Elevated Urea Levels Research Articles

Anti-Nephrotoxic effect of green synthesized Actiniopteris radiata silver nanoparticles (AR-AgNPs) against gentamicin induced nephrotoxicity

A study on green synthesized silver nanoparticles (AgNPs) using aqueous extract of Actiniopteris radiata and investigated the effect of A. radiata biosynthesized silver nanoparticles (AR-AgNPs) against gentamicin induced nephrotoxicity. The surface plasmon resonance (SPR) peak at 440 nm in UV–visible absorbance spectrum reveals the presence of AgNPs. DLS analysis shows that the distribution of size is normal and the average size of AgNPs converges about 100 nm. SEM revealed the consistent shape, uniform distribution, and closely packed characteristics of NPs whereas EDX confirms the presence of metallic silver with a strong peak at 3 keV. The N–H and O–H stretching vibrations are observed in the FTIR spectrum around 3450 and 3423 cm−1. Gentamicin induced changes in serum parameters resulted in a significant increase in the level of serum urea, creatinine, bilurubin and uric acids. AgNPs even at modest doses (250 mg/kg), significantly reverted the level of serum markers. The gentamicin-induced AR-AgNP in mice with the levels of CAT, GPx, SOD and TBARS ensured the protection against the oxidative damage in mice which clearly implies that enhancing the antioxidant defense mechanism. Nephrotoxicity of gentamicin induced mice were demonstrated by significantly elevated levels of blood urea, serum creatinine, bilirubin, and uric acids. The exposure of AR-Ag nanoparticles leads to a substantial decrease in blood urea and serum creatinine levels and enhanced the antioxidant and anti-nephrotoxic activity.

The Prevalence of Thyroid Abnormalities in Patients With Chronic Kidney Disease: A Cross-Sectional Study at a Tertiary Care Hospital.

Background and objective Chronic kidney disease (CKD) is a clinical syndrome characterized by the irreversible loss of kidney function. It is a widespread condition affecting populations worldwide. The kidneys play a crucial role in the metabolism, breakdown, and elimination of thyroid hormone and thyroid-stimulating hormone (TSH). Consequently, thyroid dysfunction can occur as an endocrine manifestation in CKD patients. Previous studies investigating thyroid abnormalities and the severity of CKD have yielded diverse outcomes. In light of this, this study aimed to determine the prevalence of thyroid dysfunction in CKD patients and explore the association between different thyroid dysfunctions and markers of kidney function. Methods A total of 140 CKD patients who met the inclusion criteria were recruited, and their demographic details and routine investigations were recorded. Blood samples were collected for kidney function tests and thyroid function tests. The primary outcome measures included markers of kidney function [urea, creatinine, and estimated glomerular filtration rate (e-GFR)] and thyroid profile [TSH, free thyroxine (FT4), and free triiodothyronine (FT3)]. Mean and standard deviation (SD) were calculated for continuous variables, while frequencies were calculated for categorical data. Fisher's exact test was employed to evaluate the association between two categorical variables, and p-values below 0.05 were considered statistically significant. Results The mean (± SD) urea, creatinine, and e-GFR were found to be 139 (± 81.1) mg/dL, 5.33 (± 4.1) mg/dL, and 20.1 (± 15) ml/min/1.73 m2, respectively. Of note,133 (95%) patients had elevated urea levels, with the majority (n = 109, 77.8%) having urea levels between 40 and 199 mg/dL; 70 (50%) patients had creatinine levels less than 4 mg/dL, and 107 (76.4%) had e-GFR of less than 30 ml/min/1.73 m2. The mean (± SD) TSH, FT4, and FT3 levels were found to be 6.64 (± 11.2) mIU/ml, 13.6 (± 4.54) pmol/L, and 2.65 (± 1.89) pmol/L, respectively. It was observed that 18 (12.9%, 95% CI: 8.29-19.4%) of the CKD patients had hypothyroidism and 21 (15%, 95% CI: 10.02-21.8%) had subclinical hypothyroidism (SCH), while only two (1.4%, 95% CI: 0.39-5.05%) and five (3.6%, 95% CI: 1.5-8.08%) had hyperthyroidism and subclinical hyperthyroidism, respectively. Thirty-nine (27.9%, 95% CI: 21.1-35.8%) patients had low FT4 levels, whereas a considerable majority (n = 123, 87.9%, 95% CI: 81.41-92.28%) of the patients suffering from CKD were found to have low FT3 levels. The associations of urea levels with SCH, low FT4, and FT3 status were found to be statistically significant with p-values of 0.002, 0.033, and <0.001, respectively. The association between e-GFR and low FT3 status was also statistically significant, with a p-value of 0.014. Conclusion Nine out of 10 patients with CKD were discovered to have low FT3 levels, whereas one in four patients had low FT4 levels. The study participants also exhibited a significant presence of SCH and hypothyroidism, with prevalence rates of 15% and 12.9%, respectively. Urea levels and e-GFR, indicating the severity of CKD, showed a significant association with the presence of various thyroid abnormalities. Hypothyroidism in CKD patients can complicate disease progression, impact mortality rates, and affect overall quality of life. Therefore, routine screening for thyroid abnormalities should be conducted in all CKD patients.

Analysis of altered level of blood-based biomarkers in prognosis of COVID-19 patients.

Immune and inflammatory responses developed by the patients with Coronavirus Disease 2019 (COVID-19) during rapid disease progression result in an altered level of biomarkers. Therefore, this study aimed to analyze levels of blood-based biomarkers that are significantly altered in patients with COVID-19. A cross-sectional study was conducted among COVID-19 diagnosed patients admitted to the tertiary care hospital. Several biomarkers-biochemical, hematological, inflammatory, cardiac, and coagulatory-were analyzed and subsequently tested for statistical significance at P<0.01 by using SPSS version 17.0. A total of 1,780 samples were analyzed from 1,232 COVID-19 patients (median age 45 years [IQR 33-57]; 788 [63.96%] male). The COVID-19 patients had significantly (99% Confidence Interval, P<0.01) elevated levels of glucose, urea, alanine transaminase (ALT), aspartate aminotransaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), white blood cell (WBC), C-reactive protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6), ferritin, D-Dimer, and creatinine phosphokinase-MB (CPK-MB) compared to the control group. However, the levels of total protein, albumin, and platelets were significantly (P<0.01) lowered in COVID-19 patients compared to the control group. The elevated levels of glucose, urea, WBC, CRP, D-Dimer, and LDH were significantly (P<0.01) associated with in-hospital mortality in COVID-19 patients. Assessing and monitoring the elevated levels of glucose, urea, ALT, AST, ALP, WBC, CRP, PCT, IL-6, ferritin, LDH, D-Dimer, and CPK-MB and the lowered levels of total protein, albumin, and platelet could provide a basis for evaluation of improved prognosis and effective treatment in patients with COVID-19.

Hepatorenal Protective Functions of Coconut Water in Alloxan-Induced Type 1 Diabetes Mellitus

Coconut water is a natural product reported to contain antioxidant compounds with beneficial health effects. This study aimed to evaluate the antidiabetic effect of mature coconut water on some biochemical parameters of liver and kidney functions, and histological architecture of the pancreas in alloxan-induced diabetic rats. Twenty-four (24) Wistar rats were randomly divided into four groups, (n=6). Group I (negative control) rats were fed with rat chow and drinking water ad libitum and did not receive alloxan. Group II (positive control) received a single intraperitoneal dose of 150mg/kg body weight of alloxan to induce type 1 diabetes mellitus. Groups III and IV received a single intraperitoneal dose of 150mg/kg body weight of alloxan and were treated with 1ml/kg of mature coconut water for 3 weeks and 2mg/kg of glibenclamide for 3 weeks respectively by oral administration. On day 21, blood samples were collected for liver and kidney function tests. Liver function tests for Group II showed elevated aspartate transaminase (AST), alkaline phosphatase (ALP), albumin, total protein, total bilirubin, and low alanine aminotransferase (ALT) (p&lt;0.05). When compared with Group II, Group III showed elevated liver function parameters except ALT that was reduced (p&lt;0.05). Group IV showed elevated AST, total bilirubin, and reduced ALT, ALP, albumin, and total protein (p&lt;0.05). Kidney function tests showed that rats in Group II had significantly high creatinine, urea, bicarbonate, potassium, and sodium (p&lt;0.05). Group III had lowered creatinine, potassium levels, but with elevated urea, bicarbonate, and sodium levels (p&lt;0.05). Group IV had lowered creatinine, urea, bicarbonate, potassium levels, but with elevated sodium levels (p&lt;0.05). This study indicates that mature coconut water can be included in the treatment regimen for diabetes mellitus due to its hepatorenal protective functions.

Extensive multiregional urea elevations in a case-control study of vascular dementia point toward a novel shared mechanism of disease amongst the age-related dementias.

Vascular dementia (VaD) is one of the most common causes of dementia among the elderly. Despite this, the molecular basis of VaD remains poorly characterized when compared to other age-related dementias. Pervasive cerebral elevations of urea have recently been reported in several dementias; however, a similar analysis was not yet available for VaD. Here, we utilized ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) to measure urea levels from seven brain regions in post-mortem tissue from cases of VaD (n = 10) and controls (n = 8/9). Brain-urea measurements from our previous investigations of several dementias were also used to generate comparisons with VaD. Elevated urea levels ranging from 2.2- to 2.4-fold-change in VaD cases were identified in six out of the seven regions analysed, which are similar in magnitude to those observed in uremic encephalopathy. Fold-elevation of urea was highest in the basal ganglia and hippocampus (2.4-fold-change), consistent with the observation that these regions are severely affected in VaD. Taken together, these data not only describe a multiregional elevation of brain-urea levels in VaD but also imply the existence of a common urea-mediated disease mechanism that is now known to be present in at least four of the main age-related dementias.

Reproductive and Biochemical Toxicity of Biobased Silver Nanoparticles against Toxocara vitulorum

Background: Toxocara vitulorum is a common parasitic worm of buffalo and cattle, causing livestock mortality and morbidity worldwide. Several countries suffered substantial eco-nomic losses due to animal death and reduced meat and milk production. Therefore, it became nec-essary to discover a new alternative drug, especially with the emerging resistance to current medica-tions. The present study aims to evaluate the in vitro anthelmintic effect of different concentrations of biobased silver nanoparticles on T. vitulorum adults. Methods: Different concentrations of silver nanoparticles were synthesised using lemon juice. Groups of male and female adult worms were incubated in 50, 100, and 200 mg/L silver nanoparti-cles for 48 h. The parasite motility, histology, and biochemical parameters were observed and com-pared to the control. Results: The results showed that silver nanoparticles decreased the worm motility, increased mor-tality rate, induced structural damage, caused collagen disruption, and showed elevated levels of as-partate aminotransferase, alanine aminotransferase, alkaline phosphatase, albumin, total protein, urea, and creatinine, as well as reduced levels of acetylcholinesterase, lactate dehydrogenase, uric acid, total cholesterol, triglycerides, and high-density lipoprotein in a dose-dependent manner. Conclusion: Silver nanoparticles established a significant anthelmintic effect against T. vitulorum and could become one of the up-and-coming antiparasitic drugs in the future.

Therapeutic effect of melatonin-loaded chitosan/lecithin nanoparticles on hyperglycemia and pancreatic beta cells regeneration in streptozotocin-induced diabetic rats

Nanotechnology is used to overcome fundamental flaws in today's marketed pharmaceuticals that obstruct therapy, like restricted solubility and quick release of drugs into the bloodstream. In both human and animal researches, melatonin was demonstrated to regulate glucose levels. Despite the fact that melatonin is quickly transported through the mucosa, its sensitivity to be oxidized creates a difficulty in achieving the required dose. Additionally, due to its variable absorption and poor oral bioavailability necessitates the development of alternative delivery methods. The study aimed to synthesize melatonin loaded chitosan/lecithin (Mel-C/L) nanoparticles to be assessed in the treatment of streptozotocin (STZ)-induced diabetes in rats. The antioxidant, anti-inflammatory, and cytotoxicity properties of nanoparticles were estimated to determine the safety of manufactured nanoparticles for in vivo studies. In addition, Mel-C/L nanoparticles were administered to rats for eight weeks after inducing hyperglycemia. The therapeutic effect of Mel-C/L nanoparticles was assessed in all experimental groups by detecting insulin and blood glucose levels; observing improvements in liver and kidney functions as well as histological and immunohistochemical evaluation of rats’ pancreatic sections. The results proved that Mel-C/L nanoparticles showed remarkable anti-inflammatory, anti-coagulant, and anti-oxidant effects, in addition to its efficiency in reducing blood glucose levels of STZ-induced diabetic rats and great ability to promote the regeneration of pancreatic beta (β)-cells. Furthermore, Mel-C/L nanoparticles elevated the insulin level; and decreased the elevated levels of urea, creatinine and cholesterol. In conclusion, nanoparticles application decreased the administrated melatonin dose that in turn can diminish the side effects of free melatonin administration.

Analyses of Kidney Biomarkers in Patients With SARS-CoV-2 (COVID-19)

The new coronavirus was first reported in China and caused a widespread global outbreak of pneumonia that spread rapidly across this country and many other countries. Acute kidney injury is one of the important complications of COVID-19, which has been shown in some cases. Exploring the diagnostic features of biomarkers of kidney function in COVID-19 patients may lead to better patient management. We collected laboratory data from 206 people with confirmed COVID-19 disease and evaluated their renal biomarkers, Blood Urea Nitrogen (BUN), and creatinine. The age range of the patients was almost 62 years old. The mean age in the dead patients and recovered patients was 71 and 54 years old, respectively. The average LDH value was 755 U/L, and creatine phosphokinase (CPK) was 267 U/L in the patients. The average BUN was 59.1 U/L, and creatinine was 1.5 U/L in COVID-2019 patients. Among all 193 patients, laboratory results revealed that 163 (85.4 %) patients had an elevated BUN level. Based on creatinine levels for total patients, laboratory results revealed that 49 (25.4 %) patients had an elevated value. The average BUN value in dead patients was 85 mg/dL, while in recovered patients was 40.5 mg/dL (P&lt;0.0001). Also, the average creatinine level in dead patients was 1.86 mg/dL, while in recovered patients was 1.24 mg/dL (P=0.0004). Inflammation following COVID-19 disease causes kidney damage and elevated urea and creatinine levels, which may increase the risk of death in these patients.

Gallic acid and/or cerium oxide nanoparticles synthesized by gamma-irradiation protect cisplatin-induced nephrotoxicity via modulating oxidative stress, inflammation and apoptosis

Cisplatin is one of the most significant anticancer. However, its use is associated with numerous toxicities especially nephrotoxicity. The main aim of this work was to examine the protective effect of Gallic acid (GA) and/or cerium oxide nanoparticles (CONPs) synthesized by gamma-irradiation on cisplatin-induced nephrotoxicity in rats. To do that, 48 adult male albino rats were separated into eight groups and received GA (100 mg/kg orally) and/or CONPs (15 mg/kg i. p.) for 10 days before injection with a single dose of cisplatin (7.5 mg/kg i. p.). The findings showed that cisplatin treatment impaired kidney functioning as shown by elevated serum levels of urea and creatinine. Additionally, the oxidative stress indicators (MDA and NO), levels of NF-kB, pro-inflammatory cytokines (IL1-and TNF-) and pro-apoptotic proteins (BAX and caspase-3) were raised after cisplatin injection, while levels of intrinsic anti-oxidants (CAT, SOD, and GSH) and anti-apoptotic protein (Bcl-2) were reduced. Moreover, renal toxicity was confirmed by alteration in normal histological architecture of the kidneys. On the other hand, pretreatment with CONPs and/or GA ameliorated cisplatin-induced nephrotoxicity as evidenced by improvement of renal function parameters and levels of oxidative stress, inflammatory and apoptotic markers in renal tissue along with the renal histopathological changes. This study clarifies how GA and CONPs protect against cisplatin-induced nephrotoxicity and demonstrates any potential synergism between them. Therefore, they can be considered as promising nephroprotective agents during chemotherapy.

Investigations into ferroptosis in methylmercury‐induced acute kidney injury in mice

Methylmercury (MeHg) is a highly poisonous form of mercury and a risk factor for kidney impairment in humans that currently has no effective means of therapy. Ferroptosis is a non-apoptotic metabolic cell death linked to numerous diseases. It is currently unknown whether ferroptosis takes part in MeHg-induced kidney damage. Here, we established a model of acute kidney injury (AKI) in mice by gavage with different doses of MeHg (0, 40, 80, 160 μmol/kg). Serological analysis revealed elevated levels of UA, UREA, and CREA; H&E staining showed variable degrees of renal tubule injury; qRT-PCR detection displayed increased expression of KIM-1 and NGAL in the groups with MeHg treatment, indicated that MeHg successfully induced AKI. Furthermore, MDA levels enhanced in renal tissues of mice with MeHg exposure whereas GSH levels decreased; ACSL4 and PTGS2 nucleic acid levels elevated while SLC7A11 levels reduced; transmission electron microscopy illustrated that the density of the mitochondrial membrane thickened and the ridge reduced considerably; protein levels for 4HNE and TfR1 improved since GPX4 levels declined, all these results implying the involvement of ferroptosis as a result of MeHg exposure. Additionally, the observed elevation in the protein levels of NLRP3, p-p65, p-p38, p-ERK1/2, and KEAP1 in tandem with downregulated Nrf2 expression levels indicate the involvement of the NF-κB/NLRP3/MAPK/Nrf2 pathways. All the above findings suggested that ferroptosis and the NF-κB/NLRP3/MAPK/Nrf2 pathways are implicated in MeHg-induced AKI, thereby providing a theoretical foundation and reference for future investigations into the prevention and treatment of MeHg-induced kidney injury.

Spectrum of Biochemical Alterations in Patients with Covid-19

Background and objective: Millions of people worldwide have died from COVID-19, which has caused the failure of the lungs and other organs. The research assessed biochemical anomalies in COVID-19 patients to comprehend the illness and its effect better. Study Design: Retrospective longitudinal cohort analysis Place of study: ABWA Medical College Faisalabad Methods: A total of 150 adult patients (n=150) who tested positive for COVID-19 via RT-PCR were included in the study. A Roche Diagnostics Cobas C501 used spectrophotometry to measure calcium, magnesium, phosphate, lactate dehydrogenase (LDH), urea, creatinine, ferritin, and chloride in the blood. A NOVA electrolytic analyzer used Ion-selective electrodes to measure sodium, chloride, potassium, and bicarbonate. Results: In the study, 33.6% of patients had elevated urea levels, and 22.4% had elevated creatinine levels. Furthermore, 88.8% of patients had elevated ferritin levels, and 93.5% had elevated LDH levels. After 44 weeks, there was a drop in sodium-containing electrolytes, with 9% of patients experiencing a decrease in sodium, 22.4% in potassium, 53.3% in bicarbonate, 48.6% in calcium, and 23.4% in phosphorus. These changes in electrolyte levels suggest a long-term trend in electrolyte depletion among the patient population. There was no significant difference in biochemical anomalies between age groups (p &gt; 0.05). Conclusion: These results suggest that COVID-19 patients have lung illness and multi-organ involvement, which should be considered when managing these patients. These biochemical alterations warrant careful monitoring for organ failure by healthcare practitioners. More study is required to comprehend the processes causing these biochemical anomalies in COVID-19 patients. Keywords: Covid-19, Biochemical alterations, Outcomes

Nuclear Magnetic Resonance-Based Metabolomics Approach Revealed the Intervention Effect of Using Complementary and Alternative Medicine (CAM) by CKD Patients.

Chronic kidney disease (CKD) is the end point of a number of systemic chronic diseases. The prevalence of CKD is increasing worldwide and recent epidemiological studies are showing the high prevalence of renal failure in CKD patients using complementary and alternative medicines (CAMs). Clinicians believe that biochemical profiles of CKD patients using CAM (referred here to as CAM-CKD) may be different compared to those on standard clinical treatment and should be managed differently. The present study aims to explore the potential of the NMR-based metabolomics approach to reveal the serum metabolic disparity between CKD and CAM-CKD patients with respect to normal control (NC) subjects and if the differential metabolic patterns can provide rationale for the efficacy and safety of standard and/or alternative therapies. Serum samples were obtained from 30 CKD patients, 43 CAM-CKD patients, and 47 NC subjects. The quantitative serum metabolic profiles were measured using 1D 1H CPMG NMR experiments performed at 800 MHz NMR spectrometer. The serum metabolic profiles were compared using various multivariate statistical analysis tools available on MetaboAnalyst (freely available web-based software) such as partial least-squares discriminant analysis (PLS-DA) and random forest (a machine learning) classification method. The discriminatory metabolites were identified based on variable importance in projection (VIP) statistics and further evaluated for statistical significance (i.e., p < 0.05) using either Student t-test or ANOVA statistics. PLS-DA models were capable of clustering CKD and CAM-CKD with considerably high values of Q 2 and R 2. Compared to CAM-CKD patients, the sera of CKD patients were characterized by (a) elevated levels of urea, creatinine, citrate, glucose, glycerol, and phenylalanine and phenylalanine-to-tyrosine ratio (PTR) and (b) decreased levels of various amino acids (such leucine, isoleucine, valine, and alanine), high-density lipoproteins, lactate, and acetate. These changes suggested that CKD patients manifest severe oxidative stress, hyperglycemia (with dampened glycolysis), increased protein energy wasting, and reduced lipid/membrane metabolism. Statistically significant and strong positive correlation of PTR with serum creatinine levels suggested the role of oxidative stress in the progression of kidney disease. Significant differences in metabolic patterns between CKD and CAM-CKD patients were observed. With respect to NC subjects, the serum metabolic changes were more aberrant in CKD patients compared to CAM-CKD patients. The aberrant metabolic changes in CKD patients with manifestations of higher oxidative stress compared to CAM-CKD patients could explain clinical discrepancies between CKD and CAM-CKD patients and further advocate the use of different treatment strategies for CKD and CAM-CKD patients.

Ameliorative potential of Acalypha wilkesiana leaf extract (subsp. macrophylla) on cyanide-induced renal damaged Wister rats

BackgroundRecently, phytomedicine have been applied in the management of various diseases related to toxicity. In addition, attention has been on cyanide toxicity due to its harmful effects on man and animals. Thus, this research was carried out to determine the effect of Acalypha wilkesiana methanol leaf extract on cyanide induced renal damage in rats. Methods45 female Wister rats randomly divided into 7 groups were used for this study. Group 1:received neither cyanide nor methanol fraction of Acalypha wilkesiana (MFAW), 2 and 3 received different doses of MFAW respectively, 4 received cyanide only, 5 Rats received cyanide and sodium thiosulphate. 6 and 7 received cyanide and different doses of MFAW respectively. Renal markers (urea, creatinine, sodium, bicarbonate, potassium and chloride electrolytes) and antioxidant status (superoxide dismutase, malonaldehyde, catalase, gluthathione peroxidase) were assessed in the kidneys using standard biochemical procedures. ResultsRenal markers showed significant elevated levels of creatinine, urea and serum electrolytes in the untreated rats. However, treatment with methanol leaf extract of Acalypha wilkesiana significantly (p<0.05) reduced the cyanide-induced increase of creatinine, urea, serum electrolytes levels of sodium ion, potassium ion, bicarbonate and chlorine ion irrespective of the dose. Additionally, antioxidant status indicated a significant increase in lipid peroxidation and glutathione peroxidase with a concomitant decrease in catalase, superoxide dismutase as well as reduced glutathione and glutathione S-transferase, in untreated rats. However, treatment using the leaf extract modulated the cyanide induced mop up of these antioxidants and the rising glutathione peroxidase and lipid peroxidation in the kidney of rats exposed to cyanide irrespective of the dose of the extract. ConclusionsThe present study indicated that methanolic leaf extract of Acalypha wilkesiana conferred protection to the kidney of rats against chronic cyanide toxicity by ameliorating renal indices and up regulating antioxidant response.

Risk factors of maternal and failed maternal mortality, prediction of severe obstetric conditions

Objective. To determine the priority risk factors for maternal mortality (MM) and failed maternal mortality (FMM) on the basis of clinical and epidemiological features and to develop scientifically based patient-centered models for predicting severe obstetric conditions.&#x0D; Materials and methods. Primary documentation of successful and dysfunctional maternal outcomes that occurred at the levels I, II, III of medical organizations in Perm and the territories of Perm Krai from 2007 to 2018. Using random sampling, two observation groups were formed: women with failed maternal mortality, deceased women and the control group. Analytical epidemiological "case-control" studies were carried out, which included the determination of confidence intervals, etiological accuracy using Epi Info and Excel 2016 MSO programs, a package of applied electronic tables Stat2015 of the author ( V.S. Sheludko, 20012016), the MedCalc 15.8 Portable program.&#x0D; Results. Socio-behavioral, general somatic, obstetric-gynecological risk factors, the frequency of occurrence of which among women with failed maternal mortality was 1,44,3; 1,225,5; 1,17,6 times more often, and in the group of deceased mothers 1,99,0; 1,729,5; 2,89,0 times higher than in the group of healthy participants. The "indicators of maternal death" have been identified, which increase the risk of a failed maternal death turning into maternal death. Early clinical and laboratory signs of severe obstetric conditions are the following: high leukocyte intoxication index (LII), elevated levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine, decreased levels of fibrinogen, prothrombin index (PTI), prolongation of thrombin time (TT). Infectious-inflammatory, hypertensive complications, comorbidity, a high percentage of premature births and, accordingly, severe perinatal conditions are significantly more common in groups with unfavorable outcomes.&#x0D; Conclusions. In the course of the study, reliably significant risk factors were identified, on the basis of which scientifically based models for assessing the probability of developing critical obstetric conditions were worked out.

Rutin and Hesperidin Alleviate Paclitaxel-Induced Nephrocardiotoxicity in Wistar Rats via Suppressing the Oxidative Stress and Enhancing the Antioxidant Defense Mechanisms.

Paclitaxel is a primary chemotherapy agent that displays antitumor activity against a variety of solid tumors. However, the clinical effectiveness of the drug is hampered by its nephrotoxic and cardiotoxic side effects. Thus, this investigation aimed at assessing the protective effects of rutin, hesperidin, and their combination to alleviate nephrotoxicity caused by paclitaxel (Taxol), cardiotoxicity in male Wistar rats, as well as oxidative stress. Rutin (10 mg/kg body weight), hesperidin (10 mg/kg body weight), and their mixture were given orally every other day for six weeks. Rats received intraperitoneal injections of paclitaxel twice weekly, on the second and fifth days of the week, at a dose of 2 mg/kg body weight. In paclitaxel-treated rats, the treatment of rutin and hesperidin decreased the elevated serum levels of creatinine, urea, and uric acid, indicating a recovery of kidney functions. The cardiac dysfunction in paclitaxel-treated rats that got rutin and hesperidin treatment also diminished, as shown by a substantial reduction in elevated CK-MB and LDH activity. Following paclitaxel administration, the severity of the kidney and the heart's histopathological findings and lesion scores were markedly decreased by rutin and hesperidin administration. Moreover, these treatments significantly reduced renal and cardiac lipid peroxidation while markedly increased GSH content and SOD and GPx activities. Thus, paclitaxel likely induces toxicity in the kidney and the heart by producing oxidative stress. The treatments likely countered renal and cardiac dysfunction and histopathological changes by suppressing oxidative stress and augmenting the antioxidant defenses. Rutin and hesperidin combination was most efficacious in rescuing renal and cardiac function as well as histological integrity in paclitaxel-administered rats.

Intraperitoneal hepato-renal toxicity of zinc oxide and nickel oxide nanoparticles in male rats: biochemical, hematological and histopathological studies.

In recent years, zinc oxide (ZnO) and nickel oxide (NiO) nanoparticles (NPs) have become more prevalent in commercial and industrial products. However, questions have been raised regarding their potential harm to human health. Limited studies have been conducted on their intraperitoneal toxicity in rats, and their co-exposure effects remain uncertain. Therefore, this study aimed to investigate some biological responses induced by a single intraperitoneal injection of ZnO-NPs (200 mg/kg) and/or NiO-NPs (50 mg/kg) in rats over time intervals. Blood and organ samples were collected from 36 male rats for hematological, biochemical, oxidative stress, and histological analysis. Results showed that the administration of NPs reduced the body and organ weights as well as red blood cell (RBC) indices and altered white blood cell (WBC) and platelet (PLT) counts. The experimental groups exhibited elevated levels of aspartate aminotransferase (AST), alanine transaminase (ALT), creatinine (CREA), urea, lipid profile, glucose (GLU), total protein (TP), albumin (ALB) and malondialdehyde (MDA), and decreased uric acid (UA), superoxide dismutase (SOD), and glutathione (GSH). Histological observations also revealed architectural damages in liver and kidneys. These alterations were time-dependent and varied in their degree of toxicity. Co-exposure of NPs initially lessened the damage but increased it afterwards compared to individual exposure. In conclusion, intraperitoneal injection of ZnO-NPs and/or NiO-NPs alters biological processes and induces oxidative stress in rats' liver and kidneys in a time-dependent manner, with NiO-NPs being more potent than ZnO-NPs. Furthermore, co-exposed NPs initially appeared to be antagonistic to one another while further aiming toward synergism.

PS-C16-3: HYPERTENSION AND RISK FACTORS ASSOCIATED WITH IN-HOSPITAL DEATH IN PATIENTS WITH COVID-19

Objective: To explore the prevalence of hypertension and the common risk factors associated with increased death rate among (Covid-19) patients. Design and method: This is a retrospective cohort study using de-identified data retrieved from clinical records of patients from two COVID 19 isolation centers. Medical history, demographic data, self-reported comorbidities, symptoms, disease complications and laboratory investigations were extracted from clinical records of 406 confirmed COVID 19 hospitalized patients between Feb 2020 and July 2021. The outcomes of interest were death or discharge from the hospital. Logistic regression analysis was used to assess the impact of age, gender, associated comorbidities and some laboratory abnormalities on increased death rate among in-hospital (Covid-19) patients. Results: The prevalence of hypertension, was 59.6%, followed by diabetes (47.3%). COVID-19 patients with hypertension were older (67.0 ± 10.7vs 65.0 ± 13.0 P = 0.001). 70.4% were males. Undiagnosed high blood pressure was detected among 14.5%. Overall mortality was 46.2%, while mortality among normotensives, known hypertensives and undiagnosed hypertension was 47.7%, 54.7% and 37.6%, respectively (p &lt; 0.005). Death was significantly higher among the age group &gt; 65 years compared to ≦ 65 years old (53.6% % vs 39.0% (P = 0.005) irrespective of their blood pressure. Severe respiratory and gastrointestinal symptoms were significantly higher among hypertensives. Type I Respiratory failure 22.1%, and acute kidney injury 11.8% were the most typical complications among hypertensives. Leucocytosis (24.2%), Lymphopenia (56.8%) and higher levels of D-Dimer (47.7%) and C-reactive protein (49.7%) were mainly observed among hypertensive patients. Logistic Regression analysis after adjusting for age significantly showed age OR: 1.81, 95% CI: (1.12: 2.73, p = 0.01), undiagnosed HTN OR: 5.65, 95% CI: (2.04:15.67, p = 0.00), low platelets count OR: 6.53, 95% CI, (1.23:35.23, p = 0.02), higher levels of urea OR:1.67, 95% CI, (1.04:2.63, p = 0.03) and creatinine OR:1.71, 95% CI, (1.063:2.70, p = 0.02), were associated with worse prognosis and in-hospital death among Covid- 19 patients. Conclusion: The age group, more than 65 years with undiagnosed BP of more than 140/90, is significantly associated with higher in-hospital death. Thrombocytopenia and elevated urea and creatinine levels were the most prominent laboratory markers and may be used as a potential indicator for prognosis and outcome among Covid 19 hypertensives.

Protective effect of cinnamon oil against ciprofloxacin toxicity on liver and kidney of male Wistar rats

Cinnamon zeylanicum is one of many herbal medications. This herb contains different materials like, cumarin, cinnamaldehyde and cinnamic acid. The plant plays a role as antiallergic, antiviral, antimicrobial, anti-inflammatory and antioxidant and other health conditions. This study focused on the therapeutic effect of cinnamon oil on hepatorenal toxicity induced by ciprofloxacin in male rats. Forty rats were housed in the animal house of the College of Pharmacy, University of Kerbala, Karbala city, Iraq. The animals were separated into four groups: Group 1. Control group (not taken drug nor cinnamon oil), Group 2. Ciprofloxacin group (drenched 250 mg/kg/day of ciprofloxacin for 30 days), Group 3. Cinnamon oil group (drenched 1ml/kg/day of cinnamon oil for 30 days) and Group 4. Cinnamon+ciprofloxacin group (drenched 1ml/kg/day of cinnamon + 250 mg/kg/day of ciprofloxacin for 30 days). Finally, 2ml of blood was collected from each rat and the serum was separated for estimating the biochemical parameters of the liver like, Aspartate transaminase (AST), alanine transaminase(ALT) and alkaline phosphatase(ALP) and the kidney (Creatinine, Urea and albumin) . The results proved that ciprofloxacin significantly elevates the parameters of the liver and kidney (p≤0.05). The results also proved the benefit of cinnamon oil in improving health by reducing the toxic effect of ciprofloxacin by lowering the elevated levels of (liver enzymes, creatinine, urea and albumin). The study showed that this oil reduced the toxic effect of ciprofloxacin on the kidney and liver.

Comparative study of extension area based methods for spectrophotometric determination of desmopressin acetate in the presence of its acid-induced degradation products

Desmopressin acetate (DPA) is a synthetic analogue of vasopressin used in the treatment of diabetes insipidus, bedwetting, hemophilia A, and elevated levels of urea in the blood. Sensitive and selective stability-indicating methods are needed to be developed and validated for its assay pure and pharmaceutical dosage forms in the presence of its degradation products as no method has been reported for its determination in the presence of its degradants. This work describes a comparative study of five simple stability-indicating spectrophotometric techniques for determination of DPA in presence of its acid-degradation products (acid-degradants) without prior separation. The proposed spectrophotometric techniques (First derivative, Derivative ratio, Ratio difference, Mean centering and Dual wavelength) were developed and validated according to ICH guidelines. Acid degradation was carried out with 0.1 N HCl; the acid-degradants were separated on TLC plates and the acidic degradation pathway was established by IR, H-NMR and MS techniques. The TLC method was based on the separation of DPA and its acid-induced degradation products on silica gel plates using methanol: water (80:20, v/v) as a developing system and UV detection at 254 nm. All assay suggested methods were successfully applied for quantitation of DPA in pure and tablet forms. They are specific, sensitive, precise and accurate. They showed good linearity in the concentration range of 1–14 µg/mL with good correlation coefficients, and limit of detection (LOD) of 0.304, 0.274, 0.167, 0.248 and 0.199 and limit of quantitation (LOQ) of 0.920, 0.829, 0.506, 0.751 and 0.604) for each method, respectively. These methods were successfully applied for the simultaneous determination of DPA in its pure and tablet dosage form in the presence of its acid-degradants. The results obtained were statistically comparable with those of reported HPLC assay method; no significant differences were observed with relevance to accuracy and precision. All the methods are sensitive, selective and can be used for the routine analysis of DPA in its pure and dosage forms.

Angiotensin-converting enzyme gene (ACE) polymorphisms are associated with dysregulation of biochemical parameters in hypertensive patients.

The genetic component, including genes and their variants, plays a significant role in the pathophysiology of arterial hypertension (AH). Thus, clinical, epidemiological and genetic studies have been carried out to improve the understanding of disease mechanisms, improve diagnostic quality and contribute to prevention. To determine the association of risk factors, biochemical parameters and different ACE gene polymorphisms with AH. The case-control study was carried out in the population of Ouro Preto, Brazil. The subjects answered a questionnaire containing clinical and sociodemographic data. The ACE gene polymorphisms rs4291, rs4363 and rs4335 were evaluated by real time-polymerase chain reaction (real-time PCR) in 310 people (155 hypertensive and 155 normotensive patients), in addition to biochemical parameters. A multivariate logistic regression model was used to identify factors associated with AH. Analysis of continuous variables was performed using the Kruskal-Wallis test to assess significance between groups and Dunn's post-test for multiple comparisons. The results showed that AH was associated with age, education, smoking, obesity and high levels of triglycerides, sodium, glucose and uric acid. Regarding the biochemical parameters, in hypertensive patients, the rs4363 and rs4335 polymorphisms were associated with high levels of triglycerides, urea and glucose; the rs4291 polymorphism was associated with elevated urea and glucose levels. No association was detected between SNPs and HA. AH was associated with socioeconomic status, lifestyle habits and biochemical parameters. ACE polymorphisms may have influenced the levels of triglycerides, urea and glucose in hypertensive patients.