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2. Results of untargeted analysis using the SOMAscan proteomics platform indicates novel associations of circulating proteins with risk of progression to kidney failure in diabetes

Author

Kobayashi, Hiroki, Looker, Helen C., Satake, Eiichiro, Saulnier, Pierre Jean, Md Dom, Zaipul I., O’Neil, Kristina, Ihara, Katsuhito, Krolewski, Bozena, Galecki, Andrzej T., Niewczas, Monika A., Wilson, Jonathan M., Doria, Alessandro, Duffin, Kevin L., Nelson, Robert G., and Krolewski, Andrzej S.

Published
2022
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3. A Genome-Wide Association Study of Diabetic Kidney Disease in Subjects With Type 2 Diabetes

Author

van Zuydam, Natalie R, Ahlqvist, Emma, Sandholm, Niina, Deshmukh, Harshal, Rayner, N William, Abdalla, Moustafa, Ladenvall, Claes, Ziemek, Daniel, Fauman, Eric, Robertson, Neil R, McKeigue, Paul M, Valo, Erkka, Forsblom, Carol, Harjutsalo, Valma, Perna, Annalisa, Rurali, Erica, Marcovecchio, M Loredana, Igo, Robert P, Salem, Rany M, Perico, Norberto, Lajer, Maria, Käräjämäki, Annemari, Imamura, Minako, Kubo, Michiaki, Takahashi, Atsushi, Sim, Xueling, Liu, Jianjun, van Dam, Rob M, Jiang, Guozhi, Tam, Claudia HT, Luk, Andrea OY, Lee, Heung Man, Lim, Cadmon KP, Szeto, Cheuk Chun, So, Wing Yee, Chan, Juliana CN, Ang, Su Fen, Dorajoo, Rajkumar, Wang, Ling, Clara, Tan Si Hua, McKnight, Amy-Jayne, Duffy, Seamus, Pezzolesi, Marcus G, Marre, Michel, Gyorgy, Beata, Hadjadj, Samy, Hiraki, Linda T, Ahluwalia, Tarunveer S, Almgren, Peter, Schulz, Christina-Alexandra, Orho-Melander, Marju, Linneberg, Allan, Christensen, Cramer, Witte, Daniel R, Grarup, Niels, Brandslund, Ivan, Melander, Olle, Paterson, Andrew D, Tregouet, David, Maxwell, Alexander P, Lim, Su Chi, Ma, Ronald CW, Tai, E Shyong, Maeda, Shiro, Lyssenko, Valeriya, Tuomi, Tiinamaija, Krolewski, Andrzej S, Rich, Stephen S, Hirschhorn, Joel N, Florez, Jose C, Dunger, David, Pedersen, Oluf, Hansen, Torben, Rossing, Peter, Remuzzi, Giuseppe, Brosnan, Mary Julia, Palmer, Colin NA, Groop, Per-Henrik, Colhoun, Helen M, Groop, Leif C, McCarthy, Mark I, Koivula, S, Uggeldahl, T, Forslund, T, Halonen, A, Koistinen, A, Koskiaho, P, Laukkanen, M, Saltevo, J, Tiihonen, M, Forsen, M, Granlund, H, Jonsson, A-C, Nyroos, B, Kinnunen, P, Orvola, A, Salonen, T, Vähänen, A, Paldanius, Kotka R, and Riihelä, M

Subjects
Diabetes, Genetics, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Case-Control Studies, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Kidney Failure, Chronic, Male, Middle Aged, Polymorphism, Single Nucleotide, Renal Insufficiency, Chronic, Finnish Diabetic Nephropathy Study, Hong Kong Diabetes Registry Theme-based Research Scheme Project Group, Warren 3 and Genetics of Kidneys in Diabetes (GoKinD) Study Group, GENIE (GEnetics of Nephropathy an International Effort) Consortium, Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) Research Group, SUrrogate markers for Micro- and Macrovascular hard endpoints for Innovative diabetes Tools (SUMMIT) Consortium, Medical and Health Sciences, Endocrinology & Metabolism
Abstract

Identification of sequence variants robustly associated with predisposition to diabetic kidney disease (DKD) has the potential to provide insights into the pathophysiological mechanisms responsible. We conducted a genome-wide association study (GWAS) of DKD in type 2 diabetes (T2D) using eight complementary dichotomous and quantitative DKD phenotypes: the principal dichotomous analysis involved 5,717 T2D subjects, 3,345 with DKD. Promising association signals were evaluated in up to 26,827 subjects with T2D (12,710 with DKD). A combined T1D+T2D GWAS was performed using complementary data available for subjects with T1D, which, with replication samples, involved up to 40,340 subjects with diabetes (18,582 with DKD). Analysis of specific DKD phenotypes identified a novel signal near GABRR1 (rs9942471, P = 4.5 × 10-8) associated with microalbuminuria in European T2D case subjects. However, no replication of this signal was observed in Asian subjects with T2D or in the equivalent T1D analysis. There was only limited support, in this substantially enlarged analysis, for association at previously reported DKD signals, except for those at UMOD and PRKAG2, both associated with estimated glomerular filtration rate. We conclude that, despite challenges in addressing phenotypic heterogeneity, access to increased sample sizes will continue to provide more robust inference regarding risk variant discovery for DKD.

Published
2018

4. A dominant negative ADIPOQ mutation in a diabetic family with renal disease, hypoadiponectinemia, and hyperceramidemia

Author

Simeone, Christopher A., Wilkerson, Joseph L., Poss, Annelise M., Banks, James A., Varre, Joseph V., Guevara, Jose Lazaro, Hernandez, Edgar Javier, Gorsi, Bushra, Atkinson, Donald L., Turapov, Tursun, Frodsham, Scott G., Morales, Julio C. Fierro, O’Neil, Kristina, Moore, Barry, Yandell, Mark, Summers, Scott A., Krolewski, Andrzej S., Holland, William L., and Pezzolesi, Marcus G.

Published
2022
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8. Integrated analysis of blood DNA methylation, genetic variants, circulating proteins, microRNAs, and kidney failure in type 1 diabetes.

Author

Chen, Zhuo, Satake, Eiichiro, Pezzolesi, Marcus G., Md Dom, Zaipul I., Stucki, Devorah, Kobayashi, Hiroki, Syreeni, Anna, Johnson, Adam T., Wu, Xiwei, Dahlström, Emma H., King, Jaxon B., Groop, Per-Henrik, Rich, Stephen S., Sandholm, Niina, Krolewski, Andrzej S., and Natarajan, Rama

Subjects
TYPE 1 diabetes, KIDNEY failure, DNA methylation, GENETIC variation, DNA analysis, CIRCULATING tumor DNA
Abstract

Variation in DNA methylation (DNAmet) in white blood cells and other cells/tissues has been implicated in the etiology of progressive diabetic kidney disease (DKD). However, the specific mechanisms linking DNAmet variation in blood cells with risk of kidney failure (KF) and utility of measuring blood cell DNAmet in personalized medicine are not clear. We measured blood cell DNAmet in 277 individuals with type 1 diabetes and DKD using Illumina EPIC arrays; 51% of the cohort developed KF during 7 to 20 years of follow-up. Our epigenome-wide analysis identified DNAmet at 17 CpGs (5′-cytosine-phosphate-guanine-3′ loci) associated with risk of KF independent of major clinical risk factors. DNAmet at these KF-associated CpGs remained stable over a median period of 4.7 years. Furthermore, DNAmet variations at seven KF-associated CpGs were strongly associated with multiple genetic variants at seven genomic regions, suggesting a strong genetic influence on DNAmet. The effects of DNAmet variations at the KF-associated CpGs on risk of KF were partially mediated by multiple KF-associated circulating proteins and KF-associated circulating miRNAs. A prediction model for risk of KF was developed by adding blood cell DNAmet at eight selected KF-associated CpGs to the clinical model. This updated model significantly improved prediction performance (c-statistic = 0.93) versus the clinical model (c-statistic = 0.85) at P = 6.62 × 10−14. In conclusion, our multiomics study provides insights into mechanisms through which variation of DNAmet may affect KF development and shows that blood cell DNAmet at certain CpGs can improve risk prediction for KF in T1D. Editor's summary: Individuals with type 1 diabetes (T1D) are at increased risk of developing kidney disease, and a proportion of those who do then progress to kidney failure. Chen et al. examined the genomic DNA methylation of blood cells from patients with diabetic kidney disease and found methylation at specific CpGs that positively or negatively associated with subsequent kidney failure over the following years or decades. Some of these methylation sites were validated in a similar but independent patient cohort, suggesting that such sites may be useful for identifying individuals with T1D who are at risk of progressing to end-stage kidney disease. —Catherine Charneski [ABSTRACT FROM AUTHOR]

Published
2024
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9. A signature of circulating inflammatory proteins and development of end-stage renal disease in diabetes

Author

Niewczas, Monika A., Pavkov, Meda E., Skupien, Jan, Smiles, Adam, Md Dom, Zaipul I., Wilson, Jonathan M., Park, Jihwan, Nair, Viji, Schlafly, Andrew, Saulnier, Pierre-Jean, Satake, Eiichiro, Simeone, Christopher A., Shah, Hetal, Qiu, Chengxiang, Looker, Helen C., Fiorina, Paolo, Ware, Carl F., Sun, Jennifer K., Doria, Alessandro, Kretzler, Matthias, Susztak, Katalin, Duffin, Kevin L., Nelson, Robert G., and Krolewski, Andrzej S.

Published
2019
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12. Neuroblastoma suppressor of tumorigenicity 1 is a circulating protein associated with progression to end-stage kidney disease in diabetes

Author

Kobayashi, Hiroki, primary, Looker, Helen C., additional, Satake, Eiichiro, additional, D’Addio, Francesca, additional, Wilson, Jonathan M., additional, Saulnier, Pierre Jean, additional, Md Dom, Zaipul I., additional, O’Neil, Kristina, additional, Ihara, Katsuhito, additional, Krolewski, Bozena, additional, Badger, Hannah S., additional, Petrazzuolo, Adriana, additional, Corradi, Domenico, additional, Galecki, Andrzej, additional, Wilson, Parker C., additional, Najafian, Behzad, additional, Mauer, Michael, additional, Niewczas, Monika A., additional, Doria, Alessandro, additional, Humphreys, Benjamin D., additional, Duffin, Kevin L., additional, Fiorina, Paolo, additional, Nelson, Robert G., additional, and Krolewski, Andrzej S., additional

Published
2022
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19. Association of Coding Variants in Hydroxysteroid 17-beta Dehydrogenase 14 (HSD17B14) with Reduced Progression to End Stage Kidney Disease in Type 1 Diabetes

Author

Mychaleckyj, Josyf C., primary, Valo, Erkka, additional, Ichimura, Takaharu, additional, Ahluwalia, Tarunveer S., additional, Dina, Christian, additional, Miller, Rachel G., additional, Shabalin, Ivan G., additional, Gyorgy, Beata, additional, Cao, JingJing, additional, Onengut-Gumuscu, Suna, additional, Satake, Eiichiro, additional, Smiles, Adam M., additional, Haukka, Jani K., additional, Tregouet, David-Alexandre, additional, Costacou, Tina, additional, O’Neil, Kristina, additional, Paterson, Andrew D., additional, Forsblom, Carol, additional, Keenan, Hillary A., additional, Pezzolesi, Marcus G., additional, Pragnell, Marlon, additional, Galecki, Andrzej, additional, Rich, Stephen S., additional, Sandholm, Niina, additional, Klein, Ronald, additional, Klein, Barbara E., additional, Susztak, Katalin, additional, Orchard, Trevor J., additional, Korstanje, Ron, additional, King, George L., additional, Hadjadj, Samy, additional, Rossing, Peter, additional, Bonventre, Joseph V., additional, Groop, Per-Henrik, additional, Warram, James H., additional, and Krolewski, Andrzej S., additional

Published
2021
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23. Comprehensive Search for Novel Circulating miRNAs and Axon Guidance Pathway Proteins Associated with Risk of ESKD in Diabetes

Author

Satake, Eiichiro, primary, Saulnier, Pierre-Jean, additional, Kobayashi, Hiroki, additional, Gupta, Manoj K., additional, Looker, Helen C., additional, Wilson, Jonathan M., additional, Md Dom, Zaipul I., additional, Ihara, Katsuhito, additional, O’Neil, Kristina, additional, Krolewski, Bozena, additional, Pipino, Caterina, additional, Pavkov, Meda E., additional, Nair, Viji, additional, Bitzer, Markus, additional, Niewczas, Monika A., additional, Kretzler, Matthias, additional, Mauer, Michael, additional, Doria, Alessandro, additional, Najafian, Behzad, additional, Kulkarni, Rohit N., additional, Duffin, Kevin L., additional, Pezzolesi, Marcus G., additional, Kahn, C. Ronald, additional, Nelson, Robert G., additional, and Krolewski, Andrzej S., additional

Published
2021
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24. Association of coding variants in hydroxysteroid 17-beta dehydrogenase 14 (HSD17B14) with reduced progression to end stage kidney disease in type 1 diabetes

Author

Mychaleckyj, Josyf C., Valo, Erkka, Ichimura, Takaharu, Ahluwalia, Tarunveer S., Dina, Christian, Miller, Rachel G., Shabalin, Ivan G., Gyorgy, Beata, Cao, Jing Jing, Onengut-Gumuscu, Suna, Satake, Eiichiro, Smiles, Adam M., Haukka, Jani K., Tregouet, David Alexandre, Costacou, Tina, O’Neil, Kristina, Paterson, Andrew D., Forsblom, Carol, Keenan, Hillary A., Pezzolesi, Marcus G., Pragnell, Marlon, Galecki, Andrzej, Rich, Stephen S., Sandholm, Niina, Klein, Ronald, Klein, Barbara E., Susztak, Katalin, Orchard, Trevor J., Korstanje, Ron, King, George L., Hadjadj, Samy, Rossing, Peter, Bonventre, Joseph V., Groop, Per Henrik, Warram, James H., Krolewski, Andrzej S., Mychaleckyj, Josyf C., Valo, Erkka, Ichimura, Takaharu, Ahluwalia, Tarunveer S., Dina, Christian, Miller, Rachel G., Shabalin, Ivan G., Gyorgy, Beata, Cao, Jing Jing, Onengut-Gumuscu, Suna, Satake, Eiichiro, Smiles, Adam M., Haukka, Jani K., Tregouet, David Alexandre, Costacou, Tina, O’Neil, Kristina, Paterson, Andrew D., Forsblom, Carol, Keenan, Hillary A., Pezzolesi, Marcus G., Pragnell, Marlon, Galecki, Andrzej, Rich, Stephen S., Sandholm, Niina, Klein, Ronald, Klein, Barbara E., Susztak, Katalin, Orchard, Trevor J., Korstanje, Ron, King, George L., Hadjadj, Samy, Rossing, Peter, Bonventre, Joseph V., Groop, Per Henrik, Warram, James H., and Krolewski, Andrzej S.

Abstract

Background Rare variants in gene coding regions likely have a greater impact on disease-related phenotypes than common variants through disruption of their encoded protein. We searched for rare variants associated with onset of ESKD in individuals with type 1 diabetes at advanced kidney disease stage. Methods Gene-based exome array analyses of 15,449 genes in five large incidence cohorts of individuals with type 1 diabetes and proteinuria were analyzed for survival time to ESKD, testing the top gene in a sixth cohort (n52372/1115 events all cohorts) and replicating in two retrospective case-control studies (n51072 cases, 752 controls). Deep resequencing of the top associated gene in five cohorts confirmed the findings. We performed immunohistochemistry and gene expression experiments in human control and diseased cells, and in mouse ischemia reperfusion and aristolochic acid nephropathy models. Results Protein coding variants in the hydroxysteroid 17-b dehydrogenase 14 gene (HSD17B14), predicted to affect protein structure, had a net protective effect against development of ESKD at exome-wide significance (n54196; P value53.3 3 1027). The HSD17B14 gene and encoded enzyme were robustly expressed in healthy human kidney, maximally in proximal tubular cells. Paradoxically, gene and protein expression were attenuated in human diabetic proximal tubules and in mouse kidney injury models. Expressed HSD17B14 gene and protein levels remained low without recovery after 21 days in a murine ischemic reperfusion injury model. Decreased gene expression was found in other CKD-associated renal pathologies. Conclusions HSD17B14 gene is mechanistically involved in diabetic kidney disease. The encoded sex steroid enzyme is a druggable target, potentially opening a new avenue for therapeutic development.

Published
2021

26. Early progressive renal decline precedes the onset of microalbuminuria and its progression to macroalbuminuria

Author

Krolewski, Andrzej S., Niewczas, Monika A., Skupien, Jan, Gohda, Tomhito, Smiles, Adam, Eckfeldt, Jan H., Doria, Alessandro, and Warram, James H.

Subjects
Cholesterol, Diabetes -- Development and progression, Health
Abstract

OBJECTIVE Progressive decrease in the glomerular filtration rate (GFR), or renal decline, in type 1 diabetes (TID) is observed in patients with macroalbuminuria. However, it is unknown whether this decline [...]

Published
2014
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27. The pseudokinase tribbles homolog 3 interacts with ATF4 to negatively regulate insulin exocytosis in human and mouse β cells

Author

Liew, Chong Wee, Bochenski, Jacek, Kawamori, Dan, Hu, Jiang, Leech, Colin A., Wanic, Krzysztof, Malecki, Maciej, Warram, James H., Qi, Ling, Krolewski, Andrzej S., and Kulkarni, Rohit N.

Subjects
Pancreatic beta cells -- Genetic aspects, Insulin -- Dosage and administration, Type 2 diabetes -- Development and progression -- Drug therapy -- Genetic aspects, Health care industry
Abstract

Insufficient insulin secretion and reduced pancreatic β cell mass are hallmarks of type 2 diabetes (T2DM). Here, we confirm that a previously identified polymorphism (rs2295490/Q84R) in exon 2 of the [...]

Published
2010
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29. Mutations at the BLK locus linked to maturity onset diabetes of the young and [beta]-cell dysfunction

Author

Borowiec, Maciej, Liew, Chong W., Thompson, Ryan, Boonyasrisawat, Watip, Hu, Jiang, Mlynarski, Wojciech M., Khattabi, Ilham El, Kim, Sung-Hoon, Marselli, Lorella, Rich, Stephen S., Krolewski, Andrzej S., Bonner-Weir, Susan, Sharma, Arun, Sale, Michele, Mychaleckyj, Josyf C., Kulkarni, Rohit N., and Doria, Alessandro

Subjects
Diabetes -- Development and progression, Diabetes -- Genetic aspects, Pancreatic beta cells -- Genetic aspects, Pancreatic beta cells -- Health aspects, Science and technology
Abstract

Maturity-onset diabetes of the young (MODY) is a subtype of diabetes defined by an autosomal pattern of inheritance and a young age at onset, often before age 25. MODY is genetically heterogeneous, with 8 distinct MODY genes identified to date and more believed to exist. We resequenced 732 kb of genomic sequence at 8p23 in 6 MODY families unlinked to known MODY genes that showed evidence of linkage at that location. Of the 410 sequence differences that we identified, 5 had a frequency < 1% in the general population and segregated with diabetes in 3 of the families, including the 2 showing the strongest support for linkage at this location. The 5 mutations were all placed within 100 kb corresponding to the BLK gene. One resulted in an Ala71Thr substitution; the other 4 were noncoding and determined decreased in vitro promoter activity in reporter gene experiments. We found that BLK--a nonreceptor tyrosine-kinase of the src family of proto-oncogenes--is expressed in [beta]-cells where it enhances insulin synthesis and secretion in response to glucose by up-regulating transcription factors Pdx1 and Nkx6.1. These actions are greatly attenuated by the Ala71Thr mutation. These findings point to BLK as a previously unrecognized modulator of [beta]-cell function, the deficit of which may lead to the development of diabetes. beta cells | genetics | MODY | tyrosine kinase

Published
2009

30. Circulating proteins protect against renal decline and progression to end-stage renal disease in patients with diabetes

Author

Md Dom, Zaipul I., primary, Satake, Eiichiro, additional, Skupien, Jan, additional, Krolewski, Bozena, additional, O’Neil, Kristina, additional, Willency, Jill A., additional, Dillon, Simon T., additional, Wilson, Jonathan M., additional, Kobayashi, Hiroki, additional, Ihara, Katsuhito, additional, Libermann, Towia A., additional, Pragnell, Marlon, additional, Duffin, Kevin L., additional, and Krolewski, Andrzej S., additional

Published
2021
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32. A profile of multiple circulating TNF receptors associated with early progressive renal decline in Type 1 Diabetes; similar to profiles in autoimmune disorders

Author

Ihara, Katsuhito, Skupien, Jan, Krolewski, Bozena, Md Dom, Zaipul I., O’Neil, Kristina, Satake, Eiichiro, Kobayashi, Hiroki, Rashidi, Narges M., Niewczas, Monika A., and Krolewski, Andrzej S.

Subjects
Diabetes Mellitus, Type 1, Risk Factors, Disease Progression, Albuminuria, Humans, Diabetic Nephropathies, Kidney, Article, Receptors, Tumor Necrosis Factor, Glomerular Filtration Rate
Abstract

This study comprehensively evaluated the association between known circulating tumor necrosis factor (TNF) superfamily ligands and receptors and the development of early progressive renal decline (PRD) leading to end-stage kidney disease (ESKD) in Type 1 diabetes (T1D). The Macro-Albuminuria Study comprised of 198 individuals, and the Micro-Albuminuria Study consisted of 148 individuals. All individuals had normal renal function and were followed for 7–15 years to determine estimate glomerular filtration rate (eGFR) slopes and to ascertain onset of ESKD. Plasma concentrations of 25 TNF superfamily proteins were measured using proximity extension assay applied in the OLINK proteomics platform. In the both studies risk of early PRD, determined as eGFR loss greater or equal to 3 ml/min/1.73m(2)/year, was associated with elevated circulating levels of 13 TNF receptors out of 19 examined. In the Macro-Albuminuria Study, we obtained similar findings for risk of progression to ESKD. These receptors comprised: TNF-R1A, -R1B, -R3, -R4, -R6, -R6B, -R7, -R10A, -R10B, -R11A, -R14, -R21, and -R27. Serial measurements showed that circulating levels of these TNF receptors had increased before the onset of PRD. In contrast, none of the 6 measured TNF ligands showed association with risk of early PRD. The disease process that underlies PRD which leads to ESKD in T1D is enriched with up-regulated levels of multiple TNF receptors, a profile also seen in autoimmune disorders. The mechanisms of this enrichment may be causally related to the development of PRD in T1D and must be investigated further. Some of these receptors may be used as new predictors of risk of ESKD.

Published
2020

35. Association Between a Genetic Variant Related to Glutamic Acid Metabolism and Coronary Heart Disease in Individuals With Type 2 Diabetes

Author

Qi, Lu, Qi, Qibin, Prudente, Sabrina, Mendonca, Christine, Andreozzi, Francesco, di Pietro, Natalia, Sturma, Mariella, Novelli, Valeria, Mannino, Gaia Chiara, Formoso, Gloria, Gervino, Ernest V., Hauser, Thomas H., Muehlschlegel, Jochen D., Niewczas, Monika A., Krolewski, Andrzej S., Biolo, Gianni, Pandolfi, Assunta, Rimm, Eric, Sesti, Giorgio, Trischitta, Vincenzo, Hu, Frank, and Doria, Alessandro

Published
2013
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37. Regression of microalbuminuria in type 1 diabetes

Author

Perkins, Bruce A., Ficociello, Linda H., Silva, Kristen H., Finkelstein, Dianne M., Warram, James H., and Krolewski, Andrzej S.

Subjects
Diabetic nephropathies -- Development and progression, Albuminuria -- Development and progression
Abstract

Many diabetics who have a protein called albumin in their urine?will not necessarily develop diabetic kidney disease, according to a study of 386 patients. In fact, they may even stop excreting albumin in their urine. Diabetics with low blood pressure, low cholesterol levels, and low glycosylated hemoglobin levels were three times more likely to stop excreting albumin in their urine than other diabetics. Albumin in the urine is a sign that a person may be developing kidney disease.

Published
2003

42. Erratum. Profibrotic Circulating Proteins and Risk of Early Progressive Renal Decline in Patients With Type 2 Diabetes With and Without Albuminuria. Diabetes Care 2020;43:2760–2767

Author

Ihara, Katsuhito, primary, Skupien, Jan, additional, Kobayashi, Hiroki, additional, Md Dom, Zaipul I., additional, Wilson, Jonathan M., additional, O’Neil, Kristina, additional, Badger, Hannah S., additional, Bowsman, Lenden M., additional, Satake, Eiichiro, additional, Breyer, Matthew D., additional, Duffin, Kevin L., additional, and Krolewski, Andrzej S., additional

Published
2020
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43. Profibrotic circulating proteins and risk of early progressive renal decline in Type 2 Diabetes patients with and without albuminuria

Author

Ihara, Katsuhito, primary, Skupien, Jan, primary, Kobayashi, Hiroki, primary, Dom, Zaipul I. Md, primary, Wilson, Jonathan M., primary, O’Neil, Kristina, primary, Badger, Hannah S., primary, Bowsman, Lenden M., primary, Satake, Eiichiro, primary, Breyer, Matthew D., primary, Duffin, Kevin L., primary, and Krolewski, Andrzej S., primary

Published
2020
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44. Profibrotic Circulating Proteins and Risk of Early Progressive Renal Decline in Patients With Type 2 Diabetes With and Without Albuminuria

Author

Ihara, Katsuhito, primary, Skupien, Jan, additional, Kobayashi, Hiroki, additional, Md Dom, Zaipul I., additional, Wilson, Jonathan M., additional, O’Neil, Kristina, additional, Badger, Hannah S., additional, Bowsman, Lenden M., additional, Satake, Eiichiro, additional, Breyer, Matthew D., additional, Duffin, Kevin L., additional, and Krolewski, Andrzej S., additional

Published
2020
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49. Genome-Wide Association Scan for Diabetic Nephropathy Susceptibility Genes in Type 1 Diabetes

Author

Pezzolesi, Marcus G., Poznik, G. David, Mychaleckyj, Josyf C., Paterson, Andrew D., Barati, Michelle T., Klein, Jon B., Ng, Daniel P.K., Placha, Grzegorz, Canani, Luis H., Bochenski, Jacek, Waggott, Daryl, Merchant, Michael L., Krolewski, Bozena, Mirea, Lucia, Wanic, Krzysztof, Katavetin, Pisut, Kure, Masahiko, Wolkow, Pawel, Dunn, Jonathon S., Smiles, Adam, Walker, William H., Boright, Andrew P., Bull, Shelley B., Doria, Alessandro, Rogus, John J., Rich, Stephen S., Warram, James H., and Krolewski, Andrzej S.

Published
2009

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