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Kidney Diseases (kidney + diseases)
Selected AbstractsPost-transplantation growth among pediatric recipients of liver transplantationPEDIATRIC TRANSPLANTATION, Issue 4 2005Idris V.R. Evans Abstract:, Improving a patient's quality-of-life (QOL) post-liver transplantation is of great importance. An aspect of improved QOL is the restoration of normal growth patterns in pediatric patients. To describe the post-transplantation growth patterns of 72 children included in the National Institute of Diabetes and Digestive and Kidney Diseases , Liver Transplantation Database (NIDDK-LTD), multilevel models were used, according to which children who waited more than a year for transplantation were smaller, compared with age and sex matched peers, at transplantation than children who waited less than a year while children who were growth retarded at transplantation experienced a larger yearly comparison height increase than children who were not growth retarded. The analysis also showed that boys older than 2 yr and younger than 13 yr at transplantation and girls older than 2 yr and younger than 11 yr at transplantation were significantly less growth retarded at transplantation than boys and girls under the age of 2 yr at transplantation. [source] The burden of kidney disease in Indigenous children of Australia and New Zealand, epidemiology, antecedent factors and progression to chronic kidney diseaseJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 9 2010Andrew White Aims: To review and present the most important issues related to kidney disease in Aboriginal, Torres Strait Islander, Maori and Pacific Islander children from Australia and New Zealand. Methods: A review of medical literature about: 1. incidence of kidney disease in Indigenous children in Australia and New Zealand, especially where rates are different from the general populations, 2. factors in early life which increase risk for chronic kidney disease in adult life, and 3. early identification and primary and secondary interventions in childhood which may prevent chronic kidney disease in adults. Results: Kidney diseases, both acute and chronic are more common in Maori, Pacific Islander, Australian Aboriginal and Torres Strait Islander people. The reasons are multiple and include genetic, environmental and socio-economic factors. In childhood post streptococcal glomerulonephritis, haemolytic uraemic syndrome, renal stones and acute kidney injury all occur at higher frequency in at least some of the Indigenous populations. Chronic kidney disease CKD occurs more commonly, and at a younger age in Indigenous than non Indigenous people. Factors involved may include reduced nephron endowment at birth, and subsequent insults including nephritis, obesity, and early onset type 2 diabetes, as well as underlying socioeconomic and environmental determinants. Conclusion: A lifecourse understanding allows one to conceptualise multiple risk factors and target interventions. [source] QTc-interval abnormalities in a forensic populationCRIMINAL BEHAVIOUR AND MENTAL HEALTH, Issue 2 2007Sobhi Girgis Background,Antipsychotic drugs have been linked to sudden death among psychiatric patients, with a suggestion that prolongation of the QT-interval detectable on a standard electrocardiogram may be linked to fatal cardiac arrhythmias in these circumstances. Patients in secure forensic psychiatric facilities may be particularly likely to be on high-dose antipsychotic medication, and yet, as far as the authors are aware, no study of QT-intervals among such patients has been reported. Aim,To investigate the prevalence of QT-interval abnormalities and associated known risk factors for fatal cardiac arrhythmias in a sample of forensic patients. Method,Participants had a 12-lead electrocardiogram taken at 50 mm/s. Information was collected on their age, gender, psychiatric diagnosis, history of cardiovascular, liver and kidney diseases, and smoking, on all medications and on history of seclusion over the previous 12 months. Analysis was carried out using binary logistic regression. Results,Lower rates of QT-interval abnormalities than might be expected for this population were found. It was also found that a high dose of antipsychotics was associated with QTc prolongation (Adjusted OR = 9.5, 95% CI 2.6,34.2), a result consistent with previous literature. Conclusion,Forensic patients need not be at increased risk of QTc abnormality provided risk factors are properly managed. A high dose of antipsychotic medication increases the risk of QTc prolongation. Copyright © 2007 John Wiley & Sons, Ltd. [source] From kidney to cardiovascular diseases: NGAL as a biomarker beyond the confines of nephrologyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2010D. Bolignano Eur J Clin Invest 2010; 40 (3): 273,276 Abstract Neutrophil gelatinase-associated lipocalin (NGAL), a small 25 kDa stress-protein released from injured tubular cells after various damaging stimuli, is already known by nephrologists as one of the most promising biomarkers of incoming Acute Kidney Injury. Moreover, recent studies seem to suggest a potential involvement of this factor also in the genesis and progression of chronic kidney diseases. This brief review explores the new interesting involvement of NGAL in the experimental and clinical field of cardiovascular diseases, such as the pathogenesis and clinical manifestations of atherosclerosis, acute myocardial infarction and heart failure. It does not seem difficult that, in the next future, NGAL may become a new missing link between the kidney and the cardiovascular system. [source] Obesity,hypertension: an ongoing pandemicINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2 2007E. A. Francischetti Summary Considerable evidence has suggested that excessive weight gain is the most common cause of arterial hypertension. This association has been observed in several populations, in different regions of the world. Obesity,hypertension, a term that underscores the link between these two deleterious conditions, is an important public health challenge, because of its high frequency and concomitant risk of cardiovascular and kidney diseases. The obesity,hypertension pandemic imposes a considerable economic burden on societies, directly reflecting on healthcare system costs. Increased renal sodium reabsorption and blood volume expansion are central features in the development of obesity,hypertension. Overweight is also associated with increased sympathetic activity. Leptin, a protein expressed in and secreted by adipocytes, is the main factor linking obesity, increased sympathetic nervous system activity and hypertension. The renin,angiotensin,aldosterone system has also been causally implicated in obesity,hypertension, because angiotensinogen is expressed in and secreted by adipose tissue. Hypoadiponectinemia, high circulating levels of free fatty acids and increased vascular production of endothelin-1 (ET-1) have been reported as potential mechanisms for obesity,hypertension. Lifestyle changes are effective in obesity,hypertension control, though pharmacological treatment is frequently necessary. Despite the consistency of the mechanistic approach in explaining the causal relation between hypertension and obesity, there is yet no evidence that one class of drug is superior to the others in controlling obesity,hypertension. In this review, we present the current knowledge and research in obesity,hypertension, exploring the epidemiologic evidence of the association, its probable pathophysiological mechanisms and treatment issues. [source] C3 and C4 hypocomplementemia and associated diseases in ArabiansINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 3 2005Emad A. KOSHAK Abstract Background:, Hypocomplementemia, which is a state of decrease in the complement (C) proteins in the serum, is frequently encountered in a wide range of diseases. Objective:, To explore the diversity of C3 and C4 hypocomplementemia and associated diseases in patients seen at King Abdulaziz University Hospital (KAUH), Jeddah, Kingdom of Saudi Arabia. Methods:, Serum samples send to the clinical immunology laboratory with requests for the measurements of C3 and C4 tests by nephelometry were studied. Files of patients with C3 and/or C4 hypocomplementemia were reviewed for demographic and diagnostic data. Results:, Out of 270 complement tests, C3 and/or C4 hypocomplementemia was found in 196 different tests (72.6%), and only 175 tests were studied. Their ages ranged between 1 week and 81 years (mean 26 ± 17 SD), and female sex was predominant in 143 tests (81.3%). Hypocomplementemia was detected as follows: C3 in 64 tests (23.7%) with sole C3 in 3 tests only (1.5%); C4 in 193 samples (71.5%) with sole C4 in 132 tests (67.3%); and combined C3 with C4 hypocomplementemia in 61 tests (22.6%). Cross-tabulation revealed that 95% of C3 hypocomplementemia were significantly associated with C4 hypocomplementemia (P < 0.001). Conversely, only 31% of C4 hypocomplementemia were significantly associated with C3 hypocomplementemia (P < 0.001). SLE was the predominant disease associated with hypocomplementemia in 104 tests (53.1%), followed by kidney diseases in 20 tests (10.2%) and chronic liver disease in eight tests (4.1%). Conclusion:, C4 hypocomplementemia was a common laboratory verdict in patients at KAUH. Of interest, most of C3 hypocomplementemia tests were associated with C4 hypocomplementemia and lone C3 hypocomplementemia is rare. The diagnosis of systemic lupus erythematosus was the predominant disease associated with hypocomplementemia. Supplementary awareness of immunopathological mechanisms leading to involvement of complement proteins in many diseases is essential to enhance its clinical utility. [source] HYPERTENSION MANAGEMENT: LIFESTYLE INTERVENTIONS IN A TRANSCULTURAL CONTEXTJOURNAL OF RENAL CARE, Issue 4 2009Tai Mooi Ho SUMMARY Hypertension is a risk factor for cardiovascular and kidney diseases. According to estimation, the prevalence of hypertension will increase unless extensive and effective preventive measures are implemented. The diversity of languages and cultures of the hypertensive patients requiring adequate blood pressure control make communications difficult in many instances. Nursing intervention for patients to adopt a healthy lifestyle requires effective communication. But the communication problems encountered in a culturally diverse context can result in undesirable outcomes for the patients and the health-care team. This paper describes the production of a document to assist staff address the difficulty in intercultural communication, which could be used anywhere in the world. This document can facilitate nursing intervention to achieve optimal hypertension management in a transcultural context, responding to the challenge regarding preventive measures to halt increase in hypertension prevalence. [source] Statins and progressive renal diseaseMEDICINAL RESEARCH REVIEWS, Issue 1 2002Michele Buemi Abstract Thanks to the administration of hypocholesterolemic drugs, important advances have been made in the treatment of patients with progressive renal disease. In vitro and in vivo findings demonstrate that statins, the inhibitors of HMG-CoA reductase, can provide protection against kidney diseases characterized by inflammation and/or enhanced proliferation of epithelial cells occurring in rapidly progressive glomerulonephritis, or by increased proliferation of mesangial cells occurring in IgA nephropathy. Many of the beneficial effects obtained occur independent of reduced cholesterol levels because statins can directly inhibit the proliferation of different cell types (e.g., mesangial, renal tubular, and vascular smooth muscle cells), and can also modulate the inflammatory response, thus inhibiting macrophage recruitment and activation, as well as fibrosis. The mechanisms underlying the action of statins are not yet well understood, although recent data in the literature indicate that they can directly affect the proliferation/apoptosis balance, the down-regulation of inflammatory chemokines, and the cytogenic messages mediated by the GTPases Ras superfamily. Therefore, as well as reducing serum lipids, statins and other lipid-lowering agents may directly influence intracellular signaling pathways involved in the prenylation of low molecular weight proteins that play a crucial role in cell signal transduction and cell activation. Statins appear to have important potential in the treatment of progressive renal disease, although further studies are required to confirm this in humans. © 2001 John Wiley & Sons, Inc. Med Res Rev, 22, No. 1, 76,84, 2002 [source] Anti-glycative and anti-inflammatory effects of caffeic acid and ellagic acid in kidney of diabetic miceMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 3 2010Che-yi Chao Abstract Protective effects of caffeic acid (CA) and ellagic acid (EA) in kidney of diabetic mice were examined. CA or EA at 2.5 and 5% was mixed in diet and supplied to diabetic mice for 12,wk. Results showed that the intake of CA or EA increased renal content of these compounds, alleviated body weight loss, decreased urine output, increased plasma insulin and decreased blood glucose levels at weeks 6 and 12 (p<0.05). The intake of these compounds dose dependently reduced plasma blood urea nitrogen and elevated creatinine clearance (p<0.05). CA or EA at 5% significantly decreased the levels of plasma HbA1c, urinary glycated albumin, renal carboxymethyllysine, pentosidine, sorbitol and fructose (p<0.05), and significantly diminished renal activity of aldose reductase and sorbitol dehydrogenase, as well as suppressed renal aldose reductase mRNA expression (p<0.05). CA or EA dose dependently lowered renal levels of IL-6, IL-1,, tumor necrosis factor (TNF)-, and monocyte chemoattractant protein 1 (MCP-1) (p<0.05). Furthermore, CA or EA dose dependently down-regulated tumor necrosis factor-, and monocyte chemoattractant protein-1 mRNA expression in kidney (p<0.05). Based on the observed anti-glycative and anti-inflammatory effects, the supplement of CA or EA might be helpful for the prevention or attenuation of diabetic kidney diseases. [source] Review: The role of microRNAs in kidney diseaseNEPHROLOGY, Issue 6 2010JORDAN YZ LI ABSTRACT MicroRNAs (miRNAs) are short non-coding RNAs that modulate physiological and pathological processes by inhibiting target gene expression via blockade of protein translation or by inducing mRNA degradation. These miRNAs potentially regulate the expression of thousands of proteins. As a result, miRNAs have emerged rapidly as a major new area of biomedical research with relevance to kidney disease. MiRNA expression has been shown to differ between the kidney and other organs as well as between different kidney regions. Furthermore, miRNAs have been found to be functionally important in models of podocyte development, diabetic nephropathy and polycystic kidney disease. Of particular interest, podocyte-specific deletion of Dicer, a key enzyme in the biogenesis of miRNA, results in proteinuria and severe renal impairment in mice. One miRNA (miR-192) can also act as an effector of transforming growth factor-, activity in the high-glucose environment of diabetic nephropathy. Differential expression of miRNAs has been reported in kidney allograft rejection. It is anticipated that future studies involving miRNAs will generate new insights into the complex pathophysiology underlying various kidney diseases, generate diagnostic biomarkers and might be of value as therapeutic targets for progressive kidney diseases. The purpose of this review is to highlight key miRNA developments in kidney diseases and how this might influence the diagnosis and management of patients with kidney disease in the future. [source] Urinary proteins from patients with nephrotic syndrome alters the signalling proteins regulating epithelial,mesenchymal transitionNEPHROLOGY, Issue 1 2010QIONG WEN ABSTRACT: Aim: Proteinuria plays an important role in the progression of tubulointerstitial fibrosis, but the mechanism for the differential renal damage induced by proteinuria is unknown. This study examined the effects of urinary proteins from patients with idiopathic minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) on several epithelial,mesenchymal transition (EMT)-related marker proteins in cultured proximal tubular HK-2 cells. Methods: Urinary proteins from MCD and FSGS patients were extracted by ultrafiltration and incubated with HK-2 cells; the expression of the cytokeratin-18, ,-smooth muscle actin (,-SMA) and vimentin were assessed. p38 and extracellular regulated kinase (ERK) activation were measured by western blotting, and SB203580 (a p38 inhibitor) and PD98059 (an ERK1/2 inhibitor) were used to inhibit their activation. Results: It was observed that urinary proteins from FSGS patients more significantly induced the expression of ,-SMA and vimentin and reduced cytokeratin-18 expression than those from MCD patients in HK-2 cells. Both ERK1/2 and p38 were activated by urinary proteins from MCD or FSGS patients. Pretreatment of the cells with SB203580 or PD98059 abolished the effect of urinary proteins from FSGS patients on the expression of ,-SMA, vimentin and cytokeratin-18, while only SB203580 elicited this effect when cells were treated with urinary proteins from MCD patients. Conclusion: The urinary proteins from MCD and FSGS patients induced significant changes of EMT-related proteins through activation of distinct mitogen-activated protein kinase-related signalling pathways. Quality of proteinuria may play an important role in determining the severity and progression of tubular injury associated with different kidney diseases. [source] Prevalence of hypouricaemia and SLC22A12 mutations in healthy Korean subjectsNEPHROLOGY, Issue 8 2008JOO HOON LEE SUMMARY: Aim: Mutations in the SLC22A12 gene, which encodes a uric acid transporter, URAT1, are associated with renal hypouricaemia. This study was designed to measure serum uric acid (Sua) levels and allele frequencies of two common mutations in SLC22A12, W258X and R90H, in healthy Korean subjects. Methods: A total of 909 unrelated Korean adults (male : female, 1:1.23; mean age, 48.4 ± 11.0 years) were recruited among those who had taken a routine health check-up in a health centre in 2003. None of them had hypertension, diabetes mellitus, kidney diseases or liver diseases. Genotyping for W258X and R90H was performed using the TaqMan method. Results: The prevalences of hyperuricaemia (Sua levels, >416 µmol/L) and hypouricaemia (Sua levels, <178 µmol/L) were 4.6% and 3.3%, respectively. A marked male preponderance in the hyperuricaemic group was noted, and the men revealed higher Sua than the women. The Sua showed a positive correlation with serum creatinine level and blood pressure. In the hypouricaemic group, the allele frequencies of W258X and R90H were 11.7% and 6.7%, respectively, and the proportion of subjects with one or both of the mutant alleles was 33.3%. Hyperuricaemic subjects never had either mutation. Conclusion: The W258X and/or R90H mutations in the SLC22A12 gene are one of the major factors responsible for hypouricaemia, and one-third of the hypouricaemic subjects had one or both of the mutant alleles. [source] Effects of interleukin 18 on injury and activation of human proximal tubular epithelial cellsNEPHROLOGY, Issue 1 2007DONG LIANG SUMMARY: Background/Aims: Injury and activation of tubular proximal epithelial cells (TEC) play central roles in renal tubulointerstitial fibrosis (TIF), but its mechanisms remain obscure. Interleukin 18 (IL-18) is overproduced during chronic kidney diseases (CKD), but how IL-18 affects the biological behaviour of TEC is not clear. The aim of the present study is to reveal the role of IL-18 in renal TIF. Methods: The expressions of IL-18 and IL-18 receptor in TEC were detected by immunohistochemical staining in vivo and by reverse transcriptase polymerase chain reaction (RT-PCR) in vitro. TEC line (HK-2 cells) were incubated without or with IL-18. Cell proliferation and cell cycle were evaluated by methyl thiazolyl tetrazolium assay and flow cytometric analysis, respectively. Cell apoptosis was assessed by Hoechst 33258 staining. Expression of ,-smooth muscle actin was evaluated by RT-PCR, immunocytochemical staining and flow cytometric analysis, respectively. Type I collagen, fibronectin, MCP-1 and RANTES in cultured supernatants were measured by enzyme-linked immunosorbent assay. Results: IL-18 expression in TEC increased significantly in CKD state. IL-18 receptor was constitutively expressed in normal proximal TEC, and its expression increased strongly in CKD state. Proliferation and cell cycle of HK-2 cells were not affected by IL-18. Cell apoptosis, ,-smooth muscle actin expression, type I collagen and fibronectin production as well as MCP-1 secretion were promoted by IL-18 in dosage- and/or time-dependent manners, but RANTES secretion was not affected. Conclusion: IL-18 may play a crucial role in the process of TIF by promoting TEC injury and activation, and could be a target of the therapeutic approaches against TIF. [source] Transforming growth factor-, and Smad signalling in kidney diseasesNEPHROLOGY, Issue 1 2005Review Article SUMMARY: Extensive studies have demonstrated that transforming growth factor-beta (TGF-,) plays an important role in the progression of renal diseases. TGF-, exerts its biological functions mainly through its downstream signalling molecules, Smad2 and Smad3. It is now clear that Smad3 is critical for TGF-,'s pro-fibrotic effect, whereas the functions of Smad2 in fibrosis in response to TGF-, still need to be determined. Our recent studies have demonstrated that Smad signalling is also a critical pathway for renal fibrosis induced by other pro-fibrotic factors, such as angiotensin II and advanced glycation end products (AGE). These pro-fibrotic factors can activate Smads directly and independently of TGF-,. They can also cause renal fibrosis via the ERK/p38 MAP kinase,Smad signalling cross-talk pathway. In contrast, blockade of Smad2/3 activation by overexpression of an inhibitory Smad7 prevents collagen matrix production induced by TGF-,, angiotensin II, high glucose and AGE and attenuates renal fibrosis in various animal models including rat obstructive kidney, remnant kidney and diabetic kidney diseases. Results from these studies indicate that Smad signalling is a key and final common pathway of renal fibrosis. In addition, TGF-, has anti-inflammatory and immune-regulatory properties. Our most recent studies demonstrated that TGF-, transgenic mice are protected against renal inflammation in mouse obstructive and diabetic models. Upregulation of renal Smad7, thereby blocking NF.,B activation via induction of I,B,, is a central mechanism by which TGF-, inhibits renal inflammation. In conclusion, TGF-, signals through Smad2/3 to mediate renal fibrosis, whereas induction of Smad7 inhibits renal fibrosis and inflammation. Thus, targeting Smad signalling by overexpression of Smad7 may have great therapeutic potential for kidney diseases. [source] Cystic kidney diseases and planar cell polarity signalingCLINICAL GENETICS, Issue 2 2009RL Bacallao Renal cystic diseases are a major clinical concern as they are the most common genetic cause of end-stage renal disease. While many of the genes causing cystic disease have been identified in recent years, knowing the molecular nature of the mutations has not clarified the mechanisms underlying cyst formation. Recent research in model organisms has suggested that cyst formation may be because of defective planar cell polarity (PCP) and/or ciliary defects. In this review, we first outline the clinical features of renal cystic diseases and then discuss current research linking our understanding of cystic kidney disease to PCP and cilia. [source] | |||||||||||||