We studied GFR, RPF and renal kallikrein in rats fed 9%, 25%, or 50% protein (casein) diets for 8 to 13 days. CFR and RPF increased progressively with increasing dietary protein. Renal excretion of active kallikrein (microgram/day) was 128 +/- 9, 174 +/- 11 and 228 +/- 14 in 9%, 25%, and 50% protein-fed rats, respectively (P less than 0.02 or less between groups). Prokallikrein excretion in these groups was 23 +/- 7, 77 +/- 11 and 118 +/- 15 micrograms/day, respectively (P less than 0.005 or less between groups). The in vivo renal kallikrein synthesis rate, relative to total protein synthesis, was reduced in 9% protein-fed rats (2.74 +/- 0.24) compared to rats fed 25% (3.93 +/- 0.34, P less than 0.02) or 50% protein (4.41 +/- 0.30, P less than 0.001). These changes in synthesis and excretion rates were not accompanied by changes in renal tissue levels of active or prokallikrein. In all groups, GFR and RPF correlated directly with the renal excretion of active kallikrein, prokallikrein or total kallikrein (r = 0.41 to 0.66, P less than 0.01). Treatment of 50% protein-fed rats with aprotinin, a kallikrein inhibitor, markedly lowered renal and urinary kallikrein-like esterase activity. Left kidney GFR and RPF were significantly reduced in aprotinin-treated rats compared to vehicle-treated rats (1.54 +/- 0.15 and 4.86 +/- 0.38 ml/min vs. 1.89 +/- 0.10 and 5.93 +/- 0.22 ml/min, GFR and RPF, respectively, P less than 0.05 or less).(ABSTRACT TRUNCATED AT 250 WORDS)
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http://dx.doi.org/10.1038/ki.1989.294 | DOI Listing |
Diabetes Obes Metab
February 2025
Division of Diabetes, Department of Medicine, University of Texas Health and Texas Diabetes Institute, University Health System, San Antonio, Texas, USA.
Aims: To investigate the effect of sodium-glucose co-transporter 2 inhibitor [SGLT-2i] therapy on renal haemodynamics in T2D patients with glomerular hyperfiltration.
Materials And Methods: Sixty T2D patients with elevated [HYPER] and normal [NORMO] GFR were randomized to dapagliflozin 10 mg/day [DAPA/HYPER, n = 15; DAPA/NORMO, n = 15] or to metformin/glipizide [CONTROL/HYPER, n = 15; CONTROL/NORMO, n = 15] to reach similar glycaemic control after 4 months. GFR was measured with Iohexol and hyperfiltration was empirically defined as >125 mL/min/1.
J Hypertens
November 2024
Department of Nephrology and Hypertension.
Background And Hypothesis: Obesity aggravates the risk to develop chronic kidney disease in hypertensive patients. Whether pre-obesity already impairs renal function, renal perfusion and intraglomerular hemodynamics in hypertensive patients is unknown.
Methods: Renal hemodynamic profiles were measured using steady state input clearance (infusion of para-amino-hippuric acid and inulin) in 36 patients with primary arterial hypertension stage 1-2 without antihypertensive medication.
Kidney360
May 2024
Department of Nephrology, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.
Nutr Metab Cardiovasc Dis
March 2024
Department of Nephrology and Hypertension, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Germany.
Background And Aims: Obesity has been shown to be an independent risk factor for the development of CKD. Little is known about pathways of interaction of visceral fat mass estimated by waist circumference (WC) and metabolic factors with the renal and intraglomerular hemodynamic profile in healthy, non-obese individuals.
Methods And Results: The study population of this post-hoc analysis in 80 healthy individuals, who participated in a randomized, controlled clinical trial (www.
Int J Mol Sci
July 2023
Department of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel.
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