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1.
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Introduction
| Chinese-herb nephropathy (CHN) was initially reported as a progressiverenal interstitial fibrosis caused by the regular intake ofChinese herbal medicine belonging to the Aristolochia speciescontaining nephrotoxic and carcinogenic aristolochic acid (AA)[1–3]. Prior exposure to AA was attested by the detectionof specific DNA adducts formed by AA metabolites in kidneysand ureters of patients suffering from end-stage renal disease(ESRD) due to CHN [4–6]. Among these patients, a highprevalence of upper urinary tract carcinoma was observed [5,7]. 相似文献
2.
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Introduction
| Autosomal dominant polycystic kidney disease (ADPKD) is a systemicdisease with renal and extra renal, cystic and non-cystic manifestations.The cystic disease involves kidney, liver, pancreas, seminalvesicles and meninges. Non-cystic manifestations include aneurysmsand dolichoectasias (intracranial, thoracic aorta, coronaryand other arteries), valvular heart disease, hernias and possiblyintestinal diverticula [1]. Hypertension, arterial vasospasm,and extensive remodelling of small renal arteries and arteriolesat early stages of cystic disease are also evident [2–5].Cardiovascular complications are the leading cause of deathin ADPKD. Here, we report eight cases of retinal arterial and/orvenous occlusions in patients with ADPKD and propose that theseconditions may be part of the generalized vasculopathy 相似文献
3.
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Introduction
| In this edition of NDT, Manlucu et al. [1] present results froma systematic review they performed on dose reducing of histamine2 receptor antagonists (H2RA) in the presence of renal failure.Fundamentally, they demonstrate that H2RA should be given inlower doses as renal function deteriorates. These results inthemselves are not surprising as H2RA are primarily excretedin the urine unchanged, and there is substantial evidence thatclearance is reduced with renal failure [2–4]. The moresurprising result is that these authors managed to identify16 published clinical 相似文献
4.
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Introduction
| Calcific uremic arteriolopathy (CUA) [1] refers to calcificationof the media of small terminal arteries and arterioles and associatedfibrotic intimal thickening and lumen narrowing, thereby increasingthe risk of ischaemic necrosis. As the term suggests, CUA isreported in patients with chronic kidney disease (CKD) ‘nearlyexclusively’ [2]. Identical clinical and pathologic featureshave developed with hyperphosphataemia from other causes [3–7]. CUA develops silently [1,5,8], sometime presenting only withsubcutaneous plaques and/or nodules. But with ischaemic complicationsit presents acutely with foci with discoloured skin progressingto necrosis and deep ulcers; hereafter designated 相似文献
5.
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Introduction
| BK-virus-induced interstitial nephritis (BK nephropathy) isa recently recognized condition affecting renal allografts thatmay lead to graft failure [1]. BK-virus infection is endemicworldwide with seroprevalence rates in normal adults of 60–80%[1]. Risk factors for BK nephropathy include high levels ofimmunosuppression, particularly involving tacrolimus [2]. Thereis no established treatment other than reduction of immunosuppressionto aid viral clearance, which risks acute irreversible rejection[3]. There are in vitro data showing that cidofovir inhibitsBK virus replication, but there are 相似文献
6.
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Introduction
| Impaired control of the complement system activation due tomutations in complement factor H (CFH) has been described intwo apparently unrelated human diseases, membranoproliferativeglomerulonephitis type II (MPGN2) and non-Shiga toxin-associatedhaemolytic uraemic syndrome (non-Stx-HUS). Mouse models of thesediseases have been developed by Pickering et al., by knocking-outCfh gene (MPGN2) and by subsequently transferring a mutatedCfh gene in the Cfh –/– background (non-Stx-HUS).The data obtained from the two models provided precious informationto clarify the mechanisms that cause the disparate phenotypesunderlying CFH genetic defect.
MPGN2
| MPGN2 is a rare cause of chronic nephritis characterized bythe presence of dense deposits within the glomerular basementmembrane (GBM), capillary wall thickening, mesangial cell proliferationand glomerular fibrosis [1,2].
Non-Stx-HUS
| Non-Shiga toxin-associated haemolytic uraemic syndrome (non-Stx-HUS)is a rare disease with manifestations of haemolytic anaemia,thrombocytopenia and renal failure. The clinical outcome isunfavourable, 相似文献
7.
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Introduction
| Nephrogenic fibrosing dermopathy (NFD) was first described byCowper et al. [1] as a cutaneous fibrosing disorder associatedwith renal dysfunction. In the last 3 years there has been agrowing body of literature regarding NFD. Clinically, skin isthickened or oedematous with indurated papules and plaques.The pathogenesis of NFD is largely unknown. Several authorshave discussed a reaction against the PVC materials used indialysis, but NFD has also occurred in patients without dialysis[2–4]. Spontaneous healing of NFD has not been documentedpreviously; however restitutio ad integrum after improvementof the renal situation has been reported [2]. The therapy ofNFD has to be regarded as 相似文献
8.
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Introduction
| It is well known that late referral to a nephrologist is associatedwith many adverse outcomes [1–4], and indeed has beenthe subject of a recent review in this journal [5]. Some ofthe more important negative outcomes include more rapid onsetof end-stage renal disease (ESRD), progression of co-morbidconditions such as anaemia and cardiovascular disease, suboptimalvascular access at initiation of dialysis, increased use ofcentre-based haemodialysis (HD), increased hospital utilization,increased cost and worse survival. The literature has many examplesof suboptimal chronic kidney disease (CKD) care provided byprimary care physicians prior to referral, and also shows clearlythat care provided by nephrologists is better [6,7]. There isa consensus within the renal community that early referral isdesirable [5,8–10].M
Multidisciplinary team-based CKD care
| There is much less consensus 相似文献
9.
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Introduction
| Heavy chain deposition disease (HCDD) is a rare manifestationof plasma cell dyscrasia. Only 11 cases have been describedin the literature [1]. The clinical picture is variable, butin all patients renal biopsy showed a nodular sclerosing glomerulopathy[1–5]. We report a patient with rapidly progressive glomerulonephritisin whom the renal biopsy showed mainly intracapillary proliferativeglomerulonephritis due to HCDD.
Case
| The patient is a 55-year-old musician with an uneventful medicalhistory except ankylosing spondylitis diagnosed at the age of47. Six weeks before admission he noticed foamy urine, at 2weeks he developed generalized swelling, dyspnoea and a severeheadache. Upon admission 相似文献
11.
Nephronophthisis (NPHP) is an autosomal recessive kidney disease characterized by tubular basement membrane disruption, interstitial
infiltration, and tubular cysts. NPHP leads to end-stage renal failure (ESRD) in the first three decades of life and is the
most frequent genetic cause of chronic renal failure in children and young adults. Extrarenal manifestations are known, such
as retinitis pigmentosa, brainstem and cerebellar anomalies, liver fibrosis, and ocular motor apraxia type Cogan. We report
on a Turkish family with clinical signs of nephronophthisis. The phenotype occurred in two generations and therefore seemed
to be inherited in an autosomal dominant pattern. Nevertheless, a deletion analysis of the NPHP1 gene on chromosome 2 was performed and showed a homozygous deletion. Analysis of the family pedigree indicated no obvious
consanguinity in the last three generations. However, haplotype analysis demonstrated homozygosity on chromosome 2 indicating
a common ancestor to the parents of all affected individuals. NPHP1 deletion analysis should always be considered in patients with apparently dominant nephronophthisis. Furthermore, three out
of four patients developed ESRD between 27 and 43 years of age, which may be influenced by yet unknown modifier genes. 相似文献
12.
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Introduction
| Renal vein thrombosis (RVT) is a common clinical condition amongpatients with nephrotic syndrome, with a relatively high prevalence(20–48%). It is most common in patients with membranousglomerulonephritis followed by membrano-proliferative glomerulonephritisand minimal change nephrosis [1]. However, there are other initiatingconditions including diabetic nephropathy and trauma [1]. Inpatients with malignancy, RVT may be secondary to direct extensionof tumour thrombus into the renal vein or may be due to a hypercoagulablestate [2]. Presenting signs and symptoms of RVT include oliguria,haematuria, flank pain and azotaemia [2]. Thrombosis of theadjacent inferior vena 相似文献
13.
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Introduction
| Familial lecithin–cholesterol acyltransferase (LCAT) deficiencyis a rare autosomal recessive disease caused by mutation inthe LCAT gene, located on chromosome 16q22 (GenBank accessionnos: genomic DNA X04981, cDNA NM_000229). LCAT catalyses theformation of cholesteryl esters via the hydrolysis and transferof sn-2 fatty acid from phosphatidylcholine to the 3-hydroxylgroup of cholesterol. A deficiency of this enzyme leads to increasedlevels of phosphatidylcholine and unesterified cholesterol inthe blood and to the formation of an abnormal lipoprotein (called‘lipoprotein-X’) rich in both phosphatidylcholineand unesterified cholesterol. As a consequence, progressivelipid deposition occurs in various tissues, including the kidney[1], resulting in progressive glomerular sclerosis which becomesclinically manifest in the third to fourth decade of life andeventually leads to end-stage renal disease [2]. To date, 13 affected families have been found in Italy (includingthe one 相似文献
14.
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Introduction
| Anti-glomerular basement membrane (GBM) disease is a disordercharacterized by antibodies against an epitope of type IV collagenfound on the GBM. The major clinical sequela is rapidly progressiveglomerulonephritis, which may be accompanied by pulmonary haemorrhage(Goodpasture's syndrome). Glomerulonephritis secondary to anti-GBMdisease frequently progresses to end-stage renal disease (ESRD)in the subset of patients who present with markedly impairedrenal function. Renal transplantation is performed for ESRDdue to anti-GBM disease, although most centres delay transplantationuntil patients are anti-GBM antibody negative for at least 12months. Although early case series showed frequent recurrencein the allograft [1], modern therapeutic approaches have maderecurrent disease very rare, and only four cases have been reported[2–5]. The effect of therapy for recurrent allograft diseaseis not well described. We 相似文献
15.
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Introduction
| Bisphosphonates currently are important antiresorptive agentsused in the treatment of metabolic bone diseases, includingtumour-associated osteolysis and hypercalcaemia, Paget's diseaseand osteoporosis. These drugs cause a loss of the osteoclastruffled border, disruption of the osteoclast cytoskeleton andinhibition of actin ring formation, sufficient to prevent boneresorption [1]. Several studies have demonstrated that highconcentrations of bisphosphonates can cause apoptotic cell deathof mouse, rat and rabbit osteoclasts in vitro and in vivo byinhibiting the mevalonate pathway and protein prenylation [2].Bisphosphonates are excreted unchanged via the kidneys. Thehigh drug levels attained in the kidney may cause renal toxicitythrough a mechanism similar to that described in osteoclasts. Short-term [3] and long-term [4–6] tubular toxicity ofpamidronate were reported in humans. Recently, an associationbetween collapsing glomerulopathy 相似文献
16.
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Background
| Recently increased attention for chronic renal failure has stimulatednew interest in renal function assessment by direct measurementas well as by algorithms or formulas [1–3]. In the failingrenal graft, a situation in which pharmacological therapy mayinterfere with the complex adaptation mechanisms of renal failure,the assessment of renal function may be particularly difficult[4]. Studies of patients with liver or heart transplantationand advanced kidney disease suggest that creatinine-based indexesmay be poor indicators of residual renal function under calcineurininhibitors [5,6]. The following two cases, displaying a discrepancybetween creatinine and urea 相似文献
17.
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Introduction
| Wegener's granulomatosis is a rare, protean disease, with evensex distribution and higher incidence in Caucasians. Its yearlyincidence is 5–12 per 1 000 000 [1] and it displays awide range of clinical presentations from a mild, localisedlesion to widespread severe disease [2]. The age range is wide, with the peak in the 40s. Women in thechildbearing age group are not spared, and pregnancy presentsa critical condition both for the onset of the disease and forits flare-ups [2,3]. The decision of a patient with Wegener's granulomatosis to becomepregnant presents a clinical dilemma [3]. To face it 相似文献
18.
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Introduction
| Fibrosis, defined as an abnormal increase of tissue collagenfibres, is an important component of cardiac remodelling inpatients with hypertension. Cardiac remodelling may in turnlead to increased myocardial stiffness, left ventricular (LV)dysfunctions, and ultimately to heart failure. A growing bodyof evidence indicates that the renin–angiotensin–aldosteronesystem (RAAS) plays an important role in the development ofcardiac fibrosis [1–8]. Furthermore, experimental datasuggest that angiotensin II (Ang II) and aldosterone can stimulatecardiac fibrosis independent of haemodynamic mechanisms throughdirect trophic effects on the myocardium, and probably alsoby inhibiting interstitial collagenases, thereby reducing collagendegradation [1,2,7,8]. However, less is known about the influenceof the RAAS on cardiac fibrosis in humans. We report here thecase of a patient with 相似文献
19.
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Introduction
| Secondary hypertension is responsible for 5–10% of causesof hypertension in the general population [1,2]. It is rarelypossible to reverse/cure secondary hypertension, but if thepatient is relatively young, and the causation of the raisedblood pressure is diagnosed early enough a cure can be effected.This is most typically after renal arterial intervention forfibromuscular dysplasia, or after removal of an endocrinologicallyactive tumour. We describe three cases of a rare cause of secondary hypertension(sometimes as here with acute renal failure), the ‘Pagekidney’, where there is sustained renal parenchymal compressionleading to ischaemia and activation of the renin–angiotensin–aldosteronesystems. We then discuss the definition and pathophysiologyof the ‘Page kidney’ phenomenon [3]. In addition,we include a mini-review of the literature regarding the reportedcauses, 相似文献
20.
BACKGROUND: The influence of hydroxyethyl starch (HES) solutions on renalfunction is controversial. We investigated the effect of HESadministration on renal function in critically ill patientsenrolled in a large multicentre observational European study. METHODS: All adult patients admitted to the 198 participating intensivecare units (ICUs) during a 15-day period were enrolled. Prospectivelycollected data included daily fluid administration, urine output,sequential organ failure assessment (SOFA) score, serum creatininelevels, and the need for renal replacement therapy (RRT) duringthe ICU stay. RESULTS: Of 3147 patients, 1075 (34%) received HES. Patients who receivedHES were older [mean (SD): 62 (SD 17) vs 60 (18) years, P = 0.022], more likely to be surgical admissions, had a higherincidence of haematological malignancy and heart failure, higherSAPS II [40.0 (17.0) vs 34.7 (16.9), P < 0.001] and SOFA[6.2 (3.7) vs 5.0 (3.9), P < 0.001] scores, and less likelyto be receiving RRT (2 vs 4%, P < 0.001) than those who didnot receive HES. The renal SOFA score increased significantlyover the ICU stay independent of the type of fluid administered.Although more patients who received HES needed RRT than non-HESpatients (11 vs 9%, P = 0.006), HES administration was not associatedwith an increased risk for subsequent RRT in a multivariableanalysis [odds ratio (OR): 0.417, 95% confidence interval (CI):0.05–3.27, P = 0.406]. Sepsis (OR: 2.03, 95% CI: 1.37–3.02, P < 0.001), cardiovascular failure (OR: 6.88, 95% CI: 4.49–10.56, P < 0.001), haematological cancer (OR: 2.83, 95% CI: 1.28–6.25, P = 0.01), and baseline renal SOFA scores > 1 ( P < 0.01for renal SOFA 2, 3, and 4 with renal SOFA = 0 as a reference)were all associated with a higher need for RRT. CONCLUSIONS: In this observational study, haematological cancer, the presenceof sepsis, cardiovascular failure, and baseline renal functionas assessed by the SOFA score were independent risk factorsfor the subsequent need for RRT in the ICU. The administrationof HES had no influence on renal function or the need for RRTin the ICU. 相似文献
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