Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reflux nephropathy is known to be a major cause of renal failure in children. Vesico-ureteral reflux is usually diagnosed by voiding cysto-urethrography (VCG). However, it has been observed that conventional VCG is not always reliable for the diagnosis of ureteral reflux. In the case of a 5 year old girl with recurrent febrile urinary tract infection, VCG showed no ureteral reflux. Urodynamic study revealed a large bladder capacity and significant residual urine. Renal scintigram delineated a right renal scar. Simple ultrasound examination with videotape recording during voiding definitely demonstrated the presence of significant ureteral reflux when she voided, that is, there was marked dilatation of the right distal ureter and ballooning of the right renal pelvis on voiding, and quick refilling of the bladder concomitantly with the disappearance of the pelvic ballooning. Therefore, an ultrasound during voiding may be useful for diagnosing ureteral reflux in patients where a VCG does not reveal reflux.
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PMID:A case of ureteral reflux identified by ultrasound. 884 May 49

Reflux nephropathy i. e. renal scarring associated with vesico-ureteric reflux and urinary tract infection is primarily a diagnosis based on renal imaging. It is well known to be associated with hypertension and renal failure. This has led to regular long-term follow-up of patients, clinically and radiologically. We report the findings of renal imaging in a cohort of 37 patients with reflux nephropathy 15 or more years after successful surgical correction of vesico-ureteric reflux. The degree of renal scarring had been assessed and recorded at the beginning of the study utilizing a score on the original X-ray films. The scar scores of the current intravenous urography (IVU) imaging underestimate the degree of scarring in 35% of cases when compared with the previously recorded scar scores of the original IVU images suggesting a reduction in the renal scar score in some cases over the years. In the current review, concomitant renal images obtained by IVU and 99mTc dimercapto succinic acid (DMSA) scanning were in agreement for scar scoring in only 50% of cases. The original scar score by IVU or the current scar score by either technique does not correlate with blood pressure, urine albumin excretion or glomerular filtration rate (GFR). We conclude that serial long-term two-dimensional renal imaging in children with damaged kidneys who no longer have vesico-ureteric reflux, does not provide additional information that will alter clinical management. However, the changes in renal volume and echogenicity were not assessed in this study.
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PMID:15-year follow-up of reflux nephropathy by imaging. 979 67

Hypertension is one of the main risk factors of mortality for children on renal replacement therapy. It has also been recognised as one of the major risk factors for progression of renal failure. The aim of the study was to define the prevalence of hypertension in children with chronic renal failure, treated in a single centre, and to assess the efficacy of its diagnosis and management. Hypertension was present in 27% of 40 children before the onset of chronic renal failure, increasing to 57% with the development of CRF, and reaching 86% at onset of dialysis. Reflux nephropathy, hemolytic-uraemic syndrome and glomerular disease were most frequently associated with severe hypertension. ACE inhibitors (70%), diuretics (52%), and calcium channel blockers were the most frequently used antihypertensives with 49% of the children being on monotherapy. Despite therapy 43% of children had elevated blood pressure levels and 16% had echocardiographic signs of LVH. A 24 hour ambulatory blood pressure measurements were more sensitive in diagnosing hypertension and assessing adequacy of blood pressure control. Early and intensified treatment should prevent end organ damage though optimal blood pressure values to aim obtain are still to be defined.
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PMID:[Hypertension in children with chronic renal failure]. 1089 39

The first specialized haemodialysis (HD) paediatric centre in former Yugoslavia was established at the University Children's Hospital in Belgrade in January 1980. A total of 194 children (F: 98, M: 96), aged less than 19 years (10.12 +/- 4.23), were treated for renal replacement therapy (RRT) over 20 years. Average annual incidence rate was 1.59 per million of child population (pmcp) aged less than 19 years for the period 1980-1990 (former Yugoslavia) and 2.85 pmcp aged less than 19 years for the period 1990-2000 (present Yugoslavia). Reflux nephropathy was the most frequent underlying disease and accounted for 37.06% of total cases, while other primary renal diseases were: glomerulonephritis (GN) 17.26%, cystic/hereditary familial nephropathy 12.69%, congenital disease 11.68%, interstitial nephritis 5.58%, non-recovered tubular necrosis 3.55%, secondary GN 1.52% and 10.66% remained with doubtful diagnosis. HD was the first RRT in 84.02%, peritoneal dialysis (PD) in 14.43% and pre-emptive transplantation in 1.55% of all patients. A total of 53 patients (27.3% of total terminal renal failure (TRF) patients) received 56 kidney transplants (58.93% live related, 37.50% cadaveric, 3.57% live-non related). Actual survival in RRT was 64.53% 5 in years; 51.68% in 10 and 48.23% in 15 years. Patient survival in HD was significantly better over the last ten-year period than in the first ten-year period (35.88% vs. 75.75%; p < 0.005) as well as the survival of transplanted patients in the same two periods (67.62% vs. 95.45%). Graft survival was 79.85% in 5 and 70.50% in 10 years. Cardiovascular complications were the most common cause of death of patients on RRT (56.10 posto) followed by infection (24.39). On December 31, 1999, 54 patients on RRT were alive less than 19 years: 75.92% in HD; 22.22% with functioning graft and 1.85% on automatic PD. This is the first national-wide long-term study of incidence and aetiology of paediatric TRF and outcome of paediatric RRT in Yugoslavia.
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PMID:[20 years' experience in the treatment of children with terminal renal insufficiency in Yugoslavia]. 1133 14

Reflux nephropathy (RN) is recognized as a major cause of end-stage renal failure in children and young adults. Inhibition of nitric oxide (NO) exacerbates and enhanced production ameliorates tubulointerstitial fibrosis (TIF) in experimental obstructive uropathy. NO is synthesised by NO synthase (NOS), three distinct isoforms of which have been identified: inducible (iNOS), endothelial (eNOS), and neuronal (nNOS). It has been reported that iNOS induces immunologic injury to glomerular cells and enhances accumulation of extracellular matrix in the glomerulus and tubulointerstitial space. Furthermore, it has been suggested that nNOS and eNOS have beneficial effects in ameliorating TIF. We investigated the expression of different isoforms of NOS in severe refluxing kidneys in order to further understand the pathogenesis of RN in kidney specimens from nine children with severe RN obtained at nephrectomy. Control material included normal kidney specimens from three adult patients undergoing partial nephrectomy for small kidney tumours. Histochemistry for NO was performed using nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase. Single-label immunofluorescence histochemistry was carried out using polyclonal antibodies to nNOS, iNOS, eNOS, and transforming growth factor (TGF)-beta 1 employing laser-scanning confocal microscopy. The TUNEL method was used to assess tubular apoptosis. Strong NADPH staining was observed in the proximal tubules of RN kidneys compared to controls, where there was weak staining. Control kidneys demonstrated weak immunoreactivity for iNOS in the proximal tubules and a lack of immunoreactivity for nNOS and eNOS. RN kidneys demonstrated strong immunoreactivity for nNOS in the tubulointerstitial space, for eNOS in the glomerulus, and for iNOS in the glomerulus and proximal tubules. Strong immunoreactivity for TGF beta 1 was seen in the glomerulus and proximal tubules identical to iNOS. Increased immunoreactivity for iNOS and TGF-beta 1 strongly correlated with the severity of apoptosis in RN. Our data demonstrate that NO derived from nNOS, iNOS, and eNOS is strongly expressed in RN. The selective shunting of NO via iNOS may induce renal fibrosis in RN. The upregulation of nNOS and eNOS in RN appears to be a compensatory mechanism of ameliorating TIF.
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PMID:The role of nitric oxide in reflux nephropathy. 1247 80

Reflux nephropathy (RN) is the cause of end-stage renal failure in 3%-25% of children and 10%-15% of adults. Angiotensin-converting enzyme (ACE) converts the inactive decapeptide angiotensin I (Ang I) to the active octapeptide angiotensin II (Ang II), a potent vasoconstrictor. ACE is localized in highest concentrations on the luminal surface of endothelial cells, but is also found in several other cell types, including the epithelial cells of the proximal renal tubule. Recent studies have suggested that ACE increases production of the components of extracellular matrix (ECM) such as fibronectin (Fib) mediated through Ang II. Since RN is a primary tubulointerstitial disease, we hypothesized that local overexpression of ACE may induce renal fibrosis via up-regulation of Ang II. In this study, we investigated the expression of ACE in severely refluxing kidneys from eight patients (age range 6 months-14 years) with severe RN secondary to primary high-grade vesicoureteral reflux at nephrectomy. Control material included normal kidney specimens obtained from three adult patients during partial nephrectomy for an incidentaloma. Soluble enzyme immunohistochemistry was carried out using polyclonal antibodies to ACE and Fib. In-situ hybridization (ISH) was performed utilizing biotin-labelled antisense oligonucleotide probe. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to evaluate the relative amount of ACE mRNA. In the refluxing kidney, there was strong ACE immunoreactivity in the glomerulus and proximal tubules and moderate-to-strong immunoreactivity in the distal tubules accompanied by strong Fib immunoreactivity in the glomerulus, proximal tubule, and interstitial space. There was strong ACE mRNA expression in the glomerulus and proximal tubules and moderate expression in the distal tubules. In the control kidneys, homogeneous weak ACE immunoreactivity and mRNA expression was demonstrated only in the proximal tubules. RT-PCR showed strong ACE expression in the refluxing kidneys compared to controls. Up-regulation of ACE in RN accompanied by an increase in ECM in the tubulointerstitial space suggests that ACE is involved in the pathogenesis of the renal parenchymal damage in patients with RN. Pharmacologic blockade of ACE may be helpful in preventing the renal fibrosis associated with RN.
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PMID:Up-regulation of angiotensin-converting enzyme (ACE) gene expression induces tubulointerstitial injury in reflux nephropathy. 1247 81

Reflux nephropathy (RN) is a major cause of end-stage renal failure in children and young adults. Intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein, has a role in the regulation of interaction among immune cells. It has been demonstrated that increased levels of tubular ICAM-1 correlate with an extent of tubular damage in diabetic nephropathy. We hypothesized that ICAM-1 local synthesis is altered in reflux nephropathy and therefore designated this study to investigate ICAM-1 expression in RN. The kidney specimens from six patients with severe reflux nephropathy secondary to primary vesicoureteral reflux were obtained at the time of nephrectomy. Control materials included normal kidney specimens obtained from three adult patients during partial nephrectomy for an incidentaloma. Fluorescent immunohistochemistry was carried out using monoclonal antibodies to ICAM-1 utilizing confocal laser scanning microscopy. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to evaluate the relative amount of ICAM-1. In the control kidneys, there was lack of ICAM-1 immunoreactivity in the interstitium and proximal tubules and moderate immunoreactivity in the glomerulus. In the refluxing kidney there was strong ICAM-1 immunoreactivity in the glomerulus, interstitium and proximal tubules. The RT-PCR showed strong ICAM-1 mRNA expression in the refluxing kidneys and absent or weak ICAM-1 expression in the controls. Our findings of increased expression of ICAM-1 in the severe reflux nephropathy kidney suggests that ICAM-1 may play a role in the pathogenesis of renal parenchymal damage associated with RN.
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PMID:ICAM-1 expression is upregulated in reflux nephropathy. 1275 65

Reflux nephropathy i.e. renal scarring associated with vesico-ureteric reflux (VUR) and urinary tract infection (UTI) was originally considered an acquired disease. The renal scarring seems to get worse with recurrent urine infections especially in the young. Therefore, in the past much effort was undertaken to correct the VUR surgically and minimize the number of recurrent urinary tract infections by antibiotic prophylaxis with the hope of reducing if not arresting the onset of complications that follow i.e. hypertension and renal failure. However, it is now becoming clear that reflux nephropathy encompass at least two major categories of disease; "acquired" renal scarring secondary to UTI and VUR predominantly affecting females and "congenital" scarring with dysplastic features associated with prenatal VUR but with no infection and predominantly affecting boys. The latter is much less common but is disproportionately represented in the group of patients with reflux nephropathy that go on to develop renal failure. Unfortunately, the susceptibility to renal scarring, the onset of hypertension and progression to renal failure seems to be significantly influenced by genetic factors and hence measures undertaken to prevent recurrence of UTI may not change the ultimate outcome although it will certainly improve the comfort of the individual. Therefore, the extensive investigation and management routines adopted today in these children may not be cost-effective in preventing end stage renal disease in VUR. The progression to renal failure, however, can be delayed but not halted with adequate control of high blood pressure and hence the need for life long follow-up.
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PMID:Vesicoureteric reflux and reflux nephropathy. 1278 97

This case-report emphasizes an uncommon cause of hypertension in an adolescent: reflux nephropathy. Reflux nephropathy is a frequent hypertension and renal failure etiology. Medical treatment is unknown from cardiologist.
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PMID:[Reflux nephropathy and arterial hypertension]. 1471 46

Chronic peritoneal dialysis (CPD) has been utilized in the treatment of children since 1989 in Turkey. The aims of this study were to summarize our experience with CPD in children and to establish a pediatric registry data system in Turkey. Standard questionnaires were sent to all pediatric CPD centers. 514 patients treated between 1989 and 2002 in 12 pediatric centers were enrolled in the study. Reflux nephropathy was the most common (18.1%) cause of renal failure. Mean age at dialysis initiation was 10.1+/-4.6 years. Mean duration of dialysis was 24.1+/-20.5 months. Continuous ambulatory peritoneal dialysis (CAPD) was the first CPD modality for 476 (92.6%) patients, 142 of whom switched to automated peritoneal dialysis (APD) during follow-up. Currently, 47.3% of the patients are still on CPD, 15.4% were transplanted, 13.2% switched to hemodialysis, 16.7% died. The patient and technique survivals were 90% and 95% at one year and 70% and 69% at five years, respectively. The survival was significantly shorter in the youngest age group (0-24 months) compared to those in older age groups (p=0.000). We herein report the first results of the TUPEPD study providing information on demographic data and survival of pediatric CPD patients. As opposed to clear recommendations in favor of APD, there is a clear preponderance of CAPD in our pediatric CPD population. That vesicoureteral reflux (VUR) is still the leading cause of renal failure is a distressing finding. Remarkably lower survival rates and transplantation ratios are as striking and distressing as the high incidence of VUR among the causes of ESRD. We conclude that we must make a great effort to achieve better results and to change these undesirable events.
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PMID:Chronic peritoneal dialysis in Turkish children: a multicenter study. 1571 62


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