced age, preoperative renal dysfunction, antihypertensive, diuretics, or statin use, operation time, total blood loss, type of anesthetic, and body mass index were not significant risk factors.
Conclusion: Diabetes mellitus and use of nonsteroidal anti-inflammatory drugs were controllable risks, and multidisciplinary approaches are a reasonable means of minimising peri-operative acute kidney injury or acute deterioration of kidney function.
MATERIALS AND METHODS: An e-mail invitation to participate in an online survey was sent to hospital laboratories in Malaysia (n=140). Questions regarding methods for measuring creatinine, equations for calculating eGFR, eGFR reporting, the terminology used in reporting urine albumin, types of samples and the cut-off values used for normal albuminuria.
RESULTS: A total of 42/140 (30%) laboratories answered the questionnaire. The prevalent method used for serum creatinine measurement was the Jaffé method (88.1%) traceable to isotope-dilution mass spectrometry. eGFR was reported along with serum creatinine by 61.9% of laboratories while 33.3% of laboratories report eGFR on request. The formula used for eGFR reporting was mainly MDRD (64.3%) and results were reported as exact numbers even when the eGFR was <60 ml/min/1.73m2. The term microalbumin is still used by 83.3% of laboratories. There is a large heterogeneity among the labs regarding the type of sample recommended for measuring urine albumin, reference interval and reporting units.
CONCLUSION: It is evident that the laboratory assessment of chronic kidney disease in Malaysia is not standardised. It is essential to provide a national framework for standardised reporting of eGFR and urine albumin. Recommendations developed by the MACB CKD Task Force, if adopted by all laboratories, will lead to a reduction in this variability.
METHODS: A population-based study was conducted on a total of 890 respondents who were representative of the adult population in Malaysia, i.e., aged ≥18 years old. Respondents were randomly selected using a stratified cluster method. The estimated glomerular filtration rate (eGFR) was estimated from calibrated serum creatinine using the CKD-EPI equation. CKD was defined as eGFR
SETTINGS: A validation study among people living with HIV(PLHIV) aged ≥18 years among the cohorts in the Asia-Pacific region.
METHODS: PLHIV with baseline eGFR>60 mL/min/1.73m were included for validation of the D:A:D CKD full version and the short version without cardiovascular risk factors. Those with <3 eGFR measurements from baseline or previous exposure to potentially nephrotoxic antiretrovirals were excluded. Kaplan-Meier methods were used to estimate the probability of CKD development. Area Under the Receiver Operating Characteristics (AUROC) was also used to validate the risk score.
RESULTS: We included 5,701 participants in full model(median 8.1 [IQR 4.8-10.9] years follow-up) and 9,791 in short model validation(median 4.9 [IQR 2.5-7.3] years follow-up). The crude incidence rate of CKD was 8.1 (95%CI 7.3-8.9) per 1,000 person-years(PYS) in the full model cohort and 10.5 (95%CI 9.6-11.4) per 1,000 PYS in the short model cohort. The progression rates for CKD at 10 years in the full model cohort were 2.7%, 8.9% and 26.1% for low-, medium- and high-risk groups, and 3.5%, 11.7% and 32.4% in the short model cohort. The AUROC for the full and short risk score was 0.81 (95%CI 0.79-0.83) and 0.83 (95%CI 0.81-0.85), respectively.
CONCLUSION: The D:A:D CKD full- and short-risk score performed well in predicting CKD events among Asian PLHIV. These risk prediction models may be useful to assist clinicians in identifying individuals at high risk of developing CKD.
METHOD: The meta-analysis included all studies that examined the effect of prebiotic, probiotic, and synbiotic supplements on one or more renal function parameters and had a control group. We searched July 1967 through to March 2016 MEDLINE, Scopus, and Google Scholar databases.
RESULTS: Of 437 studies, 13 were eligible for inclusion in the meta-analysis. GFR levels tended to be reduced; whereas creatinine levels increased in the intervention group compared with the placebo group, both in a non-significant manner. The pooled effect on BUN demonstrated a significant decline compared with the placebo group (MD, -1.72 mmol/L; 95% confidence interval [CI], -2.93 to -0.51; P = 0.005). Urea significantly decreased after intervention (-0.46 mmol/L; 95% CI, -0.60 to -0.32; P <0.0001). The UA levels significantly increased in the intervention group compared with the placebo group (12.28 µmol/L; 95% CI, 0.85-23.71; P = 0.035).
CONCLUSION: This study showed a significant increase in UA and a decrease in urea and BUN. The use of prebiotic, probiotic, and synbiotic supplements among those with compromised renal function or those at risk for renal failure should be limited until large-scale, well-designed randomized controlled trials prove the safety and efficacy of these supplements in improving renal function.
METHODS: The study comprised 106 chronic kidney disease (CKD) patients and 203 control subjects. Conventional ultrasound was performed to measure the kidney length and cortical thickness. SWE imaging was performed to measure renal parenchymal stiffness. Diagnostic performance of SWE and conventional ultrasound were correlated with serum creatinine, urea levels and eGFR.
RESULTS: Pearson's correlation coefficient revealed a negative correlation between YM measurements and eGFR (r = -0.576, p < 0.0001). Positive correlations between YM measurements and age (r = 0.321, p < 0.05), serum creatinine (r = 0.375, p < 0.0001) and urea (r = 0.287, p < 0.0001) were also observed. The area under the receiver operating characteristic curve for SWE (0.87) was superior to conventional ultrasound alone (0.35-0.37). The cut-off value of less or equal to 4.31 kPa suggested a non-diseased kidney (80.3% sensitivity, 79.5% specificity).
CONCLUSION: SWE was superior to renal length and cortical thickness in detecting CKD. A value of 4.31 kPa or less showed good accuracy in determining whether a kidney was diseased or not. Advances in knowledge: On SWE, CKD patients show greater renal parenchymal stiffness than non-CKD patients. Determining a cut-off value between normal and diseased renal parenchyma may help in early non-invasive detection and management of CKD.
METHODS: This cross-sectional study was performed at Hue Central Hospital from 2012-2016 on 176 CKD and 64 control subjects. ADMA levels were measured by using the enzyme linked immunosorbent assay (ELISA) method.
RESULTS: Mean ADMA level was markedly higher (p<0.001) in all patients combined (0.73±0.24μmol/L) than in control subjects (0.47±0.13μmol/L). Mean ADMA levels in advanced kidney disease were higher than control subjects. ADMA levels correlated inversely and relatively strictly to estimated glomerular filtration rate (eGFR) (r = -0.689; p<0.001), haemoglobin (r = -0.525; p<0.001) and haematocrit (r = - 0.491; p<0.001); correlated favourably and relatively strictly to serum creatinine (r = 0.569; p<0.001) and serum urea (r = 0.642; p<0.001). ADMA elevation was predicted simultaneously by eGFR<60 mL/min/1.73m2 (p<0.001), anaemia (p=0.002), body mass index (BMI) (p=0.011) and high sensitivity C-reactive protein (hs-CRP) (p=0.041). Cutoff of ≥0.68μmol/L, ADMA levels predict reduction of eGFR<60 mL/min/1.73m2, sensitivity of 86.9 %, specificity of 82.6%, area under ROC 92.4% (95%CI: 88.6-96.1%).
METHODS: In this 24-month, open-label study, de novo kidney transplant recipients (KTxRs) were randomized (1:1) to receive EVR+rCNI or MPA+sCNI, along with induction therapy and corticosteroids.
RESULTS: Of the 2037 patients randomized in the TRANSFORM study, 293 were Asian (EVR+rCNI, N = 136; MPA+sCNI, N = 157). At month 24, EVR+rCNI was noninferior to MPA+sCNI for the binary endpoint of estimated glomerular filtration rate (eGFR)