Jack F M Wetzels

Radboud University Medical Centre (Radboudumc), Nymegen, Gelderland, Netherlands

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Publications (380)2049.98 Total impact

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    ABSTRACT: . Urinary excretion of alpha-1-microglobulin (α1m) and beta 2-microglobulin (β2m) reflects tubular damage and predicts outcome in patients with idiopathic membranous nephropathy (iMN) with reasonable accuracy. Urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) are novel biomarkers of tubular damage. We investigated if these markers could improve prediction of outcome in iMN. . We measured KIM-1 and NGAL in urine samples from patients with iMN, who had nephrotic proteinuria and normal renal function. Excretion of α1m and β2m had been measured previously. Progression was defined as a serum creatinine rise > 30%, a rise in serum creatinine to an absolute value of ⩾ 135 µmol/L, or a clinical decision to start immunosuppressive therapy. Remission was defined as proteinuria < 3.5 g/day and > 50% reduction from baseline. . Sixty-nine patients were included. Median follow up was 35 months (interquartile range 18 - 63 months). Progression occurred in 30 patients (44%), and spontaneous remission in 36 (52%). KIM-1 and NGAL excretion rates were significantly correlated with each other, and with α1m and β2m. The areas under the receiver operating characteristic curves for progression were 0.75 (0.62 - 0.87) for KIM-1 and 0.74 (0.62 - 0.87) for NGAL. In multivariate analysis with either α1m or β2m, KIM-1 and NGAL did not independently predict outcome. . KIM-1 and NGAL excretion rates correlated with excretion rates of other tubular damage markers and predicted outcome in patients with iMN. They did not add prognostic value compared to measurement of either α1m or β2m. KEY: WORDS: : Membranous nephropathy; KIM-1; NGAL; Nephrotic syndrome; Biomarkers; Prognosis. © 2015 Sage Publications, Inc.
    Annals of Clinical Biochemistry 03/2015; DOI:10.1177/0004563215579694 · 2.08 Impact Factor
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    ABSTRACT: The Modification of Diet in Renal Disease (MDRD) formula is widely used in clinical practice to assess the correct drug dose. This formula is based on serum creatinine levels which might be influenced by chronic diseases itself or the effects of the chronic diseases. We conducted a systematic review to determine the validity of the MDRD formula in specific patient populations with renal impairment: elderly, hospitalized and obese patients, patients with cardiovascular disease, cancer, chronic respiratory diseases, diabetes mellitus, liver cirrhosis and human immunodeficiency virus. We searched for articles in Pubmed published from January 1999 through January 2014. Selection criteria were (1) patients with a glomerular filtration rate (GFR) < 60 ml/min (/1.73m2), (2) MDRD formula compared with a gold standard and (3) statistical analysis focused on bias, precision and/or accuracy. Data extraction was done by the first author and checked by a second author. A bias of 20% or less, a precision of 30% or less and an accuracy expressed as P30% of 80% or higher were indicators of the validity of the MDRD formula. In total we included 27 studies. The number of patients included ranged from 8 to 1831. The gold standard and measurement method used varied across the studies. For none of the specific patient populations the studies provided sufficient evidence of validity of the MDRD formula regarding the three parameters. For patients with diabetes mellitus and liver cirrhosis, hospitalized patients and elderly with moderate to severe renal impairment we concluded that the MDRD formula is not valid. Limitations of the review are the lack of considering the method of measuring serum creatinine levels and the type of gold standard used. In several specific patient populations with renal impairment the use of the MDRD formula is not valid or has uncertain validity.
    PLoS ONE 03/2015; 10(3):e0116403. DOI:10.1371/journal.pone.0116403 · 3.53 Impact Factor
  • Jack F.M. Wetzels, Nicole C.A.J. van de Kar
    American Journal of Kidney Diseases 02/2015; 65(2). DOI:10.1053/j.ajkd.2014.04.039 · 5.76 Impact Factor
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    ABSTRACT: Cardiovascular risk is increased in patients with chronic kidney disease (CKD). Fibroblast growth factor 23 (FGF23) has emerged as an important, independent predictor of outcome in CKD patients. High FGF23 may, however, be a reflection of renal tissue resistance to its actions, reflected by low fractional excretion of phosphate (FePi). We evaluated the modifying effect of FePi on the association between FGF23 and outcome in patients with CKD stage 3-4. An analysis was performed in a subset of 166 adult patients of two participating centers of the MASTERPLAN trial of whom urine samples at baseline were available to calculate FePi. Outcome was defined as a composite of death, renal failure (defined as need for renal replacement therapy or doubling of serum creatinine) and cardiovascular events (myocardial infarction, cerebrovascular accident, percutaneous transluminal coronary angioplasty or coronary artery bypass graft. Patients were categorized by FGF23 and FePi. A product term was added to Cox regression and RERIs were calculated. Patients had a median estimated glomerular filtration rate (eGFR) of 36 ml/min/1.73 m(2) [interquartile range (IQR) 27-44], serum phosphate 1.04 mmol/l (IQR 0.92-1.20), FGF23 140 RU/ml (IQR 81-236) and FePi 0.32 (IQR 0.25-0.44). A total of 96 events occurred during 5 years of follow up. LnFGF23 was a significant, independent predictor for the composite outcome [hazard ratio (HR) 2.13, 95 % confidence interval (CI) 1.53-2.95]. FePi did not modify the relation between FGF23 and outcome in these patients with CKD. Our study shows that FGF23 itself, but not its renal tissue resistance as reflected by FePi, is an important risk factor for clinical events in subjects with CKD stage 3-4.
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    ABSTRACT: Since the beginning of living donor kidney transplantation, physicians have expressed concern about the possibility that unilateral nephrectomy can be harmful to a healthy individual. To investigate if the elevated intra-abdominal pressure (IAP) during laparoscopic donor nephrectomy causes early damage to the remaining kidney we evaluated urine biomarkers after laparoscopic donor nephrectomy. We measured albumin and alpha-1-microglobulin (α-1-MGB) in urine samples collected during and after open and laparoscopic donor nephrectomy and laparoscopic cholecystectomy and colectomy. Additionally, kidney injury molecule 1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) were measured in urine samples collected during and after laparoscopic donor nephrectomy and colectomy. The same biomarkers were studied in patients randomly assigned to standard or low IAP during laparoscopic donor nephrectomy. We observed a peak in urinary albumin excretion during all procedures. Urine α-1-MGB rose in the post-operative period with a peak on the third postoperative day after donor nephrectomy. Urine α-1-MGB did not increase after laparoscopic cholecystectomy and colectomy. After laparoscopic nephrectomy we observed slight increases in urine KIM 1 during surgery and in urine NGAL at day 2-3 after the procedure. After laparoscopic colectomy both KIM-1, and NGAL were increased in the postoperative period. There were no differences between the high and low pressure procedure. Elevated urinary α-1-MGB suggests kidney damage after donor nephrectomy, occurring irrespective of IAP during the laparoscopic procedure. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Transplant International 01/2015; DOI:10.1111/tri.12523 · 3.16 Impact Factor
  • Rutger J Maas, Jeroen K Deegens, Jack F Wetzels
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    ABSTRACT: The term idiopathic nephrotic syndrome (iNS) traditionally covers minimal change disease and primary focal segmental glomerulosclerosis (FSGS), now thought to be separate disease entities. Clinical and experimental evidence suggest that circulating permeability factors are involved in their pathogenesis. In the past four decades, many investigators have searched for the responsible factors, thus far with little success. The recent report of the soluble urokinase plasminogen activator receptor as a causative factor in FSGS has received much attention, but again the initially promising findings were not confirmed. We describe the history of the search for permeability factors, discuss the pitfalls that are likely responsible for the lack of success and propose criteria that should be used in future studies when evaluating candidate permeability factors. © The Author 2014. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
    Nephrology Dialysis Transplantation 12/2014; 29(12):2207-2216. DOI:10.1093/ndt/gfu355 · 3.49 Impact Factor
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    ABSTRACT: Background & AimSeveral trials have demonstrated that somatostatin analogues decrease liver volume in mixed populations of patients with autosomal dominant polycystic kidney disease (ADPKD) and isolated polycystic liver disease. Chronic renal dysfunction in ADPKD may affect treatment efficacy of lanreotide and possibly enhances risk for adverse events. The aim of this open-label clinical trial (RESOLVE trial) was to assess efficacy of 6 months lanreotide treatment 120 mg subcutaneously every 4 weeks in ADPKD patients with symptomatic polycystic liver disease.Methods Primary outcome was change in liver volume after 6 months, secondary outcomes were changes in kidney volume, eGFR, symptom relief and health-related quality of life (Euro-Qol5D). We excluded patients with an estimated glomerular filtration rate (eGFR) < 30 ml/min/1.73m2. We used the Wilcoxon signed-rank test or paired two-sided t-test to analyze within-group differences.ResultsWe included 43 ADPKD patients with polycystic liver disease (84% female, median age 50 years, mean eGFR 63 ml/min/1.73m2). Median liver volume decreased from 4,859 ml to 4,595 ml (-3.1%;p<0.001), and median kidney volume decreased from 1,023 ml to 1,012 ml (-1.7%;p=0.006). eGFR declined 3.5% after the first injection, remained stable up to study end, to decline again after lanreotide withdrawal. Lanreotide significantly relieved postprandial fullness, shortness of breath and abdominal distension. Three participants had a suspected episode of hepatic or renal cyst infection during the study.Conclusion Lanreotide reduced polycystic liver and kidney volumes and decreases symptoms in ADPKD patients. Moreover, eGFR decreased acutely after starting lanreotide, stabilized thereafter and declined again after withdrawal.This article is protected by copyright. All rights reserved.
    Liver international: official journal of the International Association for the Study of the Liver 11/2014; 35(5). DOI:10.1111/liv.12726 · 4.41 Impact Factor
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    ABSTRACT: In rodents, parietal epithelial cells (PECs) migrating onto the glomerular tuft participate in the formation of focal segmental glomerulosclerosis (FSGS) lesions. We investigated whether immunohistologic detection of PEC markers in the initial biopsies of human patients with first manifestation of idiopathic nephrotic syndrome with no immune complexes can improve the sensitivity to detect sclerotic lesions compared with standard methods. Ninety-five renal biopsies were stained for claudin-1 (PEC marker), CD44 (activated PECs), and LKIV69 (PEC matrix); 38 had been diagnosed as early primary FSGS and 57 as minimal change disease. PEC markers were detected on the tuft in 87% of the biopsies of patients diagnosed as primary FSGS. PEC markers were detected in FSGS lesions from the earliest stages of disease. In minimal change disease, no PEC activation was observed by immunohistology. However, in 25% of biopsies originally diagnosed as minimal change disease the presence of small lesions indicative of a sclerosing process were detected, which were undetectable on standard periodic acid-Schiff staining, even though only a single histologic section for each PEC marker was evaluated. Staining for LKIV69 detected lesions with the highest sensitivity. Two novel PEC markers A-kinase anchor protein 12 and annexin A3 exhibited similar sensitivity. In summary, detection of PECs on the glomerular tuft by immunostaining improves the differentiation between minimal change disease and primary FSGS and may serve to guide clinical decision making.
    American Journal Of Pathology 10/2014; DOI:10.1016/j.ajpath.2014.08.007 · 4.60 Impact Factor
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    ABSTRACT: The haemolytic uraemic syndrome (HUS) is part of a spectrum of thrombotic microangiopathies. The most common etiologies of HUS are the ones seen in childhood caused by an infection of Shiga toxin-producing Escherichia coli, HUS caused by an infection with Streptococcus pneumoniae and HUS due to abnormalities in the alternative pathway of the complement system. In the past decade, enormous progress has been made in understanding the pathogenesis in the latter group of patients. The analysis of genes that encode for complement regulatory proteins and the development of assays for measuring the activity of ADAMTS13 and the detection of antibodies against factor H contributed significantly to the diagnostic tools in patients with HUS. These assays have made it possible to clearly differentiate between thrombotic thrombocytopenic purpura and various forms of HUS. With the introduction of eculizumab, a monoclonal anti-C5 inhibitor, in the clinical arena as effective treatment of most complement-mediated forms of HUS, a new era of treatment in HUS has begun. We review the recent advances in HUS, with the focus on treatment. We discuss unsolved questions, which should be addressed in future studies.
    Nephrology Dialysis Transplantation 09/2014; 29(suppl 4):iv131-iv141. DOI:10.1093/ndt/gfu235 · 3.49 Impact Factor
  • Jeroen Deegens, Jack Wetzels
    Nature Reviews Nephrology 08/2014; DOI:10.1038/nrneph.2014.113-c2 · 8.37 Impact Factor
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    ABSTRACT: The optimal timing and duration of immunosuppressive therapy for idiopathic membranous nephropathy (iMN) have been debated. This study aimed to evaluate whether measuring the antibody against the phospholipase A2 receptor (PLA2R-ab) at start and end of therapy predicts long-term outcome and therefore may inform this debate.DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This observational study included all consecutive high-risk patients with progressive iMN observed from 1997 to 2005 and treated with oral cyclophosphamide (CP) or mycophenolate mofetil (MMF) in combination with corticosteroids for 12 months. Patients were prospectively followed, and outcome was ascertained up to 5 years after completion of immunosuppressive therapy. Serum samples were collected before and after completion of therapy. PLA2R antibodies were determined retrospectively in stored samples using ELISA.RESULTS: In total, 48 patients (37 men) were included. The median age was 55 years (range, 34-75), and the median serum creatinine level was 1.60 mg/dl (range, 0.98-3.37 mg/dl). Twenty-two patients received MMF and 26 received CP. At baseline, PLA2R-abs were present in 34 patients (71%). Baseline characteristics and outcome did not significantly differ between patients negative or positive for PLA2R-ab. In PLA2R-ab-positive patients, treatment resulted in a rapid decrease of antibodies: median anti-PLA2R-ab, 428 U/ml (range, 41-16,260 U/ml) at baseline and 24 U/ml (range, 0-505 U/ml) after 2 months. The PLA2R-ab levels at baseline did not predict initial response, but antibody status at end of therapy predicted long-term outcome: After 5 years, 14 of 24 (58%) antibody-negative patients were in persistent remission compared with 0 of 9 (0%) antibody-positive patients (P=0.003).CONCLUSIONS: These data suggest that in PLA2R-ab-positive patients, measuring PLA2R-abs at the end of therapy predicts the subsequent course.
    Clinical Journal of the American Society of Nephrology 07/2014; 9(8). DOI:10.2215/CJN.10471013 · 5.25 Impact Factor
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    ABSTRACT: Background Activating mutations in the Transient Receptor Potential channel C6 (TRPC6) cause autosomal dominant focal segmental glomerular sclerosis (FSGS). TRPC6 expression is upregulated in renal biopsies of patients with idiopathic membranous glomerulopathy (iMN) and animal models thereof. In iMN, disease progression is characterized by glomerulosclerosis. In addition, a context-dependent TRPC6 overexpression was recently suggested in complement-mediated podocyte injury in e.g. iMN. Hence, we hypothesized that genetic variants in TRPC6 might affect susceptibility to development or progression of iMN. Methods & Results Genomic DNA was isolated from blood samples of 101 iMN patients and 292 controls. By direct sequencing of the entire TRPC6 gene, 13 single nucleotide polymorphisms (SNPs) were identified in the iMN cohort, two of which were causing an amino acid substitution (rs3802829; Pro15Ser and rs36111323, Ala404Val). No statistically significant differences in genotypes or allele frequencies between patients and controls were observed. Clinical outcome in patients was determined (remission n = 26, renal failure n = 46, persistent proteinuria n = 29, follow-up median 80 months {range 51–166}). The 13 identified SNPs showed no association with remission or renal failure. There were no differences in genotypes or allele frequencies between patients in remission and progressors. Conclusions Our data suggest that TRPC6 polymorphisms do not affect susceptibility to iMN, or clinical outcome in iMN.
    PLoS ONE 07/2014; 9(7):e102065. DOI:10.1371/journal.pone.0102065 · 3.53 Impact Factor
  • Jeroen K Deegens, Jack F Wetzels
    Nature Reviews Nephrology 06/2014; DOI:10.1038/nrneph.2014.113 · 8.37 Impact Factor
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    ABSTRACT: Cyclophosphamide treatment improves renal survival in patients with idiopathic membranous nephropathy. However, use of cyclophosphamide is associated with cancer. The incidence of malignancies in patients with idiopathic membranous nephropathy was evaluated, and the cancer risk associated with cyclophosphamide use was estimated.DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Patients who attended the clinic were included prospectively from 1995 on. A crude incidence ratio for the occurrence of malignancy was calculated. Incidence ratios were subsequently standardized to potential confounders. Latency between cyclophosphamide therapy and the occurrence of cancer was estimated by stratifying for time since the start of treatment. Finally, Poisson regression was used to obtain a multiple adjusted incidence ratio and investigate the dose-response relationship between cyclophosphamide and cancer.RESULTS: Data were available for 272 patients; the mean age was 51 years, and 70% of the patients were men. Median follow-up was 6.0 years (interquartile range=3.6-9.5), and 127 patients were treated with cyclophosphamide. Cancer incidence was 21.2 per 1000 person-years in treated patients compared with 4.6 per 1000 person-years in patients who did not receive cyclophosphamide, resulting in crude and adjusted incidence ratios of 4.6 (95% confidence interval, 1.5 to 18.8) and 3.2 (95% confidence interval, 1.0 to 9.5), respectively.CONCLUSION: Cyclophosphamide therapy in idiopathic membranous nephropathy gives a threefold increase in cancer risk. For the average patient, this finding translates into an increase in annual risk from approximately 0.3% to 1.0%. The increased risk of malignancy must be balanced against the improved renal survival.
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    Nephrology Dialysis Transplantation 05/2014; 29 Suppl 3:iii79-iii89. DOI:10.1093/ndt/gfu142 · 3.49 Impact Factor
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    ABSTRACT: Achtergrond In de eerste lijn komt chronische nierschade onder patiënten met diabetes of hypertensie veel voor. Deze cardiovasculaire risicofactor wordt echter vaak onvoldoende aangepakt. Een samenwerkingsmodel waarin huisartsen en praktijkondersteuners via internet een nefroloog kunnen consulteren, zou dat kunnen verbeteren. Methode Wij voerden een cluster-RCT uit in negen huisartsenpraktijken, onder patiënten met diabetes of hypertensie en chronische nierschade (geschatte glomerulaire filtratiesnelheid < 60ml/min/1,73 m2), Vijf praktijken pasten een jaar lang het samenwerkingsmodel toe en vier praktijken leverden reguliere zorg. Onze belangrijkste uitkomstmaten waren de gemiddelde bloeddrukverlaging en het percentage deelnemers dat de streefbloeddruk (≤ 130/80 mmHg) bereikte. Resultaten Wij analyseerden de gegevens van 90 patiënten in de interventiegroep en 74 in de controlegroep. De kans dat een patiënt een systolische bloeddruk van 130 mmHg bereikte, was in de interventiegroep 2,9 keer zo groot als in de controlegroep (95%-BI 1,4 tot 5,8), de kans op een diastolische bloeddruk van 90 mmHg was 2,5 keer zo groot (95%-BI 1,3 tot 4,7). In de interventiegroep nam de systolische bloeddruk af met 8,1 mmHg (95%-BI 4,8 tot 11,3), de diastolische met 1,1 mmHg (95%-BI –1,0 tot 3,2), tegenover –0,2 mmHg (95%-BI –3,8 tot 3,3) respectievelijk –0,5 mmHg (95%-BI –2,9 tot 1,8) in de controlegroep. In de interventiegroep lag bovendien het gebruik van lipidenverlagende middelen, RAS-remmers en vitamine D hoger en waren de concentraties parathormoon lager. Conclusie Een samenwerkingsmodel waarin huisarts, praktijkondersteuner en nefroloog samenwerken in de begeleiding van patiënten met diabetes of hypertensie en chronische nierschade, leidt tot een significant lagere systolische bloeddruk dan reguliere zorg.
    Huisarts en wetenschap 05/2014; 57(5):232-235. DOI:10.1007/s12445-014-0123-9
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    ABSTRACT: Despite the increasing use of pre- and posthydration protocols and low-osmolar instead of high-osmolar iodine-containing contrast media, the incidence of contrast-induced nephropathy (CIN) is still significant. There is evidence that contrast media cause ischemia-reperfusion injury of the medulla. Remote ischemic preconditioning (RIPC) is a non-invasive, safe, and low-cost method to reduce ischemia-reperfusion injury. The RIPCIN study is a multicenter, single-blinded, randomized controlled trial in which 76 patients at risk of CIN will receive standard hydration combined with RIPC or hydration with sham preconditioning. RIPC will be applied by four cycles of 5 min ischemia and 5 min reperfusion of the forearm by inflating a blood pressure cuff at 50 mmHg above the actual systolic pressure. The primary outcome measure will be the change in serum creatinine from baseline to 48 to 72 h after contrast administration. A recent pilot study reported that RIPC reduced the incidence of CIN after coronary angioplasty. The unusual high incidence of CIN in this study is of concern and limits its generalizability. Therefore, we propose a randomized controlled trial to study whether RIPC reduces contrast-induced kidney injury in patients at risk for CIN according to the Dutch guidelines.Trial registration: Current Controlled Trials ISRCTN76496973.
    Trials 04/2014; 15(1):119. DOI:10.1186/1745-6215-15-119 · 2.12 Impact Factor
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    ABSTRACT: Slit diaphragm and podocyte damage is crucial in proteinuria pathogenesis in diabetic nephropathy (DNP). Gain-of-function mutations in TRPC6, a slit diaphragm-associated ion channel, cause glomerulosclerosis; TRPC6 expression is increased in acquired glomerular disease. Hyperglycemia and high intrarenal angiotensin II (AngII) levels could contribute to podocyte injury in DNP. We determined whether glucose regulates TRPC6 expression and TRPC6-mediated Ca(2+) influx into the podocyte and whether these effects are AngII dependent. High glucose levels increased TRPC6 mRNA and protein expression in cultured podocytes; however, TRPC1 and TRPC5 mRNA expression was unaltered. AngII and induced podocyte injury also specifically increased TRPC6 expression. Angiotensin receptor blockade and inhibition of local AngII production through angiotensin-converting enzyme inhibition prevented glucose-mediated increased TRPC6 expression. In addition, high glucose concentration pretreatment enhanced Ca(2+) influx in podocytes, which was prevented by concomitant angiotensin receptor blockade application and TRPC6 knockdown. Studies with a TRPC6 luciferase promoter construct demonstrated a glucose concentration-dependent effect on TRPC6 promoter activity. In vivo, podocyte TRPC6 protein expression was increased in proteinuric streptozotocin-induced diabetic rats. These data suggest that glucose can activate a local renin-angiotensin system in the podocyte, leading to increased TRPC6 expression, which enhances TRPC6-mediated Ca(2+) influx. Regulation of TRPC6 expression could be an important factor in podocyte injury due to chronic hyperglycemia and the antiproteinuric effect of angiotensin receptor blockade or angiotensin-converting enzyme inhibition in DNP.
    American Journal Of Pathology 04/2014; DOI:10.1016/j.ajpath.2014.02.008 · 4.60 Impact Factor
  • Julia M Hofstra, Jack F M Wetzels
    Journal of the American Society of Nephrology 03/2014; 25(6). DOI:10.1681/ASN.2014010091 · 9.47 Impact Factor

Publication Stats

6k Citations
2,049.98 Total Impact Points

Institutions

  • 1988–2015
    • Radboud University Medical Centre (Radboudumc)
      • Department of Human Genetics
      Nymegen, Gelderland, Netherlands
  • 1986–2014
    • Radboud University Nijmegen
      • • Department of Nephrology
      • • Department of General Internal Medicine
      • • Department of Physiology
      Nymegen, Gelderland, Netherlands
    • St. Joseph's Hospital
      Savannah, Georgia, United States
  • 2013
    • Bridgeport Hospital
      Bridgeport, Connecticut, United States
    • VU University Medical Center
      • Department of Nephrology
      Amsterdamo, North Holland, Netherlands
    • Mayo Clinic - Rochester
      Рочестер, Minnesota, United States
  • 2012
    • Oxford University Hospitals NHS Trust
      • Department of Radiology
      Oxford, ENG, United Kingdom
  • 2010–2012
    • University Medical Center Utrecht
      • Department of Nephrology
      Utrecht, Provincie Utrecht, Netherlands
  • 2011
    • Canisius-Wilhelmina Ziekenhuis
      Nymegen, Gelderland, Netherlands
  • 2009–2011
    • University Hospital RWTH Aachen
      • Division of Internal Medicine
      Aachen, North Rhine-Westphalia, Germany
  • 2008
    • Slingeland Ziekenhuis
      Doetinchem, Gelderland, Netherlands
  • 2005
    • Rijnstate Hospital
      Arnheim, Gelderland, Netherlands
  • 2003
    • Gelderse Vallei Hospital
      • Department of Internal Medicine
      Ede, Gelderland, Netherlands
  • 1998
    • University Hospital Essen
      Essen, North Rhine-Westphalia, Germany
  • 1992–1995
    • University of Colorado Hospital
      • Department of Medicine
      Denver, Colorado, United States