Publications by authors named "Bjørn Egil Vikse"

45 Publications

A woman in her fifties with abdominal pain and severe lactic acidosis.

Tidsskr Nor Laegeforen 2021 05 27;141(7). Epub 2021 Apr 27.

Background: Pheochromocytoma is referred to as 'the great mimic' with a broad spectrum of presenting symptoms. In the following case, the diagnosis had an unusual presentation as a medical emergency - pheochromocytoma crisis.

Case Presentation: A previously healthy woman in her fifties was admitted due to abdominal pain and dyspnoea. At admission she was haemodynamically stable, with stable respiration, but arterial blood gas showed serious lactic acidosis with pH 6.8 (7.35-7.45), HCO3 3 mmol/l (22-26) and lactate 28 mmol/L (0.4-1.8). Her haemoglobin level was 12 g/dl (11,7-17,0). Further examination with CT and gastroscopy confirmed a duodenal bleeding. The lactic acidosis was corrected quickly, but the patient developed acute kidney injury, rhabdomyolysis and increased liver enzymes. The complex composition of organ manifestations could not be explained by the duodenal bleeding alone. An adrenal mass with high density was identified through re-evaluation of the CT scans. In the following case, a duodenal bleeding provoked catecholamine-induced haemodynamic instability and end-organ damage in a patient with an undiagnosed pheochromocytoma.

Interpretation: Endocrine emergencies are important differential diagnoses in critically ill patients. Pheochromocytoma crisis most commonly presents as hypertensive crisis or catecholamine cardiomyopathy but can also lead to lactic acidosis and multi-organ failure.
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http://dx.doi.org/10.4045/tidsskr.20.0669DOI Listing
May 2021

Blood Pressure Treatment in Kidney Transplant Recipients-Can We Improve?

Transplant Direct 2021 Apr 25;7(4):e688. Epub 2021 Mar 25.

Department of Transplantation Medicine, Oslo University Hospital-Rikshospitalet, Oslo, Norway.

Hypertension in kidney transplant (KTx) recipients is common, affecting both patient and graft survival. Annual data from the Norwegian Renal Registry reveal that <50% of adult (>18 y) KTx recipients reach target blood pressure (BP) ≤130/80 mm Hg. The aim of this study was to identify the determinants of failure to achieve BP control.

Methods: In conjunction with the 2018 annual data reporting, additional questions were added for recipients with BP >130/80 mm Hg (treating physician´s target BP for each patient, reasons for not achieving target, method of measurement).

Results: Annual forms were received from 98% (3407 of 3486) of KTx recipients, with 1787 (52%) reporting a BP >130/80 mm Hg ("above-target" group). These recipients were older, mostly male, with higher body mass index and serum creatinine levels ( < 0.05) compared with patients with controlled hypertension ("on-target" group). Valid survey answers were available for 84% of the "above-target" group (Surv) with no significant demographic differences versus nonresponders (Surv). Among Surv, 32% were under antihypertensive dose titration, whereas dose-limiting side effects were reported in 7%. Target BP was confirmed to 130/80 mm Hg for 60% of Surv. In recipients for whom the treating physician set target BP >130/80 mm Hg, 51% did not reach these individual targets. The number of antihypertensive drugs was significantly higher in the "above-target" group versus "on-target" group (mean 2.1 ± 1.2 versus 1.8 ± 1.3) and 36% versus 25% used ≥3 antihypertensive drugs ( < 0.05). Automatic attended BP measurement was utilized by 51%.

Conclusions: In KTx recipients, a higher BP target achievement seems possible, potentially in the range of 75%-80%.
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http://dx.doi.org/10.1097/TXD.0000000000001142DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7997102PMC
April 2021

Low birthweight is associated with lower glomerular filtration rate in middle-aged mainly healthy women.

Nephrol Dial Transplant 2020 Dec 13. Epub 2020 Dec 13.

Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: Low birthweight (LBW) has been shown to increase the risk of severe kidney disease. Studies have also shown associations between LBW and lower estimated glomerular filtration rate (GFR) in young adults. In this study we investigated whether LBW associates with measured GFR (mGFR) in middle-aged mainly healthy adults.

Methods: We invited individuals with LBW (1100-2300 g) and individuals with normal BW (NBW; 3500-4000 g) ages 41-52 years. GFR was measured using plasma clearance of iohexol. BW and BW for gestational age (BWGA) were obtained from the Medical Birth Registry of Norway and tested as main predictors. GFR was the main outcome.

Results: We included 105 individuals (57 LBW and 48 NBW). The mean GFR was 95 ± 14 mL/min/1.73 m2 in the LBW group and 100 ± 13 mL/min/1.73 m2 in the NBW group (P = 0.04). There was a significant sex difference: in women the mean GFR was 90 ± 12 versus 101 ± 14 mL/min/1.73 m2 in the LBW and NBW groups, respectively (P = 0.006), whereas corresponding values for men were 101 ± 15 versus 100 ± 11 mL/min/1.73 m2 (P = 0.7). Using linear regression, we found the GFR was 4.5 mL/min/1.73 m2 higher per 1 kg higher BW for women (P = 0.02), with a non-significant 1.2 mL/min/1.73 m2 lower GFR for men (P = 0.6). In analyses of BWGA, there was also a significant association for women, but not for men.

Conclusions: Middle-aged mainly healthy women with LBW had lower mGFR as compared with women with NBW. No such difference was found for men.
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http://dx.doi.org/10.1093/ndt/gfaa306DOI Listing
December 2020

Intrauterine Growth Restriction and Risk of Diverse Forms of Kidney Disease during the First 50 Years of Life.

Clin J Am Soc Nephrol 2020 10 17;15(10):1413-1423. Epub 2020 Aug 17.

Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background And Objectives: Previous studies have shown that individuals with low birth weight (LBW) or small for gestational age (SGA) have higher risk of kidney failure. This study investigates birth-related exposures and risk of CKD and other kidney diagnoses.

Design, Setting, Participant, & Measurements: The Medical Birth Registry of Norway has registered extensive medical data on all births in Norway since 1967. The Norwegian Patient Registry has registered diagnostic codes for all admissions and outpatient visits to Norwegian hospitals since 2008. Data from these registries were linked, and risk of CKD and other groups of kidney disease were analyzed using logistic regression statistics. LBW (below the tenth percentile), SGA (birth weight below the tenth percentile for gestational age), and preterm birth (<37 weeks) were analyzed as exposures.

Results: A total of 2,663,010 individuals were included. After a mean follow-up of 26 years (maximum 50 years), 4495 had been diagnosed with CKD and 12,818 had been diagnosed with other groups of kidney disease. LBW was associated with an odds ratio (OR) for CKD of 1.72 (95% confidence interval [95% CI], 1.60 to 1.90), SGA with an OR of 1.79 (95% CI, 1.65 to 1.94), and preterm birth with an OR of 1.48 (95% CI, 1.33 to 1.66). Analyses using diagnosis of CKD at stages 3-5 as end point showed similar results. Results were similar for men and women. We analyzed adjusted ORs for other groups of kidney disease and found that LBW was associated with an adjusted OR of 1.44 (95% CI, 1.33 to 1.56) for acute kidney disease, 1.24 (95% CI, 1.14 to 1.36) for GN, 1.35 (95% CI, 1.17 to 1.56) for cystic kidney disease, and 1.15 (95% CI, 1.06 to 1.25) for kidney disease resulting from kidney or urinary tract malformations.

Conclusions: LBW, SGA, and preterm birth are associated with higher risk of CKD in the first 50 years of life. Risk of other groups of kidney disease was less pronounced.

Podcast: This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2020_08_17_CJN04080320.mp3.
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http://dx.doi.org/10.2215/CJN.04080320DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7536758PMC
October 2020

Intrauterine growth restriction, preterm birth and risk of end-stage renal disease during the first 50 years of life.

Nephrol Dial Transplant 2020 07;35(7):1157-1163

Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: Low birth weight (LBW) is associated with a higher risk of end-stage renal disease (ESRD). The relative impacts of absolute birth weight, birth weight in relation to gestational age and preterm birth are, however, uncertain.

Methods: The Medical Birth Registry of Norway has since 1967 recorded data on all births. All patients with ESRD since 1980 have been registered in the Norwegian Renal Registry. Data from these registries were linked. All individuals registered in the Medical Birth Registry were included and the development of ESRD was used as endpoint in Cox regression statistics. LBW and LBW for gestational age [small for gestational age (SGA)] according to the 10th percentiles were used as the main predictor variables.

Results: Of the 2 679 967 included subjects, 1181 developed ESRD. Compared with subjects without LBW, subjects with LBW had an adjusted hazard ratio (aHR) for ESRD of 1.61 (1.38-1.98). SGA had an aHR of 1.44 (1.22- 1.70). Further analyses showed that as compared with subjects who had none of the risk factors LBW, SGA and preterm birth, subjects with one risk factor had an aHR of 1.05 (0.84-1.31), subjects with two risk factors had an aHR of 1.67 (1.40-1.98) and subjects with three risk factors had an aHR of 2.96 (1.84-4.76).

Conclusions: We conclude that LBW was associated with increased risk for ESRD during the first 50 years. Our analyses add to previous knowledge showing that only subjects with at least two of the risk factors LBW, SGA or preterm birth have increased risk.
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http://dx.doi.org/10.1093/ndt/gfaa001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417009PMC
July 2020

Measurement of renal functional response using iohexol clearance-a study of different outpatient procedures.

Clin Kidney J 2021 Jan 26;14(1):181-188. Epub 2019 Nov 26.

Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: Glomerular filtration rate (GFR) increases after a heavy protein load; an increase termed renal functional response (RFR). Decreased RFR could be a marker of early kidney damage, but published methods are cumbersome in the outpatient setting. The present study investigates the use of iohexol clearance to measure RFR in outpatients using both one- and two-sample methods.

Methods: Fourteen healthy volunteers with a mean ± SD age of 42 ± 12 years were included (six males and eight females). GFR was measured using plasma iohexol clearance with one- and two-sample methodologies. Four measurements in each individual were performed: one baseline test and three protein loading tests containing 80 g protein (commercially available protein supplementations from Myo Nutrition and Proteinfabrikken and 350 g chicken breast). RFR was calculated as percentage increase in GFR from the baseline test.

Results: Mean RFR was 11.4 ± 5.4% and 12.1 ± 6.4% using one- and two-sample methods, respectively. The three different protein loads resulted in similar mean RFR but there was considerable intra-individual variability. One- and two-sample methods for measurement of RFR showed similar results with near-identical means, but there was some intra-individual variation that was similar for different protein loads. The overall 95% limit of agreement between one- and two-sample methods for calculating RFR was -8.7 to 7.3.

Conclusions: RFR can be investigated using plasma iohexol clearance in an outpatient setting. Protocols using commercially available protein supplementation showed a mean RFR of about 12%. One- and two-sample methods for measuring RFR yield similar results.
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http://dx.doi.org/10.1093/ckj/sfz167DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7857819PMC
January 2021

Characterization of glomerular extracellular matrix in IgA nephropathy by proteomic analysis of laser-captured microdissected glomeruli.

BMC Nephrol 2019 11 14;20(1):410. Epub 2019 Nov 14.

Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: IgA nephropathy (IgAN) involves mesangial matrix expansion, but the proteomic composition of this matrix is unknown. The present study aimed to characterize changes in extracellular matrix in IgAN.

Methods: In the present study we used mass spectrometry-based proteomics in order to quantitatively compare protein abundance between glomeruli of patients with IgAN (n = 25) and controls with normal biopsy findings (n = 15).

Results: Using a previously published paper by Lennon et al. and cross-referencing with the Matrisome database we identified 179 extracellular matrix proteins. In the comparison between IgAN and controls, IgAN glomeruli showed significantly higher abundance of extracellular matrix structural proteins (e.g periostin, vitronectin, and extracellular matrix protein 1) and extracellular matrix associated proteins (e.g. azurocidin, myeloperoxidase, neutrophil elastase, matrix metalloproteinase-9 and matrix metalloproteinase 2). Periostin (fold change 3.3) and azurocidin (3.0) had the strongest fold change between IgAN and controls; periostin was also higher in IgAN patients who progressed to ESRD as compared to patients who did not.

Conclusion: IgAN is associated with widespread changes of the glomerular extracellular matrix proteome. Proteins important in glomerular sclerosis or inflammation seem to be most strongly increased and periostin might be an important marker of glomerular damage in IgAN.
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http://dx.doi.org/10.1186/s12882-019-1598-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6854890PMC
November 2019

Prevalence and prognostic ability of the GOLD 2017 classification compared to the GOLD 2011 classification in a Norwegian COPD cohort.

Int J Chron Obstruct Pulmon Dis 2019 23;14:1639-1655. Epub 2019 Jul 23.

Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Rationale: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 is based on an ABCD assessment tool of symptoms and exacerbation history and grade 1-4 of airflow limitation severity, facilitating classification either into 4 groups (ABCD) or 16 groups (1A-4D). We aimed to compare the GOLD 2011, GOLD 2017 ABCD, and GOLD 2017 1A-4D classifications in terms of their distribution and prediction of mortality and hospitalizations.

Methods: In the GenKOLS study, 912 COPD patients with FEV1 less than 80% of the predicted answered questionnaires and performed lung function testing in 2003-2005. The patients were recruited from a hospital patient registry (n=662) and from the general population (n=250), followed up until 2011 with respect to all-cause and respiratory mortality, and all-cause and respiratory hospitalizations. We performed logistic regression and receiver operating curve (ROC) analyses for the different classifications with estimations of area under the curve (AUC) for comparisons.

Results: Mean age at baseline was 60 years (SD 11), 55% were male. Mean duration of follow-up was 91 months. By GOLD 2011, 21% were classified as group A, 29% group B, 6% group C, and 43% as group D, corresponding percentages for GOLD 2017 were: 25%, 52%, 3%, and 20%. The GOLD 2011 classification had higher AUC values than the GOLD 2017 group ABCD classification for respiratory mortality and hospitalization, but after inclusion of airflow limitation severity in GOLD 2017 groups 2A-4D, AUC values were significantly higher with GOLD 2017.

Conclusion: In a clinically relevant sample of COPD patients, the GOLD 2017 classification doubles the prevalence of group B and halves the prevalence of groups C and D as compared to the GOLD 2011 classification. The prediction of respiratory mortality and respiratory hospitalization was better for GOLD 2017 2A-4D taking airflow limitation severity into account, as compared to GOLD 2017 ABCD and GOLD 2011.
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http://dx.doi.org/10.2147/COPD.S194019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6662162PMC
February 2020

Transcriptome-proteome integration of archival human renal cell carcinoma biopsies enables identification of molecular mechanisms.

Am J Physiol Renal Physiol 2019 05 6;316(5):F1053-F1067. Epub 2019 Mar 6.

Department of Clinical Medicine, University of Bergen , Bergen , Norway.

Renal cell cancer is among the most common forms of cancer in humans, with around 35,000 deaths attributed to kidney carcinoma in the European Union in 2012 alone. Clear cell renal cell carcinoma (ccRCC) represents the most common form of kidney cancer and the most lethal of all genitourinary cancers. Here, we apply omics technologies to archival core biopsies to investigate the biology underlying ccRCC. Knowledge of these underlying processes should be useful for the discovery and/or confirmation of novel therapeutic approaches and ccRCC biomarker development. From partial or full nephrectomies of 11 patients, paired core biopsies of ccRCC-affected tissue and adjacent ("peritumorous") nontumor tissue were both sampled and subjected to proteomics analyses. We combined proteomics results with our published mRNA sequencing data from the same patients and with published miRNA sequencing data from an overlapping patient cohort from our institution. Statistical analysis and pathway analysis were performed with JMP Genomics and Ingenuity Pathway Analysis (IPA), respectively. Proteomics analysis confirmed the involvement of metabolism and oxidative stress-related pathways in ccRCC, whereas the most affected pathways in the mRNA sequencing data were related to the immune system. Unlike proteomics or mRNA sequencing alone, a combinatorial cross-omics pathway analysis approach captured a broad spectrum of biological processes underlying ccRCC, such as mitochondrial damage, repression of apoptosis, and immune system pathways. Sirtuins, immunoproteasome genes, and CD74 are proposed as potential targets for the treatment of ccRCC.
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http://dx.doi.org/10.1152/ajprenal.00424.2018DOI Listing
May 2019

Low birth weight associates with glomerular area in young male IgA nephropathy patients.

BMC Nephrol 2018 10 22;19(1):287. Epub 2018 Oct 22.

Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Background: In a recent study we demonstrated that low birth weight (LBW) was associated with increased risk of progressive IgA nephropathy (IgAN). In the present study we investigate whether this could be explained by differences in glomerular morphological parameters.

Methods: The Medical Birth Registry of Norway has registered all births since 1967 and the Norwegian Kidney Biopsy Registry has registered all kidney biopsies since 1988. Patients diagnosed with IgAN, registered birth weight and estimated glomerular filtration rate above 60 ml/min/1.73m at time of diagnosis were eligible for inclusion. Patients were included in a case-control manner based on whether or not they had LBW or were small for gestational age (SGA). Glomerular area, volume and density were measured using high resolution digital images and differences were compared between groups.

Results: We included 51 IgAN patients with a mean age of 23.6 years, 47.1% male. Compared to IgAN patients without LBW or SGA, IgAN patients with LBW and/or SGA had larger glomerular area (16,235 ± 3744 vs 14,036 ± 3502 μm, p-value 0.04). This was significant for total cohort and male but not female. On separate analysis by gender, glomerular area was significantly larger only in males (17,636 ± 3285 vs 13,346 ± 2835 μm, p-value 0.004). Glomerular density was not different between groups. In adjusted linear regression analysis, glomerular area was negatively associated with birth weight.

Conclusion: Among young adult IgAN patients, low birth weight is associated with having larger glomerular area, especially in males. Larger glomeruli may be a sign of congenital nephron deficit that may explain the increased risk of progressive IgAN.
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http://dx.doi.org/10.1186/s12882-018-1070-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6198493PMC
October 2018

Long-term outcome in 145 patients with assumed benign immunoglobulin A nephropathy.

Nephrol Dial Transplant 2017 Nov;32(11):1841-1850

Renal Research Group, Department of Clinical Medicine, University of Bergen, Norway.

Background: Patients with immunoglobulin A nephropathy (IgAN) who present with mild to moderate proteinuria and normal renal function are assumed to have excellent short-term renal prognosis, but the long-term prognosis is uncertain.

Methods: Patients were selected from the Norwegian Kidney Biopsy Registry based on the following criteria: diagnostic renal biopsy performed in the period 1988-99, with estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2 and proteinuria <1 g/24 h at the time of biopsy. Patients were invited for a nephrological examination with a review of medical history and investigation of blood pressure, urinary findings and eGFR.

Results: A total of 145 patients attended the examination, performed by the first author, after a median of 22 (interquartile range 19-25) years after diagnosis. At the examination, 27 patients (18.6%) had a ≥50% decrease in GFR, of whom 4 (2.8%) had developed end-stage renal disease (ESRD). The mean duration from renal biopsy to ≥ 50% decrease in GFR was 17.3 ± 5.1 years in our cohort. Clinical remission was observed in 42 (29.0%) patients. Renal biopsies were re-examined utilizing the Oxford classification criteria. Mesangial hypercellularity was found in 12.3%, endocapillary proliferation was detected in 10.7% and segmental glomerulosclerosis was observed in 23.8%. All biopsies were scored as T0 (tubular atrophy in < 25% of the cortical area). None of the clinical or histopathological variables recorded at the time of biopsy could identify patients with progressive disease. Cumulative risks of ≥50% decrease in eGFR were 2.1% after 10 years, 4.1% after 15 years, 13.9% after 20 years and 24.7% after 25 years.

Conclusions: We have shown that 18.6% of patients with assumed benign IgAN had progressive disease after a median duration of 22 years and that these patients could not be predicted at the time of biopsy. Our study demonstrates that an extended follow-up period is needed when assessing prognosis in this group of patients.
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http://dx.doi.org/10.1093/ndt/gfx242DOI Listing
November 2017

Glomerular abundance of complement proteins characterized by proteomic analysis of laser-captured microdissected glomeruli associates with progressive disease in IgA nephropathy.

Clin Proteomics 2017 14;14:30. Epub 2017 Aug 14.

Department of Medicine, Haugesund Hospital, Postbox 2170, 5504 Haugesund, Norway.

Background: The clinical course of IgA nephropathy (IgAN) is variable and complement activation may predict prognosis. The present study investigated whether glomerular abundance of complement proteins associates with progression to end-stage renal disease (ESRD) in patients for whom prognosis could not be predicted based on clinical variables.

Methods: Based on data from the Norwegian Kidney Biopsy Registry and the Norwegian Renal Registry, three groups were included: IgAN patients with (n = 9) or without (n = 16) progression to ESRD during 10 years, and controls (n = 15) with a normal kidney biopsy. IgAN patients had eGFR > 45 ml/min/1.73 m and non-nephrotic proteinuria at time of biopsy. Using stored formalin-fixed paraffin embedded kidney biopsy tissue, about 100 glomerular cross sections were microdissected for each patient. Samples were analyzed by liquid chromatography-tandem mass spectrometry and relative abundances of complement proteins were compared between groups.

Results: Proteomic analyses quantified 2018 proteins, of which 28 proteins belong to the complement system. As compared to IgAN patients without progressive disease, glomeruli from patients with progressive IgAN had significantly higher abundance of components of the classical and the terminal complement pathways, and inhibitory factors such as Factor H and factor H related proteins. Abundance of complement proteins classified progressors from non-progressors with an area under ROC curve of 0.91 ( = 0.001). Clinical and morphological data were similar between the two patient groups and could not predict progressive IgAN.

Conclusions: In conclusion, higher glomerular abundance of complement proteins was associated with a progressive clinical course in IgAN and are candidate biomarkers to predict prognosis.
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http://dx.doi.org/10.1186/s12014-017-9165-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557313PMC
August 2017

Exposure to Mycophenolate and Fatherhood.

Transplantation 2017 07;101(7):e214-e217

1 Department of Transplantation Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 2 Department of Pharmacology, Oslo University Hospital, Oslo, Norway. 3 Department of Pharmaceutical Biosciences, School of Pharmacy, University of Oslo, Oslo, Norway. 4 Norwegian Renal Registry, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 5 Department of Clinical Medicine, University of Bergen, Bergen, Norway. 6 Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: Mycophenolic acid (MPA) is the active immunosuppressive substance in both mycophenolate mofetil and mycophenolate sodium, and it is widely used after organ transplantation. In women, taking MPA is teratogenic and may also influence spermatogenesis. There is a lack of knowledge regarding outcome of pregnancies fathered by men exposed to MPA.

Methods: We compared outcomes in pregnancies fathered by renal transplant men per whether they had been exposed to MPA or not at time of conception. A nationwide population-based retrospective cohort study was performed. Data from the Norwegian Renal Registry with all renal transplanted men alive between January 1, 1995 and December 31, 2015 were included, and relevant outcome data were extracted from the Medical Birth Registry of Norway.

Results: During the given time, 230 immunosuppressed renal transplanted men fathered 350 children (155 on MPA/195 not on MPA). There were no significant increased risks of malformation (3.9% vs. 2.6%, P = 0.49) in MPA exposed versus unexposed cohorts of children. The average dose (±SD) of mycophenolate was 1.42 ± 0.3 g/day and the individual median MPA trough concentration in the time period of anticipated conception and pregnancy was 2.8 ± 1.6 mg/L. Birth weight was similar in exposed and unexposed cohorts of children; 3381 ± 681 g vs. 3429 ± 714 g (P = 0.53).

Conclusions: Paternal exposure to MPA did not increase the risk of adverse birth outcomes in children fathered by male kidney transplanted patients. These results are reassuring and support the continuation of paternal MPA treatment before, during, and after conception.
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http://dx.doi.org/10.1097/TP.0000000000001747DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482562PMC
July 2017

End Stage Renal Disease Predicts Increased Risk of Death in First Degree Relatives in the Norwegian Population.

PLoS One 2016 9;11(11):e0165026. Epub 2016 Nov 9.

Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Background: Increased risk of end stage renal disease (ESRD) and death in Norwegian living kidney donors has been reported, most of the donors were related to the recipient. The present study investigates risk of death in first degree relatives of ESRD patients.

Methods: The Norwegian Population Registry, The Norwegian Cause of Death Registry and the Norwegian Renal Registry were linked. All citizens born in Norway, alive in 1960 and with at least one registered first degree relative were included; individuals who died during the first year of life were excluded. A cohort-design was used, ESRD in a first degree relative was the main exposure variable and death and causes of death were the main outcome variables. Cox regression statistics were used to investigate mortality risks.

Results: 5 130 600 individuals were included, 27 508 had at least one first degree relative with ESRD. 828 022 died during follow-up, of whom 4105 had a first degree relative with ESRD. Adjusted hazard ratio (aHR) for death was 1.13 (1.09-1.16) in individuals with a relative with ESRD compared to those without a relative with ESRD. Excluding known hereditary renal disease, aHR decreased to 1.12 (1.09-1.15). Cardiovascular death aHR was 1.15 (1.10-1.21), of which cerebrovascular death 1.34 (1.22-1.50). aHR for death due to non-hereditary renal/ureteric disease was 2.29 (1.81-2.91) with renal failure 1.80 (1.26-2.56) and glomerular disease 5.69 (3.88-8.34) as main contributors. Diabetes mellitus death aHR was 1.68 (1.35-2.10). Absolute mortality risks increased most for the oldest cohorts with excess mortality of 148 per 100.000 person years for the cohort born 1920-39 and 218 for the cohort born 1900-1919.

Conclusions: ESRD in first degree relatives was associated with increased hazard ratio for death. Death due to cardiovascular disease, renal disease and diabetes mellitus increased the most.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0165026PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102372PMC
July 2017

Low Birth Weight and Risk of Progression to End Stage Renal Disease in IgA Nephropathy--A Retrospective Registry-Based Cohort Study.

PLoS One 2016 19;11(4):e0153819. Epub 2016 Apr 19.

Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Background: Low Birth Weight (LBW) is a surrogate for fetal undernutrition and is associated with impaired nephron development in utero. In this study, we investigate whether having been born LBW and/or small for gestational age (SGA) predict progression to ESRD in IgA nephropathy (IgAN) patients.

Study Design: Retrospective registry-based cohort study.

Settings & Participants: The Medical Birth Registry has recorded all births since 1967 and the Norwegian Renal Registry has recorded all patients with ESRD since 1980. Based on data from the Norwegian Kidney Biopsy Registry we included all patients diagnosed with IgAN in Norway from 1988-2013. These registries were linked and we analysed risk of progression to ESRD associated with LBW (defined as birth weight less than the 10th percentile) and/or SGA (defined as birth weight less than the 10th percentile for gestational week) by Cox regression statistics.

Results: We included 471 patients, of whom 74 developed ESRD. As compared to patients without LBW, patients with LBW had a hazard ratio (HR) of 2.0 (95% confidence interval 1.1-3.7) for the total cohort, 2.2 (1.1-4.4) for males and 1.3 (0.30-5.8) for females. Corresponding HRs for SGA were 2.2 (1.1-4.2), 2.7 (1.4-5.5) and 0.8 (0.10-5.9). Further analyses showed that as compared to patients with neither LBW nor SGA, patients with either SGA or LBW did not have significantly increased risks (HRs of 1.3-1.4) but patients who were both LBW and SGA had an increased risk (HR 3.2 (1.5-6.8).

Limitation: Mean duration of follow-up only 10 years and maximum age only 46 years.

Conclusion: Among IgAN patients, LBW and/or SGA was associated with increased risk for progression to ESRD, the association was stronger in males.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0153819PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836690PMC
September 2016

[A woman in her 80s with reduced general condition and hypercalcemia].

Tidsskr Nor Laegeforen 2016 Jan 12;136(1):41-4. Epub 2016 Jan 12.

Medisinsk klinikk Haugesund sjukehus.

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http://dx.doi.org/10.4045/tidsskr.15.0448DOI Listing
January 2016

Familial Factors, Low Birth Weight, and Development of ESRD: A Nationwide Registry Study.

Am J Kidney Dis 2016 Apr 31;67(4):601-8. Epub 2015 Dec 31.

Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: Previous studies have demonstrated that low birth weight (LBW) is associated with higher risk for end-stage renal disease (ESRD). However, both LBW and ESRD cluster in families. The present study investigates whether familial factors explain the association between LBW and ESRD.

Study Design: Retrospective registry-based cohort study.

Setting & Participants: Since 1967, the Medical Birth Registry of Norway has recorded medical data for all births in the country. Sibling data are available through the Norwegian Population Registry. Since 1980, all patients with ESRD in Norway have been registered in the Norwegian Renal Registry. Individuals registered in the Medical Birth Registry with at least 1 registered sibling were included.

Predictor: LBW in the participant and/or LBW in at least 1 sibling.

Outcome: ESRD.

Results: Of 1,852,080 included individuals, 527 developed ESRD. Compared with individuals without LBW and with no siblings with LBW, individuals without LBW but with a sibling with LBW had an HR for ESRD of 1.20 (95% CI, 0.91-1.59), individuals with LBW but no siblings with LBW had an HR of 1.59 (95% CI, 1.18-2.14), and individuals with LBW and a sibling with LBW had an HR of 1.78 (95% CI, 1.26-2.53). Similar results were observed for individuals who were small for gestational age (SGA). Separate analyses for the association of age 18 to 42 years and noncongenital ESRD showed stronger associations for SGA than for LBW, and the associations were not statistically significant for age 18 to 42 years for LBW.

Limitations: Follow-up only until 42 years of age.

Conclusions: LBW and SGA are associated with higher risk for ESRD during the first 40 years of life, and the associations were not explained by familial factors. Our results support the hypothesis that impaired intrauterine nephron development may be a causal risk factor for progressive kidney disease.
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http://dx.doi.org/10.1053/j.ajkd.2015.11.015DOI Listing
April 2016

Proteomic Analysis of Minimally Damaged Renal Tubular Tissue from Two-Kidney-One-Clip Hypertensive Rats Demonstrates Extensive Changes Compared to Tissue from Controls.

Nephron 2016 9;132(1):70-80. Epub 2016 Jan 9.

Background: Tubular atrophy and interstitial fibrosis mark the final stage in most forms of progressive kidney diseases. Little is known regarding changes in the tubular proteome. In this study, we investigated changes in the tubular proteome of normal or minimally damaged tubular tissue in the non-clipped kidney from rats with two-kidney one-clip (2K1C) hypertension.

Methods: Formalin-fixed paraffin-embedded kidney sections from four 2K1C rats with hypertensive kidney damage and 6 sham rats were used. Tubulointerstitial tissue without discernable interstitial expansion or pronounced tubular alterations was microdissected and this was assumed to represent an early stage of chronic tubular damage in 2K1C. Samples were analyzed by mass spectrometry and relative protein abundances were compared between 2K1C and sham.

Results: A total of 1,160 proteins were identified with at least 2 unique peptides, allowing for relative quantitation between samples. Among these, 151 proteins were more abundant, and 192 proteins were less abundant in 2K1C compared with sham. Transgelin, vimentin and creatine kinase B-type were among the proteins that were most increased in 2K1C. Ingenuity Pathway Analysis showed increased abundance of proteins related to Rho signaling and protein turnover (eIF2 signaling and protein ubiquitination), and decreased abundance of proteins related to fatty acid β-oxidation.

Conclusion: Tubular tissue from normal or minimally damaged hypertensive kidney damage demonstrate extensive proteomic changes with upregulation of pathways associated with progressive kidney damage, such as Rho signaling and protein turnover. Thus, proteomics presents itself to be a promising tool for the discovery of early damage markers from not yet morphologically visible tubular damage.
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http://dx.doi.org/10.1159/000442825DOI Listing
October 2016

Addition of eGFR and Age Improves the Prognostic Absolute Renal Risk-Model in 1,134 Norwegian Patients with IgA Nephropathy.

Am J Nephrol 2015 9;41(3):210-9. Epub 2015 Apr 9.

Renal Research Group, Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Background: Predicting outcome in individual patients with IgA nephropathy (IgAN) is difficult but important. For this purpose, the absolute renal risk (ARR) model has been developed in a French cohort to calculate the risk of end-stage renal disease (ESRD) and death. ARR (0-3) is scored in individual IgAN patients based on the presence of proteinuria ≥1 g/24 h, hypertension, and severe histopathological lesions (1 point per risk factor). We have validated the ARR model in a Norwegian cohort of IgAN patients and tested whether adding data on initial estimated glomerular filtration rate (eGFR) and age improved prediction.

Methods: IgAN patients diagnosed between 1988 and 2012 were identified in the Norwegian Kidney Biopsy Registry, and endpoints were identified by record linkage with the Norwegian Renal Registry (ESRD) and the Population Registry (deaths).

Results: We identified 1,134 IgAN patients. The mean duration of follow-up was 10.2 years (range 0.0 to 25.7 years). Two hundred and fifty one patients developed ESRD and there were 69 pre-ESRD deaths. The ARR model significantly stratified the IgAN cohort according to risk of ESRD/death. The inclusion of eGFR and age significantly improved the ARR prognostic model; in the receiver operator characteristics (ROC) analysis, area under the curve (AUC) at 10-years of follow-up increased from 0.79 to 0.89, p < 0.001.

Conclusions: ARR is a suitable prognostic model for stratifying IgAN patients according to the risk of ESRD or death. Including initial eGFR and age in the model substantially improved its accuracy in our nationwide cohort.
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http://dx.doi.org/10.1159/000381403DOI Listing
May 2016

Proteomic analysis of formalin-fixed paraffin-embedded glomeruli suggests depletion of glomerular filtration barrier proteins in two-kidney, one-clip hypertensive rats.

Nephrol Dial Transplant 2014 Dec 16;29(12):2217-27. Epub 2014 Aug 16.

Department of Clinical Medicine, University of Bergen, Bergen, Norway Department of Medicine, Haukeland University Hospital, Bergen, Norway Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background: It is well known that hypertension may cause glomerular damage, but the molecular mechanisms involved are still incompletely understood.

Methods: In the present study, we used formalin-fixed paraffin-embedded (FFPE) tissue to investigate changes in the glomerular proteome in the non-clipped kidney of two-kidney one-clip (2K1C) hypertensive rats, with special emphasis on the glomerular filtration barrier. 2K1C hypertension was induced in 6-week-old Wistar Hannover rats (n = 6) that were sacrificed 23 weeks later and compared with age-matched sham-operated controls (n = 6). Tissue was stored in FFPE tissue blocks and later prepared on tissue slides for laser microdissection. Glomeruli without severe morphological damage were isolated, and the proteomes were analysed using liquid chromatography-tandem mass spectrometry.

Results: 2K1C glomeruli showed reduced abundance of proteins important for slit diaphragm complex, such as nephrin, podocin and neph1. The podocyte foot process had a pattern of reduced abundance of transmembrane proteins but unchanged abundances of the podocyte cytoskeletal proteins synaptopodin and α-actinin-4. Lower abundance of important glomerular basement membrane proteins was seen. Possible glomerular markers of damage with increased abundance in 2K1C were transgelin, desmin and acyl-coenzyme A thioesterase 1.

Conclusions: Microdissection and tandem mass spectrometry could be used to investigate the proteome of isolated glomeruli from FFPE tissue. Glomerular filtration barrier proteins had reduced abundance in the non-clipped kidney of 2K1C hypertensive rats.
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http://dx.doi.org/10.1093/ndt/gfu268DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240179PMC
December 2014

Familial clustering of ESRD in the Norwegian population.

Clin J Am Soc Nephrol 2014 Oct 4;9(10):1692-700. Epub 2014 Aug 4.

Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Medicine, Haugesund Hospital, Haugesund, Norway.

Background And Objectives: Studies and clinical experience suggest that kidney disease clusters in families, but few population-based studies have been performed. This study investigates risks and causes of ESRD in Norwegians with and without a first-degree relative with ESRD.

Design, Setting, Participants, & Measurements: On the basis of data from the Norwegian Population Registry, first-degree relatives for most Norwegians were identified. All Norwegians with ESRD (defined as chronic RRT) since 1980 have been registered in the Norwegian Renal Registry. All Norwegians born in Norway who were alive in 1980 and had at least one registered relative were included. For this study, data on ESRD were available through 2009, and individuals without ESRD were censored at December 31, 2009. Data were analyzed in a cohort design, with ESRD in a first-degree relative of the included person as the main explanatory variable. Risks of ESRD and different causes of ESRD were analyzed using Cox regression statistics.

Results: In total, 5,119,134 individuals were included, of whom 8203 individuals developed ESRD during follow-up and 27,046 individuals had a first-degree relative with ESRD. Compared with individuals without a first-degree relative with ESRD, individuals with a first-degree relative with ESRD had a relative risk of ESRD of 7.2 (95% confidence interval, 6.5 to 8.1). Similar analyses showed that relative risk of ESRD caused by nonhereditary causes was 3.7 (95% confidence interval, 3.1 to 4.4), relative risk of ESRD caused by glomerular disease was 5.2 (95% confidence interval, 4.1 to 6.6), relative risk of ESRD caused by interstitial disease was 4.7 (95% confidence interval, 3.1 to 7.3), relative risk of ESRD caused by diabetic nephropathy was 2.6 (95% confidence interval, 1.6 to 4.1), and relative risk of ESRD caused by hypertensive nephrosclerosis was 2.6 (95% confidence interval, 1.6 to 4.1). Relative risk of nonhereditary parenchymal renal disease was 3.8 (95% confidence interval, 3.1 to 4.7).

Conclusions: As expected, ESRD clusters in families. Interestingly, ESRD without known hereditary cause also clusters in families.
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http://dx.doi.org/10.2215/CJN.01680214DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186510PMC
October 2014

Preeclampsia in healthy women and endothelial dysfunction 10 years later.

Am J Obstet Gynecol 2013 Dec 27;209(6):569.e1-569.e10. Epub 2013 Jul 27.

Renal Research Group, Institute of Medicine, University of Bergen, Bergen, Norway. Electronic address:

Objective: Recent studies have shown that women with a history of preeclampsia have an increased risk of cardiovascular disease. The present study investigated cardiovascular risk factors 10 years after preeclampsia in previously healthy women.

Study Design: Based on data from the Medical Birth Registry in Norway, we selected 182 women with and 180 women without preeclampsia in their first pregnancy 9-11 years earlier, excluding women with cardiovascular or renal disease before pregnancy. Flow-mediated dilation of the brachial artery (FMD) and intima-media thickness (IMT) of the carotid artery were measured and blood samples were drawn. Blood samples were analyzed for cardiovascular risk markers and for circulating markers of endothelial function.

Results: A total of 89 women with previous preeclampsia and 69 women without preeclampsia participated, an overall attendance rate of 44%. FMD and IMT were similar between groups. Women with previous preeclampsia more often had urate and soluble fms-like tyrosine kinase values above the 75th percentile (odds ratio [OR], 2.4; P = .03, and OR, 2.4; P = .04, respectively) and high-density lipoprotein cholesterol values below the 25th percentile (OR, 2.3; P = .04). Women with preeclampsia with low birthweight offspring were associated with asymmetric dimethylarginine, L-arginine, and homoarginine above the 75th percentile, whereas the women with preeclampsia with normal-weight offspring were associated with urate and soluble fms-like tyrosine kinase above the 75th percentile.

Conclusion: Preeclampsia was not associated with impaired FMD or increased IMT 10 years after pregnancy in previously healthy women, but preeclampsia was associated with changes in circulating markers that might represent early endothelial dysfunction.
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http://dx.doi.org/10.1016/j.ajog.2013.07.024DOI Listing
December 2013

Mortality in patients with IgA nephropathy.

Am J Kidney Dis 2013 Nov 21;62(5):883-90. Epub 2013 Jun 21.

Department of Clinical Medicine, Renal Research Group, University of Bergen, Bergen, Norway; Department of Medicine, Haukeland University Hospital, Bergen, Norway.

Background: Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis globally. Few studies have investigated mortality in patients with IgAN compared with the age- and sex-adjusted general population.

Study Design: Cohort study with record linkage between the Norwegian Kidney Biopsy Registry, Norwegian Cause of Death Registry, and Norwegian Renal Registry.

Setting & Participants: 633 patients diagnosed with IgAN in 1988-2004.

Predictor: Estimated glomerular filtration rate (eGFR), age, and sex.

Outcomes: Deaths and causes of death before and after the onset of end-stage renal disease through 2008.

Results: Mean follow-up was 11.8 (range, 0-20.8) years. During the observation period, the observed number of deaths was 80 and the expected number was 42.1, resulting in a standardized mortality ratio (SMR) of 1.9 (95% CI, 1.5-2.4). Risk stratification based on initial eGFR showed that SMR was 1.0 (95% CI, 0.6-1.6) if eGFR was ≥60 mL/min/1.73 m(2), 1.9 (95% CI, 1.3-2.8) if eGFR was 30-60 mL/min/1.73 m(2), and 3.6 (95% CI, 2.6-5.0) in patients with eGFR <30 mL/min/1.73 m(2). Renal replacement therapy (RRT) was initiated in 146 patients and 35 of the 80 deaths occurred after the start of RRT. The age- and sex-adjusted SMR was not increased significantly in the pre-RRT period (1.3; 95% CI, 1.0-1.7), but was increased after initiation of RRT (4.9; 95% CI, 3.5-7.0). The most common cause of death was cardiovascular disease, accounting for 45% of all deaths.

Limitations: Treatment during follow-up is not known.

Conclusions: Mortality in patients with IgAN was twice the expected rate, but not significantly increased before RRT. The risk of end-stage renal disease was substantially higher than risk of death.
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http://dx.doi.org/10.1053/j.ajkd.2013.04.019DOI Listing
November 2013

Pre-eclampsia and the risk of kidney disease.

Lancet 2013 Jul 31;382(9887):104-6. Epub 2013 May 31.

Department of Clinical Medicine, University of Bergen, Bergen, Norway.

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http://dx.doi.org/10.1016/S0140-6736(13)60741-2DOI Listing
July 2013

Preeclampsia and prevalence of microalbuminuria 10 years later.

Clin J Am Soc Nephrol 2013 Jul 30;8(7):1126-34. Epub 2013 May 30.

Renal Research Group, Institute of Medicine, University of Bergen, Bergen, Norway.

Background And Objectives: A recent meta-analysis found that about 30% of women with a previous preeclamptic pregnancy had persistent microalbuminuria at follow-up. The analysis was, however, based on small studies, and more data are needed.

Design, Setting, Participants, & Measurements: Using data from the Medical Birth Registry in Norway, this study identified women with or without preeclampsia in their first pregnancy 9-11 years previously (1998-2000). Women with diabetes, rheumatic disease, essential hypertension, or renal disease before first pregnancy and/or preeclampsia in later pregnancies were excluded. Eighty-nine women with and 69 women without preeclampsia participated in the study. Urinary albumin-to-creatinine ratio (ACR) was measured in three morning urine samples. Estimated GFR (eGFR) was calculated using the CKD-Epidemiology Collaboration formula.

Results: Median urinary ACR in follow-up urine samples was 0.53 mg/mmol for women with and 0.50 mg/mmol for women without preeclampsia (P=0.54). Only one woman (1%) with previous preeclampsia had urinary ACR >2.5 mg/mmol in two of three urine samples. Preeclampsia was not associated with urinary ACR above the 75th percentile. Women with preeclampsia did not have significantly higher eGFR than women without preeclampsia (107.9 versus 104.9 ml/min per 1.73 m(2); P=0.12), but preterm preeclampsia was significantly associated with eGFR above the 75th percentile (P=0.03).

Conclusions: In this population-based study of otherwise healthy women, preeclampsia 10 years earlier was not associated with increased risk of persisting microalbuminuria. Estimated GFR was not significantly different between women with and those without preeclampsia, but preterm preeclampsia was associated with high normal eGFR.
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http://dx.doi.org/10.2215/CJN.10641012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700700PMC
July 2013

Agalsidase benefits renal histology in young patients with Fabry disease.

J Am Soc Nephrol 2013 Jan;24(1):137-48

Renal Research Group, Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway.

The effect of early-onset enzyme replacement therapy on renal morphologic features in Fabry disease is largely unknown. Here, we evaluated the effect of 5 years of treatment with agalsidase alfa or agalsidase beta in 12 consecutive patients age 7-33 years (median age, 16.5 years). We performed renal biopsies at baseline and after 5 years of enzyme replacement therapy; 7 patients had additional biopsies after 1 and 3 years. After a median of 65 months, biopsy findings from all patients showed total clearance of glomerular endothelial and mesangial cell inclusions, and findings from 2 patients showed complete clearance of inclusions from epithelial cells of the distal tubule. The 4 patients who received the highest dose of agalsidase exhibited substantial clearance of podocyte inclusions, and the youngest patient had nearly complete clearance of these inclusions. Linear regression analysis showed a highly significant correlation between podocyte globotriaocylceramide clearance and cumulative agalsidase dose (r=0.804; P=0.002). Microalbuminuria normalized in five patients. In summary, long-term enzyme replacement therapy in young patients can result in complete globotriaocylceramide clearance of mesangial and glomerular endothelial cells across all dosage regimens, and clearance of podocyte inclusions is dose-dependent.
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http://dx.doi.org/10.1681/ASN.2012030316DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3537211PMC
January 2013

Cardiovascular mortality after pre-eclampsia in one child mothers: prospective, population based cohort study.

BMJ 2012 Nov 27;345:e7677. Epub 2012 Nov 27.

Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway.

Objective: To assess the association of pre-eclampsia with later cardiovascular death in mothers according to their lifetime number of pregnancies, and particularly after only one child.

Design: Prospective, population based cohort study.

Setting: Medical Birth Registry of Norway.

Participants: We followed 836,147 Norwegian women with a first singleton birth between 1967 and 2002 for cardiovascular mortality through linkage to the national Cause of Death Registry. About 23,000 women died by 2009, of whom 3891 died from cardiovascular causes. Associations between pre-eclampsia and cardiovascular death were assessed by hazard ratios, estimated by Cox regression analyses. Hazard ratios were adjusted for maternal education (three categories), maternal age at first birth, and year of first birth

Results: The rate of cardiovascular mortality among women with preterm pre-eclampsia was 9.2% after having only one child, falling to 1.1% for those with two or more children. With term pre-eclampsia, the rates were 2.8% and 1.1%, respectively. Women with pre-eclampsia in their first pregnancy had higher rates of cardiovascular death than those who did not have the condition at first birth (adjusted hazard ratio 1.6 (95% confidence interval 1.4 to 2.0) after term pre-eclampsia; 3.7 (2.7 to 4.8) after preterm pre-eclampsia). Among women with only one lifetime pregnancy, the increase in risk of cardiovascular death was higher than for those with two or more children (3.4 (2.6 to 4.6) after term pre-eclampsia; 9.4 (6.5 to 13.7) after preterm pre-eclampsia). The risk of cardiovascular death was only moderately elevated among women with pre-eclamptic first pregnancies who went on to have additional children (1.5 (1.2 to 2.0) after term pre-eclampsia; 2.4 (1.5 to 3.9) after preterm pre-eclampsia). There was little evidence of additional risk after recurrent pre-eclampsia. All cause mortality for women with two or more lifetime births, who had pre-eclampsia in first pregnancy, was not elevated, even with preterm pre-eclampsia in first pregnancy (1.1 (0.87 to 1.14)).

Conclusions: Cardiovascular death in women with pre-eclampsia in their first pregnancy is concentrated mainly in women with no additional births. This association might be due to health problems that discourage or prevent further pregnancies rather than to pre-eclampsia itself. As a screening criterion for cardiovascular disease risk, pre-eclampsia is a strong predictor primarily among women with only one child-particularly with preterm pre-eclampsia.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508198PMC
http://dx.doi.org/10.1136/bmj.e7677DOI Listing
November 2012

Familial factors in the association between preeclampsia and later ESRD.

Clin J Am Soc Nephrol 2012 Nov 6;7(11):1819-26. Epub 2012 Sep 6.

Renal Research Group, Institute of Medicine, University of Bergen, Bergen, Norway.

Background And Objectives: Women with preeclampsia have increased risk of developing ESRD. This study assessed whether this can be explained by preeclampsia itself or by familial aggregation of common risk factors.

Design, Setting, Participants, & Measurements: Since 1967, the Medical Birth Registry of Norway has registered data on all births in the country. By linkage with the Norwegian Population Registry, different, but overlapping, cohorts were defined: the first and second cohorts included women and a sibling (first cohort) or child (second cohort) with a registered first birth between 1967 and 2008. Similar cohorts were defined for men. The Norwegian Renal Registry provided data on ESRD from 1980 to June 2009.

Results: Cohort 1 was used for the main analyses and included 570,675 women, 291 of whom developed ESRD after a median 18.2 years. Compared with women without preeclampsia and no siblings with preeclampsia, women without preeclampsia but a sibling with preeclampsia had a relative risk (RR) of ESRD of 0.96 (95% confidence interval, 0.59-1.6), women with preeclampsia but no siblings with preeclampsia had a RR of 6.0 (4.4-8.1), and women with preeclampsia and a sibling with preeclampsia had a RR of 2.8 (0.88-8.6). Further analyses of women showed no increased risk of ESRD if a child had preeclampsia in first pregnancy.

Conclusions: Familial aggregation of risk factors does not seem to explain increased ESRD risk after preeclampsia. These findings support the hypothesis that preeclampsia per se may lead to kidney damage.
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http://dx.doi.org/10.2215/CJN.01820212DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488941PMC
November 2012

[A man in his fifties with fever, cough and anuria].

Tidsskr Nor Laegeforen 2012 Aug;132(14):1621-4

Medisinsk avdeling, Haukeland universitetssykehus, Norway.

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http://dx.doi.org/10.4045/tidsskr.11.0356DOI Listing
August 2012
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