Physiopathology glomerular hyperfiltration in diabetes. Part 1
Glomerular hyperfiltration (HF) in diabetic kidney disease is a complex hemodynamic phenomenon which occurs in early stages of the disease’s progress and probably has negative influences, regarding the progression to the occurrence of microalbuminuria and the progress of evident diabetic nephropathy...
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| Format: | Article |
| Language: | Spanish |
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Asociación Regional de Diálisis y Trasplantes Renales de Capital Federal y Provincia de Buenos Aires
2014-09-01
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| Series: | Revista de Nefrología, Diálisis y Trasplante |
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| Online Access: | http://www.revistarenal.org.ar/index.php/rndt/article/view/116 |
| _version_ | 1811342983773028352 |
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| author | Claudio A. Mascheroni |
| author_facet | Claudio A. Mascheroni |
| author_sort | Claudio A. Mascheroni |
| collection | DOAJ |
| description | Glomerular hyperfiltration (HF) in diabetic kidney disease is a complex hemodynamic phenomenon which occurs in early stages of the disease’s progress and probably has negative influences, regarding the progression to the occurrence of microalbuminuria and the progress of evident diabetic nephropathy (DN). Factors involved in its physiopathology are numerous, they include: diabetic biochemical environment and several humoral factors like nitric oxide, prostaglandins, renin-angiotensin-aldosterone system, atrial natriuretic peptide, reactive oxygen species, other humoral and growth factors. These factors cause or enhance the vasodilatation of the afferent arteriole (AA). Factors with vasoconstriction function over the efferent arteriole, all considered primary vascular factors. However, these factors cannot explain other observed alterations and they constitute primary tubular abnormalities such as the increased reabsorption at the proximal tubule, probably conditioned by kidney growth in DBT and by the overexpression of the SGLT2 cotransporter. This higher proximal reabsorption would produce a lower arrival of solutes to the macula densa (MD). This would be incompatible with an action of the tubuloglomerular balance system, but it would be compatible with an action performed by the tubuloglomerular feedback system (TGFB) that senses the decrease of the ClNa concentration at the MD. Also deactivating the TGFB and causing vasodilatation of the AA, resulting in an increase of glomerular filtration (GF) and renal plasma flow (RPF), characteristic of the HF process. These two processes (vascular and tubular) could act in synergy or simultaneously, depending on the metabolic and progressing conditions of the diabetic kidney disease. Similar mechanisms could explain the salt paradox, whereby a lowsalt diet would exacerbate the HF phenomenon and a high-salt diet would decrease the GF and the RPF, which could result in unexpected clinical implications. The common therapy measures for HF strict metabolic control, a low-protein diet, and the wide clinical use of IECA or AT1 blockers (not clinically tested for this purpose) seem to be added to the new specific inhibitors of the SGLT2 cotransporter, which have shown beneficial effects in several aspects of the diabetic management. There are already some works with specific effect over the HF that seem to be encouraging. There is less experience with the potential use of C-peptide, as a therapeutic tool in these clinical situations. Clearly, defining the mechanisms involved in this complex phenomenon, will allow a better knowledge of it and a better therapeutic approach. |
| first_indexed | 2024-04-13T19:21:39Z |
| format | Article |
| id | doaj.art-b008428d43254723aa0657d2395f544f |
| institution | Directory Open Access Journal |
| issn | 0326-3428 2346-8548 |
| language | Spanish |
| last_indexed | 2024-04-13T19:21:39Z |
| publishDate | 2014-09-01 |
| publisher | Asociación Regional de Diálisis y Trasplantes Renales de Capital Federal y Provincia de Buenos Aires |
| record_format | Article |
| series | Revista de Nefrología, Diálisis y Trasplante |
| spelling | doaj.art-b008428d43254723aa0657d2395f544f2022-12-22T02:33:31ZspaAsociación Regional de Diálisis y Trasplantes Renales de Capital Federal y Provincia de Buenos AiresRevista de Nefrología, Diálisis y Trasplante0326-34282346-85482014-09-01343130154116Physiopathology glomerular hyperfiltration in diabetes. Part 1Claudio A. Mascheroni0Nefrología San Pedro, Buenos AiresGlomerular hyperfiltration (HF) in diabetic kidney disease is a complex hemodynamic phenomenon which occurs in early stages of the disease’s progress and probably has negative influences, regarding the progression to the occurrence of microalbuminuria and the progress of evident diabetic nephropathy (DN). Factors involved in its physiopathology are numerous, they include: diabetic biochemical environment and several humoral factors like nitric oxide, prostaglandins, renin-angiotensin-aldosterone system, atrial natriuretic peptide, reactive oxygen species, other humoral and growth factors. These factors cause or enhance the vasodilatation of the afferent arteriole (AA). Factors with vasoconstriction function over the efferent arteriole, all considered primary vascular factors. However, these factors cannot explain other observed alterations and they constitute primary tubular abnormalities such as the increased reabsorption at the proximal tubule, probably conditioned by kidney growth in DBT and by the overexpression of the SGLT2 cotransporter. This higher proximal reabsorption would produce a lower arrival of solutes to the macula densa (MD). This would be incompatible with an action of the tubuloglomerular balance system, but it would be compatible with an action performed by the tubuloglomerular feedback system (TGFB) that senses the decrease of the ClNa concentration at the MD. Also deactivating the TGFB and causing vasodilatation of the AA, resulting in an increase of glomerular filtration (GF) and renal plasma flow (RPF), characteristic of the HF process. These two processes (vascular and tubular) could act in synergy or simultaneously, depending on the metabolic and progressing conditions of the diabetic kidney disease. Similar mechanisms could explain the salt paradox, whereby a lowsalt diet would exacerbate the HF phenomenon and a high-salt diet would decrease the GF and the RPF, which could result in unexpected clinical implications. The common therapy measures for HF strict metabolic control, a low-protein diet, and the wide clinical use of IECA or AT1 blockers (not clinically tested for this purpose) seem to be added to the new specific inhibitors of the SGLT2 cotransporter, which have shown beneficial effects in several aspects of the diabetic management. There are already some works with specific effect over the HF that seem to be encouraging. There is less experience with the potential use of C-peptide, as a therapeutic tool in these clinical situations. Clearly, defining the mechanisms involved in this complex phenomenon, will allow a better knowledge of it and a better therapeutic approach.http://www.revistarenal.org.ar/index.php/rndt/article/view/116fisiopatologíahiperfiltración glomerulardiabetesnefropatía diabéticaenfermedades glomerulares |
| spellingShingle | Claudio A. Mascheroni Physiopathology glomerular hyperfiltration in diabetes. Part 1 Revista de Nefrología, Diálisis y Trasplante fisiopatología hiperfiltración glomerular diabetes nefropatía diabética enfermedades glomerulares |
| title | Physiopathology glomerular hyperfiltration in diabetes. Part 1 |
| title_full | Physiopathology glomerular hyperfiltration in diabetes. Part 1 |
| title_fullStr | Physiopathology glomerular hyperfiltration in diabetes. Part 1 |
| title_full_unstemmed | Physiopathology glomerular hyperfiltration in diabetes. Part 1 |
| title_short | Physiopathology glomerular hyperfiltration in diabetes. Part 1 |
| title_sort | physiopathology glomerular hyperfiltration in diabetes part 1 |
| topic | fisiopatología hiperfiltración glomerular diabetes nefropatía diabética enfermedades glomerulares |
| url | http://www.revistarenal.org.ar/index.php/rndt/article/view/116 |
| work_keys_str_mv | AT claudioamascheroni physiopathologyglomerularhyperfiltrationindiabetespart1 |