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Tubular reabsorption and diabetes-induced glomerular hyperfiltration Persson P; Hansell P; Palm FActa Physiol (Oxf) 2010[Sep]; 200 (1): 3-10Elevated glomerular filtration rate (GFR) is a common observation in early diabetes mellitus and closely correlates with the progression of diabetic nephropathy. Hyperfiltration has been explained to be the result of a reduced load of sodium and chloride passing macula densa, secondarily to an increased proximal reabsorption of glucose and sodium by the sodium-glucose co-transporters. This results in an inactivation of the tubuloglomerular feedback (TGF), leading to a reduced afferent arteriolar vasoconstriction and subsequently an increase in GFR. This hypothesis has recently been questioned due to the observation that adenosine A(1)-receptor knockout mice, previously shown to lack a functional TGF mechanism, still display a pronounced hyperfiltration when diabetes is induced. Leyssac demonstrated in the 1960s (Acta Physiol Scand58, 1963:236) that GFR and proximal reabsorption can work independently of each other. Furthermore, by the use of micropuncture technique a reduced hydrostatic pressure in Bowman's space or in the proximal tubule of diabetic rats has been observed. A reduced pressure in Bowman's space will increase the pressure gradient over the filtration barrier and can contribute to the development of diabetic hyperfiltration. When inhibiting proximal reabsorption with a carbonic anhydrase inhibitor, GFR decreases and proximal tubular pressure increases. Measuring intratubular pressure allows a sufficient time resolution to reveal that net filtration pressure decreases before TGF is activated which highlights the importance of intratubular pressure as a regulator of GFR. Taken together, these results imply that the reduced intratubular pressure observed in diabetes might be crucial for the development of glomerular hyperfiltration.|*Glomerular Filtration Rate[MESH]|Absorption[MESH]|Animals[MESH]|Diabetic Nephropathies/genetics/*metabolism/physiopathology[MESH]|Feedback, Physiological[MESH]|Hemodynamics[MESH]|Humans[MESH]|Hydrostatic Pressure[MESH]|Kidney Glomerulus/*metabolism/physiopathology[MESH]|Kidney Tubules/*metabolism/physiopathology[MESH]|Mice[MESH]|Mice, Transgenic[MESH]|Models, Animal[MESH]|Up-Regulation[MESH] |
