Diabetic Proteinuria Revisited: Updated Physiologic Perspectives
Albuminuria, a hallmark of diabetic nephropathy, reflects not only injury and dysfunction of the filtration apparatus, but is also affected by altered glomerular hemodynamics and hyperfiltration, as well as by the inability of renal tubular cells to fully retrieve filtered albumin. Albuminuria furth...
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| Format: | Article |
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MDPI AG
2022-09-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/11/18/2917 |
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| author | Samuel N. Heyman Itamar Raz Jamie P. Dwyer Roni Weinberg Sibony Julia B. Lewis Zaid Abassi |
| author_facet | Samuel N. Heyman Itamar Raz Jamie P. Dwyer Roni Weinberg Sibony Julia B. Lewis Zaid Abassi |
| author_sort | Samuel N. Heyman |
| collection | DOAJ |
| description | Albuminuria, a hallmark of diabetic nephropathy, reflects not only injury and dysfunction of the filtration apparatus, but is also affected by altered glomerular hemodynamics and hyperfiltration, as well as by the inability of renal tubular cells to fully retrieve filtered albumin. Albuminuria further plays a role in the progression of diabetic nephropathy, and the suppression of glomerular albumin leak is a key factor in its prevention. Although microalbuminuria is a classic manifestation of diabetic nephropathy, often progressing to macroalbuminuria or overt proteinuria over time, it does not always precede renal function loss in diabetes. The various components leading to diabetic albuminuria and their associations are herein reviewed, and the physiologic rationale and efficacy of therapeutic interventions that reduce glomerular hyperfiltration and proteinuria are discussed. With these perspectives, we propose that these measures should be initiated early, before microalbuminuria develops, as substantial renal injury may already be present in the absence of proteinuria. We further advocate that the inhibition of the renin–angiotensin axis or of sodium–glucose co-transport likely permits the administration of a normal recommended or even high-protein diet, highly desirable for sarcopenic diabetic patients. |
| first_indexed | 2024-03-10T00:25:58Z |
| format | Article |
| id | doaj.art-b39f2f42a00c422fb02df1b62a7c0b7c |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-10T00:25:58Z |
| publishDate | 2022-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-b39f2f42a00c422fb02df1b62a7c0b7c2023-11-23T15:34:24ZengMDPI AGCells2073-44092022-09-011118291710.3390/cells11182917Diabetic Proteinuria Revisited: Updated Physiologic PerspectivesSamuel N. Heyman0Itamar Raz1Jamie P. Dwyer2Roni Weinberg Sibony3Julia B. Lewis4Zaid Abassi5Department of Medicine, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem 9765422, IsraelFaculty of Medicine, Hebrew University of Jerusalem, Jerusalem 9765422, IsraelClinical and Translational Science Institute, University of Utah Health, Salt Lake City, UT 84112, USAFaculty of Medicine, Ben-Gurion University, Beer Sheva 84105, IsraelDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN 37232, USADepartment of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 3200003, IsraelAlbuminuria, a hallmark of diabetic nephropathy, reflects not only injury and dysfunction of the filtration apparatus, but is also affected by altered glomerular hemodynamics and hyperfiltration, as well as by the inability of renal tubular cells to fully retrieve filtered albumin. Albuminuria further plays a role in the progression of diabetic nephropathy, and the suppression of glomerular albumin leak is a key factor in its prevention. Although microalbuminuria is a classic manifestation of diabetic nephropathy, often progressing to macroalbuminuria or overt proteinuria over time, it does not always precede renal function loss in diabetes. The various components leading to diabetic albuminuria and their associations are herein reviewed, and the physiologic rationale and efficacy of therapeutic interventions that reduce glomerular hyperfiltration and proteinuria are discussed. With these perspectives, we propose that these measures should be initiated early, before microalbuminuria develops, as substantial renal injury may already be present in the absence of proteinuria. We further advocate that the inhibition of the renin–angiotensin axis or of sodium–glucose co-transport likely permits the administration of a normal recommended or even high-protein diet, highly desirable for sarcopenic diabetic patients.https://www.mdpi.com/2073-4409/11/18/2917diabetes mellitusdiabetic nephropathyalbuminuriaglomerulartubularrenal reserve |
| spellingShingle | Samuel N. Heyman Itamar Raz Jamie P. Dwyer Roni Weinberg Sibony Julia B. Lewis Zaid Abassi Diabetic Proteinuria Revisited: Updated Physiologic Perspectives Cells diabetes mellitus diabetic nephropathy albuminuria glomerular tubular renal reserve |
| title | Diabetic Proteinuria Revisited: Updated Physiologic Perspectives |
| title_full | Diabetic Proteinuria Revisited: Updated Physiologic Perspectives |
| title_fullStr | Diabetic Proteinuria Revisited: Updated Physiologic Perspectives |
| title_full_unstemmed | Diabetic Proteinuria Revisited: Updated Physiologic Perspectives |
| title_short | Diabetic Proteinuria Revisited: Updated Physiologic Perspectives |
| title_sort | diabetic proteinuria revisited updated physiologic perspectives |
| topic | diabetes mellitus diabetic nephropathy albuminuria glomerular tubular renal reserve |
| url | https://www.mdpi.com/2073-4409/11/18/2917 |
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