Trivalent Chromium Based Conversion Coating Contains Zinc/Zn(OH)2 on Iron Substrates for the Detection of Uric Acid in Biological Samples and Control of Dyeing

This study evaluated the microalbumin, cystatin C, creatinine and uric acid levels in HIV patients in Nnamdi Azikiwe University Teaching Hospital, Nnewi (NAUTH). A total of one hundred (100) male and female HIV positive and control participants who were aged between 18 and 60 years attending the voluntary counseling and testing unit (VCT) and antiretroviral therapy unit (ART) of NAUTH were randomly recruited for the study and grouped thus: Group A (HIV positive symptomatic participants on long term ART (HPSPLTART) (n= 25); Group B (HIV positive symptomatic participants on short term ART (HPSPSTART) (n= 25); Group C: Asymptomatic HIV positive participants NOT on ART (AHPPNART) (n=25) and Group D: control (n=25).6mls of blood sample and 10mls of freshly voided urine samples were collected from each of the participants for the evaluation of biochemical parameters using standard laboratory methods. Results showed significantly higher BMI and SBP in HPSPSTART than in control (p=0.04; 0.02). SBP was significantly higher in HPSPLTART than in AHPPNART and Control (p=0.00). DBP was significantly higher in HPSPLTART than in HPSPSTART and control respectively (p=0.00). There were significantly higher plasma creatinine and Cys-C levels in both male HIV positives and male HIV positive participants on ART than in both females respectively (p0.00; 0.02). Also, BMI, creatinine, uric acid and Cystatin C levels were significantly higher in male HIV negative participants than in female HIV negative participants (p=0.00; 0.04; 0.02; 0.01). This study has revealed greater risk for renal disease among the HIV participants studied.

Download Full-text

TO STUDY THE CORRELATION OF URINARY URIC ACID AND CREATININE RATIO IN BIRTH ASPHYXIA

10.36106/ijsr/0127075 ◽

2021 ◽

pp. 53-54

Author(s):

B Revanth Reddy ◽

Gauri Chauhan ◽

Anand Kumar Bhardwaj ◽

Sasanka Chakrabarti

Keyword(s):

Uric Acid ◽

Apgar Score ◽

Perinatal Asphyxia ◽

Birth Asphyxia ◽

Control Group ◽

P Value ◽

Creatinine Ratio ◽

Spot Urine ◽

Spot Urine Sample ◽

And Control

Introduction: Perinatal asphyxia is one of the leading causes of perinatal morbidity and mortality. Feasible and early biochemical markers to diagnose and predict the neurologic outcome is a great need of time as APGAR score alone is inuenced by various factors. The present study was performed to determine the urinary uric acid to creatinine ratio in perinatal asphyxia and its correlation with APGAR score and compare urinary uric acid to creatinine ratio with Sarnat and Sarnat staging. Materials and Methods: This study was carried out on 100 term neonates with an equal number of cases and control 50 each, control group being the neonates with Apgar score ≥ 7 at 1 minute of life and cases being the neonates who suffered from perinatal asphyxia with Apgar < 7 at 1 minute of life. The spot urine sample was collected within 24 hours of birth and their uric acid and creatinine levels were measured and the ratio calculated. Asphyxiated neonates were classied according to Sarnat and Sarnat staging. We Compare UA/Cr ratio with Apgar score and HIE staging using Sarnat and Sarnat staging.Results: On comparison of UUA/Cr among cases and controls we found that ratio was signicantly higher in asphyxiated neonates as compared to non asphyxiate neonates. (Control vs. Cases Group: 2.4 ± 1 vs. 3.6 ± 1.5; p –value < 0.0001). On comparison of UUA/Cr among cases with Sarnat and Sarnat staging of HIE, there is a signicant difference observed in mean UA/Cr ratio across Sarnat and Sarnat staging of HIE (F – Value = 68.760; p – value = 0.0001). Conclusion: Urinary uric acid and creatinine ratio can be used as markers for perinatal asphyxia for screening in centers where other markers for assessing perinatal asphyxia are not available. Urinary uric acid and creatinine ratio is a non-invasive, cheap and easily available marker for assessing the severity perinatal asphyxia.

Download Full-text

Comparative Study of Level of Serum Uric Acid in Type 2 Diabetes Mellitus Associated with Hypertension

Anwer Khan Modern Medical College Journal ◽

10.3329/akmmcj.v9i2.39202 ◽

2018 ◽

Vol 9 (2) ◽

pp. 96-101

Author(s):

Roksana Yeasmin ◽

MA Muttalib ◽

Nazneen Sultana ◽

Md Jamil Hasan Karami ◽

Ayatunnessa ◽

...

Keyword(s):

Diabetes Mellitus ◽

Blood Pressure ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Uric Acid ◽

Serum Uric Acid ◽

Exercise Time ◽

The Mean ◽

And Control

Background: The role of uric acid in the progression of prediabetes to diabetes has been known. Serum uric acid has been shown to beassociated with cardiovascular disease, hypertension, and chronic kidney disease. However, conflicting data exist asregards the serum uric acid (UA) levels in type 2 diabetes mellitus, which are associated with risk factors andcomplications.Material & Methods: The present study was designed to look for any association of serum uric acid with hypertension in type 2diabetes mellitus, taking into consideration the relevant clinical, biochemical and the anthropometric data. 110 patientswith type 2 male diabetes mellitus as case and 100 healthy malecontrols were included in this study.Results: This study shows that there were significant differences in mean of age, duration of DM, exercise time, waist hip ratio, systolic blood pressure and diastolic blood pressure within case and control but no significant differences of mean BMI was found between and control. The mean age, duration of DM, exercise time, waist hip ratio, systolic blood pressure and diastolic blood pressure and BMI were (51.83±9.911 years, 6.87±5.54 years, 1.94±.831 hours, .92±.03, 140±6.75 mm of Hg,90±2.41 mm of Hg and 25.43±3.19 Kg/m2 respectively), where as in controls these were (44.81±9.66 yrs, 00 years, 1.12±.327 hours, .91±.03, 130±1.28 mm of Hg, 80±6.18 mm of Hg and 24.96±3.02 Kg/m2 respectively). This table also shows that significant differences in mean of FBS, ABF, HbA1C and S. Uric acid between case and control, but there was no significant differences of mean TG, Cholesterol, HDL and LDL. The mean of FBS, ABF, HbA1C and S. Uric acid among the cases were (8.19±2.48 mmol/L, 11.29±3.47 mmol/L, 7.96±6.04 mg%, 189.72±111.36 mg/dl, 179±43 mg/dl, 38.38±13.77 mg/dl, 102.10±35.79 mg/dl and 8.39±2.61 mg/dl respectively, on the other hand among the control these were 5.91±1.13 mmol/L, 9.19±1.95 mmol/L, 5.93±1.01 mg%, 200±104.49 mg/dl, 183±42.25 mg/dl, 38.14±5.52 mg/dl, 110±33.23 mg/dl and 5.14±.84 mg/dl respectively.Anwer Khan Modern Medical College Journal Vol. 9, No. 2: Jul 2018, P 96-101

Download Full-text

P0690CORRELATIONS BETWEEN OPG/RANKL/RANK AXIS, VITAMIN D STATUS, PTH AND VASCULAR CALCIFICATION IN AN ADENINE-INDUCED MODEL OF CHRONIC KIDNEY DISEASE

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0690 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Beata Sieklucka ◽

Tomasz Domaniewski ◽

Marta Zieminska ◽

Malgorzata Galazyn-Sidorczuk ◽

Anna Pawlak ◽

...

Keyword(s):

Gene Expression ◽

Chronic Kidney Disease ◽

Uric Acid ◽

Kidney Disease ◽

Vascular Calcification ◽

Control Group ◽

Urea Nitrogen ◽

And Control ◽

Rank Gene

Abstract Background and Aims Chronic kidney disease (CKD) is a major public health problem worldwide and refers to a wide range of disorders in bone and mineral metabolism, abnormalities of biochemical parameters and pathological calcification of the blood vessels. Vascular calcification (VC) is a common complication in CKD patients, contributes to cardiovascular disease (CVD), and associates with increased mortality and morbidity. The precise mechanism of VC in CKD is not yet fully understood. Recently discovered molecules such as osteoprotegerin (OPG), its ligand receptor activator of nuclear factor NF-κB ligand (RANKL) and RANK are not only well-known to play a crucial role in bone homeostasis, but they has also been implicated in the process of development of vascular complications However the exact role of OPG/RANKL/RANK axis in the process of VC has not been yet fully assessed. Thus, the aim of this work is to evaluate the role of OPG/RANKL/RANK axis in the process of calcification in CKD. Method Seventy two male Wistar rats weighing 260-290 g (8-weeks old) were initially divided into 6 groups containing 12 animals in each group. Rats were divided into six groups: control rats (K4, K6, K8) and CKD rats (B4, B6, B8). Control group rats received standard diet, whereas CKD rats were fed a low adenine – diet containing 0.3 % adenine, 1.0 % Ca, 1.2 % Pi through 4 (K4, B4), 6 (K6, B6) and 8 (K8, B8) weeks. Subsequently, CKD and control rats were sacrificed at weeks 4 (n=24), 6 (n=24) and 8 (n=24). One day before being killed, the rats were placed in metabolic cages for 24-hour urine collection. Thereafter, the rats were anesthetized and samples of blood, as well as aortas were collected. Next, the OPG, RANKL, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxy vitamin D3 1,25(OH)2D3 concentrations were determined using appropriate ELISA kits. Then the sRANKL/OPG ratio was calculated. The OPG, RANK and RANKL gene expression was assessed using real-time PCR (RT-PCR). The VC was quantified by measurement of the arterial calcium (Ca) and phosphate (Pi) content using flame atomic absorption. Serum levels of urea nitrogen, creatinine, uric acid, Ca, Pi and urinary levels of creatinine, Ca and Pi were measured. Results There was a progressive increase in serum urea nitrogen, creatinine, uric acid and PTH of CKD rats in comparison to control values. We also observed significantly decreased levels of 25(OH)D, 1,25(OH)2D and serum Ca. Total Ca content in the aorta was significantly increased in CKD rats in comparison with control group, whereas total Pi content in the aorta was significantly increased only in B8 group in comparison to appropriate controls. There were no differences in serum OPG and sRANKL levels between CKD and control rats. In contrast, we observed decreased OPG, RANKL and RANK gene expression in a B4 group in comparison to appropriate controls, whereas in a B6 group we noticed increased OPG, RANKL and decreased RANK gene expression. B8 group revealed increased RANKL and RANK gene expression, but there were no differences in OPG gene expression between CKD rats and control group. Furthermore, we observed positive correlations between serum sRANKL and OPG and RANK gene expression. Ca and P content in the aorta inversely corelated with RANKL gene expression, whereas positively with OPG gene expression. Serum 25(OH)D concentrations correlated inversely with Ca in aorta. PTH was positively correlated with serum RANKL and OPG and gene expression these cytokines. Conclusion Our results suggest that OPG/RANK/RANKL axis may be involved in the process of vascular calcification in chronic kidney disease. However, its role and evaluation of precise mechanism in this field requires further evaluation.

Download Full-text

Trivalent chromium conversion coating formation on aluminium

Surface and Coatings Technology ◽

10.1016/j.surfcoat.2015.09.024 ◽

2015 ◽

Vol 280 ◽

pp. 317-329 ◽

Cited By ~ 67

Author(s):

J.-T. Qi ◽

T. Hashimoto ◽

J.R. Walton ◽

X. Zhou ◽

P. Skeldon ◽

...

Keyword(s):

Trivalent Chromium ◽

Conversion Coating ◽

Coating Formation

Download Full-text

Renal excretion of allantoin in rats: a micropuncture and clearance study

AJP Renal Physiology ◽

10.1152/ajprenal.1977.233.5.f373 ◽

1977 ◽

Vol 233 (5) ◽

pp. F373-F381 ◽

Cited By ~ 4

Author(s):

J. P. Briggs ◽

M. F. Levitt ◽

R. G. Abramson

Keyword(s):

Uric Acid ◽

Renal Excretion ◽

Rat Kidney ◽

Chromatographic Technique ◽

Experimental Conditions ◽

Clearance Studies ◽

Fluid Collections ◽

And Control ◽

Clearance Study ◽

Column Chromatographic

Free-flow micropuncture and clearance studies were performed to evaluate the transport of allantoin inthe rat kidney. Inn all studies [2-14C]uric acid and [methoxy-3H]inulin were administered. With a two-step column chromatographic technique, radiolabeled uric acid and allantoin were separated in plasma, urine, and tubular fluid, and the [2-14C]allantoin concentration was determined. Tubular fluid collections were obtained under hydropenic and control coneated animals in the control and volume-expanded states. Clearance data were obtained in oxonic acid-treated animals under the same experimental conditions. These studies indicate that allantoin is not bound to plasma protein and is, therefore, freely filterable. Neither net reabsorption nor net secretion of allantoin was evident along the length of the nephron. The bubular handling of allantoin was demonstrated to be dissociated from that of uric acid in all experimental states. No significant intrarenal production of allantoin from uric acid was observed.

Download Full-text