Biochemical predictors of chronic kidney disease in children recovering from acute kidney injury

The pressing question today is to find early informative markers for kidney interstitial injury in reconvalescents of acute kidney injury (AKI). The aim of the study was to determine the informativeness of transferrin (TF), ceruloplasmin (CP) presence and activity level of lysosomal enzymes in urine as predictors of chronic kidney disease. Materials and methods. The contents of TF, CP and N-acetyl-β-Dgluosaminindase (NAG) and β-galactosidase (ß-GAL) in the urine of 41 children after AKI were determined. All patients were divided into 2 groups depending on the disease duration – group 1 included 22 patients with 12 months’ duration, group 2 – 19 children with the disease duration of 2 years and more. The control group consisted of 28 conditionally healthy children. Results. The levels of NAG and ß-GAL were 8 and 3 times increased, respectively, in the patients from group 1 in comparison with the control group (P < 0.001). In the group 2 children, the enzyme levels were 4 times higher than the control, and albuminuria was observed at normal GFR (P < 0.001). An inverse correlation was established between GFR indices and activity levels of NAG (r = -0.473) and ß-GAL (r = -0.333), and a direct correlation between activity indices of GAG and ß-GAL (r = 0.845). The presence and high levels of TF in 18.8 % of children in group 1 and in 21.0 % in group 2, as well as urine CP in 72.7 % of patients in group 1 and in 78.9 % in group 2, is indicative of a progressive damage to the kidney glomerular apparatus. Conclusions. The presence and increased quantitative parameters of TF and CP in the urine of children after AKI are early signs of damage to the kidney glomerular apparatus. Four times increased levels of the enzyme activity and albuminuria at unchanged GFR indicate an interstitial kidney injury (P < 0.001). The examinations conducted are non-invasive, relatively low cost and easy to use for children of all ages.

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Urinary N-Acetyl-Beta-D-Glucosaminidase Activity in Rat Experimental Ischemic and Toxic Models of Acute Kidney Injury

Bulletin of University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca Veterinary Medicine ◽

10.15835/buasvmcn-vm:12618 ◽

2017 ◽

Vol 74 (1) ◽

pp. 105

Author(s):

Razvan Andrei CODEA ◽

Mircea MIRCEAN ◽

Sidonia Alina BOGDAN ◽

Andras Laszlo NAGY ◽

Alexandra BIRIS ◽

...

Keyword(s):

Acute Kidney Injury ◽

Experimental Model ◽

Wistar Rats ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Control Group ◽

Tubular Injury ◽

Group 2 ◽

Group 1

The identification of a suitable prevention method which facilitates limiting the deleterious effects of acute kidney injuries is highly required. In order to identify a proper treatment for acute kidney injuries, a suitable experimental model that replicates the structural, metabolic and inflammatory lesions that occur in the natural acute injured kidney is highly necessary. Intense urinary NAG activity can be found in a variety of renal disease such as toxic nephropathies, ischemic renal injury following cardiac surgery or renal transplantation but also in glomerular disease especially in diabetic nephropathy. Rises in urinary NAG enzyme activity strongly suggests tubular cell damage and support NAG enzyme as a biomarker of renal tubular injury. The aim of this paper is to obtain a stable in vivo acute kidney injury experimental model, in Wistar, rats and to evaluate the urinary activity of N-acetyl-Î²-D-glucosaminidase (NAG) enzyme, blood levels of urea and creatinine and microstructural renal alterations induced by ischemia/reperfusion injury respectively gentamicin nephrotoxicity. For this purpose we have used a rat experimental model. Adult male Wistar rats weighing 250-300 g were randomly divided into 3 groups with 8 rats in each group. Group 1 served as a model for the renal ischemia/reperfusion injury experiment, group 2 served for toxic kidney injury experimental model and group 3 served as control group. All individuals in both groups 1 and 2 presented marked elevations in blood urea and creatinine at the moment of euthanasia (day 3 for group 1 and day 9 for group 2) compared to the control group where biochemical values remained within normal limits. Urine analysis of both group 1 and 2 showed marked urinary NAG index activity which suggests acute tubular injury, suggestion confirmed by histological evaluation of the renal parenchyma sampled from this subjects

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Metabolomic and biochemical characterization of a new model of the transition of acute kidney injury to chronic kidney disease induced by folic acid

PeerJ ◽

10.7717/peerj.7113 ◽

2019 ◽

Vol 7 ◽

pp. e7113

Author(s):

Marlene Marisol Perales-Quintana ◽

Alma L. Saucedo ◽

Juan Ricardo Lucio-Gutiérrez ◽

Noemí Waksman ◽

Gabriela Alarcon-Galvan ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Acute Kidney Injury ◽

Folic Acid ◽

Kidney Disease ◽

Biochemical Parameters ◽

Kidney Injury ◽

Renal Diseases ◽

Control Group ◽

Organic Osmolytes ◽

Histological Classification

Background Renal diseases represent a major public health problem. The demonstration that maladaptive repair of acute kidney injury (AKI) can lead to the development of chronic kidney disease (CKD) and end-stage renal disease has generated interest in studying the pathophysiological pathways involved. Animal models of AKI–CKD transition represent important tools to study this pathology. We hypothesized that the administration of multiple doses of folic acid (FA) would lead to a progressive loss of renal function that could be characterized through biochemical parameters, histological classification and nuclear magnetic resonance (NMR) profiling. Methods Wistar rats were divided into groups: the control group received a daily intraperitoneal (I.P.) injection of double-distilled water, the experimental group received a daily I.P. injection of FA (250 mg kg body weight−1). Disease was classified according to blood urea nitrogen level: mild (40–80 mg dL−1), moderate (100–200 mg dL−1) and severe (>200 mg dL−1). We analyzed through biochemical parameters, histological classification and NMR profiling. Results Biochemical markers, pro-inflammatory cytokines and kidney injury biomarkers differed significantly (P < 0.05) between control and experimental groups. Histology revealed that as damage progressed, the degree of tubular injury increased, and the inflammatory infiltrate was more evident. NMR metabolomics and chemometrics revealed differences in urinary metabolites associated with CKD progression. The main physiological pathways affected were those involved in energy production and amino-acid metabolism, together with organic osmolytes. These data suggest that multiple administrations of FA induce a reproducible model of the induction of CKD. This model could help to evaluate new strategies for nephroprotection that could be applied in the clinic.

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Changes in Glomerular Filtration Rate and Its Relation to Serum Calcium Level in Advanced Stages of Chronic Kidney Disease

Journal of National Institute of Neurosciences Bangladesh ◽

10.3329/jninb.v1i1.22942 ◽

2015 ◽

Vol 1 (1) ◽

pp. 15-17

Author(s):

Gobinda Chandra Saha ◽

M Akhtaruzzaman ◽

Ekramul Mustafa ◽

Asif Mahmud ◽

Sunil Kumar Sikder

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Serum Creatinine ◽

Serum Calcium ◽

Control Group ◽

Control Serum ◽

Advanced Stages ◽

Group 3 ◽

Group 2 ◽

Group 1

Background: The progression of CKD occurs in five different stages in which there are gradual changes of GFR, serum creatinine and serum calcium.Objective: The study was undertaken to determine GFR in advanced stages of CKD and its relation with s. creatinine and s. calcium and also to find out the correlation between s. creatinine and s. calcium.Methodology: This study was carried out in the departments of Physiology and Nephrology, Rajshahi Medical College. All the advanced stage chronic kidney disease patients were taken as comparison. Apparently healthy persons were taken as control. Serum Creatinine was measured by alkaline picrate method; estimation of GFR was done by using Cockcroft- Gault formula and serum calcium was performed by analyzer.Result: In this study a total number of 120 subjects were included, out of which 30 were healthy control and 90 were diagnosed cases of advanced stages of CKD. Among the patients, 55 (61.12%) were male and 35 (38.88%) were female. Mean age (±SD) of the patients were 45 ± 11.16 (Range 20-65 years). While comparing between groups of CKD patients, it was found that s. creatinine of control group was significantly lower than that of group 1. Again s. creatinine of Group 1 was significantly lower than that of group 2 and similarly, s. creatinine of group 2 was significantly lower than that of group 3. On the other hand, s. calcium of control group was significantly higher than group 1, likewise s. calcium of group 1 was significantly higher than that of group 2 and s. calcium of group 2 was significantly higher than that of group 3.Conclusion: From this study the inference could be drawn that serum calcium had a positive correlation with GFR and a negative correlation with s. creatinine.J. Natl Inst. Neurosci Bangladesh 2015;1(1):15-17

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Inhibition of PTEN Activity Aggravates Post Renal Fibrosis in Mice with Ischemia Reperfusion-Induced Acute Kidney Injury

Cellular Physiology and Biochemistry ◽

10.1159/000484070 ◽

2017 ◽

Vol 43 (5) ◽

pp. 1841-1854 ◽

Cited By ~ 14

Author(s):

Jun Zhou ◽

Jiying Zhong ◽

Sen Lin ◽

Zhenxing Huang ◽

Hongtao Chen ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Acute Kidney Injury ◽

Kidney Disease ◽

Renal Fibrosis ◽

Smooth Muscle Actin ◽

Ischemia Reperfusion ◽

Specific Inhibitor ◽

Kidney Injury ◽

Control Group ◽

Kidney Fibrosis

Background: Renal fibrosis is a common pathophysiological feature of chronic kidney disease. Acute kidney injury (AKI) is defined as an independent causal factor of chronic kidney disease, with a pathological representation of post renal fibrosis. However, the etiopathogenesis underlying post renal fibrosis induced by AKI is not completely understood. Methods: BALB/c mice were treated with bpv or vehicle controls and were, respectively, the ischemia reperfusion (IR) model group and control group. All of the animals had blood taken from the orbital venous plexus at 24 hours after IR. Six mice in each group were randomly chosen and euthanized 7 days after IR treatment, and the remaining six mice in each group were euthanized 14 days after IR treatment. We examined the effect on post kidney fibrosis of inhibiting PTEN activity in mice in an IR induced AKI experimental model. Results: Compared with vehicle mice, bpv-(PTEN specific inhibitor) treated mice accumulated more bone marrow-derived fibroblasts and myofibroblasts in the kidneys. Inhibition of PTEN activity increased the expression of α-smooth muscle actin and extracellular matrix proteins and post kidney fibrosis. Furthermore, inhibition of PTEN activity resulted in more inflammatory cytokines in the kidneys of mice subjected to IR-induced renal fibrosis. Moreover, inhibition of PTEN activity up-regulated PI3K protein expression and Akt phosphorylation. Conclusions: Our study demonstrated that PTEN played an important role in post renal fibrosis in mice with ischemia reperfusion-induced AKI. These results indicated that the PTEN/PI3K/Akt signaling pathway may serve as a novel therapeutic target for AKI-induced chronic kidney disease.

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Mild Stage 1 post-operative acute kidney injury: association with chronic kidney disease and long-term survival

Clinical Kidney Journal ◽

10.1093/ckj/sfz197 ◽

2020 ◽

Author(s):

Thorir Einarsson Long ◽

Dadi Helgason ◽

Solveig Helgadottir ◽

Gisli Heimir Sigurdsson ◽

Runolfur Palsson ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Acute Kidney Injury ◽

Kidney Disease ◽

Kidney Injury ◽

Control Group ◽

Term Survival ◽

Absolute Increase ◽

Long Term Survival ◽

Stage 1

Abstract Background Mild cases of acute kidney injury (AKI) are identified by a small rise in serum creatinine (SCr) according to the KDIGO AKI definition. The aim of this study was to examine the long-term outcomes of individuals with mild AKI. Methods This was a retrospective cohort study of all adult patients who underwent abdominal, cardiothoracic, vascular or orthopaedic surgery at Landspitali–The National University Hospital of Iceland in 1998–2015. Incident chronic kidney disease (CKD), progression of pre-existing CKD and long-term survival were compared between patients with mild Stage 1 AKI (defined as a rise in SCr of ≥26.5 μmol/L within 48 h post-operatively without reaching 1.5× baseline SCr within 7 days), and a propensity score-matched control group without AKI stratified by the presence of CKD. Results Pre- and post-operative SCr values were available for 47 333 (42%) surgeries. Of those, 1161 (2.4%) had mild Stage 1 AKI and 2355 (5%) more severe forms of AKI. Mild Stage 1 AKI was associated with both incident CKD and progression of pre-existing CKD (P < 0.001). After exclusion of post-operative deaths within 30 days, mild Stage 1 AKI was not associated with worse 1-year survival in patients with preserved kidney function (94% versus 94%, P = 0.660), and same was true for patients with pre-operative CKD (83% versus 82%, P = 0.870) compared with their matched individuals. Conclusions Mild Stage 1 AKI is associated with development and progression of CKD, but not with inferior 1-year survival. These findings support the inclusion of a small absolute increase in SCr in the definition of AKI.

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Effect of ADMA levels on severity of erectile dysfunction in chronic kidney disease and other risk factors

Canadian Urological Association Journal ◽

10.5489/cuaj.3170 ◽

2016 ◽

Vol 10 (1-2) ◽

pp. 41 ◽

Cited By ~ 2

Author(s):

Kaan Gökçen ◽

Hakan Kılıçarslan ◽

Burhan Coşkun ◽

Alparslan Ersoy ◽

Onur Kaygısız ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Erectile Dysfunction ◽

Kidney Disease ◽

Erectile Function ◽

Serum Prolactin ◽

Control Group ◽

Total Testosterone ◽

Group 2 ◽

And Control ◽

Group 1

Introduction: Hormonal, neurogenic, vasculogenic, and psychogenic impairments, as well as endothelial dysfunction may play a role in erectile dysfunction (ED) in patients with chronic kidney disease (CKD). Asymmetrical dimethylarginine (ADMA) is an inhibitor of nitric oxide, which is the key element of ED. ADMA levels are increased in CKD. We aimed to evaluate the effect of serum ADMA, prolactin, testosterone, and hemoglobin levels on erectile function of patients with CKD and control subjects.Methods: A total of 42 men with CKD and 25 age-matched controls were enrolled. The patients with CKD were categorized into group 1 and group 2 based on whether they had ED according to their response to International Index of Erectile Function questionnaire (IIEF-EFD). Group 3 was a control group. Serum ADMA, total testosterone prolactin, and hemoglobin levels of the patients were evaluated.Results: Serum ADMA, testosterone, and hemoglobin levels were similar between group 1 and 2, serum prolactin level was significantly high in group 1 than in group 2 or 3 (control group). There was no correlation between ADMA levels and IIEF-EFD scores of patients with CKD.Conclusions: The results of this study suggest serum ADMA level is not related with ED in patients with CKD. Also, low testosterone and hemoglobin levels were not significant factors. High levels of serum prolactin are related with ED in patients with CKD.

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