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Entries Tagged as 'J Nephrol'

Estimate of renal function in oldest old inpatients by MDRD study equation, Mayo Clinic equation and creatinine clearance.

June 23rd, 2010 · Start a Discussion

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Estimate of renal function in oldest old inpatients by MDRD study equation, Mayo Clinic equation and creatinine clearance.

J Nephrol. 2010 May-Jun;23(3):306-13

Authors: Carnevale V, Pastore L, Camaioni M, Mellozzi M, Sabatini M, Arietti E, Fusilli S, Scillitani A, Pontecorvi M

BACKGROUND: Patients older than 85 years are increasingly admitted to hospital care settings. Despite this, the clinical employment of equations for estimating glomerular filtration rate (GFR) has been scarcely investigated so far in this age group. Our study compared 2 commonly employed equations to estimate GFR, as well as measured 24-hour creatinine clearance (CrCl), in patients aged >or=85 years. METHODS: Seventy-three patients consecutively admitted over 4 months to our Internal Medicine Department had an accurate 24-hour urinary collection, as well as serum and urinary creatinine determinations. Measured CrCl was compared with the GFR values estimated by the Modification of Diet in Renal Disease (MDRD) Study and Mayo Clinic quadratic (MCQ) equations. RESULTS: GFR values derived by MDRD and MCQ equations and CrCl significantly differed from each other in the whole sample. CrCl negatively correlated with age (r=-0.389, p<0.001), at variance with GFR levels obtained by both the MDRD and the MCQ equations. The 3 estimates of renal function significantly correlated with each other, these correlations persisting after correcting for age, serum albumin and 24-hour urinary creatinine. Despite the visual impression of Bland and Altman plots, the overall agreement between methods was poor. Moreover, the proportion of patients classified by the 3 GFR estimates into each stage of kidney disease as specified in the Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines significantly differed. CONCLUSIONS: In patients older than 85 years, the tested equations for estimation of GFR and the measured 24-hour CrCl provide significantly different results, so that they may not be used interchangeably in clinical practice.

PMID: 20155719 [PubMed - indexed for MEDLINE]

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Contrast-induced nephropathy and its prevention: What do we really know from evidence-based findings?

September 2nd, 2009 · Start a Discussion

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Contrast-induced nephropathy and its prevention: What do we really know from evidence-based findings?

J Nephrol. 2009 May-Jun;22(3):333-51

Authors: Reddan D, Laville M, Garovic VD

INTRODUCTION: Contrast-induced acute kidney injury, also referred to as contrast-induced nephropathy (CIN), is a potentially serious renal complication associated with the use of iodinated contrast media (CM) in patients at risk. With the dramatic growth in contrast-enhanced imaging services worldwide, including procedures involving exposure to iodinated CM, efforts to reduce the occurrence of CIN have received considerable attention in recent years. To date, these efforts have met with little success since the 12% prevalence of CIN today remains unchanged from 2 decades ago. METHODS: We conducted a systematic literature review of the most recent evidence available from published reports of contemporary (2000-2008) prospective, randomized, controlled trials that have investigated CIN either by comparing CM or by comparing preventive strategies. The objective was to critically review the findings in light of several aspects of study design and then to establish a set of parameters for consideration in the planning of future CIN trials so as to optimize the strength of evidence obtained. RESULTS: Whether future CIN trials are investigating comparative CM nephrotoxicity or dealing with prophylactic strategies for risk reduction, the complexities that must be addressed include a standardized definition of CIN, appropriate timing of SCr measurements with timing standardized for all subjects in a given study population, awareness of study population risk profile, hydration protocols, and pharmacological prophylactic strategies. CONCLUSIONS: Large, well-designed trials (ideally with hard clinical outcome measures) that consider all the complexities involved in CIN and its prevention are needed before the clinical community has the evidence-based direction required for optimized patient care.

PMID: 19557710 [PubMed - indexed for MEDLINE]

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Nephrogenic systemic fibrosis an unsolved riddle.

July 6th, 2009 · Start a Discussion

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Nephrogenic systemic fibrosis an unsolved riddle.

J Nephrol. 2009 Mar-Apr;22(2):203-7

Authors: Graziani G, Montanelli A, Brambilla S, Balzarini L

Nephrogenic systemic fibrosis (NSF) is an emergent scleroderma-like disease progressively inducing a skin and joint severe dermal fibrosis. Until now there have been about 215 cases reported in NSF registry, linked to the use of Gadolinium as contrast agent for Magnetic Resonance. The pathogenesis of NSF is unexplained, and the factor or factors triggering the onset of the disease are a matter of debate. The toxic Gd effect on tissues of uremic patients may be linked to the long Gd half-life. Alternatively, according to the transmetallation theory, Gd may easily be released from linear versus cyclic chelating agents exchanged with other metals. Despite many studies indicating exposure to Gd in end-stage renal disease (ESRD) or hemodialysis as a trigger of NSF, a certain cause-effect relationship has still not been found. Other epidemiological studies report cases of NSF without previous Gd infusion. Another intriguing hypothesis is the possible role of lanthanum carbonate, which like Gd is a rare earth element. The lanthanum toxicity theory may explain the diffusion of Gd-induced NSF only in countries where the use of lanthanum carbonate was introduced some years ago (e.g., United States and northern Europe). In spite of the tight linkage reported between Gd infusion and NSF occurrence in ESRD and HD patients,the prevalence of this dermal severe disease ranges from 0.4 to 0.7%. Therefore the nephrologist, must keep this in mind and advise patients that the risk of renal impairement induced by iodinated contrast media infusion, is exceedingly more elevated than the occurrence of Gd-induced NSF which is below 1%.

PMID: 19384837 [PubMed - indexed for MEDLINE]

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Catastrophic antiphospholipid syndrome: report of 4 cases.

March 24th, 2008 · Start a Discussion

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Catastrophic antiphospholipid syndrome: report of 4 cases.

J Nephrol. 2007 Nov-Dec;20(6):739-44

Authors: Sinico RA, Di Toma L, Sabadini E, Renoldi P, Li Vecchi M

Catastrophic antiphospholipid syndrome (CAPS), described by Asherson in 1992, is a rare form of antiphospholipid syndrome resulting in multiorgan failure with a mortality rate of about 50%. The syndrome occurs in patients with either systemic lupus erythematosus and other rheumatic diseases (systemic sclerosis, rheumatoid arthritis, primary Sjogren syndrome) or alone. Whereas in “classic” antiphospholipid syndrome (APS), medium-large vessels are involved, a diffuse small vessel ischemia and thrombosis (microangiopathic disease) leading to a severe multiorgan dysfunction is predominant in CAPS. “Trigger” factors have been demonstrated in 45% of patients, but in the majority, they remain unknown. Not infrequently, CAPS arises in patients without any previous thrombotic history. The kidney is the organ most commonly affected, followed by the lung, the central nervous system, the heart and the skin. Disseminated intravascular coagulation occurs in approximately 13% of patients. The present study reports the clinical and serological features of 4 patients affected by this rare form of antiphospholipid syndrome. Nephrologists should be aware of the possibility of this syndrome as a cause of multiorgan failure since prompt recognition is essential for effective treatment.

PMID: 18046677 [PubMed - indexed for MEDLINE]

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Tags: J Nephrol