292 results about "Kidney Glomerulus" patented technology

The invention relates to an adjusting system applied to continuous kidney replacement treatment of acute kidney injury patients. Comprising the following steps: capturing the blood flow velocity and vascular endothelial permeability of glomerular capillaries in real time by using a micro sensor or a nano-scale optical imaging technology; the method comprises the following steps: pre-judging a risk time point of insufficient tissue perfusion through dynamic modeling of a capillary structure and a functional relationship; combining the microcirculation data with conventional biochemical indexes of the patient to create an early intervention model; when it is monitored that microcirculation perfusion is greatly reduced or kidney oxygen supply is insufficient, continuous renal replacement therapy CRRT parameter fine adjustment is triggered in advance; the method comprises the following steps: collecting plasma toxins of different patients at clinical and molecular levels, and constructing a common toxin map of the acute kidney injury AKI; whether the specific toxin concentration exceeds the standard or not is judged by combining a real-time sensor, and the removal priority is output in real time; a membrane material with an adjustable aperture or a special coating is adopted, so that inflammatory mediators and bacterial endotoxin molecules are adsorbed or intercepted, and the permeability of micromolecular electrolyte is kept.

The invention discloses a method and a system for constructing a renal function automatic estimation model based on plain-scan CT (Computed Tomography). The method comprises the following steps: S1, collecting image data of a patient suffering from renal atrophy or hydronephrosis; s2, training a kidney parenchyma and hydronephrosis region automatic segmentation model based on UNETR by using kidney parenchyma and hydronephrosis regions manually described by a radiologist; s3, image omics features are extracted from the images, and data are screened; s4, constructing a renal function index regression model, wherein the renal function index regression model comprises a GFR regression model and an SRF regression model; s5, verifying an estimated value of the regression model; and S6, calculating GFR and SRF by using the renal function index regression model, and distinguishing kidneys in different health states. By adopting the method, the glomerular filtration rate and the lateral renal function of each kidney can be automatically estimated. A rapid, convenient and low-cost renal function evaluation method is provided for treating patients with renal atrophy or hydronephrosis.

The invention belongs to the technical field of disease risk assessment, and discloses a hearing loss disease risk prediction method, system and device and a medium, and the method comprises the steps: obtaining hearing test data, serum creatinine detection data and genetic typing data of a tester; calculating estimated glomerular filtration rate data based on the serum creatinine detection data; screening SNP (Single Nucleotide Polymorphism) sites related to hearing loss in the genetic typing data, and calculating multi-gene risk scoring data on the basis of the SNP sites; based on a statistical method, combining the hearing test data, the estimated glomerular filtration rate data, the polygene risk scoring data and the basic feature data of the test personnel to construct a hearing loss disease risk prediction model; and predicting the hearing loss of the person to be predicted and the illness risk probability of the severity of the hearing loss based on the constructed hearing loss illness risk prediction model. According to the technical scheme, genetic and non-genetic factors are comprehensively considered, and the hearing loss disease risk can be evaluated more comprehensively and accurately.

The present invention relates to RNAi agents, e.g., double stranded RNA (dsRNA) agents, targeting the complement component C3 gene (C3). The invention also relates to methods of using such RNAi agents to inhibit expression of a C3 gene and to methods of preventing and treating a C3-associated disorder, e.g., cold agglutinin disease (CAD), warm autoimmune hemolytic anemia, and paroxysmal nocturnal hemoglobinuria (PNH), lupis nephritis (LN), bullous pemphigoid, Pemphigus, e.g., Pemphigus vulgaris (PV) and Pemphigus foliaceus (PF), and C3 glomerulopathy.

The instant invention relates to a process for the preparation of a pharmaceutical composition in sustained-release tablet form comprising from 600 milligrams to 2400 milligrams of Pirfenidone (PFD), in such a way that the drug is bioavailable during an extended period of time of 12 hours from its administration. In this way, the anti-fibrotic and anti-inflammatory action of the drug Pirfenidone is optimized. Moreover, the instant invention offers advantages and a higher therapeutic efficacy compared to other pharmaceutical forms of Pirfenidone for oral administration and its therapeutic application in the regression of chronic renal failure secondary to primary glomerulosclerosis; it shows a better activity with regard to the reduction and / or regression of deleterious effects in breast capsular contracture observed after the surgical implantation of breast implants in humans and has an important anti-TNF-α and anti-TGF-β1 action for the treatment of hepatic fibrosis.

The invention relates to a cardiovascular disease risk assessment system and method. On the basis of fully considering the influence of dimension index information of kidney-related risk factors on the occurrence risk of cardiovascular diseases, heart and kidney metabolic indexes are integrated. And a mathematical model Fine-Gray is used for screening predictive factors by a step-by-step method. On the premise that traditional cardiovascular disease risk factors are reserved, in order to give consideration to the accuracy and easy generalization of risk assessment, prediction factors are simplified through strict calculation and derivation; the method is constructed based on a small amount of clinically ubiquitous detection index information such as age, sex, smoking or not, systolic pressure (SBP), fasting blood glucose (FBG), non-high density lipoprotein cholesterol (non-HDL-C) and estimated glomerular filtration rate (eGFR) as predictive factors. The method has the advantages of simplicity and convenience in operation, less required information and low professional requirement. Meanwhile, the risk of the outcome of various clinical cardiovascular diseases (including CVD, ASCVD and HF) can be evaluated at the same time, and the method can be suitable for various scenes such as primary medical care and clinical diagnosis and treatment.

The invention provides a glomerular senescence evaluation method, system and device, and relates to the technical field of glomerular senescence evaluation.The evaluation method mainly comprises the steps that based on a low-abundance proteomics result of an aged mouse plasma sample, core expression protein related to glomerular senescence is screened out, a prediction model aiming at glomerular senescence is constructed, and the prediction model is used for predicting the glomerular senescence; the prediction model comprises a glomerular senescence index; detecting core expression protein data of a to-be-detected plasma sample, and calculating the glomerular senescence index of the to-be-detected plasma sample according to the prediction model. According to the scheme, aiming at the specificity of glomerular senescence, core expression protein can be screened out and a prediction model can be constructed through methods such as low-abundance proteomics results, so that the glomerular senescence can be evaluated simply, conveniently, reliably and quickly; the scheme is helpful for follow-up efficient research and evaluation of anti-glomerular senescence drugs, and is helpful for follow-up efficient research and explanation of the effect of glomerular senescence in CKD progress.

The invention relates to application of targeted intervention FBP2mRNA in preparation of a medicine for preventing and treating diabetic nephropathy, and belongs to the technical field of biomedicine. The invention provides an application of FBP2mRNA as a therapeutic target in preparation of a medicine for preventing and treating diabetic nephropathy. The NCBI (National Center of Biotechnology Information) login number of the FBP2mRNA is NM003837.4. The invention also provides an application of the shRNA for specifically interfering with the expression of the FBP2mRNA in the preparation of a medicine for preventing and treating diabetic nephropathy, wherein the nucleotide sequence of the shRNA is shown as SEQ ID NO. 1. It is found for the first time that targeted inhibition of the expression level of FBP2mRNA can effectively reduce the lipid level in mouse glomerular podocytes, reduce the expression level of lipid synthesis related genes and reduce the activity of lipid synthesis protein, and then the effect of treating diabetic nephropathy is achieved, so that FBP2mRNA can be used as a drug treatment target, and the treatment effect of diabetic nephropathy is improved. The application is applied to research, development and preparation of diabetic nephropathy prevention and treatment medicines.

To provide a technique capable of facilitating prediction of a tendency of future changes in estimated glomerular filtration rate (eGFR).SOLUTION: An information processing device includes: acquisition means for acquiring time-series medical insurance information of a specific person; and prediction means for predicting a tendency of future changes in estimated glomerular filtration rate (eGFR) of the specific person based on time-series medical insurance information by using a trained machine learning model. The machine learning model predicts the tendency of the future changes in eGFR of the specific person using time-series eGFR and time-series measurements other than eGFR contained in the time-series medical insurance information.SELECTED DRAWING: Figure 2

Systemic lupus erythematosus (SLE) is an autoimmune disease in which circulating immune complexes can cause different types of glomerulonephritis, according to immune deposits and to the type of glomerular cell injury. Proliferative lesions represent the most severe form of lupus nephritis (LN) and often lead to kidney failure and death. Mucosal-associated invariant T (MAIT) are a subset of innate-like T cells that recognize microbial-derived ligands from the riboflavin synthesis pathway. Now the inventors analyzed the phenotype and function of peripheral blood MAIT cells by flow cytometry in 26 patients with LN and in a control group of 16 healthy volunteers. The inventors found that MAIT cell frequencies are markedly reduced in blood of LN patients. More particularly, among LN patients, baseline MAIT cell frequency, Ki-67 expression evaluating proliferative activity and granzyme B production measuring cytotoxicity represent promising prognostic factors of renal response one year after induction therapy. In conclusion, the inventors showed that baseline frequency and cytotoxic profile of MAIT cells may represent a promising prognostic factor of renal remission one year after induction therapy.

The invention provides application of AQP1 protein as a target spot in preparation of a diagnostic reagent and a therapeutic drug for hypoglycaemia nephropathy, and belongs to the technical field of biological medicines.The AQP1 protein is used as the target spot, AQP1 protein expression is reduced by adopting an inhibitor, and the hypoglycaemia nephropathy is obtained. According to the present invention, with the application of the kit, the effects of reducing the renal tubule injury markers in the urine, reducing the glomerular filtration rate or relieving the kidney tissue hypoxia can be achieved, the new idea is provided for the early prevention and treatment of the diabetic nephropathy (DKD), and the early recognition and the effective treatment of the kidney injury of the diabetic patient can be well achieved.

The invention provides a binding protein specifically bound with a glomerular basement membrane, a preparation method and application, and relates to the technical field of biology. The binding protein contains a heavy chain variable region and a light chain variable region, wherein a complementary determining region of the heavy chain variable region comprises amino acid sequences consistent with VH-CDR1, VH-CDR2 and VH-CDR3 of the heavy chain variable region shown as SEQ ID NO.1; the complementarity determining region of the light chain variable region comprises amino acid sequences which are consistent with the amino acid sequences of VL-CDR1, VL-CDR2 and VL-CDR3 of the light chain variable region as shown in SEQ ID NO.2. The binding protein has good specific binding capacity with a glomerular basement membrane antigen, and can be used for identification of an anti-glomerular basement membrane antibody or the glomerular basement membrane antigen, and diagnosis and detection of anti-glomerular basement membrane antibody positive diseases and / or vasculitis or auxiliary diagnosis and detection of the anti-glomerular basement membrane antibody positive diseases and / or vasculitis.

The application discloses a fusion protein NGF2 with improved in-vivo half-life and application thereof, and belongs to the technical field of medical biological engineering, and comprises ABD and FGF2, and the gene and protein sequence thereof are respectively composed of the sequences shown in SEQ ID NO:1, SEQ ID NO:2, SEQ ID NO:3, SEQ ID NO:5, SEQ ID NO:6 and SEQ ID NO:7, and the complete gene and protein sequence thereof is shown in SEQ ID NO:4 and SEQ ID NO:8. The fusion protein NGF2 can keep activity for more than 7 days in an environment of 37 DEG C, and the half-life of the fusion protein in solution is prolonged. In addition, the ABD is combined with HAS to form a complex, and the total molecular weight reaches 90kDa, which is higher than the cut-off molecular weight of glomerular filtration, so that the in-vivo half-life of the fusion protein is effectively prolonged.

The invention belongs to the technical field of biological medicine, and particularly relates to an in-vitro fusion technology for multi-lineage human kidney organs and application thereof. The invention provides a method for realizing culture of multilineage kidney organs by fusing kidney units and ureteral bud organs in vitro. According to the in-vitro fusion technology of the kidney organoid reported by the invention, two organoid with different pedigree sources, namely the kidney unit and the ureteral bud, can be efficiently fused, a UB tubular structure is integrated into the kidney unit organoid, and the UB tubular structure starts from a single ureteral bud and is wrapped by kidney unit precursor cells in a similar in-vivo development process, and finally develops into a kidney with glomerulus and a plurality of kidney cells. The multi-lineage renal organ comprises a catheter, a proximal tube, a marrow tab thin section, a distal tube, a connecting tube and a ureteral bud with a single outlet. A framework is provided for an engineered renal unit and a smooth collection system, and the method is an important step for generating the functional renal tissue from the beginning.

The invention provides a glomerular crescent lesion multi-task semantic segmentation and classification system, which relates to the technical field of medical image processing and comprises an input module, an encoder module, a decoder module, a boundary branch module, a main output module and a processing module. The input module is used for receiving images; the encoder module adopts a symmetric topological structure and is used for carrying out multi-stage down-sampling operation on an input image and outputting feature maps of different scales; the decoder module is used for fusing the feature maps from the corresponding stages of the encoder and carrying out up-sampling step by step; the boundary branch module is connected behind the lowest layer output feature at the tail end of the decoder; the main output module is located at the tail end of the decoder; and the processing module is used for calculating a composite loss function and performing back propagation to update parameters of the encoder module, the decoder module and the boundary branch module, and is used for outputting a final segmentation and classification result of the lesion region of the crescent body. The system provided by the invention can realize accurate segmentation and category prediction of the lesion area of the crescent body.

The invention discloses a novel compound and application thereof in preparation of a medicine for treating systemic lupus erythematosus. In-vitro experiments show that the compound provided by the invention can further inhibit the secretion of anti-dsDNA IgG + B cell subtype mediated autoantibody by inhibiting the process that B cells are differentiated into plasmoblasts; in-vivo experiments show that the compound provided by the invention can effectively reduce the content of total IgG and anti-dsDNA-IgG in peripheral blood of a systemic lupus erythematosus model mouse, inhibit splenomegaly and peripheral lymph node hyperplasia of the mouse, slow down urine protein increment of the mouse, inhibit glomerular lesion and renal tubule lesion of the mouse and inhibit IFN-gamma generation of the mouse kidney; differentiation of spleen and peripheral lymph node plasmablasts of mice is inhibited, that is, differentiation and function development (antibody secretion) processes of B cells are directly acted. Therefore, the compound provided by the invention has a prospect of being developed into drugs for treating systemic lupus erythematosus.

The invention relates to nucleic acid products that interfere with complement factor B (CFB) gene expression or inhibit its expression. The nucleic acids are preferably for use in the prophylaxis or treatment of complement associated diseases, disorders or syndromes, particularly C3 glomerulopathy (C3G), paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), lupus nephritis, IgA nephropathy (IgA N), myasthenia gravis (MG), and primary membranous nephropathy.

The present invention relates to RNAi agents, e.g., double stranded RNA (dsRNA) agents, targeting a complement component C3 (C3) gene. The invention also relates to methods of using such RNAi agents to inhibit expression of a C3 gene and to methods of preventing and treating a C3-associated disorder, e.g., paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), atypical hemolytic uremic syndrome (aHUS), neuromyelitis optica (NMO), multifocal motor neuropathy (MMN), myasthenia gravis (MG), C3 glomerulonephritis, or systemic lupus erythmatosis.

The present application relates to a kind of pharmaceutical composition for treating type 2 diabetes and its application.The pharmaceutical composition includes icariin, hydroxymethyl coumarin and cinnamaldehyde, by three-component synergistic effect, simultaneously act on insulin resistance, pancreatic beta cell apoptosis and systemic metabolic inflammation three type 2 diabetes core pathological links, auxiliary reduce serum lipid level, and reduce drug-related liver injury risk, good safety.Animal experiment results show that three-drug combination group can effectively reduce blood sugar (decrease about 50%), significantly improve islet structure atrophy, restore hepatocyte index arrangement, reduce glomerular hypertrophy, significantly reduce serum TG and CHOL level (P<0.05) and inflammatory factor IL-6 and TNF-alpha level (P<0.05), and avoid the hepatotoxicity risk (ALT / AST restores to close to normal level) of hydroxymethyl coumarin.The present application is composed of three kinds of natural monomers with clear structure, and has clear components and controllable quality, which provides a more optimal comprehensive treatment strategy for the treatment of type 2 diabetes and its complications.

Disclosed are methods for treating focal segmental glomerulosclerosis (FSGS), comprising administering to a patient in need thereof a pharmaceutically effective amount of a compound of formula (I), wherein R1 to R7, A, L and Y are as defined herein. Also disclosed are pharmaceutical compositions comprising the compound of formula (I) and their use for treating FSGS.

The disclosure provides at least one compound, tautomer, deuterated derivative, or pharmaceutically acceptable salt chosen from compounds of Formula I, tautomers thereof, deuterated derivatives of those compounds or tautomers, and pharmaceutically acceptable salts of any of the foregoing, compositions comprising the same, and methods of using the same, including uses in treating APOL1-mediated diseases, including pancreatic cancer, focal segmental glomerulosclerosis (FSGS), and / or non-diabetic kidney disease (NDKD).

Disclosed herein is a method for treating immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN) with the factor B inhibitor iptacopan or a pharmaceutically acceptable salt thereof (e.g., iptacopan hydrochloride).

The disclosure provides at least one entity chosen from compounds of formula (I), solid state forms of the same, compositions comprising the same, and methods of using the same, including use in treating focal segmental glomerulosclerosis (FSGS) and / or non-diabetic kidney disease (NDKD).

This invention relates to the fields of biomedical technology and biological model construction technology, and discloses an ANCA-associated vasculitis glomerular endothelial cell injury model, its construction method and application, and the application of BACH1 inhibitors. The method includes: (1) activating neutrophils sequentially with tumor necrosis factor α and immunoglobulin G to obtain a culture medium containing activated neutrophils; wherein the immunoglobulin G is immunoglobulin G isolated and purified from the plasma of patients with ANCA-associated vasculitis; (2) co-culturing the culture medium containing activated neutrophils with human glomerular endothelial cells to obtain the cell injury model. The cell injury model provided by this invention can verify the role of neutrophil adhesion characteristics in endothelial cell injury, and at the same time, the cell injury model can better simulate the immune microenvironment of ANCA-associated vasculitis glomerular endothelial cells in vivo.

A phosphodiesterase type 5 inhibitor is used in the preparation of a medicament for resisting fibrotic diseases. Experiments in animal models of ischemia-reperfusion (UIRI)-induced renal fibrosis, unilateral ureteral obstruction (UUO)-caused kidney fibrosis and idiopathic pulmonary fibrosis show that a PDE5 inhibitor such as tadalafil, sildenafil and vardenafil can significantly inhibit the expression of multiple fibrosis iconic proteins such as fibronectin, collagen I, renal injury molecule-1, and α-skeletal muscle actin in UIRI and UUO renal fibrosis lesions, improves glomerulopathy, degree of renal tubular distension, renal interstitial collagen fiber deposition and inflammatory cell infiltration, reduces the fibrotic area within the lesion, and significantly inhibits the progression of renal fibrosis; and the PDE5 inhibitor can significantly improve smooth muscle proliferation and inflammatory cell infiltration in bronchioles and pulmonary arterioles of idiopathic pulmonary fibrosis lesion, improve damage condition of alveolar tissue, and significantly inhibit the progression of pulmonary fibrosis.

The application discloses a marker for determining the severity of IgAN kidney tissue lesions and application thereof, and inventors find that ACTN4, ACADS and COL1A1 are significantly differentially expressed proteins in kidney tissues. The significant down-regulation of ACTN4 may cause the change of actin cytoskeleton of IgAN glomerular podocytes; the significant down-regulation of ACAD may indirectly participate in the occurrence process of abnormal structure and function of IgAN renal tubular epithelial cells by affecting fatty acid metabolism in the cells; and the significant up-regulation of COL1A1 may participate in the accumulation of extracellular matrix in the renal interstitium of IgAN, and play a certain role in promoting the renal interstitial fibrosis. The combination of ACTN4, ACADS and COL1A1 has good prediction efficiency for the diagnosis of the severity of IgAN kidney tissue lesions, and the area under the ROC curve is 0.815, P 0.043. In addition, the immunohistochemical results also confirm the expression trend of the three proteins ACTN4, ACADS and COL1A1 in the corresponding kidney tissue substructures in proteomics.

The present disclosure is directed to method of generating human glomeruli endothelial cells (HGECs) from human endothelial cells (ECs), comprising expressing in human ECs an exogenous nucleic acid encoding a T-box transcription factor 3 (Tbx3), alone or in combination with one or more of PR domain zinc finger protein 1 (Prdm1), GATA Binding Protein 5 (Gata5) and Pre-B-Cell Leukemia Transcription Factor 1 (Pbx1). Disclosed also are HGECs produced by the methods of the instant disclosure, as well as methods for using the same.

In an illustrative embodiment, systems and methods for treating kidney disease in a human patient are disclosed. A method includes advancing a collapsible array of RF electrodes through a urinary tract of the patient in collapsed form and into a position in or near a renal pelvis. The effector is deployed to an expanded form to engage at least a portion of an interior wall of the renal pelvis. RF energy delivered through the array of electrodes target afferent nerves proximate the interior wall of the renal pelvis to inhibit or destroy their function. eGFR of the patient can be raised after treatment according to the method.

Described herein are methods of treating immune complex mediated membrane proliferative glomerulonephritis (IC-MPGN) with a factor B inhibitor ipropam or a pharmaceutically acceptable salt thereof, e.g., ipropam hydrochloride.

The mechanisms driving the development of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly understood. A key question is how parietal epithelial cells (PECs) invade glomerular capillaries, thereby promoting injury and kidney failure. Here the inventors show that expression of the tetraspanin CD9 increases markedly in PECs in mouse models of CGN and FSGS, and in kidneys from individuals diagnosed with these diseases. Cd9 gene targeting in PECs prevents glomerular damage in CGN and FSGS mouse models. Mechanistically, CD9 deficiency prevents the oriented migration of PECs into the glomerular tuft and their acquisition of CD44 and β1 integrin expression. These findings highlight a critical role for de novo expression of CD9 as a common pathogenic switch driving the PEC phenotype in CGN and FSGS, while offering a potential therapeutic avenue to treat these conditions. Accordingly, CD9 represents a reliable biomarker and as well as a biotargets in glomerulonephritides.