1,721,121 research outputs found

    Cardiorenal syndrome: causes, diagnosis and treatment of congestive nephropathy

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    Zusammenfassung Die kongestive Nephropathie (CN) ist eine Entität des kardiorenalen Syndroms, die wesentlich auf dem Boden einer venösen Kongestion und neurohormonellen Aktivierung entsteht. Eine Herzinsuffizienz, pulmonalarterielle Hypertonie, isolierte Trikuspidalklappeninsuffizienz und angeborene Herzfehler sind die häufigsten Ursachen. Es gibt bis dato keine allgemein akzeptierten diagnostischen Kriterien, jedoch scheint das Erfassen des intrarenalen venösen Blutflusses mittels Dopplersonographie die geeignetste Methode zu sein. Mit dieser Technik kann ein kontinuierlicher venöser Fluss (keine Kongestion) von den diskontinuierlichen Flussmustern pulsatil (leichte Kongestion), biphasisch (moderate Kongestion) und monophasisch (schwere Kongestion) differenziert werden. Der Venous Impedance Index und der Renal Venous Stasis Index sind zusätzliche dopplersonographische Kriterien zum Erfassen einer CN. Therapien mit Schleifendiuretika und/oder Natrium-Glukose-Kotransporter-2(SGLT-2)-Inhibitoren können eine venöse Kongestion nachweislich verbessern.Abstract Congestive nephropathy (CN) is an entity of the cardiorenal syndrome that essentially arises from venous congestion and neurohormonal activation. The most common underlying causes include heart failure, pulmonary arterial hypertension, isolated tricuspid valve insufficiency and congenital heart defects. Currently, there are no universally accepted diagnostic criteria; however, the most suitable method appears to be the recording of intrarenal venous blood flow using Doppler sonography. A distinction can be made between continuous venous flow (no congestion) and discontinuous flow patterns, categorized as pulsatile (mild), biphasic (moderate) and monophasic (severe congestion). The venous impedance index (VII) and the renal venous stasis index (RVSI) are additional Doppler sonographic criteria for detecting CN. Evidence supports the efficacy of loop diuretics and/or the administration of sodium-glucose cotransporter 2 (SGLT2) inhibitors in the management of venous congestion.Zusammenfassung Die kongestive Nephropathie (CN) ist eine Entität des kardiorenalen Syndroms, die wesentlich auf dem Boden einer venösen Kongestion und neurohormonellen Aktivierung entsteht. Eine Herzinsuffizienz, pulmonalarterielle Hypertonie, isolierte Trikuspidalklappeninsuffizienz und angeborene Herzfehler sind die häufigsten Ursachen. Es gibt bis dato keine allgemein akzeptierten diagnostischen Kriterien, jedoch scheint das Erfassen des intrarenalen venösen Blutflusses mittels Dopplersonographie die geeignetste Methode zu sein. Mit dieser Technik kann ein kontinuierlicher venöser Fluss (keine Kongestion) von den diskontinuierlichen Flussmustern pulsatil (leichte Kongestion), biphasisch (moderate Kongestion) und monophasisch (schwere Kongestion) differenziert werden. Der Venous Impedance Index und der Renal Venous Stasis Index sind zusätzliche dopplersonographische Kriterien zum Erfassen einer CN. Therapien mit Schleifendiuretika und/oder Natrium-Glukose-Kotransporter-2(SGLT-2)-Inhibitoren können eine venöse Kongestion nachweislich verbessern.Abstract Congestive nephropathy (CN) is an entity of the cardiorenal syndrome that essentially arises from venous congestion and neurohormonal activation. The most common underlying causes include heart failure, pulmonary arterial hypertension, isolated tricuspid valve insufficiency and congenital heart defects. Currently, there are no universally accepted diagnostic criteria; however, the most suitable method appears to be the recording of intrarenal venous blood flow using Doppler sonography. A distinction can be made between continuous venous flow (no congestion) and discontinuous flow patterns, categorized as pulsatile (mild), biphasic (moderate) and monophasic (severe congestion). The venous impedance index (VII) and the renal venous stasis index (RVSI) are additional Doppler sonographic criteria for detecting CN. Evidence supports the efficacy of loop diuretics and/or the administration of sodium-glucose cotransporter 2 (SGLT2) inhibitors in the management of venous congestion

    Decompensated Heart Failure and Renal Failure: What Is the Current Evidence?

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    PURPOSE OF REVIEW Acute decompensated heart failure (ADHF) is one of the biggest challenges in the management of chronic heart failure. Despite several advances in medical and device therapy, high readmission and mortality rates continue to be a burden on healthcare systems worldwide. The aim of the current review is to provide an overview on current as well as future approaches in cardiorenal interactions in patients with ADHF. RECENT FINDINGS One of the strongest predictors of adverse outcomes in ADHF is renal dysfunction, referred to as cardiorenal syndromes (CRS) or cardiorenal interactions. Patients with ADHF frequently develop worsening of renal function (WRF) and/or acute kidney injury (AKI). Recent studies brought new information about biomarkers in diagnosing and predicting prognosis of CRS. Among others, dry weight at hospital discharge is considered a surrogate marker of successful treatment in ADHF patients with/without renal dysfunction. The etiology of WRF appears to be an important factor for determining risk related to WRF as well as clinical management. The hypertonic saline used as adjunctive therapy for intravenous loop diuretics and/or induction of aquaresis (e.g., using tolvaptan) may be promising and efficient approaches in the future

    Immunoadsorption in steroid-refractory multiple sclerosis

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    Multiple sclerosis (MS) is an autoimmune disorder, with involvement of both the humoral and cellular components of the immune system. The use of plasma exchange (PE) in steroid-refractory relapses has become an integral part of national and international guidelines for the treatment of steroid-resistant relapses of MS with an efficacy of 40-70%. So far, 6 studies of immunoadsorption (IA) treatment in different forms of MS have been published, 4 of them in steroid-refractory MS relapses. These 4 studies revealed a significant clinical improvement in 73-85% of patients with steroid-refractory MS relapses. However in MS patients with non-active relapsing-remitting or secondary progressive course, there was no clinical improvement. Despite the limited number of patients and studies, these data suggest a reasonably similar efficacy of IA in the treatment of steroid-refractory MS relapses compared to PE. More prospective trials are needed to confirm and extend these results. (C) 2012 Elsevier Ireland Ltd. All rights reserved.Diamed (Cologne, Germany

    Decrease in serum tacrolimus level and rise in serum creatinine under late addition of Cinacalcet in a renal transplant recipient with hyperparathyroidism: A case report

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    Cinacalcet is a calcimimetic drug that has been approved for treatment of secondary and tertiary hyperparathyroidism in patients with renal failure requiring renal replacement therapy. A few cases of successful treatment in renal transplant patients immunosuppressed with cyclosporine have been reported. Herein we have reported the case of a 48-year-old renal transplant recipient presenting with secondary hypercalcemic hyperparathyroidism (parathyroid hormone [PTH] 896 pg/mL; total calcium, up to 3.3 mmol/L) under immunosuppressive therapy with tacrolimus. Owing to substantial comorbidity and a high operative risk, we decided to initiate a therapeutic trial with cinacalcet. Using a daily dose of 30 mg of Cinacalcet, normal calcium levels and a mild fall in PTH levels (decline of 62 pg/mL) were achieved within the first week of treatment. At this point, we also observed a marked decrease in tacrolimus levels (from 6.3 to 2.6 mg/dL) without any change in concomitant medications. Thus, we adapted the tacrolimus dosage. Concurrent with cinacalcet therapy, there was a rise in serum creatinine levels (from 3.9 to 4.9 mg/dL before discontinuation of cinacalcet), which was not reversible after termination of 3 weeks of treatment with cinacalcet, but continued. Cinacalcet and tacrolimus are both metabolized via cytochrome P 450. The documented decrease in tacrolimus serum levels, suggested a drug- drug interaction between tacrolimus and cinacalcet. The irreversible deterioration in renal function may be attributed to nephrotoxic properties of cinacalcet, but may also indicate an acceleration of the natural course of chronic allograft nephropathy

    Plasma Exchange or Immunoadsorption in Demyelinating Diseases: A Meta-Analysis

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    Multiple sclerosis (MS) is an inflammatory disease mainly affecting the central nervous system. In MS, abnormal immune mechanisms induce acute inflammation, demyelination, axonal loss, and the formation of central nervous system plaques. The long-term treatment involves options to modify the disease progression, whereas the treatment for the acute relapse has its focus in the administration of high-dose intravenous methylprednisolone (up to 1000 mg daily) over a period of three to five days as a first step. If symptoms of the acute relapse persist, it is defined as glucocorticosteroid-unresponsive, and immunomodulation by apheresis is recommended. However, several national and international guidelines have no uniform recommendations on using plasma exchange (PE) nor immunoadsorption (IA) in this case. A systematic review and meta-analysis was conducted, including observational studies or randomized controlled trials that investigated the effect of PE or IA on different courses of MS and neuromyelitis optica (NMO). One thousand, three hundred and eighty-three patients were included in the evaluation. Therapy response in relapsing-remitting MS and clinically isolated syndrome was 76.6% (95%CI 63.7–89.8%) in PE- and 80.6% (95%CI 69.3–91.8%) in IA-treated patients. Based on the recent literature, PE and IA may be considered as equal treatment possibilities in patients suffering from acute, glucocorticosteroid-unresponsive MS relapses

    Impact of LDL-Apheresis on inflammation and microcirculation

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    Lipid-apheresis (LIPID-A) is highly effective in reduction of pro-atherosclerotic LDL-cholesterol and lipoprotein (a). It has been demonstrated in prospective and retrospective analyses to reduce major cardiovascular events. In addition to improvement of pro-atherosclerotic lipoprotein milieu, LIPID-A exerts pleiotropic effects on inflammation and micro-circulation. Several pro-inflammatory cyto- and chemokines as well as adhesion molecules are cleared by distinct LIPID-A methods. Moreover, a single LIPID-A can induce proliferative activity of circulating endothelial progenitor cells and by this way, enhance vascular repair capacity. Microcirculation is modified by LIPID-A by influencing the balance of vasoconstrictory and -dilatative mediators, plasma viscosity and erythrocyte aggregation resulting in an activation of functional capillary reserve and blood flow
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