Association of Noise Annoyance with Measured Renal Hemodynamic Changes

<b><i>Background:</i></b> Chronic mental stress is recognized as a modifiable risk factor for cardiovascular disease. The aim of this study was to demonstrate that noise annoyance-induced stress is associated with changes in renal hemodynamics. <b><i>Methods:</i></b> Renal hemodynamic parameters were measured using steady-state input clearance with infusion of para-aminohippuric acid and inulin in individuals with normal, high normal, and elevated blood pressure. All individuals ranked subjective annoyance due to noise in everyday life on a 7-grade Likert scale. The median of all rankings was used as a cutoff point to divide the group into noise-annoyed and non-noise-annoyed individuals. Different renal hemodynamic parameters were calculated based on the Gomez equation. <b><i>Results:</i></b> Noise-annoyed individuals (<i>n</i> = 58) showed lower renal plasma flow (599 ± 106 vs. 663 ± 124 mL/min, <i>p</i> = 0.009), lower renal blood flow (1,068 ± 203 vs. 1,172 ± 225 mL/min, <i>p</i> = 0.047), higher filtration fraction (22.7 ± 3.3 vs. 21.3 ± 3.0, <i>p</i> = 0.012), higher renal vascular resistance (88.9 ± 25.6 vs. 75.8 ± 22.9 mm Hg/[mL/min], <i>p</i> = 0.002), and higher resistance of afferent arteriole (2,439.5 ± 1,253.4 vs. 1,849.9 ± 1,242.0 dyn s⁻¹ cm⁻⁵, <i>p</i> = 0.001) compared to non-noise-annoyed individuals (<i>n</i> = 55). There was no difference in measured glomerular filtration rate (133 ± 11.8 vs. 138 ± 15 mL/min, <i>p</i> = 0.181), resistance of efferent arteriole (2,419.4 ± 472.2 vs. 2,245.8 ± 370.3 dyn s⁻¹ cm⁻⁵, <i>p</i> = 0.060), and intraglomerular pressure (64.0 ± 3.1 vs. 64.6 ± 3.5 mm Hg, <i>p</i> = 0.298) between the groups. After adjusting for age, renal plasma flow, renal blood flow, and renal vascular resistance remained significantly different between the groups, with a trend in increased afferent arteriolar resistance and filtration fraction. <b><i>Conclusion:</i></b> In this study, noise annoyance was associated with reduced renal perfusion attributed to increased renal vascular resistance predominantly at the afferent site. Long-term consequences of this renal hemodynamic pattern due to noise annoyance need to be investigated.

Dysregulation mechanism of the influence of water of negative redox potential on kidney function

Elucidate the dysregulatory mechanism of the effect of water load of negative redox potential in comparison with induced diuresis with ordinary tap water on the functional state of the kidneys.Material and methods. The experiments were carried out on 40 male white nonlinear rats weighing 0.16-0.18 kg with the analysis of the effect of water loading with a negative redox potential on renal function, which was obtained by treating tap water with microhydrin. The redox potential of water and urine was determined with an ORP meter. From the indicators of renal function studied: protein excretion, glomerular filtration, filtration fraction of sodium ions, its absolute and proximal reabsorption. Statistical processing of the data obtained, including multivariate regression analysis, was carried out using the Statgrafics, Statistica, and Excel 2003 programs.Results. Comparative multivariate analysis of the effect of water loading of negative redox potential in comparison with induced diuresis with ordinary tap water revealed an ambiguous nature of reliable correlations (p <0.05) between the studied indicators of renal function and the redox potential of urine, which is due to the simultaneous presence of both protective mechanisms of negative redox potential influence (improvement of energy supply, antioxidant effect), and damaging (transient renal ischemia due to activation of the basal tone mechanism due to an increase in the contractile function of the heart as a result of improving its energy supply), the final result will depend on the dominance of classical or dysregulation mechanisms in this particular situation. Conclusion. The dysregulation mechanism of the effect of water of negative redox potential on renal function is due to the initial mobilization of defense reactions with improved contractile function of the heart, which is subsequently transformed into an injury response due to increased basal renal vascular tone with the development of transient ischemia and renal dysfunction, decrease оf glomerular filtration, filtration fraction of sodium ions, its absolute and proximal reabsorption and development of proteinuria.

The utility of magnetic resonance imaging for noninvasive evaluation of diabetic nephropathy

Background Noninvasive quantitative measurement of fibrosis in chronic kidney disease (CKD) would be desirable diagnostically and therapeutically but standard radiologic imaging is too variable for clinical usage. By applying a vibratory force, tissue shear wave stiffness can be measured by magnetic resonance elastography (MRE) that may correlate with progression of kidney fibrosis. Since decreased kidney perfusion decreases tissue turgor and stiffness, we combined newly available three-dimensional MRE shear stiffness measurements with MR arterial spin labeling (ASL) kidney blood flow rates to evaluate fibrosis in diabetic nephropathy. Methods Thirty individuals with diabetes and Stage 0–5 CKD and 13 control individuals without CKD underwent noncontrast MRE with concurrent ASL blood flow measurements. Results MRE cortical shear stiffness at 90 Hz was decreased significantly below controls in all CKD stages of diabetic nephropathy. Likewise, ASL blood flow decreased progressively from 480 ± 136 mL/min/100 g of cortical tissue in controls to 302 ± 95, 229 ± 7 and 152 ± 32 mL/min/100 g in Stages 3, 4 and 5 CKD, respectively. A magnetic resonance imaging (MRI) surrogate for the measured glomerular filtration fraction [surrogate filtration fraction = estimated glomerular filtration rate (eGFR)/ASL] decreased progressively from 0.21 ± 0.07 in controls to 0.16 ± 0.04 in Stage 3 and 0.10 ± 0.02 in Stage 4–5 CKD. Conclusions In this pilot study, MRI with ASL blood flow rates can noninvasively measure decreasing kidney cortical tissue perfusion and, with eGFR, a decreasing surrogate filtration fraction in worsening diabetic nephropathy that appears to correlate with increasing fibrosis. Differing from the liver, MRE shear stiffness surprisingly decreases with worsening CKD, likely related to decreased tissue turgor from lower blood flow rates.

Relaxin-mediated renal vasodilation in the rat is associated with falls in glomerular blood pressure

Relaxin (RLX) is a pleiotropic peptide hormone with marked renal vasodilatory actions that are physiologically important during pregnancy. RLX also has potent antifibrotic actions and is being tested therapeutically in various fibrotic diseases, including chronic kidney disease (CKD). Since renal vasodilation may expose the glomerulus to increased blood pressure [glomerular capillary pressure (PGC)], which exacerbates progression of CKD, we assessed the glomerular hemodynamic actions of acute (0.89 µg·100 g body wt−1·h−1 iv over 75 min) and chronic (1.5 µg·100 g body wt−1·h−1 sc) administration of RLX. Both acute and chronic RLX produced marked renal vasodilation and increased renal plasma flow (RPF) in euvolemic, anesthetized male rats. Glomerular filtration rate also increased with RLX, but the magnitude of the rise was much less than the increase in RPF due to concomitant decreases in filtration fraction. The fall in filtration fraction was the result of significant decreases in PGC, despite a slight increase in mean arterial blood pressure (MAP) with acute RLX and no net change in MAP with chronic RLX. This fall in PGC occurred because of the “in-series” arrangement of the afferent and efferent arteriolar resistance vessels, which can regulate PGC independently of MAP. With both acute and chronic RLX, efferent arteriolar resistance vessels relaxed to a greater extent than afferent arteriolar resistance vessels, thus producing falls in PGC. Based on this finding, RLX has a beneficial hemodynamic impact on the kidney, which, together with the antifibrotic actions of RLX, suggests a strong therapeutic potential for use in CKD.

Influence of sex on hyperfiltration in patients with uncomplicated type 1 diabetes

The aim of this analysis was to examine sex-based differences in renal segmental resistances in healthy controls (HCs) and patients with type 1 diabetes (T1D). We hypothesized that hyperfiltration—an early hemodynamic abnormality associated with diabetic nephropathy—would disproportionately affect women with T1D, thereby attenuating protection against the development of renal complications. Glomerular hemodynamic parameters were evaluated in HC ( n = 30) and in normotensive, normoalbuminuric patients with T1D and either baseline normofiltration [ n = 36, T1D-N, glomerular filtration rate (GFR) 90–134 ml·min−1·1.73 m2] or hyperfiltration ( n = 32, T1D-H, GFR ≥ 135 ml·min−1·1.73 m2) during euglycemic conditions (4–6 mmol/l). Gomez’s equations were used to derive efferent (RE) and afferent (RA) arteriolar resistances, glomerular hydrostatic pressure (PGLO) from inulin (GFR) and paraaminohippurate [effective renal plasma flow (ERPF)] clearances, plasma protein and estimated ultrafiltration coefficients (KFG). Female patients with T1D with hyperfiltration (T1D-H) had higher RE (1,985 ± 487 vs. 1,381 ± 296 dyne·sec−1·cm−5, P < 0.001) and filtration fraction (FF, 0.20 ± 0.047 vs. 0.16 ± 0.03 P < 0.05) and lower ERPF (876 ± 245 vs. 1,111 ± 298 134 ml·min−1·1.73 m2 P < 0.05) compared with male T1D-H patients. Overall, T1D-H patients had higher PGLO and lower RA vs. HC subjects, although there were no sex-based differences. In conclusion, female T1D-H patients had higher RE and FF and lower ERPF than their male counterparts with no associated sex differences in RA. Prospective intervention studies should consider sex as a modifier of renal hemodynamic responses to renal protective therapies.