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1.
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Introduction
| A patient developed direct renal tubular toxicity on high-doseHMG-CoA reductase inhibitor (statin) therapy. Considerable renaldamage was present by the time the injury became apparent. Urineabnormalities regressed after stopping the drug and reappearedafter about 2 weeks following re-challenge. Although tubulardamage may be slight and relatively difficult to detect, itis possible that cumulative injury in susceptible individualsover a period of years may result in significant renal damage. HMG-CoA reductase inhibitors (statins) reduce morbidity andmortality from coronary heart disease, prevent strokes and possiblyreduce renal disease as the result of cholesterol lowering,improved endothelial function, reduced inflammation and reducedoxidative stress [1]. Significant side effects associated with statins are infrequent.Myalgia and arthralgia are common (1–7%) but frank rhabdomyolysis 相似文献
2.
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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
3.
Rhabdomyolysis in deceased donors usually causes acute renal failure (ARF), which may be considered a contraindication for kidney transplantation. From January 2012 to December 2016, 30 kidneys from 15 deceased donors with severe rhabdomyolysis and ARF were accepted for transplantation at our center. The peak serum creatinine (SCr) kinase, myoglobin, and SCr of the these donors were 15 569±8597 U/L, 37 092±42 100 μg/L, and 422±167 μmol/L, respectively. Two donors received continuous renal replacement therapy due to anuria. Six kidneys exhibited a discolored appearance (from brown to glossy black) due to myoglobin casts. The kidney transplant results from the donors with rhabdomyolysis donors were compared with those of 90 renal grafts from standard criteria donors (SCD). The estimated glomerular filtration rate at 2 years was similar between kidney transplants from donors with rhabdomyolysis and SCD (70.3±14.6 mL/min/1.73 m 2 vs 72.3±15.1 mL/min/1.73 m 2). We conclude that excellent graft function can be achieved from kidneys donors with ARF caused by rhabdomyolysis. 相似文献
4.
Background and aimThe current study investigated the effects of treatment with 300 mg/kg valproic acid on rhabdomyolysis and acute kidney injury induced by intramuscular injection of hypertonic glycerol in rats. MethodsFour groups of male wistar rats: control and hypertonic glycerol, valproic acid and valproic acid + hypertonic glycerol treated groups were used. Blood urea nitrogen, serum creatinine, creatinine kinase (CK) and CK MB, myoglobin and renal reduced glutathione (GSH) levels were measured. Histopathological examination of the kidneys was carried out to evaluate the degree of renal injury in each group. The expression of interleukin-1 beta “IL-1β” in renal tissue was detected using immunohistochemistry. ResultsHypertonic glycerol administration led to severe renal tubular damage with a significant elevation of blood urea nitrogen, serum creatinine, creatinine kinase, CK MB and myoglobin levels and overexpression of IL-1β compared to control group. Valproic acid administration attenuated both the muscle injury and the acute kidney injury induced by hypertonic glycerol, estimated through a significant reduction of creatinine kinase, myoglobin, and serum creatinine. Valproic acid administration caused a significant increase in GSH in the hypertonic glycerol + valproic acid group compared to the hypertonic glycerol group. A significant decrease in tubular necrosis grade, and expression of IL-1β in hypertonic glycerol + valproic acid group compared to the hypertonic glycerol group was observed. ConclusionThis study demonstrates, for the first time to the best of our knowledge, that valproic acid could ameliorate the rhabdomyolysis and the related acute kidney injury in rats. 相似文献
5.
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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
6.
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Introduction
| Kaposi's sarcoma (KS) is a cancer of connective and fibroustissue such as cartilage, bone, fat, muscle, blood vessels,tendons and ligaments [1–3]. It was first described bydermatologist Moritz Kaposi as a disease characterized by ‘... idiopathic multiple pigmented lesions of the skin ... ’.For decades KS has been regarded as an uncommon disease thatmostly affects elderly men of Mediterranean or Jewish heritage,young adult African men and organ transplanted patients [1].
Case report
| Here we describe a case of a 42-year-old black African malewho developed KS a few months after renal transplantation. The cause and the onset of renal insufficiency was unknown.Haemodialysis treatment started in 1992. Clinical history duringrenal replacement therapy was unremarkable. In January 2002,the patient underwent a cadaveric renal transplantation; thedonor 相似文献
7.
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Introduction
| Familial juvenile hyperuricaemic nephropathy (FJHN; OMIM 162000)is considered a rare cause of end-stage renal disease (ESRD).FJHN is characterized by hyperuricaemia and gout after adolescenceand the slow development of renal insufficiency, leading toESRD in adulthood. The disorder is characterized by a renalunder-secretion of urate, which may be detected already duringearly childhood [1]. The histological lesions in affected subjectsare characterized by unspecific tubulo-interstitial nephropathy.FJHN is inherited in an autosomal dominant pattern with a highpenetrance. Recently, the gene(s) for FJHN was localized toa candidate interval at the short arm of chromosome 16 [2,3].
Case
| We report a Caucasian four-generation family with FJHN withoutconsanguinity between spouses and a clustering of 相似文献
8.
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Introduction
| Nephronophthisis (NPHP) is an autosomal recessive disease withprevalent renal manifestations, characterized by occasionalcysts in medulla and severe tubulo-interstitial fibrosis, evolvingto end-stage renal failure [1]. It represents the most frequentcause of uraemia in children, with major clinical, physiologicaland social consequences including high costs for substitutiveapproaches and renal transplant. NPHP is a clinical and geneticheterogeneous disease with at least five genes ( NPHP1–5)identified and variable extra-renal manifestations [2–6].Retinal dysfunction constituting Senior Loken syndrome (SLS1–5)is the most common association [1]. Other organ defects identifyspecific subsets such as liver fibrosis in NPHP3 and situs inversusin NPHP2. NPHP1 [OMIM 相似文献
9.
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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
10.
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Why measure risk factors for vascular disease?
| Identifying cardiovascular risk factors among patients withchronic kidney disease (CKD) is potentially useful for two mainreasons. First, such risk factors may be used to predict thefuture risk of an event, which may help physicians to plan treatment.Second, they may be targets for intervention to prevent suchevents. It is now clear that a large number of risk factorsindependently predict the risk of cardiovascular outcomes amongdialysis patients [1] and among patients with lesser degreesof renal impairment [2]. But, although a risk score based onindependent risk factors can be assembled without particularregard to whether they are causal, treatments which modify aparticular risk factor will only be effective for the preventionof vascular disease if that risk factor is a cause of such disease.
Limitations of dialysis studies for identifying causes of vascular disease
| The starting point for identifying risk factors that might proveto be 相似文献
11.
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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
12.
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Introduction
| Sarcoidosis is a systemic granulomatous disorder of unknownetiology, characterized by chronic non-caseating epitheloidgranulomatous inflammation with tissue destruction [1,2]. Renalinvolvement affects 20% of patients with sarcoidosis [1,2] andcan be found in patients with no other localizations of thedisease [3]. A common cause of renal dysfunction is hypercalcaemiaand hypercalciuria leading to nephrocalcinosis [2]. Granulomatousinterstitial nephritis (GIN) is also a cause of renal dysfunction,in which the clinical picture and laboratory evidence of tubulardefects point to tubulo-interstitial nephritis [4]. Sarcoidosisis a systemic disease, affecting many organs. However, largevessel involvement such as 相似文献
13.
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Introduction
| Paradoxical embolism is a rare cause of severe renal arteryocclusion and is frequently under-diagnosed [1]. Rapid endovascular intervention with minimal morbidity may makeclot removal possible and reverse organ function [2,3]. We present here the case of a patient with an acute renal failuredue to a bilateral renal artery paradoxical embolism that wassuccessfully treated by a modified standard technique of anendovascular procedure, with a rapid mechanical and local pharmacologicalthrombolysis. The patient partially recovered her renal functionand was able to stop dialysis.
Case report
| A 70-year-old female with a past medical history of type IIdiabetes, hypertension and dyslipidaemia was admitted for pulmonaryembolism associated with a recurrent deep vein thrombosis ofthe right lower extremity. The anti-coagulation treatment wasinitially well tolerated, but had to 相似文献
14.
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Introduction
| In 1898 Bryant and White reported features of the conditionthat was later described as calciphylaxis by Selye in 1961 becauseof a pathophysiologic resemblance to anaphylaxis [1,2]. Calciphylaxis(or calcific uraemic arteriolopathy) is characterized by medialcalcification of small arterioles, intimal proliferation, fibrosisand thrombosis resulting in ischaemia, necrosis and superinfectionof the skin and subcutis. When renal function is normal, calciphylaxishas been reported infrequently, associated with conditions suchas primary hyperparathyroidism [3]. However, amongst patientswith chronic kidney disease (CKD) on dialysis, the annual incidencehas been estimated at 1–4%, with an apparent increaseover the past decades that may reflect the increased use ofcalcium-based phosphate binders [4,5]. For patients on dialysis,mortality rates are increased 8-fold if calciphylaxis develops[6]. The mortality of non-ulcerating types is 相似文献
15.
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Introduction
| Pregnancy in women with end-stage renal disease (ESRD) undergoingdialysis treatment is uncommon but increasingly observed overthe last few years [1]. The outcome in pregnancies in dialysedwomen is greatly influenced by maternal risk factors. Duringgestation, various risks may appear including the mother's fluidoverload, hypertension, anaemia and an increased risk for fetaland perinatal complications such as neonatal mortality, prematurityand small-for-gestational-age [2,3]. Here, we report on a 40-year-oldfemale patient who developed ESRD due to an extended Stanford-B-aneurysmof the aorta 1 year prior to conception. Nonetheless, the childwas delivered successfully by caesarian section after 31 weeksof gestation.
Case
| A 39-year-old female was referred to our centre with a hypertensivecrisis, dizziness, 相似文献
16.
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Introduction
| Proteinuria is a common finding in pregnancy and usually attributableto physiological changes that concurrently reduce serum albuminby 5–10 g/l. Urinary protein loss rarely exceeds 0.4 g/day,but nephrotic levels occur in up to 0.025% of all pregnancies[1], even in the absence of features of pre-eclampsia [2] orrenal impairment. Many patients with pregnancy-associated proteinuriawill remit spontaneously and may be managed conservatively withoutrenal biopsy. Non-specific glomerular lesions may be seen inassociation with pre-eclampsia [3]. Primary glomerular disease,diabetes and renal vein thrombosis may also produce nephroticlevels of proteinuria in pregnancy. Pre-existing renal diseasepredisposes subjects to develop hypertension and further accelerated 相似文献
17.
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Introduction
| Injury to the kidney can be initiated via diverse mechanisms,such as genetic defects, autoimmune reactions, environmentalinsults and metabolic defects [1,2]. Based on the kinetics ofdisease progression, renal injury is traditionally grouped aseither being an acute or chronic effect [3,4]. While the kidneydisplays an enormous potential to regenerate after acute renalinjury, chronic renal disease is generally irreversible [1,5,6].The switch from the normal potential to repair after acute injury,to an irreversible chronic disease phase, is not yet well understood.It has been 相似文献
18.
Over the past decade, bisphosphonate use in patients with variousforms of kidney disease has become widespread. The extensivetake up-of these agents by nephrologists reflects the twin perceptionsthat bisphosphonates are generally safe in patients with kidneydisease, and that skeletal protection, readily demonstrablein bisphosphonate-treated populations without kidney disease,is also achievable in patients with chronic kidney disease (CKD)and other forms of nephropathy. Unfortunately, both of theseperceptions are based on limited evidence and somewhat tenuousextrapolations [1,2].
The case for bisphosphonates in patients with renal disease
| In the non-renal population, convincing evidence exists to showthat bisphosphonates can effectively prevent, or at least attenuate,bone loss in glucocorticoid-treated patients [3–8]. Thereis evidence of significant fracture reduction in this patientgroup. Benefit is also seen in glucocorticoid-treated patientswith normal or near normal renal function and inflammatory disease[5]. It was reasonable, therefore, 相似文献
19.
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Introduction
| Collapsing glomerulopathy (CG) is a renal injury described initiallyin association with HIV-induced nephropathy but also seen increasinglyin non-HIV-infected individuals. Some authors recognise it asa separate clinicopathological variant of focal segmental glomerulosclerosis(FSGS) associated with nephritic syndrome, rapidly progressivechronic renal failure and the histopathologic features of glomerularcapillary collapse [1,2]. It has also been linked with otherviral infections including hepatitis C, but to date not withcytomegalovirus (CMV). There may be an association with lymphoproliferativedisorders and autoimmune disease, but this is less certain [3].We report the first case 相似文献
20.
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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
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