Filtration Function Research Articles

The Age–Stiffness Relationships of Elastic and Muscular Arteries in a Control Population and in End-Stage Renal Disease Patients

Arterial dysfunction is major risk factor for cardiovascular complications, and arterial stiffness is an independent risk factor in end-stage renal disease patients. As the distance from the heart increases, arterial stiffness (pulse wave velocity) becomes progressively more marked. This generates a centrifugal stiffness gradient, which leads to partial, continuous local wave reflections, which in turn attenuate the transmission of pulsatile pressure into the microcirculation, thus limiting the potentially deleterious outcomes both upstream (on the heart: left-ventricular hypertrophy and coronary perfusion) and downstream (on the renal and cerebral microcirculation: reduced glomerular filtration and impaired cognitive functions). The impact of arterial aging is greater on the aorta and central capacitive arteries, and it is characterized by a loss or reversal of the physiological stiffness gradient between central and peripheral arteries. Recently, however, in contrast to observations on the aorta, several studies have shown less pronounced, absent, or even negative associations between muscular peripheral arteries and age–stiffness relationships, which may be associated with a decrease in or reversal of the stiffness gradient. These findings point to a potential benefit of assessing the muscular peripheral arteries to predict the risk of cardiovascular disease and suggest that reversal of the stiffness gradient may be an independent risk factor for all-cause mortality.

Relationship between vascular access and angulation of vena cava filter at placement and retrieval: a multicenter retrospective cohort study.

Inferior vena cava (IVC) filters are commonly used intravascular devices designed to prevent fatal pulmonary embolism (PE), maintaining the IVC filter as centered as possible is fundamental for achieving its filtration function. This study aimed to characterize the tilt angles of IVC filter between the vascular access of internal jugular vein (IJV) and femoral vein (FV), as well as to identify factors associated with increased or decreased tilt angles between placement and retrieval. This is a multicenter retrospective study. A multicenter retrospective study was conducted from October 2017 to March 2019. The primary outcome was the change in filter tilt between placement and retrieval. The secondary outcome was the identifications of factors associated with increased or decreased tilt angle. Relevant variables were analyzed using t-tests, Chi-square tests, Fisher's exact tests, while multivariate logistic regression analysis was used to determine risk factors. A total of 184 eligible patients were included in this study. The IJV group had a lower likelihood of tilt angle over 10° at the time of placement compared to the FVs group (0% versus 12.5%, p = 0.040). Among the 171 patients with a mean dwell time of 22.1 days, the IJV group had a higher likelihood of tilt angle over 10° than the FVs group (10.3% versus 2.3%, p = 0.080). The use of FVs access at placement was associated with a higher difference between placement and retrieval filter tilt angles (p < 0.01). Multivariate logistic regression analysis showed that hypertension [odds ratio (OR) 0.668; 95% confidence interval (CI) 0.328-1.358, p = 0.265], cardiologic artery disease (OR 0.537; 95% CI 0.136-2.130, p = 0.377), cerebral venous disease (OR 0.555; 95% CI 0.186-1.651, p = 0.290), filter types (OR 1.624; 95% CI 0.851-3.096, p = 0.141), and IVC filter thrombosis (OR 1.634; 95% CI 0.804-3.323, p = 0.175) were not associated with increased filter tilt angle. Right side (OR 0.434; 95% CI 0.202-0.930, p = 0.032) or bilateral lower extremity deep vein thrombosis (LEDVT) (OR 0.383; 95% CI 0.148-0.995, p = 0.049) were identified as protective factors. IJV access was associated with a lower filter tilt angle at the time of placement, while FVs access was linked to a higher difference between placement and retrieval tilt angles. Right side or bilateral LEDVT were identified as protective factors against increased IVC filter tilt angle.

The pan-liver network theory: From traditional chinese medicine to western medicine.

In traditional Chinese medicine (TCM), the liver is the "general organ" that is responsible for governing/maintaining the free flow of qi over the entire body and storing blood. According to the classic five elements theory, zang-xiang theory, yin-yang theory, meridians and collaterals theory, and the five-viscera correlation theory, the liver has essential relationships with many extrahepatic organs or tissues, such as the mother-child relationships between the liver and the heart, and the yin-yang and exterior-interior relationships between the liver and the gallbladder. The influences of the liver to the extrahepatic organs or tissues have been well-established when treating the extrahepatic diseases from the perspective of modulating the liver by using the ancient classic prescriptions of TCM and the acupuncture and moxibustion. In modern medicine, as the largest solid organ in the human body, the liver has the typical functions of filtration and storage of blood; metabolism of carbohydrates, fats, proteins, hormones, and foreign chemicals; formation of bile; storage of vitamins and iron; and formation of coagulation factors. The liver also has essential endocrine function, and acts as an immunological organ due to containing the resident immune cells. In the perspective of modern human anatomy, physiology, and pathophysiology, the liver has the organ interactions with the extrahepatic organs or tissues, for example, the gut, pancreas, adipose, skeletal muscle, heart, lung, kidney, brain, spleen, eyes, skin, bone, and sexual organs, through the circulation (including hemodynamics, redox signals, hepatokines, metabolites, and the translocation of microbiota or its products, such as endotoxins), the neural signals, or other forms of pathogenic factors, under normal or diseases status. The organ interactions centered on the liver not only influence the homeostasis of these indicated organs or tissues, but also contribute to the pathogenesis of cardiometabolic diseases (including obesity, type 2 diabetes mellitus, metabolic [dysfunction]-associated fatty liver diseases, and cardio-cerebrovascular diseases), pulmonary diseases, hyperuricemia and gout, chronic kidney disease, and male and female sexual dysfunction. Therefore, based on TCM and modern medicine, the liver has the bidirectional interaction with the extrahepatic organ or tissue, and this established bidirectional interaction system may further interact with another one or more extrahepatic organs/tissues, thus depicting a complex "pan-hepatic network" model. The pan-hepatic network acts as one of the essential mechanisms of homeostasis and the pathogenesis of diseases.

Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis.

Podocytes are essential components of the glomerular filtration barrier and essential for the proper filtration function of the glomerulus. Podocyte injury under various stress conditions is the primary pathogenesis and key determinant of focal segmental glomerulosclerosis (FSGS) with prominent clinical manifestations of proteinuria or nephrotic syndrome. Under physiological conditions, a highly coordinated mitochondrial quality control system, including antioxidant defenses, mitochondrial dynamics (fusion, fission, and mitophagy), and mitochondrial biogenesis, guarantees the sophisticated structure and various functions of podocytes. However, under FSGS pathological conditions, mitochondria encounter oxidative stress, dynamics disturbances, and defective mitochondrial biogenesis. Moreover, mutations in mitochondrial DNA and mitochondria-related genes are also strongly associated with FSGS. Based on these pieces of evidence, bioactive agents that function to relieve mitochondrial oxidative stress and promote mitochondrial biogenesis have been proven effective in preclinical FSGS models. Targeting the mitochondrial network is expected to provide new therapeutic strategies for the treatment of FSGS and delay its progression to end-stage renal disease. Mitochondrial dysfunction plays a key role in podocyte injury and FSGS progression. This review summarized recent advances in the study of mitochondrial homeostatic imbalance and dysfunction in FSGS and discussed the potential of mitochondria-targeted therapeutics in improving FSGS and retarding its progression to end-stage renal disease.

Cerebral microangiopathy in men with obstructive sleep apnea syndrome

To determine factors associated with the development of small vessel disease (SVD) in patients with obstructive sleep apnea syndrome (OSA). One hundred and fifty-two patients with risk factors for the development of cerebrovascular diseases were examined. Based on the results of polysomnography, patients were divided into groups with- (n=84) and without (n=68) OSA. The groups were matched by age, prevalence of arterial hypertension and diabetes mellitus. SVD was diagnosed using brain MRI. Laboratory tests included an assessment of parameters of lipid metabolism, glucose metabolism, concentration of C-reactive protein (CRP), levels of homocysteine and creatinine with the calculation of glomerular filtration rate (GFR). Patients with OSA, compared with those without OSA, were characterized by a statistically significant number of gliosis foci, with their large sizes, more frequent changes on the Fazekas scales and the Hassan scale. The most severe degree of damage according to the Hassan scale in patients with OSA was detected more often (55 (66%) and 27 (39%) OR=2.89, 95% CI 1.47-5.67, p=0.002). More pronounced atrophic changes in the brain, an increase in the size of the III ventricle and the index of the anterior horns, significantly lower GFR and higher levels of CRP were noted in the OSA group. Patients with OSA and duration of nocturnal hypoxia for more than 2 minutes were more likely to have hyperintensity of subcortical regions. In patients with OSAS, pronounced manifestations of SMD were associated with a significantly higher level of morning systolic blood pressure (MAP): 140 [120; 150] vs. 127 [120; 130] p=0.029; increased levels of blood homocysteine: 14 [11; 17.8] vs. 13 [9.7; 12.5] p=0.049; a decrease in GFR: 79 [71; 87.3] vs. 89.8 [80.3; 94] p=0.002, respectively. OSA and intermittent nocturnal hypoxia are independent risk factors for SMD. A more severe micro-focal vascular lesion in OSA is associated with a decrease in renal filtration function, an increase in morning blood pressure and an elevation in homocysteine level.

АУТОСОМНО-ДОМИНАНТНАЯ ГИПОКАЛЬЦИЕМИЯ: ОПИСАНИЕ СЕМЕЙНОГО НАБЛЮДЕНИЯ

Autosomal dominant hypocalcemia (ADH), or familial hypocalciuric hypercalcemia (FHH) is a rare hereditary disease manifested by hypocalcemia and hypercalciuria due to a malfunction of the calcium-sensitive receptor (mutations in the CASR or GNA11 genes). A familial clinical case of ADH is presented: the disease was diagnosed in a 36 y/o female and her two male children of 11 and 1.5 y/o. The disease was detected in an older child aged 7 years on the basis of convulsive syndrome, decreased blood calcium and parathyroid hormone, increased calciuria and detection of a mutation in the CASR gene (c.344-358del TTGCTCAAAACAAAA/ p.116 120delAQNKI). The initial manifestations of the disease in the form of a convulsive syndrome were observed in a child starting his 2nd day of life and were regarded as a manifestation of epilepsy, which was then followed by a long non-convulsive period. The patient needs constant therapy with alfacalcidol and has nephrocalcinosis. Based on the diagnosis made, the disease was also confirmed in his mother as the asymptomatic hypocalcemia and a mutation in the CASR gene were found. The woman does not need drug therapy, does not have nephrocalcinosis. In the youngest child, the diagnosis was suspected at birth on the basis of convulsions, hypocalcemia and was subsequently confirmed then by the detection of a mutation in the CASR gene. The course of the disease in the youngest child is severe, aggravated by the presence of perinatal CNS lesions and epilepsy. The patient has been receiving therapy with alfacalcidol since birth, has manifestations of severe nephrocalcinosis with a decrease in the filtration function of the kidneys. To stop the convulsive syndrome the patient needs to maintain a higher level of blood calcium, which is complicated due to hypercalciuria and causes chronic kidney disease. Conclusion: the observed familial case demonstrates the polymorphism of the course of the disease, and, given the rarity of the disease and the nonspecificity of manifestations, the description of this case will improve the awareness of medical practitioners of various specialties about the disease for its timely diagnosis.

Calorie Restriction Provides Kidney Ischemic Tolerance in Senescence-Accelerated OXYS Rats

Kidney diseases belong to a group of pathologies, which are most common among elderly people. With age, even outwardly healthy organisms start to exhibit some age-related changes in the renal tissue, which reduce the filtration function of kidneys and increase the susceptibility to injury. The therapy of acute kidney injury (AKI) is aggravated by the absence of targeted pharmacotherapies thus yielding high mortality of patients with AKI. In this study, we analyzed the protective effects of calorie restriction (CR) against ischemic AKI in senescence-accelerated OXYS rats. We observed that CR afforded OXYS rats with significant nephroprotection. To uncover molecular mechanisms of CR beneficial effects, we assessed the levels of anti- and proapoptotic proteins of the Bcl-2 family, COX IV, GAPDH, and mitochondrial deacetylase SIRT-3, as well as alterations in total protein acetylation and carbonylation, mitochondrial dynamics (OPA1, Fis1, Drp1) and kidney regeneration pathways (PCNA, GDF11). The activation of autophagy and mitophagy was analyzed by LC3 II/LC3 I ratio, beclin-1, PINK-1, and total mitochondrial protein ubiquitination. Among all considered protective pathways, the improvement of mitochondrial functioning may be suggested as one of the possible mechanisms for beneficial effects of CR.

Role of ion channels in the mechanism of proteinuria (Review).

Proteinuria is a common clinical manifestation of kidney diseases, such as glomerulonephritis, nephrotic syndrome, immunoglobulin A nephropathy and diabetic nephropathy. Therefore, proteinuria is considered to be a risk factor for renal dysfunction. Furthermore, proteinuria is also significantly associated with the progression of kidney diseases and increased mortality. Its occurrence is closely associated with damage to the structure of the glomerular filtration membrane. An impaired glomerular filtration membrane can affect the selective filtration function of the kidneys; therefore, several macromolecular substances, such as proteins, may pass through the filtration membrane and promote the manifestation of proteinuria. It has been reported that ion channels play a significant role in the mechanisms underlying proteinuria. Ion channel mutations or other dysfunctions have been implicated in several diseases, therefore ion channels could be used as major therapeutic targets. The mechanisms underlying the action of ion channels and ion transporters in proteinuria have been overlooked in the literature, despite their importance in identifying novel targets for treating proteinuria and delaying the progression of kidney diseases. The current review article focused on the four key ion channel groups, namely Na+, Ca2+, Cl- and K+ ion channels and the associated ion transporters.

Features of Kidney Function in Patients With Comorbidity of Arterial Hypertension and Chronic Obstructive Pulmonary Disease.

Background and objective Chronic kidney disease (CKD) and hypertension are closely linked in terms of cause and effect. Decreased renal function is usually associated with increased blood pressure, and a steady increase in blood pressure accelerates the decline in renal function. In this study, we aimed to investigate laboratory parameters of renal function - blood creatinine level, urine creatinine level, urea blood level,urine albumin level, and in particular, serum cystatin C level - as early predictors of kidney damage and assess the filtration function of the kidneys based on the glomerular filtration rate (GFR) in patients with isolated arterial hypertension,those with a comorbid pathology of hypertension and chronic obstructive pulmonary disease (COPD). and those with isolated COPD. Materials and methods Thestudy included a total of 101 patients (the final sample consisted of 88 patients) with hypertension and COPD, who were divided into three groups: Group I consisted of 38 patients with hypertension, Group IIcomprised 27 patients with hypertension and COPD, and Group III was made up of 23 patients with COPD. The average age of patients in groups -presented as mean [standard deviation (SD)] - was as follows - Group I: 55.7 (11.2) years, Group II: 59.3 (9.2) years, and Group III: 57.8 (9.1) years. For statistical data processing, the program Statistics 10 was used. Results The level of blood creatinine- presented as median (Me) and interquartile range (IQR) - was statistically significantly different between the groups, and the values in the three groups were as follows - Group I (patients with hypertension): 88.3 (84.2; 102.7) μmol/l, Group II (patients with comorbid pathology of arterial hypertension and COPD): 99.0 (80.0; 115.0) μmol/l, and Group III (patients with COPD): 84.6 (75.0; 94.2) μmol/l (p=0.008). The highest level was determined in patients with hypertension and comorbid COPD, while the lowest was in the comparison group, in patients with COPD. Urinary creatinine levels were as follows - Group I: 1081.0 (578.0; 1749.0) mg/l, Group II: 1318.5 (1124.0; 1817.0) mg/l, and Group III: 822.0 (625.0; 1320.5) mg/l (p=0.08). Blood urea values were as follows - Group I: 5.7 (5.2; 6.0) mmol/l, Group II: 5.7 (4.9; 6.6) mmol/l, Group III: 5.9 (4.4; 7.7) mmol/l. The calculation of GFR revealed a statistically significant difference between the three groups - Group I: 70.5 (56.0; 83.0) ml/min, Group II: 66.5 (57.0; 77.0) ml/min, and Group III: 81.5 (70.0; 88.0) ml/min (p=0.02). The cystatin C level was 1.16 (1.03; 1.27) mg/l in Group I, 1.3 (1.22; 1.38) mg/l in GroupII, and 1.05 (0.96; 1.05) mg/lin Group III. Conclusions In patients of all three groups, there was a decrease in renal filtration function based on the results ofcreatinine and cystatin C levels. Even in the group of patients with COPD without kidney disease,a decrease in GFR was observed. We noted a negative aggravating effect of COPD on renal function in patients with hypertension, which can be attributed to increased endothelial dysfunction and increased general inflammation in this group of patients.

Decreased Red Blood Cell Deformability Contributes to Loss of Splenic Filtration Function and Variations in Spleen Size in Children with Sickle Cell Anaemia

Decreased Red Blood Cell Deformability Contributes to Loss of Splenic Filtration Function and Variations in Spleen Size in Children with Sickle Cell Anaemia

A Study on Etiology, Clinical Features and Complications of Chronic Kidney Disease Patients

Background and Aim: Chronic kidney disease (CKD) is a major health issue that encompasses a variety of pathophysiological processes mostly related to declining rate of glomerular filtration and abnormal kidney function. Globally, the incidence of chronic kidney disease is increasing due to hypertension, diabetes, and cardiovascular disease. The present study aimed to investigate the etiology, clinical features, and complications of chronic kidney disease patients. Methodology: This cross-sectional study was conducted on 136 chronic kidney disease patients admitted to the Department of Medicine of Mamji Hospital, Karachi Pakistan from January 2021 to December 2021. Prior to study conduction, ethical approval from the research and ethical committee of the institute was taken. Informed consent was obtained from each individual. Demographic details, para-clinical and clinical features, etiology, and therapeutic features were the different outcome variables. Clinical examinations with detailed history and laboratory investigations were assessed. For laboratory examinations, urine and blood samples from each participant were taken. Data analysis with detailed descriptive statistics was carried out in SPSS version 25. Results: Out of 136 CKD patients, there were 74 (54.4%) male and 62 (45.6%) females. The overall mean age was 38.6±4.8 years. Age-wise distribution of the participants was as: 23 (16.9%) 15-25 years, 38 (27.9%) 26-35 years, 34 (25%) 36-45 years, 26 (19.1%) 46-55 years, and 15 (11.1%) &gt;55 years. The chronic kidney disease associated comorbidities were high blood pressure (HBP) 64 (47.1%), human immunodeficiency virus (HIV) 25 (18.4%), Diabetic sugar 21 (15.4%), heart disease 19 (14%), and sickle cell anemia 7 (5.1%). Lesion diagnosis was found in 61 (44.9%) patients. The most prevalent diagnosis was chronic glomerulonephritis (CGN), Glam nephropathy, and vascular nephropathies presented in 27 (19.9%), 18 (13.2%), and 16 (11.8%) respectively. Intermediate 69 (50.7%), Hypertensive nephropathy 20 (14.7%), HIV-related nephropathy 17 (12.5%), Diabetic nephropathy 15 (11%), Primary segmental and focal hyalinosis 11 (8.2%), and Autosomal dominant polycystic kidney disease 4 (2.9%) were the different etiology diagnosed in CKD patients. The chronic disease complications such as Anemia, hyperkalaemia, hyperuricemia, uremic encephalopathy, right femoral venous thrombosis, and acute pulmonary edema were seen in 107 (78.7%), 54 (39.7%), 13 (9.6%), 9 (6.6%), 2 (1.5%), and 8 (5.9%) respectively. Conclusion: The present study concluded that hypertension, cardiovascular disease, diabetes, and HIV are the different predominant risk factors for chronic kidney disease. Also, the most prevalent etiology of the CKD was chronic glomerulonephritis (CGN) followed by Diabetic nephropathy in CKD patients. Anemia was the prevalent complication followed by hyperkalemia and hyperuricemia. Swelling at lower limb and weakness were the common symptoms of chronic kidney disease. Keywords: Etiology, Clinical features, Complications, Chronic Kidney Disease.

Defect-rich covalently-crosslinked UiO-66(Zr)-NH2/PVC adsorption ultrafiltration membrane for effective phosphate ions removal from water

BackgroundPhosphorus in wastewater is a major environmental concern. Very small phosphorus inputs in the environment can cause algal blooms that can deplete the dissolved oxygen and decrease the water quality, leading to eutrophication. Furthermore, some algal blooms produce toxins and bacterial growth that can cause human illness through exposure to contaminated water. Therefore, It is necessary to remove phosphorus before it is discharged to the environment. Methodsadsorbent enhanced adsorptive ultrafiltration (UF) has recently emerged as an advanced ion recovery technology with membrane filtration function and adsorption function, and is very effective in removing cationic bisphosphate and anionic phosphate. Significant findingsHerein, a novel defect-rich and covalently-crosslinked octanoic acid (OA)-UiO-66(Zr)-NH2/PVC adsorption ultrafiltration membrane are designed for removal of phosphate ions in water. The OA-UiO-66-NH2/PVC-33 membrane achieved the adsorption capacity (∼30 mgg−1) and higher removal efficiency (∼90%). The OA-UiO-66(Zr)-NH2/PVC ultrafiltration membrane exhibited a higher water flux of 266.9 L/(m2·h·bar) compared to those of pristine PVC and UiO-66-NH2/PVC. Filtration and cyclic stability experiments reveal that OA-UiO-66(Zr)-NH2/PVC membrane can maintain a high retention capacity and exhibit excellent regeneration performance after 5 cycles.

Type 2 myocardial infarction: Diagnostic features in real clinical practice

Purpose. To determine the incidence of type 2 myocardial infarction (MI) diagnosis (according to the Fourth Universal Definition) and the features of patient management in real clinical practice.Material and Methods. A retrospective study was performed by analyzing the case histories of 153 patients diagnosed with acute coronary syndrome (ACS). Inclusion criteria were the presence of ACS at admission followed by a confirmed diagnosis of MI during the hospital period according to the Fourth Universal Definition of MI and the age of patients &gt; 18 years. Patients with severe comorbidities affecting the immediate prognosis and/or being an alternative to the diagnosis of MI were not included in the study.Results. The study showed that emergency coronary angiography was performed in 151 patients (98.7%). A decrease in the renal filtration function in the presence of chronic kidney disease was a contraindication to this study found in 1.3% of cases; 12 (8%) patients did not have coronary artery disease or had stenoses of less than 50%; these patients comprised the group of patients with type 2 MI. While analyzing the results of examination in patients with type 2 MI, ST segment elevation was detected in seven patients (58.4%) according to electrocardiography; ST segment depression was observed in one patient (8.3%); complete left bundle-branch block was found also in 1 case (8.3%), three individuals (25%) did not have any changes in the position of ST segment, but had a negative T wave. Analysis of possible etiological factors in the development of type 2 MI showed the presence of sinus tachycardia in two patients (16.7%), severe sinus bradycardia in one patient (8.3%), fl utter paroxysm and atrial fibrillation with tachysystole throughout the ventricles in two patients (16.7%), and history of atrial fibrillation in one patient (8.3%).Conclusion. Type 2 MI was diagnosed in 8% of patients with ACS with and without ST segment elevation where cardiac arrhythmias including sinus arrhythmias may be the potential etiological factors. Limited capabilities of assessing the stability of atherosclerotic plaque in the coronary artery including that in the presence of plaque thrombosis represent a significant negative factor for establishing diagnosis in routine clinical practice.

Photon count rates estimated from 1980 clinical CT scans.

All photon counting detectors have a characteristic count rate over which their performance degrades. Degradation in the clinical setting takes the form of increased noise, reduced material quantification accuracy, and image artifacts. Count rate is a function of patient attenuation, beam filtration, scanner geometry, and X-ray technique. To guide protocol and technology development in the photon counting space, knowledge of clinical count rates spanning the complete range of clinical indications and patient sizes is needed. In this paper, we use clinical data to characterize the range of computed tomography (CT) count rates. We retrospectively gathered 1980 patient exams spanning the entire body (head/neck/chest/abdomen/extremity) and sampled 36951 axial image slices. We assigned the tissue labels air/lung/fat/soft tissue/bone to each voxel for each slice using CT number thresholds. We then modeled four different bowtie filters, 70/80/100/120/140kV spectra, and a range of mA values. We forward-projected each slice to obtain detector-incident count rates, using the geometry of a GE Revolution Apex scanner. Our analysis divided the detector into thirds: the central one-third, one-third of the detector split into two equal regions adjacent to the central third, and the final one-third divided equally between the outer detector edges. We report the 99th percentile of counts to mimic the upper limits of count rates making passing through a patient as a function of patient water equivalent diameter. We also report the percentage of patient scans, by body region, over different count rate thresholds for all combinations of bowtie and beam energy. For routine exam types, we recorded count rates of approximately 3.5×108 counts/mm2 /s in the torso, extremities, and brain. For neck scans, we observed count rates near 6×108 counts/mm2 /s. Our simulations of 1000mA, appropriately mimicking the mA needs for fast pediatric, fast thoracic, and cardiac scanning, resulted in count rates of over 10×108 counts/mm2 /s for the torso, extremities, and brain. At 1000mA, for the neck region, we observed count rates close to 2×109 counts/mm2 /s. Importantly, we saw only a small change in maximum count rate needs over patient size, which we attribute to patient mis-positioning with respect to the bowtie filters. As expected, combinations of kV and bowtie filter with higher beam energies and wider/less attenuating bowtie fluence profiles lead to higher count rates relative to lower energies. The 99th-50th percentile count rate changed the most for the torso region, with a maximum variation of 3.9×108 to 1.2×107 counts/mm2 /s. The head/neck/extremity regions had less than a 50% change in count rate from the 99th to 50th percentiles. Our results are the first to use a large patient cohort spanning all body regions to characterize count rates in CT. Our results should be useful in helping researchers understand count rates as a function of body region and mA for various combinations of bowtie filter designs and beam energies. Our results indicate clinical rates >1×109 counts/mm2 /s, but they do not predict the image quality impact of using a detector with lower characteristic count rates.

CeO2 modified carbon nanotube electrified membrane for the removal of antibiotics

Electrified carbon nanotube membranes (ECM) are used as electroactive porous materials for the degradation of micropollutants. It integrated design of both electrochemical processes and filtration functions. In this study, CeO2 modified carbon nanotube electrified membrane (CeO2@CNT membrane) was prepared and activate NaClO towards degradation of antibiotics. As CeO2 with face-centered cubic (Fcc) fluorite structure was loaded onto the CNT sidewalls, the CeO2@CNT membrane showed a higher over potential and a smaller equivalent polarization resistance compared to ECM. More reactive oxygen species (ROS) and reactive chlorine species (RCS) were generated by CeO2@CNT membrane due to faster electron transfer at the solid-liquid interface. Thus, the removal efficiencies of DCF, SMX, CIP, TC and CBZ were more than 91.2%, 91.3%, 94.4%, 99.3% and 89.4% by the CeO2@CNT membrane with NaClO, respetively. And the apparent reaction rate constant (k) of the CeO2@CNT membrane was 2.9 times of that of ECM. The selective capping experiments and density functional theory (DFT) calculation showed that the oxygen vacancies of CeO2 contributed to the generation of ‧OH, and the generation of ClO‧ and ‧O2− would mainly occur on Lewis acid sites of CeO2. In addition, the CeO2@CNT membrane showed a reasonable stability to treat actual water samples and reduced disinfection byproducts (DBPs) formation, suggesting that it can potentially be combined with the conventional chlorine disinfection to degrade antibiotics in water.

Association between proteinuria and adverse pregnancy outcomes: a retrospective cohort study

Proteinuria during pregnancy is closely related to the occurrence of adverse pregnancy outcomes. One hundred and forty-two women with proteinuria during pregnancy and followed between January 2018 and December 2020 were evaluated. Based on the 24-h proteinuria value, they were divided as mild (n = 76, 300–1000 mg/day), moderate (n = 39, 1000–3500 mg/day) and severe (n = 27, >3500 mg/day) proteinuria. The rates of prematurity, low birth weight and neonatal asphyxia were significantly higher in the severe proteinuria group than in the mild and moderate groups, while the rates of foetal growth restriction and neonatal intensive care unit admission were significantly higher in the severe compared with the mild proteinuria group (all p < .05). Logistic regression analysis showed that moderate proteinuria (OR = 97.2, 95%CI: 7.1–1334.2, p = .001) and severe proteinuria (OR = 34.0, 95%CI: 1.6–711.0, p = .023) were associated with adverse perinatal outcomes. Compared with mild proteinuria, moderate and severe proteinuria are associated with adverse pregnancy outcomes in perinatal infants. Impact Statement What is already known on this subject? The production of proteinuria is closely related to the filtration function of the glomerulus, the reabsorption and secretion function of the renal tubules. For women with normal renal function before pregnancy, such physiological changes are less likely to cause adverse symptoms; however, for women with chronic kidney disease before pregnancy, especially those with significantly impaired renal function, the kidneys often cannot compensate for these physiological changes, which can lead to serious complications for both mother and infant. What do the results of this study add? In our study, logistic regression analysis showed that the severity of proteinuria was independently associated with adverse perinatal outcomes. The ROC curve showed that 24-h proteinuria had a predictive value for adverse perinatal outcomes. Therefore, for patients with urine protein quantification ≥0.3 g/24 h, regular 24-h urine protein quantification during pregnancy could help predict adverse perinatal outcomes and improve prognosis. What are the implications of these findings for clinical practice and/or further research? Proteinuria quantification can be used as one of the factors predicting adverse pregnancy outcomes. Thus, monitoring of urinary protein quantification in women during pregnancy should be strengthened for early detection of renal impairment, then interventions be used to improve maternal and infant outcomes.

The Effect of Aminophylline on Urine Output and Fluid Balance after a Single Dose in Children Admitted to the Pediatric Cardiac Intensive Care Unit

AbstractThe purpose of this retrospective study was to investigate the effects of a single dose of aminophylline on urine output and fluid balance in children admitted to the cardiac intensive care unit. A retrospective study was performed to compare variables of interest before and 24 hours after aminophylline administration in children under the age of 18 years who were admitted to the cardiac intensive care unit at our institution from January 2011 onwards. Variables of interest included age, weight, aminophylline dose, concurrently administered diuretics, specific hemodynamic parameters, and blood urea nitrogen and creatinine levels. Variables such as urine output and fluid balance were measured through a binary endpoint. Data were compared in a paired fashion and continuous variables were compared through paired t-tests. Analyses were conducted using SPSS Version 23.0. A total of 14 patients were included in the study. There was no significant change in hemodynamic parameters or creatinine levels before and after intravenous aminophylline administration of 5 mg/kg. There was a significant difference in urine output, fluid balance, and blood urea nitrogen levels from the baseline value. Concurrent usage of diuretics did not show significant association with a difference in urine output or fluid balance from baseline. No significant adverse reactions were noted 24 hours after administration of aminophylline. Use of aminophylline dosed at 5 mg/kg is safe and leads to improvement in urine output and fluid balance without negatively impacting systemic oxygen delivery or renal filtration function.

Molecular mechanisms of histone deacetylases and inhibitors in renal fibrosis progression.

Renal fibrosis is a common progressive manifestation of chronic kidney disease. This phenomenon of self-repair in response to kidney damage seriously affects the normal filtration function of the kidney. Yet, there are no specific treatments for the condition, which marks fibrosis as an irreversible pathological sequela. As such, there is a pressing need to improve our understanding of how fibrosis develops at the cellular and molecular levels and explore specific targeted therapies for these pathogenic mechanisms. It is now generally accepted that renal fibrosis is a pathological transition mediated by extracellular matrix (ECM) deposition, abnormal activation of myofibroblasts, and epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells under the regulation of TGF-β. Histone deacetylases (HDACs) appear to play an essential role in promoting renal fibrosis through non-histone epigenetic modifications. In this review, we summarize the mechanisms of renal fibrosis and the signaling pathways that might be involved in HDACs in renal fibrosis, and the specific mechanisms of action of various HDAC inhibitors (HDACi) in the anti-fibrotic process to elucidate HDACi as a novel therapeutic tool to slow down the progression of renal fibrosis.

Prospects for the Use of NGAL and KIM-1 for the Diagnosis of Acute Kidney Injury in Patients Receiving Antibacterial Therapy

The developers of Clinical Practice Guidelines for Acute Kidney Injury titled The Initiative to Improve Global Kidney Disease Outcomes (KDIGO) point at the need of new biomarkers for diagnosis acute kidney injury (AKI).The objective: to study and evaluate the diagnostic significance of the levels of neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in patients with AKI in the early postoperative period when antibiotic therapy is used.Subjects and Methods. AKI frequency was assessed in 276 patients during the early postoperative period after the antibacterial drugs had been prescribed. Serum levels of KIM-1 and NGAL, glomerular filtration rate (GFR), creatinine, protein in urine were tested before the start of antibiotic therapy, in 24–48 hours, and in patients with AKI – additionally in 72–96 hours. The normal initial renal excretory function was registered only in 36 patients (13.04%). The majority of patients (242 patients, 86.96%) were diagnosed with chronic kidney disease of various stages.Results. NGAL and KIM-1 levels were higher in the group of patients with AKI before start of antibiotic therapy versus the group of patients with preserved renal function. However, a statistically significant increase in the level of KIM-1 and NGAL was found only in the group of patients with stages 3A and 3B of CKD versus the groups of patients with stages 1 and 2 of CKD. The second important observation is that a comorbid pathology in patients led to a high AKI incidence when antibiotic therapy was used – 35.86% (30–42%; 95%CI).Conclusion. The relationship of NGAL and KIM-1 levels with glomerular filtration rate (GFR) and KIM-1 level with the presence of proteinuria as indicators of impaired renal filtration function suggests that NGAL and KIM-1 levels reflect the state of renal filtration function. Based on this observation, it should be accepted that NGAL and KIM-1 levels can be used as markers for the diagnosis of AKI in patients receiving antibiotic therapy. The prescription of antibiotic therapy in the postoperative period in patients with surgical pathology and renal dysfunction leads to a high AKI incidence. Elevated KIM-1 and NGAL levels in AKI during the antibiotic therapy suggests their involvement in the reparation process.

Case report and literature review: A de novo pathogenic missense variant in ACTN4 gene caused rapid progression to end-stage renal disease

BackgroundFocal segmental glomerulosclerosis (FSGS) is a histopathological diagnosis of the sclerosis of glomeruli and the damage to renal podocytes. FSGS affects the filtration function of the kidneys and results in nephrotic syndrome (NS) in children and adults. FSGS is a clinically and genetically heterogeneous disorder. FSGS-1 [OMIM #603278] is one of the progressive hereditary renal diseases. It is caused by heterozygous variants of the actinin alpha 4 (ACTN4) [OMIM*604638] gene on chromosome 19q13.2 in a dominant inheritance (AD) manner. With the recent development of whole-exome sequencing (WES), 22 (including our case) pathogenic or likely pathogenic variants have been identified in ACTN4 gene.Case presentationWe reported a 17-year-old Chinese girl who was hospitalized with foamy urine, nausea and vomiting. Laboratory tests revealed increased levels of serum creatinine and urea nitrogen. Ultrasonography demonstrated bilaterally reduced size of kidneys. The primary diagnoses were NS and chronic kidney disease stage 5 (CKD5). The hemodialysis was initiated in 48 h after admission. After 4 months of treatment, the patient received an allogeneic kidney transplantation from her father. A novel heterozygous missense variant c.494C > T (p.A165V) in the ACTN4 gene was found by WES in the patient. This variant was confirmed by Sanger sequencing. The computational simulation of the stability of mutant protein (p.A165V) was decreased. Interatomic interactions of the p.A165V site were increased, and it might be associated with the increased ubiquitylation in the vicinity of the mutant site.ConclusionAs per the guidelines of the American College of Medical Genetics and Genomics for interpreting sequence variants, the novel heterozygous missense variant was pathogenic (PS2 + PM1 + PM2 + PP3 + PP4). It should be noted that the early onset of severe proteinuria with a poor prognosis is an important and universal symptom for most genetic FSGS. If necessary, genetic screening is recommended.