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  • 1
    Online Resource
    Online Resource
    Random Spot Urine Protein/Creatinine Ratio Is Unreliable for Estimating 24-Hour Proteinuria in Individual Systemic Lupus Erythematosus Nephritis Patients
    S. Karger AG ; 2009
    In:  Nephron Clinical Practice Vol. 113, No. 3 ( 2009-8-12), p. c177-c182
    Details
    In: Nephron Clinical Practice, S. Karger AG, Vol. 113, No. 3 ( 2009-8-12), p. c177-c182
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Recently the American Rheumatologic Association (ARA) recommended random spot urine protein/creatinine ratio (P/C) to monitor systemic lupus erythematosus (SLE) glomerulonephritis (GN). Shortly afterward, 2 works were published, designated Study 1 and Study 2, which are the only studies to test spot P/C in SLE GN. Here we evaluate Study 1 and Study 2, which came to different conclusions. 〈 i 〉 Methods: 〈 /i 〉 Study 1 compared spot P/C to the P/C of intended 24-hour collections 〉 50% complete, which reliably estimates 24-hour proteinuria. Study 2 compared spot P/C to the protein content of intended 24-hour collections 〉 80% complete. To compare studies, Study 2 data were converted to P/C ratios. 〈 i 〉 Results: 〈 /i 〉 Study 1 and Study 2 were found to be in agreement. Both showed that spot P/C and 24-hour P/C were highly correlated, but only when compared over the entire P/C range (0–8.0) (r = 0.842). Over the P/C range 0.5–3.0 (the most common P/C range encountered in SLE GN), correlation was present, but concordance was poor, rendering random P/C ratio unreliable. 〈 i 〉 Conclusions: 〈 /i 〉 Random spot P/C ratio is unreliable for detecting moderate proteinuria change. For example, random spot P/C would not reliably diagnose British Isles Lupus Assessment Group (BILAG) Category A or B proteinuric flares.
    Type of Medium: Online Resource
    ISSN: 1660-2110
    URL: Article
    DOI: 10.1159/000232599
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2009
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  • 2
    Online Resource
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    Oral Cyclophosphamide Is on the Verge of Extinction as Therapy for Severe Autoimmune Diseases (Especially Lupus): Should Nephrologists Care?
    S. Karger AG ; 2010
    In:  Nephron Clinical Practice Vol. 117, No. 1 ( 2010-8-3), p. c8-c14
    Details
    In: Nephron Clinical Practice, S. Karger AG, Vol. 117, No. 1 ( 2010-8-3), p. c8-c14
    Abstract: Some day we will have powerful targeted therapies for autoimmune diseases. Remission will be induced efficiently. Side effects will be mere ripples. Unfortunately, that day is not imminent. Current therapies are powerful but with unintended targets and side effects that can be equivalent to a sea change. For SLE, the current competition to select the ‘gold standard’ immunosuppressant has come down to two regimens: intravenous cyclophosphamide (IVCY, standard NIH protocol or its variations) versus oral mycophenolate (MMF). Until recently, IVCY reigned as the gold standard, a title it achieved through a curious journey that did not involve rigorous head-to-head competition. Oral cyclophosphamide (POCY) has not been invited to the current competition to select the gold standard immunosuppressant despite the substantial evidence that POCY can perform at least as well as IVCY or mycophenolate, and compared to IVCY, is far less expensive, easier for the patient, and maybe more effective in African-Americans. Here, we state the case for POCY as therapy for severe autoimmune diseases. We suggest that if POCY is allowed to compete, it will not disappoint.
    Type of Medium: Online Resource
    ISSN: 1660-2110
    URL: Article
    DOI: 10.1159/000319641
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
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  • 3
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    Differential Diagnosis of Glomerular Disease: A Systematic and Inclusive Approach
    S. Karger AG ; 2013
    In:  American Journal of Nephrology Vol. 38, No. 3 ( 2013), p. 253-266
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 38, No. 3 ( 2013), p. 253-266
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Glomerular disease is a complex and evolving topic. In evaluating a specific case it is not unusual for the clinician to ask: ‘Am I missing something? Should I biopsy? When? Should I treat first, then biopsy?' This work, which is both evidence and experience based, is intended to address each of these concerns and many other issues relevant to the differential diagnosis of glomerular disease. 〈 b 〉 〈 i 〉 Summary: 〈 /i 〉 〈 /b 〉 The central approach is the use of diagnostic algorithms that are based on quantitative measures routinely obtained early in the course of the diagnostic evaluation. The algorithms are designed to be easy to navigate, systematic, and inclusive. Also provided is a detailed and prioritized list of recommended diagnostic testing, and the rationale for each test. 〈 b 〉 〈 i 〉 Key Message: 〈 /i 〉 〈 /b 〉 This work is intended to facilitate accurate diagnosis in the individual patient presenting with evidence of glomerular disease.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000354390
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2013
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  • 4
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    A Multicenter Randomized Controlled Trial of Rituximab versus Cyclosporine in the Treatment of Idiopathic Membranous Nephropathy (MENTOR)
    S. Karger AG ; 2015
    In:  Nephron Vol. 130, No. 3 ( 2015), p. 159-168
    Details
    In: Nephron, S. Karger AG, Vol. 130, No. 3 ( 2015), p. 159-168
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Idiopathic membranous nephropathy remains the leading cause of nephrotic syndrome in Caucasian adults. Immunosuppressive therapy with cyclosporine (CSA) is often successful in reducing proteinuria, but its use is associated with a high relapse rate. Rituximab, a monoclonal antibody that specifically targets CD20 on the surface of B-cells, is effective in achieving a complete remission of proteinuria in patients with idiopathic membranous nephropathy. However, whether rituximab is as effective as CSA in inducing and maintaining complete or partial remission of proteinuria in these patients is unknown. The membranous nephropathy trial of rituximab (MENTOR) hypothesizes that B-cell targeting with rituximab is non-inferior to CSA in inducing long-term remission of proteinuria. 〈 b 〉 〈 i 〉 Methods and Design: 〈 /i 〉 〈 /b 〉 Patients with idiopathic membranous nephropathy, proteinuria ≥5 g/24 h, and a minimum of 3 months of Angiotensin-II blockade will be randomized into a 12-month treatment period with IV rituximab, 1,000 mg (2 infusions, 14 days apart; repeated at 6 months if a substantial reduction in proteinuria (equal to or 〉 25%) is seen at 6 months) or oral CSA 3.5-5 mg/kg/day for 6 months (continued for another 6 months if a substantial reduction in proteinuria (equal to or 〉 25%) is seen at 6 months). The efficacy of treatment will be assessed by the remission status (based on changes in proteinuria) at 24 months from randomization. Patient safety will be assessed via collection of adverse event data and evaluation of pre- and posttreatment laboratory data. At the 6-month post-randomization visit, patients who have been randomized to either CSA or rituximab but who do not have a reduction in proteinuria ≥25% (confirmed on repeat measurements within 2 weeks) will be considered treatment failures and exit the study. 〈 b 〉 〈 i 〉 Discussion: 〈 /i 〉 〈 /b 〉 This study will test for the first time whether treatment with rituximab is non-inferior to CSA in inducing long-term remission (complete or partial) of proteinuria in patients with idiopathic membranous nephropathy.
    Type of Medium: Online Resource
    ISSN: 1660-8151 , 2235-3186
    URL: Article
    DOI: 10.1159/000430849
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
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  • 5
    Online Resource
    Online Resource
    Relapse or Worsening of Nephrotic Syndrome in Idiopathic Membranous Nephropathy Can Occur even though the Glomerular Immune Deposits Have Been Eradicated
    S. Karger AG ; 2011
    In:  Nephron Clinical Practice Vol. 119, No. 2 ( 2011-7-8), p. c145-c153
    Details
    In: Nephron Clinical Practice, S. Karger AG, Vol. 119, No. 2 ( 2011-7-8), p. c145-c153
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Relapse or worsening of nephrotic syndrome (NS) in idiopathic membranous nephropathy (IMN) is generally assumed to be due to recurrent disease. Here we document that often that may not be the case. 〈 i 〉 Subjects and Methods: 〈 /i 〉 This is a prospective study of 7 consecutive IMN patients whose renal status improved, then worsened after completing a course of immunosuppressive therapy. Each underwent detailed testing and repeat kidney biopsy. 〈 i 〉 Results: 〈 /i 〉 In 4 patients (group A), the biopsy showed recurrent IMN (fresh subepithelial deposits). Immunosuppressive therapy was begun. In the other 3 patients (group B), the biopsy showed that the deposits had been eradicated. However, the glomerular basement membrane (GBM) was thickened and vacuolated. Immunosuppressive therapy was withheld. Groups A and B were comparable except that group B had very high intakes of salt and protein, based on 24-hour urine testing. Reducing their high salt intake sharply lowered proteinuria to the subnephrotic range and serum creatinine stabilized. 〈 i 〉 Conclusion: 〈 /i 〉 This work is the first to demonstrate that relapse/worsening of NS can occur in IMN even though the GBM deposits have been eradicated. High salt and protein intake in combination with thickened and vacuolated GBM appears to be the mechanism.
    Type of Medium: Online Resource
    ISSN: 1660-2110
    URL: Article
    DOI: 10.1159/000324762
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
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  • 6
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    Online Resource
    When Size Matters: Diagnostic Value of Kidney Biopsy according to the Gauge of the Biopsy Needle
    S. Karger AG ; 2013
    In:  American Journal of Nephrology Vol. 37, No. 3 ( 2013), p. 249-254
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 37, No. 3 ( 2013), p. 249-254
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Kidney biopsy is a vital tool in the diagnosis of kidney disease. Although it has become a routine procedure, it is not complication-free. Some serious complications of percutaneous kidney biopsy include retroperitoneal hemorrhage and death. There is an increased belief that smaller biopsy needle size results in a lower complication rate. As renal pathologists, we witness an increased number of kidney biopsies performed with a small needle size (as low as gauge 22), which results in inadequate tissue sampling and often non-diagnostic biopsy results. Herein we report the diagnostic value of kidney biopsies according to the size of the biopsy needles. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We performed kidney biopsies from nephrectomy specimens using biopsy needles of different sizes. Morphologic parameters were analyzed. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 We found that biopsies performed by small needles (gauges 20 and 22) contain significantly lower numbers of glomeruli and blood vessels, which limits pathologic evaluation. Data from our institution do not show differences in kidney biopsy complication rates between 16- and 18-gauge needles. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Our data indicate that small biopsy needles do not provide sufficient material for diagnosis, and they increase the likelihood for a repeat biopsy.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000347219
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2013
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  • 7
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    Online Resource
    Warfarin Therapy That Results in an International Normalization Ratio above the Therapeutic Range Is Associated with Accelerated Progression of Chronic Kidney Disease
    S. Karger AG ; 2010
    In:  Nephron Clinical Practice Vol. 115, No. 2 ( 2010-4-22), p. c142-c146
    Details
    In: Nephron Clinical Practice, S. Karger AG, Vol. 115, No. 2 ( 2010-4-22), p. c142-c146
    Abstract: 〈 i 〉 Background/Aims: 〈 /i 〉 We had previously reported that acute kidney injury (AKI) in warfarin-treated chronic kidney disease (CKD) patients may occur shortly after an acute increase in the International Normalization Ratio (INR) 〉 3.0 with formation of occlusive red blood casts. Recovery from this warfarin-associated AKI is poor. Here we investigated whether excessive warfarin therapy could accelerate the progression of CKD. 〈 i 〉 Methods: 〈 /i 〉 We analyzed serum creatinine (SC) and INR in 103 consecutive CKD patients on warfarin therapy in our Nephrology program from 2005 to the present. 〈 i 〉 Results: 〈 /i 〉 Forty-nine patients experienced at least 1 episode of INR 〉 3.0. Of these, 18 patients (37%, Group 1) developed an unexplained increase in SC ≧0.3 mg/dl coincident with INR 〉 3.0 (mean SC increase 0.61 ± 0.44 mg/dl); 31 patients (63%, Group 2) showed stable SC (mean SC change 0.04 ± 0.19 mg/dl). Subsequent CKD progression was accelerated in Group 1, but not in Group 2. The 2 groups were not different with respect to demographics, comorbidities, blood pressure, or therapies. However, African Americans were overrepresented in Group 1 (p = 0.035). 〈 i 〉 Conclusions: 〈 /i 〉 Overanticoagulation is associated with faster progression of CKD in a high percentage of patients. Our results indicate the need for prospective trials. Nevertheless, we suggest that our findings are sufficiently compelling at this point to justi- fy extra caution in warfarin-treated CKD patients to avoid overanticoagulation.
    Type of Medium: Online Resource
    ISSN: 1660-2110
    URL: Article
    DOI: 10.1159/000312877
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
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  • 8
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    Tolerating Increases in the Serum Creatinine following Aggressive Treatment of Chronic Kidney Disease, Hypertension and Proteinuria: Pre-Renal Success
    S. Karger AG ; 2012
    In:  American Journal of Nephrology Vol. 36, No. 5 ( 2012), p. 430-437
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 36, No. 5 ( 2012), p. 430-437
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Blood pressure (BP) reduction in patients with chronic kidney disease (CKD), particularly with a renin-angiotensin system inhibitor (RASI), commonly leads to an initial decrease in glomerular filtration rate. The current clinical guideline, based on studies with single RASIs, is to tolerate an increase in the serum creatinine only up to 30%. This guideline has aptly guided CKD care for over a decade, but should be updated in the contemporary context of more aggressive RASI 〈 b 〉 〈 /b 〉 and diuretic use. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 This study is a retrospective review of 48 mostly African-American patients with CKD treated with multiple and/or high-dose renin-angiotensin system (RAS) inhibition and diuretics, targeting both low BP and reduction of urine protein. RASI was not reduced in response to initial increases in serum creatinine greater than 30%. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 A clinically well-tolerated increase in serum creatinine over 30% during the first year occurred in 41% of the patients. Treatment was unaltered, and target goals for BP and urine protein were typically achieved. After the point of maximal serum creatinine in the first year, these patients had minimal progression of disease over the next 6 years, with a long-term estimated glomerular filtration rate slope of only –0.52 ml/min/year/1.73 m 〈 sup 〉 2 〈 /sup 〉 . Only 25% progressed to end-stage renal disease or death. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 The 30% limitation to initial increases in the serum creatinine still pertains for single RASI at usual doses. However, favorable long-term outcomes suggest that initial increases over 30% should be tolerated in the context of dual goal-directed, more aggressive RASI and diuretic use.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000343453
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
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  • 9
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    Brodifacoum Induces Early Hemoglobinuria and Late Hematuria in Rats: Novel Rapid Biomarkers of Poisoning
    S. Karger AG ; 2015
    In:  American Journal of Nephrology Vol. 41, No. 4-5 ( 2015), p. 392-399
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 41, No. 4-5 ( 2015), p. 392-399
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Brodifacoum (BDF) is a superwarfarin that is used primarily as a rodenticide. There have been increasing numbers of reports of human cases of accidental or intentional BDF ingestion with high mortality rate. Its broad availability and high lethality suggest that BDF should be considered a potential chemical threat. Currently, there is no biomarker for early detection of BDF ingestion in humans; patients typically present with severe coagulopathy. Since we demonstrated earlier that warfarin can induce acute kidney injury with hematuria, we tested whether BDF would also lead to change in urinary biomarkers. 〈 b 〉 〈 i 〉 Material and Methods: 〈 /i 〉 〈 /b 〉 BDF was administered to Sprague Dawley rats via oral gavage. N-acetylcysteine (NAC) was given per os in drinking water 24 h prior to BDF. Urinalysis was performed at different times after BDF administration. Anticoagulation and serum creatinine levels were analyzed in the blood. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 We observed that within a few hours the animals developed BDF-dose-dependent transient hemoglobinuria, which ceased within 24 h. This was accompanied by a transient decrease in hematocrit, gross hemolysis and an increase in free hemoglobin in the serum. At later times, animals developed true hematuria with red blood cells in the urine, which was associated with BDF anticoagulation. NAC prevented early hemoglobinuria, but not late hematuria associated with BDF. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 We propose that transient early hemoglobinuria (associated with oxidative stress) with consecutive late hematuria (associated with anticoagulation) are novel biomarkers of BDF poisoning, and they can be used in clinical setting or in mass casualty with BDF to identify poisoned patients.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000433568
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
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