مستخلص: BACKGROUND: Untreated microangiopathic hemolytic anemia in pregnancy is associated with adverse maternal and perinatal outcomes. Accurate diagnosis is challenging owing to nonspecific clinical features and pathologic findings. Timely initiation of appropriate management is essential to optimize maternal and perinatal outcomes. CASE: A 26-year-old primiparous woman presented at 20 weeks of gestation with new-onset microangiopathic hemolytic anemia on a background of poorly controlled type 1 diabetes. She received eculizumab for presumed atypical hemolytic uremic syndrome. At 24 weeks of gestation, she developed superimposed early-onset preeclampsia; she delivered at 27 weeks of gestation after continuing eculizumab. CONCLUSION(S): Eculizumab may prolong pregnancy in early-onset preeclampsia. Additional research is needed to assess short-term and long-term maternal and newborn outcomes.Copyright © 2019 by the American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.

مصطلحات الفهرس: erythrocyte transfusion, estimated glomerular filtration rate, female, fetal well being, fetus lung maturation, fibrin deposition, fibrosing alveolitis, gene, generalized edema/dt [Drug Therapy], generalized edema/si [Side Effect], gestational age, glycemic control, headache/si [Side Effect], hemoglobin blood level, hemolytic uremic syndrome/di [Diagnosis], heterozygote, histopathology, home oxygen therapy, human, human tissue, hyperreflexia/si [Side Effect], hypertension/dt [Drug Therapy], insulin dependent diabetes mellitus/dt [Drug Therapy], insulin treatment, kidney biopsy, kidney function, kidney tubule, lactate dehydrogenase blood level, lethargy, macroalbuminuria, maternal smoking, meningococcosis, missense mutation, onset age, peripheral edema, placenta insufficiency, platelet count, preeclampsia/dt [Drug Therapy], preeclampsia/pc [Prevention], primipara, priority journal, proliferative diabetic retinopathy, prolonged pregnancy, protein urine level, proteinuria, restlessness/si [Side Effect], thrombocyte aggregation, thrombocytopenia, thrombotic thrombocytopenic purpura/di [Diagnosis], vaccination, acetylsalicylic acid/dt [Drug Therapy], albumin/ec [Endogenous Compound], antihypertensive agent/po [Oral Drug Administration], corticosteroid, creatinine/ec [Endogenous Compound], eculizumab/ae [Adverse Drug Reaction], eculizumab/dt [Drug Therapy], eculizumab/iv [Intravenous Drug Administration], furosemide/dt [Drug Therapy], haptoglobin/ec [Endogenous Compound], hemoglobin/ec [Endogenous Compound], insulin/dt [Drug Therapy], lactate dehydrogenase/ec [Endogenous Compound], magnesium sulfate, nifedipine/dt [Drug Therapy], nifedipine/po [Oral Drug Administration], penicillin derivative, placental growth factor/ec [Endogenous Compound], prednisone, protein/ec [Endogenous Compound], urea/ec [Endogenous Compound], vasculotropin receptor 1/ec [Endogenous Compound], CFI gene, hemolytic uremic syndrome/dt [Drug Therapy], adult, antibiotic prophylaxis, antihypertensive therapy, article, atrophy, blurred vision/si [Side Effect], cannabis use, case report, Caucasian, cesarean section, cigarette smoking, clinical article, creatinine urine level, diabetic nephropathy/di [Diagnosis], end stage renal disease, erythrocyte concentrate, Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/35380Test
Obstetrics and Gynecology
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مستخلص: BACKGROUND: Untreated microangiopathic hemolytic anemia in pregnancy is associated with adverse maternal and perinatal outcomes. Accurate diagnosis is challenging owing to nonspecific clinical features and pathologic findings. Timely initiation of appropriate management is essential to optimize maternal and perinatal outcomes. CASE: A 26-year-old primiparous woman presented at 20 weeks of gestation with new-onset microangiopathic hemolytic anemia on a background of poorly controlled type 1 diabetes. She received eculizumab for presumed atypical hemolytic uremic syndrome. At 24 weeks of gestation, she developed superimposed early-onset preeclampsia; she delivered at 27 weeks of gestation after continuing eculizumab. CONCLUSION(S): Eculizumab may prolong pregnancy in early-onset preeclampsia. Additional research is needed to assess short-term and long-term maternal and newborn outcomes.Copyright © 2019 by the American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.

مصطلحات الفهرس: erythrocyte transfusion, estimated glomerular filtration rate, female, fetal well being, fetus lung maturation, fibrin deposition, fibrosing alveolitis, gene, generalized edema/dt [Drug Therapy], generalized edema/si [Side Effect], gestational age, glycemic control, headache/si [Side Effect], hemoglobin blood level, hemolytic uremic syndrome/di [Diagnosis], heterozygote, histopathology, home oxygen therapy, human, human tissue, hyperreflexia/si [Side Effect], hypertension/dt [Drug Therapy], insulin dependent diabetes mellitus/dt [Drug Therapy], insulin treatment, kidney biopsy, kidney function, kidney tubule, lactate dehydrogenase blood level, lethargy, macroalbuminuria, maternal smoking, meningococcosis, missense mutation, onset age, peripheral edema, placenta insufficiency, platelet count, preeclampsia/dt [Drug Therapy], preeclampsia/pc [Prevention], primipara, priority journal, proliferative diabetic retinopathy, prolonged pregnancy, protein urine level, proteinuria, restlessness/si [Side Effect], thrombocyte aggregation, thrombocytopenia, thrombotic thrombocytopenic purpura/di [Diagnosis], vaccination, acetylsalicylic acid/dt [Drug Therapy], albumin/ec [Endogenous Compound], antihypertensive agent/po [Oral Drug Administration], corticosteroid, creatinine/ec [Endogenous Compound], eculizumab/ae [Adverse Drug Reaction], eculizumab/dt [Drug Therapy], eculizumab/iv [Intravenous Drug Administration], furosemide/dt [Drug Therapy], haptoglobin/ec [Endogenous Compound], hemoglobin/ec [Endogenous Compound], insulin/dt [Drug Therapy], lactate dehydrogenase/ec [Endogenous Compound], magnesium sulfate, nifedipine/dt [Drug Therapy], nifedipine/po [Oral Drug Administration], penicillin derivative, placental growth factor/ec [Endogenous Compound], prednisone, protein/ec [Endogenous Compound], urea/ec [Endogenous Compound], vasculotropin receptor 1/ec [Endogenous Compound], CFI gene, hemolytic uremic syndrome/dt [Drug Therapy], adult, antibiotic prophylaxis, antihypertensive therapy, article, atrophy, blurred vision/si [Side Effect], cannabis use, case report, Caucasian, cesarean section, cigarette smoking, clinical article, creatinine urine level, diabetic nephropathy/di [Diagnosis], end stage renal disease, erythrocyte concentrate, Article

URL: Obstetrics and Gynecology
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مستخلص: OBJECTIVE-The structural basis of normoalbuminuric renal insufficiency in patients with type 2 diabetes remains to be elucidated. We compared renal biopsy findings in patients with type 2 diabetes and estimated glomerular filtration rate (eGFR) and measured GFR of <60 mL/min/1.73 m2, associated with either normo-, micro-, or macroalbuminuria. RESEARCH DESIGN AND METHODS-In patients with normo- (n = 8) ormicroalbuminuria (n = 6), renal biopsies were performed according to a research protocol. In patients with macroalbuminuria (n = 17), biopsies were performed according to clinical indication. Findings were categorized according to the Fioretto classification: category 1 (C1), normal/near normal; category 2 (C2), typical diabetic nephropathy (DN)with predominantly glomerular changes; and category 3 (C3), atypical with disproportionately severe interstitial/tubular/vascular damage and with no/mild diabetic glomerular changes. RESULTS-In our study population (mean eGFR 35 mL/min/1.73 m2), typical glomerular changes (C2) of DN were observed in 22 of 23 subjects with micro- or macroalbuminuria compared with 3 of 8 subjects with normoalbuminuria (P = 0.002). By contrast, predominantly interstitial or vascular changes (C3) were seen in only 1 of 23 subjects with micro- or macroalbuminuria compared with 3 of 8 normoalbuminuric subjects (P = 0.08). Mesangial area increased progressively fromnormal controls to patients with type 2 diabetes and normo-, micro-, and macroalbuminuria. Varying degrees of arteriosclerosis, although not necessarily the predominant pattern, were seen in seven of eight subjects with normoalbuminuria. CONCLUSIONS-Typical renal structural changes of DN were observed in patients with type 2 diabetes and elevated albuminuria. By contrast, in normoalbuminuric renal insufficiency, these changes were seen less frequently, likely reflecting greater contributions from aging, hypertension, and arteriosclerosis. © 2013 by the American Diabetes Association.

مصطلحات الفهرس: diabetic nephropathy/et [Etiology], disease classification, disease course, female, glomerulonephritis/co [Complication], glomerulonephritis/di [Diagnosis], glomerulonephritis/et [Etiology], glomerulopathy/co [Complication], glomerulopathy/di [Diagnosis], glomerulopathy/et [Etiology], glomerulus filtration rate, hematuria, histopathology, human, hyaline degeneration/co [Complication], hyaline degeneration/di [Diagnosis], hyaline degeneration/et [Etiology], hypertension, immunoglobulin A nephropathy/co [Complication], immunoglobulin A nephropathy/di [Diagnosis], immunoglobulin A nephropathy/et [Etiology], kidney hypertrophy/et [Etiology], kidney structure, macroalbuminuria, male, microalbuminuria, nephrosclerosis/co [Complication], nephrosclerosis/di [Diagnosis], nephrosclerosis/et [Etiology], non insulin dependent diabetes mellitus, pathophysiology, sex difference, smoking, antinuclear antibody/ec [Endogenous Compound], glomerular basement membrane thickness/co [Complication], glomerular basement membrane thickness/di [Diagnosis], glomerular basement membrane thickness/et [Etiology], trend study, interstitial nephritis/co [Complication], interstitial nephritis/di [Diagnosis], interstitial nephritis/et [Etiology], kidney amyloidosis/co [Complication], kidney amyloidosis/di [Diagnosis], kidney amyloidosis/et [Etiology], kidney biopsy, kidney dysfunction/co [Complication], kidney dysfunction/di [Diagnosis], kidney dysfunction/et [Etiology], kidney failure/co [Complication], kidney failure/di [Diagnosis], kidney failure/et [Etiology], kidney hypertrophy/co [Complication], kidney hypertrophy/di [Diagnosis], aged, albuminuria, article, clinical article, cryoglobulinemia, diabetic nephropathy/co [Complication], diabetic nephropathy/di [Diagnosis], Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/27567Test
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مستخلص: Diabetic nephropathy is a significant cause of chronic kidney disease and end-stage renal failure globally. Much research has been conducted in both basic science and clinical therapeutics, which has enhanced understanding of the pathophysiology of diabetic nephropathy and expanded the potential therapies available. This review will examine the current concepts of diabetic nephropathy management in the context of some of the basic science and pathophysiology aspects relevant to the approaches taken in novel, investigative treatment strategies.Copyright © 2014 Lim.

مصطلحات الفهرس: diabetic nephropathy/di [Diagnosis], diabetic nephropathy/dt [Drug Therapy], diabetic nephropathy/ep [Epidemiology], diabetic nephropathy/et [Etiology], diabetic nephropathy/su [Surgery], diabetic nephropathy/th [Therapy], diet therapy, disease surveillance, drug effect, drug targeting, glycemic control, human, inflammation, intracellular signaling, kidney biopsy, kidney blood flow, kidney metabolism, kidney pancreas transplantation, lifestyle modification, medical history, molecular pathology, nonhuman, oxidative stress, risk factor, risk reduction, screening test, tea, treatment planning, aldose reductase inhibitor/dt [Drug Therapy], aldosterone antagonist/cb [Drug Combination], aldosterone antagonist/dt [Drug Therapy], aliskiren/dt [Drug Therapy], aminoguanidine/dt [Drug Therapy], angiotensin receptor antagonist/cb [Drug Combination], angiotensin receptor antagonist/dt [Drug Therapy], atrasentan/dt [Drug Therapy], avosentan/dt [Drug Therapy], bardoxolone/dt [Drug Therapy], neutrophil gelatinase associated lipocalin/ec [Endogenous Compound], palosuran/dt [Drug Therapy], phosphodiesterase inhibitor/dt [Drug Therapy], pirfenidone/dt [Drug Therapy], pyridoxamine/dt [Drug Therapy], renin inhibitor/cb [Drug Combination], renin inhibitor/dt [Drug Therapy], sulodexide/dt [Drug Therapy], transforming growth factor beta1/ec [Endogenous Compound], unclassified drug, unindexed drug, vitamin D/dt [Drug Therapy], zinc, protein L FABP/ec [Endogenous Compound], vasculotropin/ec [Endogenous Compound], biological marker/ec [Endogenous Compound], calcium channel blocking agent/cb [Drug Combination], calcium channel blocking agent/dt [Drug Therapy], connective tissue growth factor/ec [Endogenous Compound], cystatin C/ec [Endogenous Compound], cytokine/ec [Endogenous Compound], dipeptidyl carboxypeptidase inhibitor/cb [Drug Combination], dipeptidyl carboxypeptidase inhibitor/dt [Drug Therapy], fish oil, hydroxymethylglutaryl coenzyme A reductase inhibitor/dt [Drug Therapy], kidney injury molecule 1/ec [Endogenous Compound], alternative medicine, article, Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/41642Test
International Journal of Nephrology and Renovascular Disease
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مستخلص: OBJECTIVE-The structural basis of normoalbuminuric renal insufficiency in patients with type 2 diabetes remains to be elucidated. We compared renal biopsy findings in patients with type 2 diabetes and estimated glomerular filtration rate (eGFR) and measured GFR of <60 mL/min/1.73 m2, associated with either normo-, micro-, or macroalbuminuria. RESEARCH DESIGN AND METHODS-In patients with normo- (n = 8) ormicroalbuminuria (n = 6), renal biopsies were performed according to a research protocol. In patients with macroalbuminuria (n = 17), biopsies were performed according to clinical indication. Findings were categorized according to the Fioretto classification: category 1 (C1), normal/near normal; category 2 (C2), typical diabetic nephropathy (DN)with predominantly glomerular changes; and category 3 (C3), atypical with disproportionately severe interstitial/tubular/vascular damage and with no/mild diabetic glomerular changes. RESULTS-In our study population (mean eGFR 35 mL/min/1.73 m2), typical glomerular changes (C2) of DN were observed in 22 of 23 subjects with micro- or macroalbuminuria compared with 3 of 8 subjects with normoalbuminuria (P = 0.002). By contrast, predominantly interstitial or vascular changes (C3) were seen in only 1 of 23 subjects with micro- or macroalbuminuria compared with 3 of 8 normoalbuminuric subjects (P = 0.08). Mesangial area increased progressively fromnormal controls to patients with type 2 diabetes and normo-, micro-, and macroalbuminuria. Varying degrees of arteriosclerosis, although not necessarily the predominant pattern, were seen in seven of eight subjects with normoalbuminuria. CONCLUSIONS-Typical renal structural changes of DN were observed in patients with type 2 diabetes and elevated albuminuria. By contrast, in normoalbuminuric renal insufficiency, these changes were seen less frequently, likely reflecting greater contributions from aging, hypertension, and arteriosclerosis. © 2013 by the American Diabetes Association.

مصطلحات الفهرس: diabetic nephropathy/et [Etiology], disease classification, disease course, female, glomerulonephritis/co [Complication], glomerulonephritis/di [Diagnosis], glomerulonephritis/et [Etiology], glomerulopathy/co [Complication], glomerulopathy/di [Diagnosis], glomerulopathy/et [Etiology], glomerulus filtration rate, hematuria, histopathology, human, hyaline degeneration/co [Complication], hyaline degeneration/di [Diagnosis], hyaline degeneration/et [Etiology], hypertension, immunoglobulin A nephropathy/co [Complication], immunoglobulin A nephropathy/di [Diagnosis], immunoglobulin A nephropathy/et [Etiology], kidney hypertrophy/et [Etiology], kidney structure, macroalbuminuria, male, microalbuminuria, nephrosclerosis/co [Complication], nephrosclerosis/di [Diagnosis], nephrosclerosis/et [Etiology], non insulin dependent diabetes mellitus, pathophysiology, sex difference, smoking, antinuclear antibody/ec [Endogenous Compound], glomerular basement membrane thickness/co [Complication], glomerular basement membrane thickness/di [Diagnosis], glomerular basement membrane thickness/et [Etiology], trend study, interstitial nephritis/co [Complication], interstitial nephritis/di [Diagnosis], interstitial nephritis/et [Etiology], kidney amyloidosis/co [Complication], kidney amyloidosis/di [Diagnosis], kidney amyloidosis/et [Etiology], kidney biopsy, kidney dysfunction/co [Complication], kidney dysfunction/di [Diagnosis], kidney dysfunction/et [Etiology], kidney failure/co [Complication], kidney failure/di [Diagnosis], kidney failure/et [Etiology], kidney hypertrophy/co [Complication], kidney hypertrophy/di [Diagnosis], aged, albuminuria, article, clinical article, cryoglobulinemia, diabetic nephropathy/co [Complication], diabetic nephropathy/di [Diagnosis], Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/27567Test
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LibKey Link

مستخلص: Diabetic nephropathy is a significant cause of chronic kidney disease and end-stage renal failure globally. Much research has been conducted in both basic science and clinical therapeutics, which has enhanced understanding of the pathophysiology of diabetic nephropathy and expanded the potential therapies available. This review will examine the current concepts of diabetic nephropathy management in the context of some of the basic science and pathophysiology aspects relevant to the approaches taken in novel, investigative treatment strategies.Copyright © 2014 Lim.

مصطلحات الفهرس: diabetic nephropathy/di [Diagnosis], diabetic nephropathy/dt [Drug Therapy], diabetic nephropathy/ep [Epidemiology], diabetic nephropathy/et [Etiology], diabetic nephropathy/su [Surgery], diabetic nephropathy/th [Therapy], diet therapy, disease surveillance, drug effect, drug targeting, glycemic control, human, inflammation, intracellular signaling, kidney biopsy, kidney blood flow, kidney metabolism, kidney pancreas transplantation, lifestyle modification, medical history, molecular pathology, nonhuman, oxidative stress, risk factor, risk reduction, screening test, tea, treatment planning, aldose reductase inhibitor/dt [Drug Therapy], aldosterone antagonist/cb [Drug Combination], aldosterone antagonist/dt [Drug Therapy], aliskiren/dt [Drug Therapy], aminoguanidine/dt [Drug Therapy], angiotensin receptor antagonist/cb [Drug Combination], angiotensin receptor antagonist/dt [Drug Therapy], atrasentan/dt [Drug Therapy], avosentan/dt [Drug Therapy], bardoxolone/dt [Drug Therapy], neutrophil gelatinase associated lipocalin/ec [Endogenous Compound], palosuran/dt [Drug Therapy], phosphodiesterase inhibitor/dt [Drug Therapy], pirfenidone/dt [Drug Therapy], pyridoxamine/dt [Drug Therapy], renin inhibitor/cb [Drug Combination], renin inhibitor/dt [Drug Therapy], sulodexide/dt [Drug Therapy], transforming growth factor beta1/ec [Endogenous Compound], unclassified drug, unindexed drug, vitamin D/dt [Drug Therapy], zinc, protein L FABP/ec [Endogenous Compound], vasculotropin/ec [Endogenous Compound], biological marker/ec [Endogenous Compound], calcium channel blocking agent/cb [Drug Combination], calcium channel blocking agent/dt [Drug Therapy], connective tissue growth factor/ec [Endogenous Compound], cystatin C/ec [Endogenous Compound], cytokine/ec [Endogenous Compound], dipeptidyl carboxypeptidase inhibitor/cb [Drug Combination], dipeptidyl carboxypeptidase inhibitor/dt [Drug Therapy], fish oil, hydroxymethylglutaryl coenzyme A reductase inhibitor/dt [Drug Therapy], kidney injury molecule 1/ec [Endogenous Compound], alternative medicine, article, Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/41642Test
International Journal of Nephrology and Renovascular Disease
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مستخلص: Background: Diabetic nephropathy is a major global health problem. Progression to renal failure is common; however, the mechanisms are unknown. Experimental models suggest a role for macrophages. Therefore, macrophage accumulation and its relationship to the subsequent clinical course were studied. Method(s): A retrospective study of baseline histology and the subsequent clinical course over at least 5 years involving 20 consecutive patients with a histological and clinical diagnosis of diabetic nephropathy was performed. The relationship between macrophage accumulation in renal biopsy tissue (KP-1/anti-CD68+ cells), baseline measures of known predictors of progression (proteinuria, tubulointerstitial damage, myofibroblast accumulation) and progression over 5 years (plot of reciprocal of serum creatinine) was quantified. Result(s): Accumulation of macrophages was apparent in the glomeruli (2.8 + 0.7/gcs vs 1.0 + 0.2 for normals, P = not significant) and interstitium (296.9 + 63.3/mm2vs 19.0 + 1.3/mm2 for normals, P = 0.002) of patients with diabetic nephropathy. Glomerular macrophage number correlated with baseline serum creatinine (r = 0.548, P = 0.012) but not with progression of renal failure as glomerular macrophages were prevalent in early, but not advanced diabetic nephropathy. Interstitial macrophage accumulation correlated strongly with serum creatinine (r = 0.649, P = 0.002), proteinuria (r = 0.779, P < 0.0001), interstitial fibrosis (r = 0.774, P < 0.0001) and inversely with the slope of 1/serum creatinine (r = -0.531, P = 0.023). Conclusion(s): Macrophages accumulate within glomeruli and the interstitium in diabetic nephropathy and the intensity of the interstitial infiltrate is proportional to the rate of subsequent decline in renal function. These human data support animal studies that suggest a pathogenic role for the macrophage in diabetic nephropathy. © 2006 Asian Pacific Society of Nephrology.

مصطلحات الفهرس: kidney biopsy, kidney failure, kidney tubule damage, macrophage, male, myofibroblast, prevalence, priority journal, proteinuria, retrospective study, human, human tissue, interstitium, article, clinical article, creatinine blood level, diabetic nephropathy/di [Diagnosis], disease course, female, fibrosing alveolitis, glomerulus, histology, statistical significance, creatinine/ec [Endogenous Compound], adult, aged, Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/32066Test
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مستخلص: Background: Diabetic nephropathy is a major global health problem. Progression to renal failure is common; however, the mechanisms are unknown. Experimental models suggest a role for macrophages. Therefore, macrophage accumulation and its relationship to the subsequent clinical course were studied. Method(s): A retrospective study of baseline histology and the subsequent clinical course over at least 5 years involving 20 consecutive patients with a histological and clinical diagnosis of diabetic nephropathy was performed. The relationship between macrophage accumulation in renal biopsy tissue (KP-1/anti-CD68+ cells), baseline measures of known predictors of progression (proteinuria, tubulointerstitial damage, myofibroblast accumulation) and progression over 5 years (plot of reciprocal of serum creatinine) was quantified. Result(s): Accumulation of macrophages was apparent in the glomeruli (2.8 + 0.7/gcs vs 1.0 + 0.2 for normals, P = not significant) and interstitium (296.9 + 63.3/mm2vs 19.0 + 1.3/mm2 for normals, P = 0.002) of patients with diabetic nephropathy. Glomerular macrophage number correlated with baseline serum creatinine (r = 0.548, P = 0.012) but not with progression of renal failure as glomerular macrophages were prevalent in early, but not advanced diabetic nephropathy. Interstitial macrophage accumulation correlated strongly with serum creatinine (r = 0.649, P = 0.002), proteinuria (r = 0.779, P < 0.0001), interstitial fibrosis (r = 0.774, P < 0.0001) and inversely with the slope of 1/serum creatinine (r = -0.531, P = 0.023). Conclusion(s): Macrophages accumulate within glomeruli and the interstitium in diabetic nephropathy and the intensity of the interstitial infiltrate is proportional to the rate of subsequent decline in renal function. These human data support animal studies that suggest a pathogenic role for the macrophage in diabetic nephropathy. © 2006 Asian Pacific Society of Nephrology.

مصطلحات الفهرس: kidney biopsy, kidney failure, kidney tubule damage, macrophage, male, myofibroblast, prevalence, priority journal, proteinuria, retrospective study, human, human tissue, interstitium, article, clinical article, creatinine blood level, diabetic nephropathy/di [Diagnosis], disease course, female, fibrosing alveolitis, glomerulus, histology, statistical significance, creatinine/ec [Endogenous Compound], adult, aged, Article

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/32066Test
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مستخلص: Despite current therapies, many diabetic patients will suffer from declining renal function in association with progressive kidney inflammation. Recently, animal model studies have demonstrated that kidney macrophage accumulation is a critical factor in the development of diabetic nephropathy. However, specific anti-inflammatory strategies are not yet being considered for the treatment of patients with diabetic renal injury. This review highlights the chemokine monocyte chemoattractant protein-1 (MCP-1)/CC-chemokine ligand 2 as a major promoter of inflammation, renal injury, and fibrosis in diabetic nephropathy. Researchers have found that diabetes induces kidney MCP-1 production and that urine MCP-1 levels can be used to assess renal inflammation in this disease. In addition, genetic deletion and molecular blocking studies in rodents have identified MCP-1 as an important therapeutic target for treating diabetic nephropathy. Evidence also suggests that a polymorphism in the human MCP-1 gene is associated with progressive kidney failure in type 2 diabetes, which may identify patients at higher risk who need additional therapy. These findings provide a strong rationale for developing specific therapies against MCP-1 and inflammation in diabetic nephropathy. Copyright © 2008 the American Physiological Society.

مصطلحات الفهرس: nonhuman, nephritis, non insulin dependent diabetes mellitus, pathogenesis, monocyte chemotactic protein 1/ec [Endogenous Compound], biological marker/ec [Endogenous Compound], review, priority journal, diabetic nephropathy/di [Diagnosis], diabetic nephropathy/et [Etiology], diagnostic value, gene deletion, genetic polymorphism, human, kidney injury/di [Diagnosis], kidney injury/et [Etiology], Review

URL: Click here for full text options
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مستخلص: Despite current therapies, many diabetic patients will suffer from declining renal function in association with progressive kidney inflammation. Recently, animal model studies have demonstrated that kidney macrophage accumulation is a critical factor in the development of diabetic nephropathy. However, specific anti-inflammatory strategies are not yet being considered for the treatment of patients with diabetic renal injury. This review highlights the chemokine monocyte chemoattractant protein-1 (MCP-1)/CC-chemokine ligand 2 as a major promoter of inflammation, renal injury, and fibrosis in diabetic nephropathy. Researchers have found that diabetes induces kidney MCP-1 production and that urine MCP-1 levels can be used to assess renal inflammation in this disease. In addition, genetic deletion and molecular blocking studies in rodents have identified MCP-1 as an important therapeutic target for treating diabetic nephropathy. Evidence also suggests that a polymorphism in the human MCP-1 gene is associated with progressive kidney failure in type 2 diabetes, which may identify patients at higher risk who need additional therapy. These findings provide a strong rationale for developing specific therapies against MCP-1 and inflammation in diabetic nephropathy. Copyright © 2008 the American Physiological Society.

مصطلحات الفهرس: nonhuman, nephritis, non insulin dependent diabetes mellitus, pathogenesis, monocyte chemotactic protein 1/ec [Endogenous Compound], biological marker/ec [Endogenous Compound], review, priority journal, diabetic nephropathy/di [Diagnosis], diabetic nephropathy/et [Etiology], diagnostic value, gene deletion, genetic polymorphism, human, kidney injury/di [Diagnosis], kidney injury/et [Etiology], Review

URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/31429Test
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