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Glomerular charge selectivity is impaired in hypertensive nephropathy
Rolf E F Christiansen1, Olav Tenstad, Sabine Leh
1Renal Research Group, Institute of Medicine, University of Bergen, Norway. rolf.christiansen@meda.uib.no
Summary
Hypertensive nephropathy impairs the kidney's glomerular charge barrier, particularly in the inner cortex. This dysfunction in spontaneously hypertensive rats (SHR) leads to increased protein excretion, explaining proteinuria in this condition.
Area of Science:
- Nephrology
- Hypertension Research
- Renal Physiology
Background:
- Hypertensive nephropathy is characterized by morphological changes and albuminuria, often originating in the inner cortex.
- The precise mechanism driving proteinuria in hypertensive nephropathy remains unclear.
- This study investigates reduced glomerular charge selectivity in the juxtamedullary cortex of spontaneously hypertensive rats (SHR) as a potential cause of proteinuria.
Purpose of the Study:
- To evaluate the glomerular charge barrier function in the inner cortex of aged spontaneously hypertensive rats (SHR).
- To determine if impaired charge selectivity contributes to proteinuria in hypertensive nephropathy.
- To compare glomerular filtration and protein tracer clearance between SHR and normotensive Wistar-Kyoto rats (WKY).
Main Methods:
- Assessed glomerular charge barrier by measuring clearance of radiolabelled cationic and anionic chymotrypsinogen (Chym and aChym) in cortical zones of SHR and WKY.
- Determined glomerular filtration rates (GFR) using aprotinin.
- Calculated the sieving coefficient (theta) for protein tracers as glomerular clearance/GFR.
Main Results:
- Anionic chymotrypsinogen clearance (theta aChym) was significantly higher in the inner cortex of SHR compared to WKY (0.65 vs. 0.48).
- The ratio of theta aChym to theta Chym increased in the inner cortex of SHR, indicating impaired charge selectivity.
- Increased adsorption droplets in podocytes were observed in the inner cortex of SHR glomeruli.
Conclusions:
- The findings support the existence of a functional glomerular charge barrier.
- Impaired charge barrier function in the inner cortex of SHR, evidenced by increased aChym clearance, contributes to proteinuria in hypertensive nephropathy.
- This impairment offers a partial explanation for elevated protein excretion in SHR with hypertensive nephropathy.