Renal disease

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Oral Mucosal Symptoms, Signs and Lesions in the End Stage Renal Disease and Non-End Stage Renal Disease in Diabetes Mellitus Patient

Oral Mucosal Symptoms, Signs and Lesions in the End Stage Renal Disease and Non-End Stage Renal Disease in Diabetes Mellitus Patient

The present study is a Comparative study which was conducted in the Department of Oral Medicine and Radiology of Ragas Dental College and Hospital, Uthandi, Chennai and Voluntary Health Services, Adyar, Chennai. It was devised to compare the oral signs, symptoms and oral lesions type and prevalence in Diabetic patients with End Stage Renal Disease (ESRD-DM) and with Non-End Stage Renal Disease (NESRD-DM) group. The study was conducted between June 2010-March 2011 on a total of 200 diabetic patients, who are diagnosed as having End Stage Renal Disease-undergoing dialysis and Non-End Stage Renal Disease. The data obtained from the study were statistically analyzed. The results extracted are compared with various variables included in the study and are presented here.
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Angiopoietin growth factors in models of renal disease

Angiopoietin growth factors in models of renal disease

Recent studies investigate endothelial cell proliferation and remodelling in various models of renal disease. These studies tend to concentrate on models where the kidney fails to recover from the initial insult, unlike the case in ARF. Some of these animal models have an insult that concentrates its effect on the glomerulus of the kidney. The anti-glomerular basement membrane (GBM) model induces glomerulonephritis resulting from an immune initiated, leukocyte-mediated inflammatory response directed against an antigen (sheep globulin) planted in the glomerular basement membrane (Yuan et al, 2002). The injection results in a proliferative and crescentric glomerulonephritis, characterised by glomerular accumulation o f macrophages, proliferation o f intrinsic glomerular cells and fibrin deposition (Ophascharoensuk et al, 1998). Glomerular sclerosis, interstitial inflammation and renal impairment develop secondarily to the glomerular inflammatory response. Local fibrin deposition contribute to crescent formation, sclerosis and renal impairment (Drew et al, 2001) and plasminogen activators produced by endothelial cells and leukocytes play an important role in regulating this process (Kitching et al, 1997).
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Bioactive Compounds for the Treatment of Renal Disease

Bioactive Compounds for the Treatment of Renal Disease

Renal failure is a major health issues worldwide. Acute kidney injury (AKI) results in an abrupt loss of renal function with a corresponding spike in serum creatinine concentration and decrease in urine output. Although AKI is a reversible condi- tion, it can progress to chronic kidney disease (CKD), which is characterized by a reduced glomerular filtration rate. End- stage renal disease (ESRD) is devastating condition, which re- quires either renal transplantation or dialysis. Although kid- ney dialysis replaces the renal filtration function by removing toxic substances from the blood and maintains survival of ESRD patients, it does not restore other kidney functions, such as
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ON THE MECHANISM OF ACIDOSIS IN CHRONIC RENAL DISEASE

ON THE MECHANISM OF ACIDOSIS IN CHRONIC RENAL DISEASE

It has been pointed out 1 that, in terms of modern acid-base chemistry, the defects reponsible for the acidosis of renal disease could be: 1 impaired renal excretion of acid in the form [r]

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OBSERVATIONS ON PHOSPHATE TRANSPORT IN EXPERIMENTAL RENAL DISEASE

OBSERVATIONS ON PHOSPHATE TRANSPORT IN EXPERIMENTAL RENAL DISEASE

In most of these experiments, the pattern of phosphate excretion was comparable in the diseased and contralateral control kidneys, regardless of the type of experimental renal disease st[r]

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RENAL DISEASE IN MULTIPLE MYELOMA

RENAL DISEASE IN MULTIPLE MYELOMA

The patients’ dynamics showed that most of them remained at the initial stage of the CRD; only in 4 cases (10.25%) there was a permanent decrease of the glomerular filtration rate – with implicit advancement of the chronic renal disease stage. We noticed that none of these patients displayed any obstructive factors; half of them were diagnosed with recurrent urinary infections and all of them had aggravations of the pre-existing renal disease in the context of existing infections, which led to an aggravation of the renal impairment. In terms of chemotherapy schemes these patients were following, they were all on cyclophosphamide, vincristine, melphalane and prednisone.
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Nephrolithiasis-induced end stage renal disease

Nephrolithiasis-induced end stage renal disease

In our experience, nephrolithiasis related ESRD contributed 0.63% to the total series of patients who started maintenance dialysis therapy at our department of nephrology during a 15 year period. These figures are in agreement with those extracted from recent the United States Renal Data System data. Among 228,332 white patients who started renal replacement therapy in the US from 1993 to 1997, a total of 1.5% were categorized as having “nephrolithiasis, obstruction, gouty “ as the pri- mary renal disease, thus leading to an estimated incidence of 2.9 patients/year. Paul Jungers and colleagues have reported that the overall proportion of nephrolithiasis related ESRD was 3.2%. 6 Another estimation can be
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Progression of Chronic Renal Disease - An Update

Progression of Chronic Renal Disease - An Update

It may cause, as well as be a consequence of chronic renal disease. Previously it was thought that hypotension leads to glomerular sclerosis due to ischaemia where there was decreased glomenmlar perfusion resulting from renal vascular disease. More recent data has suggested that glomerular sclerosis could occur in the absence of arteriosclerotic disease and in many cases glomerular capillary hyperper fusion and hypertension could initiate glomemlar structural injury 19 . Systemic hypertension is not required for the development of glomerular capillary hyper filtration and hypertension. In diabetic rats a pathological reduction in afferent arteriolar resistance leads to an increase inglomemlarcapillary flow and allows a greater fraction of systemic blood pressure to be transmitted into the glomerular capillary network. This raises the glomerular capillary hydraulic pressure inspite of normal renal perfusion pressure 20,21 . Systemic blood pressure tends not to decline with protein rcstriction but glomerular injury is arrested 22,16 ; this emphasizes the importance of glomerular than systemic haemodynamics. Studies have also shown that it is glomerular capillary hypertension rather than hyperfiltration or hyperperfusion which is the critical detenninant of glomerular cell injury. Thus control of glomerular capillary pressure may concur renal protection even in the lace of the continued systemic hypertension. The factors that increase glomemlar capillary hydraulic pressure experimentally were: a high protein diet, dietary cholesterol supplementation 27 , administration of glucocorticoids 28 , minerallocorticoids 29,30 or erythropoitin 31 . There arc various studies %vhich defined the role of angiotensin converting enzymes inhibitors in not only controlling blood pressure but also limiting proteinurea and slowing development of glomerular sclerosis in experimental models. ACE inhibitors normalized both systemic and glomerular capillary pressure 32-37 and thereby they are most consistently beneficial in slowing progression of experimental renal disease. The role of calcium channel blocker 5 is still under study and various studies have shown conflicting result of this family of drugs 38-44 . Several other drugs like a diuretic, vasodilator or centrally acting agent or a combination of the three have also been used though there have been very good control of blood pressure with the above drugs. Renal protection has been quite variabic with this regimen 45 . Beta adrenergic blockers have also been studied widely but the results available are not very encouraging. The deleterious consequences of intra- glomemlar hypertension besides its direct destmctive effect, have been suspected to be due to glomerular endothelial damage. This in turn may precipitate intra-glomerular coagulation 46 and increase the mesangial "trafficking" of macromolecules which promote glomemlosclerosis 46 Role of Dietary Proteins
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Is the inflammasome a potential therapeutic target in renal disease?

Is the inflammasome a potential therapeutic target in renal disease?

The inflammasome is a large, multiprotein complex that drives proinflammatory cytokine production in response to infection and tissue injury. Pattern recognition receptors that are either membrane bound or cytoplasmic trigger inflammasome assembly. These receptors sense danger signals including damage-associated molecular patterns and pathogen-associated molecular patterns (DAMPS and PAMPS respectively). The best-characterized inflammasome is the NLRP3 inflammasome. On assembly of the NLRP3 inflammasome, post-translational processing and secretion of pro-inflammatory cytokines IL-1 β and IL-18 occurs; in addition, cell death may be mediated via caspase-1. Intrinsic renal cells express components of the inflammasome pathway. This is most prominent in tubular epithelial cells and, to a lesser degree, in glomeruli. Several primary renal diseases and systemic diseases affecting the kidney are associated with NLRP3 inflammasome/IL-1 β /IL-18 axis activation. Most of the disorders studied have been acute inflammatory diseases. The disease spectrum includes ureteric obstruction, ischaemia reperfusion injury, glomerulonephritis, sepsis, hypoxia, glycerol-induced renal failure, and crystal nephropathy. In addition to mediating renal disease, the IL-1/ IL-18 axis may also be responsible for development of CKD itself and its related complications, including vascular calcification and sepsis. Experimental models using genetic deletions and/or receptor antagonists/antiserum against the NLRP3 inflammasome pathway have shown decreased severity of disease. As such, the inflammasome is an attractive potential therapeutic target in a variety of renal diseases.
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Renal disease in patients with Crohn's disease

Renal disease in patients with Crohn's disease

Searches were performed in PubMed, PubMed Central (PMC), and Web of Science using the following MESH search terms: “Crohn´s disease” and “renal disease.” For PubMed and PMC, the R RISmed package was used [9]. Systematic searches were performed according to PRISMA criteria, obtaining 1002 records (from 2009 to 2019). The advanced search tool was used for Web of Science (using the Boolean operator AND among the previously mentioned terms, obtaining 415 records, from 2009 to 2019). Then the relevance of all records was evaluated according to the title and summary. If considered relevant, the entire article was examined, and 51 articles were selected using this method.
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Amyloidosis and renal disease in patients with Crohn's disease

Amyloidosis and renal disease in patients with Crohn's disease

Abstract: Crohn's disease (CD) results from an aberrant immune response against commensal microbiota in genetically susceptible hosts. However, the nature of immune defects, the microflora involved, and genetic susceptibility remain incompletely defined and controversial. This review seeks to describe the present state of association between CD and renal disease; moreover, we highlight the convergence of CD with amyloidosis that can trigger sustained inflammation, producing the pathological alteration observed in both diseases. The following MESH terms were searched in PubMed, PubMed Central (PMC), and Web of Science: “Crohn´s disease” and “renal disease.” The R RISmed package was used for PubMed and PMC. The abnormal humoral immune response is described along with alterations in immune cell migration mechanisms in CD during inflammation.
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Hyperuricemia after orthotopic liver transplantation: divergent associations with progression of renal disease, incident end-stage renal disease, and mortality

Hyperuricemia after orthotopic liver transplantation: divergent associations with progression of renal disease, incident end-stage renal disease, and mortality

The incidence of post-OLT ESRD has been previously estimated at 12.8 and 14.5 per 1000 patient-years in the pre- and post-MELD era, respectively [25]. The overall incidence of ESRD in our cohort was higher, at 20.7 per 1000 years, though only 35 patients progressed to ESRD. Some other studies have suggested various factors po- tentially contribute to the progression of renal disease and ESRD development in patients after OLT, including hyperuricemia [26]. Several studies in the general popu- lation have demonstrated an association between hyper- uricemia and ESRD [9, 27] but others did not find this association, especially in advanced stages of CKD (stage III-V) [28]. The small number of ESRD events in our study and the resultant low statistical power may par- tially explain the lack of association between hyperurice- mia and ESRD incidence in our cohort, although the associations between uric acid (as a dichotomous, quar- tile, and continuous variable) and ESRD incidence were all very close to the null. The factors associated with in- creased ESRD incidence in our study included lower
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Impact of hypertension on renal disease among renal patients.

Impact of hypertension on renal disease among renal patients.

A retrospective study to assess the impact of hypertension on renal disease among renal patients in MIOT Hospitals, Chennai. The conceptual framework of the study was developed on the basis of epidemiological triad. The study variable was hypertension with renal disease patients attending renal outpatient department MIOT Hospitals, Chennai. A quantitative research approach with retrospective design was used to achieve the objectives of the study. The study was conducted in MIOT Hospitals, Chennai, with a sample size of 150 hypertension with renal disease patients. The samples were selected through purposive sampling method for prevalence of hypertension among renal patients and convenient sampling method for impact of hypertension on renal disease. The investigator used a demographic variable proforma and with clinical data and checklist on impact of hypertension on renal disease among renal patients to collect the data. The data collection tools were validated and reliability was established. The data was collected by using an interview method and from patient clinical file.
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Renal transplant improves pulmonary hypertension in patients with end stage renal disease

Renal transplant improves pulmonary hypertension in patients with end stage renal disease

Pulmonary hypertension (PH) is seen in a significant proportion of patients with end stage renal disease (ESRD) [1-3]. The prevalence of PH has been report- ed to be as high as 48% [4]. A variety of mecha- nisms are proposed to contribute to the develop- ment of PH in uremic patients. Duration of renal re- placement therapy, extraosseous pulmonary calcifi- cation, high cardiac output due to arterio-venous fistula or other causes, anemia, fluid overload, hor- monal and metabolic imbalances associated with uremic milieu and impaired endothelial function are among various mechanisms responsible for ele- vation of pulmonary artery pressure (PAP) [4,5]. It has been shown that PH is important prognosti- cally in patients with ESRD as in other patient groups with this disorder [6,7]. It is a progressive disease. Unless diagnosed early and treated appro- priately, the course of PH is usually fatal due to the development of right ventricular failure. In addition to other comorbidities and age, it stands as an inde- pendent predictor of survival in patients with renal failure [8]. However, data about the impact of renal transplant on PH in patients with ESRD is limited. Therefore, in this study, the effect of renal transplant on PH determined by Doppler echocardiography in the pre-transplant and post-transplant period was examined.
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Mortality of Chronic Hemodialysis and Renal Transplantation in Pediatric End-Stage Renal Disease

Mortality of Chronic Hemodialysis and Renal Transplantation in Pediatric End-Stage Renal Disease

transplants, survival was 80% at three years and 76% at five years for living related transplants and 78% at three years and 70% at five years for cadaver transplant recipients.’ These c[r]

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Clinical practice guideline on pregnancy and renal disease

Clinical practice guideline on pregnancy and renal disease

In pregnancy, concern regarding the fetotoxicity of urea is likely to precede maternal indications for dialysis, which are the same as outside of pregnancy: refractory hyperkalaemia, acidosis and/or fluid overload, and ur- aemic symptoms that impact upon daily living [214]. A recommendation to initiate dialysis when maternal urea concentration is greater that 17 mmol/l is extrapolated from historical, observational data reporting high rates of fetal death in women with this level of renal dysfunc- tion [215, 216], although these data also reflect obstetric and renal practice from over 50 years ago. Contemporary practice is variable: from routine commencement of dia- lysis at a maternal urea above 17 mmol/L [217], to con- sideration of dialysis only when the urea is consistently above 20 mmol/L. [66] In addition to maternal serum biochemistry, fetal health (including growth profile and polyhydramnios) and maternal wellbeing (including fluid balance, biochemistry, blood pressure and nutrition) will influence initiation of dialysis in pregnancy. It was the consensus of the guideline committee that in the context of deteriorating renal function, a serum urea above 15 mmol/L should initiate conversations about the risks, benefits and logistics of dialysis initiation in pregnancy, weighed with the risks of preterm delivery before dialysis initiation if the gestation is approaching or more than 34 weeks.
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Recent Experience with Hemodialysis in Acute Renal Failure, Chronic Renal Disease with Reversible Features, and in Conjunction with Renal Homotransplants

Recent Experience with Hemodialysis in Acute Renal Failure, Chronic Renal Disease with Reversible Features, and in Conjunction with Renal Homotransplants

Since the development of our exist- ing artificial kidney unit, the volume of acute dialysis has likewise increased.. The first group was made up of eleven patients who[r]

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The Excretion of Acid in Unilateral Renal Disease in Man

The Excretion of Acid in Unilateral Renal Disease in Man

The proportionality between GFR and the tubular capacity to excrete acid observed in unilateral parenchymal disease was modified in the four patients with unilateral renal arterial steno[r]

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The Effect of Renal Transplantation on Respiratory Muscle Strength in Patients with End Stage Renal Disease

The Effect of Renal Transplantation on Respiratory Muscle Strength in Patients with End Stage Renal Disease

Chronic kidney disease not only deteriorates renal function, but also affects other organs, including respiratory system muscles. This, in addition to the effects of hemodialysis, may weaken the respiratory muscles of patients with CKD (1-3). In fact, patients with CKD who receive hemodialysis are less active and suffer from muscle

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NEPHRECTOMY IN JUVENILE HYPERTENSION ASSOCIATED WITH RENAL DISEASE

NEPHRECTOMY IN JUVENILE HYPERTENSION ASSOCIATED WITH RENAL DISEASE

and showed the changes of chronic atrophic pvebonephritis. There was grade 1 to grade 2 generalized narrowing of the ret- inal arterioles. The urine contained albumin and pus. Excretory [r]

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