Biochemical Markers Of Kidney Function Research Articles

Selenium prevented renal tissue damage in lipopolysaccharide-treated rats.

Kidney diseases are one of the common diseases, which are one of the main causes of death in society and impose costs on the health system of the society. A growing body of evidence has well documented that inflammatory responses and oxidative damage play a significant role in the progress of various kidney diseases. This study examined whether selenium (Sel) could prevent the detrimental influences of lipopolysaccharide (LPS) in rats. Four groups of Wistar rats were considered: control, LPS (1 mg/kg, i.p.,for 14days), LPS-Sel 1 (0.1 mg/kg, i.p.,for 14days), and LPS-Sel 2 (0.2 mg/kg, i.p.,for 14days). Sel treatment markedly attenuated oxidative stress damage in the kidney tissue in LPS-induced renal toxicity. Generally, the administration of Sel resulted in improved antioxidant indicators such as catalase (CAT) and superoxide dismutase (SOD) activities, or total thiol content, and decreased malondialdehyde (MDA) in the kidney tissue. It also decreased interleukin-6 in kidney homogenates. Furthermore, Se treatment significantly inhibited the elevation of serum biochemical markers of kidney function including serum, BUN, and creatinine. Based on the findings of the current study, it seems that the administration of Sel to LPS-treated rats improves renal function by reducing oxidative damage and inflammation in kidney tissue. However, more research is needed to reveal the accurate mechanisms for the effect of Sel on renal outcomes of LPS in human subjects.

Alterations in Biochemical Markers of Liver and Kidney Function and Oxidative Stress Indices on Sub-acute Exposure of Meloxicam in Albino Rats

Background: The study was performed to study the alterations in biochemical markers of liver and kidney function and oxidative stress indices on sub-acute exposure of meloxicam in albino rats. Methods: The study was performed in three groups of rats, consisting six rats in each group. The rats of group I were served as control. However, rats of group II, III were treated with meloxicam @ 0.2 mg/kg b.wt. meloxicam @ 0.6 mg/kg b.wt. respectively. Result: Meloxicam administration induced oxidative stress in rats as indicated by significant decrease in concentration of catalase, superoxide dismutase and reduced glutathione in blood as compared to control. However, lipid peroxidation was significantly enhanced as indicated by increased level of MDA in blood as compared to control. Meloxicam altered the functions of liver and kidney as indicated by the alteration in the biochemical markers of liver and kidney function. Meloxicam significantly enhanced the concentration of biochemical markers of liver function viz. ALT, AST, GGT, ALP, albumin and bilirubin as compared to control. The concentration of biochemical markers of kidney function viz. BUN and creatinine was significantly enhanced after meloxicam administration as compared to control.

Nephroprotective effect of AT-MSCs against cisplatin-induced EMT is improved by azilsartan via attenuating oxidative stress and TGF-β/Smad signaling

The nephrotoxicity of cisplatin (CIS) is a significant complication that challenges its clinical applicability. The epithelial to mesenchymal transition (EMT) may be included in the pathogenesis of CIS-evoked nephrotoxicity. Therefore, the current study aimed to evaluate, for the first time, the possible protective effect of AZL and/or AT-MSCs against CIS–induced EMT in rats on molecular bases. Fifty-four healthy Wistar male albino rats were used in this study. Different biochemical markers of kidney function as well as oxidative stress parameters were investigated. Additionally, renal histopathological study was performed. The expression of EMT-related proteins and genes was evaluated by western blotting and qRT-PCR. CIS markedly increased SCr, BUN, uric acid and renal MDA levels, with concomitant decrease in serum total protein, renal GSH level and SOD activity. Furthermore, it suppressed the expression of Cdh1 gene, increased the α-SMA, Acta2, Cdh2 and Vim genes expression, down regulated the expression of E-cad protein and up-regulated the α-SMA, TGF-β1, p-Smad2/3 and Snail proteins expression. Kidney tissues showed severe histopathological alterations and extensive collagen accumulation. Conversely, the treatment with either AZL or AT-MSCs significantly attenuated these alterations caused by CIS. Interestingly, the combined therapy of AZL and AT-MSCs has a superior ameliorative effect than AT-MSCs alone. In conclusion, this study, for the first time, revealed that AZL and/ or AT-MSCs successfully ameliorated the CIS-induced EMT via the inhibition of oxidative stress and TGF-β/Smad signaling pathway. Intriguingly, AZL enhanced the effect of AT-MSCs making them promising agents for kidney protection against CIS-induced EMT.

Fetal growth restriction followed by very preterm birth is associated with smaller kidneys but preserved kidney function in adolescence

BackgroundPreterm birth and fetal growth restriction (FGR) are associated with structural and functional kidney changes, increasing long-term risk for chronic kidney disease and hypertension. However, recent studies in preterm children are conflicting, indicating structural changes but normal kidney function. This study therefore assessed kidney structure and function in a cohort of adolescents born very preterm with and without verified FGR.MethodsAdolescents born very preterm with FGR and two groups with appropriate birthweight (AGA) were included; one matched for gestational week at birth and one born at term. Cortical and medullary kidney volumes and T1 and T2* mapping values were assessed by magnetic resonance imaging. Biochemical markers of kidney function and renin–angiotensin–aldosterone system (RAAS) activation were analyzed.ResultsSixty-four adolescents were included (13–16 years; 48% girls). Very preterm birth with FGR showed smaller total (66 vs. 75 ml/m2; p = 0.01) and medullary volume (19 vs. 24 ml/m2; p < 0.0001) compared to term AGA. Corticomedullary volume ratio decreased from preterm FGR (2.4) to preterm AGA (2.2) to term AGA (1.9; p = 0.004). There were no differences in T1 or T2* values (all p ≥ 0.34) or in biochemical markers (all p ≥ 0.12) between groups.ConclusionsFGR with abnormal fetal blood flow followed by very preterm birth is associated with smaller total kidney and medullary kidney volumes, but not with markers of kidney dysfunction or RAAS activation in adolescence. Decreased total kidney and medullary volumes may still precede a long-term decrease in kidney function, and potentially be used as a prognostic marker.Graphical abstractA higher resolution version of the Graphical abstract is available as Supplementary information

Critical Role of Osteopontin in Maintaining Urinary Phosphate Solubility in CKD.

Nephron loss dramatically increases tubular phosphate to concentrations that exceed supersaturation. Osteopontin (OPN) is a matricellular protein that enhances mineral solubility in solution; however, the role of OPN in maintaining urinary phosphate solubility in CKD remains undefined. Here, we examined (1) the expression patterns and timing of kidney/urine OPN changes in CKD mice, (2) if tubular injury is necessary for kidney OPN expression in CKD, (3) how OPN deletion alters kidney mineral deposition in CKD mice, (4) how neutralization of the mineral-binding (ASARM) motif of OPN alters kidney mineral deposition in phosphaturic mice, and (5) the in vitro effect of phosphate-based nanocrystals on tubular epithelial cell OPN expression. Tubular OPN expression was dramatically increased in all studied CKD murine models. Kidney OPN gene expression and urinary OPN/Cr ratios increased before changes in traditional biochemical markers of kidney function. Moreover, a reduction of nephron numbers alone (by unilateral nephrectomy) was sufficient to induce OPN expression in residual nephrons and induction of CKD in OPN-null mice fed excess phosphate resulted in severe nephrocalcinosis. Neutralization of the ASARM motif of OPN in phosphaturic mice resulted in severe nephrocalcinosis that mimicked OPN-null CKD mice. Lastly, in vitro experiments revealed calcium-phosphate nanocrystals to induce OPN expression by tubular epithelial cells directly. Kidney OPN expression increases in early CKD and serves a critical role in maintaining tubular mineral solubility when tubular phosphate concentrations are exceedingly high, as in late-stage CKD. Calcium-phosphate nanocrystals may be a proximal stimulus for tubular OPN production.

Alterations in Biochemical Markers of Kidney Function of Thyroid Disorders at Vidharbha Region, India

Background: The thyroid gland is a major endocrine gland in the body that is located in the front of the neck. Thyroid disorders cause problems on kidney function in a variety of ways. Hyperthyroidism causes an increase in both RBF and GFR. The expression of cardiac beta-adrenergic receptors may be influenced by thyroid hormones. The increased catecholamine sensitivity of beta adrenergic coupled cardiac responses in hyperthyroid patients may be due to the increased number of receptors. ROS may be one of the main causes of kidney failure in thyroid disorders, although this needs to be confirmed in the lab.&#x0D; Aim: The aim of this research was to look at the effects of thyroid disorders on kidney function and oxidative stress markers, as well as the relationship between them.&#x0D; Materials and Methods: After visiting Shalinitai Meghe hospital in Nagpur for a health check-up, a total of 350 people were chosen for the research. This was the place where the five groups were held. Subclinical Hypothyroidism: 70 subjects, Overt Hypothyroidism: 70 subjects, Subclinical Hyperthyroidism: 70 subjects, Overt Hyperthyroidism: 70 subjects. There are 70 patients in each household. Specific biochemical methods were used to quantify biochemical parameters such as T3, T4, TSH, Urea, Creatinine, and Cys C. Assay of Superoxide dismutase by Marklund and Marklund method&#x0D; ResultS: In our work, we discovered a significant positive correlation between serum creatinine and TSH in hypothyroidism and hyperthyroidism, and a significant negative correlation between serum Cystatin C and TSH in hypothyroidism and hyperthyroidism. TSH was linked to oxidative stress markers as well. When the oxidative stress markers MDA and SOD were statistically analysed, they were found to be highly associated with markers of kidney function.&#x0D; Conclusion:When the incidence of chronic kidney disease rises, all instances of hypothyroidism and hyperthyroidism should be regularly tested for worsening kidney functions, and since the study indicates that oxidative stress plays a role in nephropathy, current thyroid disorders treatment methods should include oxidative stress, which will aid clinicians in better managing kidney dysfunction.

Alterations in Biochemical Markers of Liver and Kidney Function and Oxidative Stress Indices on Sub-acute Exposure of Enrofloxacin in Albino Rats

Background: The present study was performed to evaluate Alterations in biochemical markers of liver and kidney function and oxidative stress indices on sub-acute exposure of enrofloxacin in albino rats. Methods: Albino rat weighing 200-300 gm were treated with enrofloxacin orally with the help of gavage needle and devided into three groups each group consist six rats. The rats of group I were served as control. However, rats of group II and III were treated with enrofloxacin @ 5 mg/kg b.wt., enrofloxacin @ 10 mg/kg b.wt. respectively. All the groups received medication orally, once daily for 28 days and blood samples were collected on the 28 day of experiment by the help of capillary tube and processed by laboratory methods. Result: Enrofloxacin altered the functions of liver and kidney as indicated by the alteration in the biochemical markers of liver and kidney function. Enrofloxacin significantly enhanced the concentration of biochemical markers of liver function viz. ALT, AST, GGT, ALP, albumin and bilirubin as compared to control. The concentration of biochemical markers of kidney function viz. BUN and creatinine was significantly enhanced after enrofloxacin administration as compared to control. Enrofloxacin administration induced oxidative stress in rats as indicated by significant decrease in concentration of catalase, superoxide dismutase and reduced glutathione in blood as compared to control. However, lipid peroxidation was significantly enhanced as indicated by increased level of MDA in blood as compared to controlConclusion: Thus, enrofloxacin have ability to altered the biochemical markers of liver and kidney and also have potency to induced oxidative stress in albino rats after the sub-acute exposure for 28 days.

Evaluation of biochemical markers of kidney function in patients with subclinical hypothyroidism in comparison with euthyroid people.

Background:Subclinical hypothyroidism (SCH) as a compensated or preclinical type of primary and overt hypothyroidism (OHT) can affect approximately 4–10% of the general population. Treating SCH can slowdown the progression to OHT, the formation of cardiovascular diseases, neuropsychiatric symptoms, and other miscellaneous problems.Materials and Methods:The present study is a case-control study that was conducted on 239 adults who were referred to 501 Imam Reza Hospital from March 2019 up to September 2019. Of the 239 patients and their families admitted to the hospital, 121 (50.6%) were euthyroid (as control group) and the remaining participants (118, 49.4%) were SCH (as case group). The serum levels of thyroid stimulating hormone (TSH), urea, uric acid, creatinine, T3, and T4 were asked to be determined at a single laboratory. Biochemical markers of kidney function and the level of thyroid hormones were compared between the two groups of euthyroid and SCH.Results:TSH was significantly higher in SCH (7.25 (4.4-18.15)) compared to euthyroid (1.4 (0.2-3.7)) patients (P < 0.001). Among biochemical markers, creatinine (P < 0.001) and uric acid (P = 0.006) had higher serum levels in the case group. There was no remarkable difference in the thyroxine hormone levels and urea between the euthyroid and SCH patients (P > 0.05). Within the SCH group, there was a significant positive correlation between TSH and the level of creatinine (P = 0.001, r = 0.302).Conclusion:Regular monitoring of the major function of the kidneys in patients with hypothyroidism and SCH can help early diagnosis of kidney dysfunction, thus increasing the chance of restoring normal kidney function.

Αlpha-Tocopherol Supplementation Diminishes the Renal Damage Caused by Experimental Diabetes

Background: Previous studies have shown alpha- tocopherol favorable effects on biochemical markers of kidney function and tissue damage in experimental models of diabetes. However, few reports highlight its effect in organ morphology and even less its impact during pregnancy. The main goal of this study was to evaluate the effect of alpha- tocopherol supplementation on the renal tissue morphology of diabetic pregnant rats. Methods: Diabetes was induced in female Wistar rats after intraperitoneal administration of streptozotocin. Healthy rats without any preparation were used as control subjects. Diabetic and control rats were grouped by receiving oral alpha-tocopherol 150 mg/kg/day or the vehicle during pregnancy. Euthanasia was practiced by bleeding under anesthesia at 20 days of gestation. Metabolic markers in plasma were analyzed and the kidney cortex morphology was studied by optical and electron microscopy. Statistic studies were performed using Kruskal Wallis, U Mann-Withney, Dunn and Fisher tests; significant differences were considered with p<0.05. Results: Diabetic rats presented a lower weight gain than the control group, hyperglycemia, hypercholesterolemia and morphological alterations on renal cortex, with increase in glomerular volume and 70% of tubular damage. A lower incidence of kidney lesions was observed in diabetic rats that received alpha- tocopherol, with similar glomerular volumes to the control and improved of tubular cells with only 36% of damage. Conclusions: The administration of alpha- tocopherol to diabetic rats during gestation showed a protective effect on the morphology kidney. This result would be related to the antioxidant action of alpha- tocopherol, but further studies are needed to confirm this.

Renal Effects of Non-Steroidal Anti Inflammatory Drugs in Albino Rats

Aims: Non-steroidal anti-inflammatory drugs (NSAIDs) are cyclooxygenase enzyme inhibitors used widely and frequently as analgesics, antipyretics and anti-inflammatory agents. This study investigated the comparative effects of aspirin (ASA), ibuprofen (IBF) and diclofenac sodium (DCF) on kidney function in albino rats, using biochemical parameters as indices. Study Design: Different groups of animals were to be treated with the test drugs and vehicle. Thereafter, the serum levels of biochemical markers of kidney function obtained in the experimental animals will be compared with those of the control animals. Place and Duration of Study: Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt, Port Harcourt, Nigeria, between June 2012 and November 2012. Methodology: Animals were divided into 7 groups (n=5) and administered daily with ASA (50, 100mg/kg), IBF (20, 40mg/kg), DCF (2, 4mg/kg) and vehicle by oral gavage for 28 days. Blood samples were collected and the serum levels of urea, creatinine, aspartate transaminase (AST) and total protein were measured using standard methods. Results: The results showed that ASA, IBU and DCF caused significant (P &lt; 0.05) and dose-dependent increases in serum levels of urea (39.79, 47.58 and 73.89%, respectively), creatinine (104.29, 128.00 and 133.57%, respectively) and AST (63.74, 24.18 and 32.97%, respectively) without significant (P &gt; 0.05) effect on total protein, compared to the control. Conclusion: The results obtained indicate that long administration of the NSAIDs will cause adverse renal effects in a rank order of DCF &gt; IBU &gt; ASA, which may be partly due to their inhibitory effects on prostaglandins.

Human toxicology of Mercury

This article describes the health effects of the two principal forms of mercury to which humans are exposed, namely mercury vapor and methylmercury compounds. Mercury vapor is the monatomic gas that vaporizes from liquid metallic mercury. It has a long history of human exposure dating back to ancient times. The earliest life forms on this planet may have received substantial exposure and developed defense mechanisms that we inherit to this day. Severe forms of poisoning from inhalation of mercury vapor are now rare. More commonly observed in occupational exposures are subtle neurobehavioral effects and preclinical changes in biochemical markers of kidney function. Methylmercury compounds may also date back to Archean times. The methylation of inorganic mercury by methanogenic bacteria is believed to be a protective mechanism for these cells that appeared early in evolution. Unfortunately, for life forms dependent on a central nervous system, what is protective for simple cells becomes a threat to the more complex life forms. Today, the main source of human exposure is from methylation of inorganic mercury in bodies of fresh and ocean water, the ensuing bioaccumulation in the aquatic food chain, and the consumption of fish or sea mammals by humans. Methylmercury selectively damages the brain. In adult humans, damage is focal, affecting specific cell types in certain anatomical areas such as the visual cortex and the cerebellum. Prenatal exposure disrupts the normal developmental processes of the fetal brain. Indeed, the prenatal period is widely believed to be the most susceptible stage of the life cycle. At present, two large epidemiological studies are underway to determine human health risks from methylmercury in fish. J. Trace Elem. Exp. Med. 11:303–317, 1998. © 1998 Wiley-Liss, Inc.

Human toxicology of Mercury

This article describes the health effects of the two principal forms of mercury to which humans are exposed, namely mercury vapor and methylmercury compounds. Mercury vapor is the monatomic gas that vaporizes from liquid metallic mercury. It has a long history of human exposure dating back to ancient times. The earliest life forms on this planet may have received substantial exposure and developed defense mechanisms that we inherit to this day. Severe forms of poisoning from inhalation of mercury vapor are now rare. More commonly observed in occupational exposures are subtle neurobehavioral effects and preclinical changes in biochemical markers of kidney function. Methylmercury compounds may also date back to Archean times. The methylation of inorganic mercury by methanogenic bacteria is believed to be a protective mechanism for these cells that appeared early in evolution. Unfortunately, for life forms dependent on a central nervous system, what is protective for simple cells becomes a threat to the more complex life forms. Today, the main source of human exposure is from methylation of inorganic mercury in bodies of fresh and ocean water, the ensuing bioaccumulation in the aquatic food chain, and the consumption of fish or sea mammals by humans. Methylmercury selectively damages the brain. In adult humans, damage is focal, affecting specific cell types in certain anatomical areas such as the visual cortex and the cerebellum. Prenatal exposure disrupts the normal developmental processes of the fetal brain. Indeed, the prenatal period is widely believed to be the most susceptible stage of the life cycle. At present, two large epidemiological studies are underway to determine human health risks from methylmercury in fish. J. Trace Elem. Exp. Med. 11:303–317, 1998. © 1998 Wiley-Liss, Inc.

Occupational exposure to lead, kidney function tests, and blood pressure

In the present study we examined sensitive biochemical markers of kidney function and damage in 166 workers exposed to lead and in 60 control workers. The objective was to investigate the chronic renal toxicity of lead and its possible correlation with arterial pressure. Diastolic arterial pressure was higher in the exposed group (p < 0.05), but the two groups did not differ in systolic pressure. Median activity of urinary N-acetyl-beta-D-glucosaminidase was higher in the exposed group (p < 0.001), and correlated with blood lead levels (p < 0.001) and duration of exposure (p < 0.001), but not with arterial pressure. The other indicators studied, gamma-glutamyl-transpeptidase and alanine-aminopeptidase activity, urine albumin, and total urine protein, were not higher than in the control group and were not correlated with blood lead, duration of exposure, or arterial pressure.