M J Mihatsch

Universität Basel, Basel, BS, Switzerland

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Publications (512)1755.61 Total impact

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    ABSTRACT: Das metanephrogene Adenom ist ein seltener gutartiger Nierentumor. Die Differenzialdiagnose gegenüber tubulopapillären Adenomen und papillären Nierenzellkarzinomen ist teilweise schwierig. In der vorliegenden Arbeit wird über zwei metanephrogene Adenome berichtet und ihr Immunphänotyp mit einem papillären Adenom verglichen. Die Analyse der zwei metanephrogenen Adenome und Angaben in der Literatur weisen darauf hin, dass der Nachweis der CD57-Expression und eine fehlende EMA-Expression hilfreich für die Abgrenzung gegenüber papillären Adenomen sein kann. Glomeruloide Strukturen, Psammomkörper, Nekrosen, Zytokeratin-7- und Vimentin-Expression können sowohl im metanephrogenen Adenom als auch in papillären Adenomen bzw. papillären Karzinomen auftreten. Da metanephrogene Adenome sehr groß werden können und nicht selten Nekrosen aufweisen, ist die Kenntnis des Immunprofils dieser Tumorentität für differenzialdiagnostische Entscheidungen von Bedeutung. Metanephric adenoma of the kidney is a well described tumor entity. The differential diagnosis between papillary adenoma or papillary carcinoma type 1 and metanephric adenoma of the kidney can be challenging in single cases. We report two cases of metanephric adenomas and compare their immunophenotype with a papillary adenoma. The analysis of these metanephric adenomas and a review of the literature shows that CD-57 positivity and lack of EMA expression are helpful in distinguishing metanephric adenoma from papillary adenoma and papillary carcinoma. Glomeruloid structures, Psammoma bodies, necrosis or expression of cytokeratin 7 and vimentin are common features in metanephric adenoma and papillary adenoma or papillary carcinoma. The knowledge of the immunohistochemical constellation is important, because metanephric adenoma can be very large and often have some necrosis. Metanephrogenes Adenom-Papilläres Nierenzellkarzinom-Papilläres Adenom-EMA-Leu-7 (CD57)Metanephric adenoma-Papillary carcinoma-Papillary adenoma-EMA-Leu-7 CD57
    Der Pathologe 07/2014; 23(4):303-307. DOI:10.1007/s00292-002-0548-y · 0.64 Impact Factor
  • The Lancet 07/2013; 382(9910). DOI:10.1016/S0140-6736(13)60224-X · 39.21 Impact Factor
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    ABSTRACT: Control of polyomavirus BK (BKV) is achieved by reducing immunosuppression allowing an effective BKV-specific T-cell response. The morphology of resolving BKV-associated nephropathy (PyVAN) has not been systematically investigated. Ninety-nine surveillance biopsies of 35 patients with BKV viremia treated exclusively by immunosuppression reduction were scored according to Banff criteria and grouped relative to BKV viremia as pre-, increasing, decreasing and post-BKV viremia. Thirty-four of 35 patients (97%) cleared BKV viremia after a median of 9 months posttransplantation. The tubulitis score, extent of tubules with intraepithelial lymphocytes, and interstitial inflammation significantly increased from the time of increasing to decreasing viremia. Tubulointerstitial inflammation, to a lower extent, persisted after clearance. The number of SV40+ tubules correlated with the BKV load in plasma, but SV40 immunohistochemistry was frequently negative (60%). During decreasing viremia, 31% of PyVAN cases were plasma cell-rich and 40% showed tubular HLA-DR expression. Compared to baseline 1 month posttransplantation, allograft function remained stable or improved in 29/35 patients (83%) after a median follow-up of 48 months. Within 1 year after clearance of BKV viremia, clinical rejection occurred in 2/35 patients (6%). Our data suggest that resolving PyVAN is typically characterized by a self-limiting acute interstitial nephritis, morphologically indistinguishable from interstitial rejection.
    American Journal of Transplantation 06/2013; 13(6):1474-83. DOI:10.1111/ajt.12218 · 6.19 Impact Factor
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    ABSTRACT: Immunosuppressive maintenance therapy after kidney transplantation leads to various undesired side effects such as calcineurin inhibitor (CNI)-associated nephrotoxicity or elevated cardiovascular risk due to posttransplantation diabetes and hypertension. These effects show negative impacts on long-term allograft function as well as patient morbidity and mortality. Therefore, we used an immunosuppressive regimen with early corticosteroid withdrawal (ESW), maintenance therapy containing tacrolimus, sirolimus (SRL), and mycophenolate sodium for 3 months followed by a prospective randomized trial comparing a CNI free versus a low-dose CNI therapy. The primary endpoint was 6-month graft function. Among 75 patients, ESW was performed after 4 days in 65 patients. Over the following 3 months before randomization to CNI-free maintenance therapy, we experienced a high number (25%) of SRL discontinuations due to adverse events, including leukopenia, anemia, arthritis, and pneumonitis. In addition there were significantly more allograft rejection episodes in the CNI-free group (P = .017) during the study period leading to a switch from SRL to a CNI. Despite the higher rate of rejection episodes in the CNI-free groups, glomerular filtration rates (GFR) at 6 months were comparable between the study groups (P = .25). After 1 year only 9.2% (6/65) of all patients treated with SRL remained on this drug. Conclusion, there was an unacceptably high rate of SRL intolerance using an ESW and CNI-free immunosuppressive regimen combined with a significantly higher rate of rejection episodes.
    Transplantation Proceedings 12/2012; 44(10):2961-5. DOI:10.1016/j.transproceed.2012.07.142 · 0.95 Impact Factor
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    ABSTRACT: Chronic kidney disease (CKD) represents a major health burden. Its central feature of renal fibrosis is not well understood. By exome sequencing, we identified mutations in FAN1 as a cause of karyomegalic interstitial nephritis (KIN), a disorder that serves as a model for renal fibrosis. Renal histology in KIN is indistinguishable from that of nephronophthisis, except for the presence of karyomegaly. The FAN1 protein has nuclease activity and acts in DNA interstrand cross-link (ICL) repair within the Fanconi anemia DNA damage response (DDR) pathway. We show that cells from individuals with FAN1 mutations have sensitivity to the ICL-inducing agent mitomycin C but do not exhibit chromosome breakage or cell cycle arrest after diepoxybutane treatment, unlike cells from individuals with Fanconi anemia. We complemented ICL sensitivity with wild-type FAN1 but not with cDNA having mutations found in individuals with KIN. Depletion of fan1 in zebrafish caused increased DDR, apoptosis and kidney cysts. Our findings implicate susceptibility to environmental genotoxins and inadequate DNA repair as novel mechanisms contributing to renal fibrosis and CKD.
    Nature Genetics 07/2012; 44(8):910-5. DOI:10.1038/ng.2347 · 29.65 Impact Factor
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    ABSTRACT: Fibronectin glomerulopathy (FNG) is a rare, autosomal dominant renal disease with massive mesangial, and subendothelial fibronectin deposits. It presents proteinuria, often in the nephrotic range in the third to fourth decade, and slow progression to end-stage renal disease. The risk of recurrent disease in renal allograft is uncertain. A Japanese female with end-stage renal disease because of unknown origin received a renal transplant and was referred with proteinuria and mild deterioration of renal function four months after transplantation. Five allograft biopsies were underwent from one h to 12 months after the transplantation, including a biopsy 19 d after the transplantation, which revealed dense deposits suggesting fibronectin. A biopsy 134 d after the transplantation showed a feature of lobular glomerulonephritis corresponding FNG. The diagnosis was confirmed by IST4 positive and IST9 negative immunostaining together with typical fibrillary dense deposits in the mesangium and subendothelial spaces in electron microscopy. This is the first report of recurrent FNG in Japan.
    Clinical Transplantation 07/2012; 26 Suppl 24:58-63. DOI:10.1111/j.1399-0012.2012.01644.x · 1.49 Impact Factor
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    ABSTRACT: Protocol biopsies are assigned to fixed points in time after transplantation irrespective of renal function. Usually, it is not known whether there is graft dysfunction at the time of biopsy. This study analyzes repeat protocol biopsies in the absence of any clinical signs of graft dysfunction at the time of biopsy (i.e., "true surveillance biopsy"). Observational single center study. Kidney transplant recipients with protocol biopsies after 3 and 6 months were analyzed. Three hundred seventy patients had protocol biopsies after 3 and 6 months. One hundred forty-eight patients (40%; 296 biopsies) with a median follow-up of 3.4 years (range, 0.95-7.7 years), fulfilled the criteria of repeat true surveillance biopsies. Graft survival censored for death was 100% at 1 year, 96% at the end of follow-up. One hundred eighty-four biopsies (62%) revealed pathological findings, mainly subclinical rejection (3/6 months: 41% vs. 45%; P = 0.2) and chronic lesions (3/6 months: 22% vs. 44%; P<0.001). Grafts with repeat pathological findings at 3 and 6 months had a significant decline in graft function at end of follow-up compared with grafts with no or only singular pathology (median delta estimated glomerular filtration rate: -10.24 vs. -0.19; P = 0.005). Ninety-three of 148 patients (63%) had a therapeutic intervention as a consequence of the biopsy. Less than 50% of protocol biopsies were performed in the absence of any clinical signs of graft dysfunction. A high proportion of these biopsies revealed pathological findings that were associated with a significant decrease in long-term graft function.
    Transplantation 05/2012; 93(9):908-13. DOI:10.1097/TP.0b013e318248cab0 · 3.78 Impact Factor
  • Nieren- und Hochdruckkrankheiten 01/2012; 41(01):2-8. DOI:10.5414/NHX01378
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    ABSTRACT: We assessed the long-term follow up of all the patients with fibrillary glomerulonephritis diagnosed since 1992 at our centre of reference for renal pathology in Basel. We performed a retrospective surveillance study with mail questionnaire based follow-up of all patients with the diagnosis of fibrillary glomerulonephritis found in the database of the department of renal pathology in Basel from 1992 to 2007. The outcome was assessed in terms of endstage renal disease (ESRD), death, reduction of proteinuria and improvement of estimated glomerular filtration rate (eGFR). We obtained sufficient follow up data from 16 out of 20 identified patients. The mean follow up time was 35 months (1-115.1). Six patients died (37.5%), three without having ESRD. Six patients (37.5%) reached ESRD, five of them went on hemodialysis. Thirteen patients (81.3%) received an immunosuppressive therapy with steroids, five of them in combination with cyclophosphamide. The group without immunosuppressive therapy was too small to compare the two groups. In relation to the histological pattern membranous glomerulonephritis (MGN) had a better outcome as compared to the other histological patterns. FGN is a heterogeneous disease associated with significant risk of ESRD and mortality. The histological type of the glomerulonephritis may influence the course of the disease.
    Schweizerische medizinische Wochenschrift 01/2012; 142:w13578. DOI:10.4414/smw.2012.13578 · 1.88 Impact Factor
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    M Mengel, M Mihatsch, P F Halloran
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    ABSTRACT: No histological lesions specific for renal calcineurin inhibitor toxicity exist, and this is a critical issue influencing the interpretation of all literature addressing calcineurin inhibitors as a cause for renal allograft deterioration. See article by Snanoudj et al on page 2635.
    American Journal of Transplantation 08/2011; 11(12):2549-50. DOI:10.1111/j.1600-6143.2011.03719.x · 6.19 Impact Factor
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    ABSTRACT: The etiology of nephrocalcinosis is variable. In this study, we wanted to elucidate whether the histopathological appearance of calcium phosphate deposits provides information about possible etiology. Autopsy cases from the years 1988 to 2007 and native kidney biopsies from a 50-year period (1959-2008) with nephrocalcinosis were identified. The biopsy cases were re-evaluated by light microscopy. The autopsy cases were analysed according to the underlying disease. The biopsy cases were grouped with respect to the likely etiology of nephrocalcinosis. Total number, density, localization, size and pattern of all calcification foci were documented and correlated with clinical and laboratory data. About 223 of 12,960 autopsy cases (1.7%) had nephrocalcinosis, 111 of which (49.8%) suffered from advanced malignant tumours. Nephrocalcinosis was the main diagnosis in 48 of 12,480 native kidney biopsies (0.4%). Clinicopathological correlation revealed a specific pattern of calcification associated with hyperphosphataemia and/or hyperphosphaturia: these cases showed predominant globular or shell-like calcifications (phosphate type). In contrast, the biopsies of the hypercalcaemic/hypercalciuric group had a different predominant pattern with clumpy or finely granular calcifications (calcium type). Our results indicate that hyperphosphaturia-associated cases of nephrocalcinosis can be distinguished from hypercalciuria-associated cases histopathologically.
    Nephrology Dialysis Transplantation 07/2011; 27(3):1122-31. DOI:10.1093/ndt/gfr414 · 3.37 Impact Factor
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    Stephen Batsford, John Dunn, Michael Mihatsch
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    ABSTRACT: Bacterial lipoproteins and CpG-DNA are ligands for Toll-Like-Receptors (TLR) 2 and 9 respectively. Both classes of molecules were reported to induce experimental arthritis in rodents following direct intra-articular injection. Here we studied: 1) whether arthritis induction by Outer surface (Lipo)protein A (OspA) (B.burgdorferi) involved the TLR-2 as well as the TLR-4 or the CD-14 receptors in addition, and 2) re-examined the arthritogenic potential of CpG-DNA motifs in mice.Following intra-articular injection of the test substances [20µg recombinant, lipidated OspA; 1nM(6µg) to 10nM(60µg) synthetic CpG-DNA], inflammation was monitored by (99)Tc scintigraphy (ratio left/right knee joint uptake > 1.1 indicates inflammation) and by histology.Lipoprotein OspA induced severe, acute arthritis in TLR-2(+/+) w.t. but not in TLR-2(-/-) mice (p<0.01). There were no significant differences in the severity of arthritis induced in TLR-4(+/+) w.t. and TLR-4(-/-) mutant mice, or between CD14(+/+) w.t. and CD14(-/-) mice.CpG-DNA (1or 10 nM) did not cause notable inflammation in C57BL/6 mice; (99)Tc ratios were < 1.0 and histology showed only minimal changes.Induction of arthritis by the OspA lipoprotein of B.burgdorferi involves the TLR-2 receptor, no evidence for additional participation of TLR-4 or CD14 receptors was found. Intra-articular injection of CpG-DNA did not produce manifest joint injury in mice, at variance with previous reports.
    The Open Rheumatology Journal 07/2011; 5:18-23. DOI:10.2174/1874312901105010018
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    ABSTRACT: Toll-like receptors (TLR) recognize a variety of ligands, including pathogen-associated molecular patterns and link innate and adaptive immunity. Individual receptors can be up-regulated during infection and inflammation. We examined the expression of selected TLRs at the protein level in various types of renal disease. Frozen sections of renal biopsies were stained with monoclonal antibodies to TLR-2, -4 and -9. Up-regulation of the three TLRs studied was seen, although the extent was modest. TLR-2- and -4-positive cells belonged to the population of infiltrating inflammatory cells; only in the case of TLR-9 were intrinsic glomerular cells positive in polyoma virus infection and haemolytic uraemic syndrome (HUS). Evidence for the involvement of the three TLRs tested in a variety of human renal diseases was found. These findings add to our understanding of the role of the innate immune system in kidney disease.
    Nephrology Dialysis Transplantation 04/2011; 26(4):1413-6. DOI:10.1093/ndt/gfq752 · 3.37 Impact Factor
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    ABSTRACT: In systemic lupus erythematosus patients, a strong association between the occurrence of antibodies against complement C1q (anti-C1q) and lupus nephritis can be observed. However, the predictive value of anti-C1q titres for a renal flare remains to be determined. Increasing titres of anti-C1q before the occurrence of clinical apparent nephritis might not only serve as a clinical parameter but also indicate a direct pathogenic mechanism of anti-C1q. The aim of this study was to analyse the occurrence of anti-C1q before the onset of experimental lupus nephritis in MRL/MpJ +/+ mice and to correlate anti-C1q titres with the type and severity of glomerulonephritis (GN) developing at advanced age. As judged by a number of morphological and immunological analyses, GN in MRL/MpJ +/+ mice resembled human lupus nephritis and occurred in variable degrees of severity. We also observed an abundant and early presence of anti-C1q. However, anti-C1q neither correlated with overall survival nor with any histological marker of severity of GN. The absence of a correlation between the presence of anti-C1q and the occurrence of experimental lupus nephritis contradicts the hypothesis that anti-C1q are pathogenic. However, different pathogenic mechanisms of experimental lupus nephritis and human proliferative lupus nephritis cannot be excluded.
    Nephrology Dialysis Transplantation 04/2011; 26(4):1220-8. DOI:10.1093/ndt/gfq558 · 3.37 Impact Factor
  • Helmut Hopfer, Thorsten Wiech, Michael J Mihatsch
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    ABSTRACT: Renal amyloidosis results from protein misfolding and leads to progressive renal insufficiency. Few data are available concerning the relevance of the histomorphological patterns and the dynamics of the disease process. Cases of renal amyloidosis in native kidney biopsies (n = 203) were retrospectively evaluated for the pattern of amyloid distribution, the extent of glomerular amyloid deposition and the amount of interstitial fibrosis and tubular atrophy. One hundred and fifty-eight cases were characterized by immunohistochemistry to determine the biochemical amyloid type. Morphological findings were correlated with available clinical data. According to the predominant site of amyloid deposition, 84.6% showed a glomerular, 9.4% a vascular and 6% a tubulointerstitial distribution pattern. Within the glomeruli, amyloid was initially deposited in a focal segmental fashion that became diffuse and global in later stages. Most cases were identified as AL lambda (84/158) or AA (68/158). There was no correlation between the biochemical type and the distribution pattern. Serum creatinine correlated well with interstitial fibrosis and tubular atrophy and proteinuria with the glomerular amyloid load. The relevance of the different distribution patterns is unclear at the moment, but they may be due to the physicochemical properties of the amyloid fibrils in a given patient. This may become important in future anti-fibrillar therapies.
    Nephrology Dialysis Transplantation 03/2011; 26(9):2877-84. DOI:10.1093/ndt/gfq831 · 3.37 Impact Factor
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    ABSTRACT: The virtual crossmatch (virtual-XM) has been proposed for accurate identification of donor-specific HLA-antibodies, but large prospective studies assessing its value for pretransplant risk stratification are lacking. A total of 233 consecutive renal allograft recipients were prospectively stratified according to the virtual-XM. In patients with a negative virtual-XM (n=190, 82%), prospective cytotoxicity crossmatches (CDC-XM) were omitted, and they received standard immunosuppression. Virtual-XM positive patients were only transplanted if CDC-XM were negative. They received additional induction with anti-T-lymphocyte-globulin and intravenous immunoglobulins (n=43, 18%). The cumulative incidence of clinical/subclinical antibody-mediated rejection (AMR) at 1 year was lower in the negative virtual-XM than in the positive virtual-XM group [15/190 (8%) vs. 18/43 (42%); P<0.0001]. After a median follow-up of 2.6 years, allograft loss because of AMR occurred less often in the negative virtual-XM group (1% vs. 7%; P=0.04) and death-censored allograft survival at 2 years was higher (98% vs. 91%; P=0.02). Serum creatinine was not different at the last follow-up (129 μm vs. 130 μm; P=0.58). We conclude that a negative virtual-XM defines patients at low risk for AMR and early allograft loss, while a positive virtual-XM represents a significant risk for AMR despite enhanced induction therapy. This supports the utility of the virtual-XM for risk stratification and treatment allocation.
    Transplant International 02/2011; 24(6):560-9. DOI:10.1111/j.1432-2277.2011.01235.x · 3.16 Impact Factor
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    ABSTRACT: The FOXP3 (forkhead Box p3) transcription factor is a marker for T regulatory cells (Treg). During cellular immune responses, Treg are expected to increase in number to ultimately control and limit this response. In renal transplants massive infiltration by T cells is often seen during rejection crises. This prompted us to examine changes in the numbers of FOXP3 positive T cells accompanying acute cellular rejection events. A total of 32 transplant biopsies from 23 patients were studied retrospectively, these 16 protocol biopsies and 16 biopsies taken during rejection episodes included 9 serial pairs (protocol-rejection). To quantify FOXP3 positive T cells, frozen sections were double immunostained with anti-CD3 and anti-FOXP3 antibodies. Areas revealing T cell infiltrates were measured morphometrically and the number of FOXP3 positive cells per 1,000 µm2 of CD3 positive cells was taken as an FOXP3 index. This index was 0.46 (median, range 0.00-1.00) in the 16 protocol biopsies and 0.48 (median, range 0.16-2.31) in rejection episode biopsies. The highest values were seen during rejection crises, exceeding 1.00 in 6/16 biopsies, whereas no protocol biopsies had values greater than 1.00 (0/16) (difference significant p<0.02). In serial biopsies no consistent behavior was observed; the FOXP3 index remained unchanged, fell slightly or rose to a maximum of 13 fold. Expression levels of FOXP3 could vary within weeks. No correlations were found between donor type, initial therapy, therapy at biopsy, serum creatinine at the time of biopsy, at 3 months or 1 year later, and any of the morphometric parameters (CD3 and FOXP3) studied. During rejection of renal allografts the fraction of FOXP3+ Treg cells within the infiltrating T-cell population can increase transiently. This phenomenon was not consistently seen in acute cellular rejection and the information does not appear to be of value for individual patient management in such cases.
    Clinical nephrology 02/2011; 75(2):101-6. DOI:10.2379/CNP75101 · 1.23 Impact Factor
  • Erik H Strøm, Michael J Mihatsch
    Kidney International 12/2010; 78(11):1189; author reply 1190. DOI:10.1038/ki.2010.360 · 8.52 Impact Factor
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    ABSTRACT: Early detection of polyomavirus BK (BKV) viremia and reduction of immunosuppression is recommended for preventing polyomavirus-associated nephropathy (PyVAN), but systematic histological evaluations were not performed in previous studies. We routinely screen for decoy cells and, if positive, measure plasma BKV-loads. In a cohort of 203 consecutive renal transplantations performed from 2005-2008, 38 patients (19%) developed BKV-viremia and were treated with reduction of immunosuppression. Based on subsequent allograft biopsy results and peak BKV-viremia, patients were assigned to three groups: (i) definitive PyVAN (n = 13), (ii) presumptive PyVAN defined by plasma BKV-loads of ≥ 4 log(10) copies/ml (n = 17) and (iii) low BKV-viremia (n = 8). Clearance of BKV-viremia was achieved in 35/38 patients (92%) and subsequent clinical rejection occurred in 3/35 patients (8.6%), both without any difference among the groups. Patients with definitive PyVAN had higher peak plasma BKV-loads and required longer time for clearance (8.8 vs. 4.6 vs. 2.9 months; p = 0.001). However, allograft function remained stable from baseline to last follow-up at 34 months (range 18-60) in all three groups with median serum creatinine of 1.6 mg/dl, 1.6 mg/dl and 1.3 mg/dl, respectively. We conclude that screening for BKV-replication and reduction of immunosuppression is an effective strategy to preserve medium-term allograft function even in patients developing definitive PyVAN.
    American Journal of Transplantation 12/2010; 10(12):2615-23. DOI:10.1111/j.1600-6143.2010.03310.x · 6.19 Impact Factor
  • H. Hopfer, M. J. Mihatsch
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    ABSTRACT: Zusammenfassung Das Syndrom der dünnen Basalmembranen und das Alport-Syndrom sind hereditäre Nephropathien, die die glomerulären Basalmembranen betreffen. Bei allen Patienten mit Alport-Syndrom und bei etwa 40% der Patienten mit dünnen Basalmembranen finden sich Mutationen der α3-, α4- oder α5-Kette des Kollagen Typ IV. Obwohl beide Erkrankungen einen sehr unterschiedlichen Verlauf zeigen, manifestieren sie sich initial als glomeruläre Hämaturie und sind klinisch zunächst nicht auseinanderzuhalten. Beide Erkrankungen lassen sich durch eine Nierenbiopsie diagnostizieren, vorausgesetzt, es wird eine elektronenmikroskopische Untersuchung durchgeführt. Die zusätzliche immunhistologische Darstellung der α3(IV)- und α5(IV)-Kette hilft in bis zu 80% der Fälle, das Alport-Syndrom sicher zu diagnostizieren und ermöglicht darüber hinaus auch, Alport-Konduktorinnen zu identifizieren.
    Der Nephrologe 11/2010; 5(6):508-516. DOI:10.1007/s11560-009-0381-x

Publication Stats

22k Citations
1,755.61 Total Impact Points


  • 1973–2014
    • Universität Basel
      • • Institut für Pathologie
      • • Institute of Geology and Paleontology
      Basel, BS, Switzerland
  • 1991–2013
    • Universitätsspital Basel
      • Institut für Pathologie
      Bâle, Basel-City, Switzerland
  • 1992–2012
    • Kantonsspital Liestal
      Liestal, Basel-Landschaft, Switzerland
  • 2003–2007
    • University of North Carolina at Chapel Hill
      • Department of Pathology and Laboratory Medicine
      North Carolina, United States
  • 2004
    • Nagoya Second Red Cross Hospital
      Nagoya, Aichi, Japan
    • Sun Yat-Sen University
      • Department of Gynecology
      Guangzhou, Guangdong Sheng, China
  • 1997–2003
    • Pathologie Institut Enge
      Zürich, Zurich, Switzerland
  • 1974–2003
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 2001
    • Turtle Mountain Community College
      Belcourt, North Dakota, United States
    • University of South Carolina School of Medicine - Greenville
      Greenville, South Carolina, United States
  • 1998–1999
    • National Human Genome Research Institute
      Maryland, United States
  • 1996
    • University of Oslo
      Kristiania (historical), Oslo, Norway
  • 1993–1996
    • University of California, San Francisco
      • Department of Laboratory Medicine
      San Francisco, CA, United States
  • 1995
    • Istituto Nazionale Tumori "Fondazione Pascale"
      Napoli, Campania, Italy
  • 1992–1995
    • Cantonal Hospital of Schwyz
      Schwyz, Schwyz, Switzerland
  • 1994
    • University of Zurich
      Zürich, Zurich, Switzerland
  • 1990
    • University Hospital Frankfurt
      Frankfurt, Hesse, Germany
  • 1989
    • University of Geneva
      Genève, Geneva, Switzerland
    • University of Milan
      Milano, Lombardy, Italy
    • Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico
      • Nephrology and Dialysis
      Milano, Lombardy, Italy
  • 1983
    • University of Melbourne
      • Department of Physiology
      Melbourne, Victoria, Australia
  • 1981
    • Università degli studi di Cagliari
      Cagliari, Sardinia, Italy