Intrarenal Hemodynamic Changes Research Articles

#326 Features of intrarenal hemodynamics in patients with chronic glomerulonephritis on the background of taking anticoagulants

Abstract Background and Aims Chronic glomerulonephritis (CGN)-glomerular, autoimmune kidney disease, where baseline therapy is clinically proven to be successful. The study evaluates hemodynamic disorders of renal blood flow in patients with CGN on the background of baseline treatment with the inclusion of rivaroxaban. Method We researched108 patients CGN against the background of 3-month basic therapy with the inclusion of rivaroxaban (group AC+, 55 patients) and without anticoagulant (group AC-, 53 patients). Initial and after 3 months evaluation in the mode of color Doppler mapping and pulse-wave doppler. Results In the course of 3-month therapy, the performance of dopplerography of renal arteries in patients with CGN did not change reliably. But there was a credible and clinically significant increase in the systolic blood flow rate at the level of the Interregional Artery (IA), both compared to the baseline data and towards the end of hospitalization (by 9.27 2.58% p < 0.001 the validity of the difference with the raw data, by 8.60 2.53%, p < 0.01 with the 10th day of therapy), remaining reliably lower than in control group (p < 0.001). The speed at the arc artery (АА) also increased slightly (by 2.46 1.03%, p < 0.05 reliability of the difference with the original data and the end of hospitalization), but although statistical reliability was achieved, the dynamics was clinically insignificant and was less than 2.5%. The resistivity index (RI) at both IA and AA levels did not change reliably. Conclusion In CGN patients, intrarenal hemodynamics change with decreased blood flow rates in IA and AA. In the future, against the background of 3-month basic HGH therapy, there was some improvement in blood flow at the IA level but not AA, but no qualitative changes in intrarenal hemodynamics were achieved. The supplementation of long-term anticoagulation therapy with rivaroxaban has increased the effect of therapy on hemodynamic rates, resulting in some improvement in blood flow at both IA and AA levels, but no qualitative improvement has been achieved, possible due to pronounced structural remodeling of kidney vessels in patients with CGN.

Intrarenal Doppler ultrasonography in patients with HFrEF and acute decompensated heart failure undergoing recompensation

ObjectivesRenal venous congestion due to backward heart failure leads to disturbance of renal function in acute decompensated heart failure (ADHF). Whether decongestion strategies have an impact on renal venous congestion is unknown. Objective was to evaluate changes in intrarenal hemodynamics using intrarenal Doppler ultrasonography (IRD) in patients with heart failure with reduced ejection fraction (HFrEF) and ADHF undergoing recompensation.MethodsProspective observational study in patients with left ventricular ejection fraction (LV-EF) ≤ 35% hospitalized due to ADHF. IRD measurement was performed within the first 48 h of hospitalisation and before discharge. Decongestion strategies were based on clinical judgement according to heart failure guidelines. IRD was used to assess intrarenal venous flow (IRVF) pattern, venous impedance index (VII) and resistance index (RI). Laboratory analyses included plasma creatinine, eGFR and albuminuria.ResultsA number of 35 patients with ADHF and LV-EF ≤ 35% were included into the study. IRD could be performed in 30 patients at inclusion and discharge. At discharge, there was a significant reduction of VII from a median of 1.0 (0.86–1.0) to 0.59 (0.26–1.0) (p < 0.01) as well as improvement of IRVF pattern categories (p < 0.05) compared to inclusion. Albuminuria was significantly reduced from a median of 78 mg/g creatinine (39–238) to 29 mg/g creatinine (16–127) (p = 0.02) and proportion of patients with normoalbuminuria increased (p = 0.01). Plasma creatinine and RI remained unchanged (p = 0.73; p = 0.43).DiscussionThis is the first study showing an effect of standard ADHF therapy on parameters of renal venous congestion in patients with HFrEF and ADHF. Doppler sonographic evaluation of renal venous congestion might provide additional information to guide decongestion strategies in patients with ADHF.Graphical abstract

Gray-Scale, Color Doppler, Spectral Doppler, and Contrast-Enhanced Renal Artery Ultrasound: Imaging Techniques and Features.

Renal artery stenosis (RAS) is increasingly being detected in elderly patients as life expectancy increases. RAS induces hypertension or reduces renal function. Computed tomography or magnetic resonance angiography are objective in detecting RAS but may cause iodine-induced nephrotoxicity or nephrogenic systemic fibrosis in patients with RAS. Ultrasound (US) is, by contrast, a noninvasive and real-time imaging modality useful in patients with reduced renal function. Renal US is not as sensitive for detecting RAS because this technique indirectly assesses the renal artery by analyzing intrarenal hemodynamic changes. Although, ideally, US would be used to directly evaluate the renal artery, its current utility for RAS detection remains unclear. The purpose of this review is to introduce how to assess renal artery with US, to describe imaging features of renal artery US, to compare renal artery US and renal US, and to show how to perform work-up in patients in whom RAS is suspected.

PRIMARY ALDOSTERONISM: THE RESULTS OF THE TREATMENT ACCORDING TO THE DATA OF RENAL ARTERIES DUPLEX SCANNING

&#x0D; &#x0D; &#x0D; In the structure of arterial hypertension, primary aldosteronism (РА) ranges from 5 to 15%. Changes in intrarenal hemodynamics are due to both high blood pressure and direct aldosterone level. The purpose of the study was to analyze the results of PA treatment according to ultrasound doppler scanning of renal arteries. In general, 55 patients with PA were treated. Renal arteries duplex scanning before and after the treatment was performed in 20 patients. During treatment, the normalization of Vps, Ved, S/D, PI, PI, AT, TAMX indices was recorded in patients. The RI of the interlobar arteries slightly increased, however, it remained within the reference range. The reduction of aldosterone levels led to increase of TAMX index at the level of the renal artery trunk, S/D, RI and decrease in AT at the level of the segmental arteries, as well as increase of Ved and S/D at the level of the interlobar arteries.&#x0D; &#x0D; &#x0D;

Role of doppler sonographic evaluation of intra-renal hemodynamic changes in diagnosis of obstructive uropathy and in differentiation of acute and chronic obstructive uropathy

Role of doppler sonographic evaluation of intra-renal hemodynamic changes in diagnosis of obstructive uropathy and in differentiation of acute and chronic obstructive uropathy

Evaluation of diuretic, saluretic and natriuretic activity of hydrochlorothiazide in combination with misoprostol in Wistar rats

Background: Renal vasodilatation by prostaglandins is well proven facts. Furosemide is better diuretics due to their additional effect on intrarenal hemodynamic changes brought about by increase in local prostaglandin synthesis. No such changes occur with thiazide group of diuretics. Hence, we want to analyze the diuretic effect of hydrochlorothiazide in combination with prostaglandin analog misoprostol. Aims and Objectives: This study aims to evaluate the diuretic, saluretic, and natriuretic activity of hydrochlorothiazide in combination with misoprostol. Materials and Methods: Four groups of Wistar rats with six animals in each group were grouped. One group served as the control and the other three groups received furosemide, hydrochlorothiazide, and hydrochlorothiazide with misoprostol, respectively. Urine output, urinary electrolytes, saluretic activity, and natriuretic of all groups were estimated and then compared with the standard and control groups. Results: There was a statistically difference in the urinary output between groups as determined by oneway ANOVA (F = 33.413, P ≤ 0.001 and F =260.267, P = 0.001) at 5 and 24 h, respectively. The Lipschitz value showed that standard group and test Group 4 indices were >2.0 showing potent diuretic action. There was a statistically significant difference in the urinary excretion of all the electrolytes between groups as determined by one-way ANOVA (F = 645.087, P ≤ 0.001; F = 360.49, P ≤ 0.001; and F = 366.974, P ≤ 0.001) for the levels of Na+, K+, and Cl−, respectively. It has been found that the saluretic activity was significant in all three groups when compared with control group. However, they do not show significant changes in natriuretic activity. Conclusion: This study has shown that the diuretic activity and diuretic index of hydrochlorothiazide can be increased when it is given in combination with prostaglandin analog misoprostol and also found to be almost equivalent to standard drug furosemide effect. There was also a significant effect in the excretion of electrolytes in urine and significant saluretic activity that favors their use in edematous conditions. Saluretic activity of hydrochlorothiazide with misoprostol was also similar to furosemide. Since both the drugs are already approved and safely used for many decades, we can further do a clinical trial to confirm these findings and can be used as a combination of old drugs for a new indication.

Relationship between kidney findings and systemic vascular damage in elderly hypertensive patients without overt cardiovascular disease.

Few studies have investigated the influence of age on the relationships between systemic vascular damage, kidney dysfunction, and intrarenal hemodynamic changes in patients with hypertension without overt cardiovascular disease. The authors enrolled 126 elderly patients with hypertension (aged ≥65years) and 350 nonelderly patients with hypertension (aged <65 years). Carotid intima-media thickness, renal resistive index, and aortic pulse wave velocity were performed in all patients. Elderly patients with hypertension had lower estimated glomerular filtration rates and higher albuminuria, renal resistive index, carotid intima-media thickness, and aortic pulse wave velocity compared with nonelderly patients with hypertension (P<.001). Carotid intima-media thickness independently correlated with renal resistive index and estimated glomerular filtration rate in nonelderly patients with hypertension, whereas it was significantly related to renal resistive index only in elderly patients with hypertension. Aortic pulse wave velocity was independently associated with albuminuria in nonelderly patients with hypertension, whereas it did not independently correlate with any indexes of renal damage in elderly patients with hypertension. Age is an important modifier of the relationships between renal function and renal hemodynamics with subclinical vascular involvement in elderly persons without cardiovascular disease.

OP.5B.09] RELATIONSHIP BETWEEN RENAL HEMODYNAMICS AND CORONARY ATHEROSCLEROTIC BURDEN IN PATIENTS WITH HYPERTENSION

Objective: Cardiovascular diseases recognize ischemia as the main pathogenetic prime mover and represent the final step of morphofunctional vascular changes that develop over a long period of time, mostly asymptomatically. Recent studies detected the role of intrarenal hemodynamic changes as independent predictors of cardiovascular events in different populations. No data exist about the relationship between renal hemodynamics and coronary atherosclerotic damage. The purpose of our investigation is to study the relationship between intrarenal vascular changes and coronary atherosclerotic burden in hypertensive patients.Design and method: We enrolled 130 hypertensive subjects (30–80 years) who received indication for elective coronary angiography. Duplex ultrasound of intrarenal vasculature was performed to evaluate renal resistive index (RI), renal pulsatility index (PI) and renal acceleration time (AT). Subsequently, a coronary angiography was performed to assess atherosclerotic burden through Gensini Score (GS). Carotid intima-media thickness (cIMT) was also assessed as a model of vascular damage well related with renal parameters. The population was divided into quintiles based on the GS (I quintile: GS < 9; II quintile: GS>9 and <17; III quintile: GS>17 and <30.8; IV quintile: GS>30.8 and <44; V quintile: GS>44). Statistical analysis was also performed in the population divided in 2 groups: 1) subjects with mild coronary disease (GS<30); 2) subjects with severe coronary disease (GS>30). Results: Subjects in higher quintiles had greater values of PI, RI and lower values of AT compared to the ones in lower quintiles. The correlation between GS and PI, RI or AT was not statistically significant at the univariate analysis in overall population, whereas GS, IR and IP were significantly associated with cIMT (all p < 0.01). IP and IR, but not AT, were associated to GS in the group with GS<30, whereas did not correlate in subjects with GS>30. These correlations held after adjustment for multiple confounders. Conclusions: Renal vascular changes are not significantly related to coronary atherosclerotic burden in all hypertensive patients. Nevertheless, within the complex mathematical relationship between PI (or RI) and GS (Figure 1), the relationship becomes linear and significant in patients with mild coronary disease.

Intra-Renal Hemodynamic Changes After Habitual Physical Activity in Patients with Chronic Kidney Disease.

Chronic Kidney Disease (CKD) is considered a silent epidemic with a continuously growing prevalence around the world. Due to uremia many functional and morphological abnormalities occur in almost all systems. Mostly affected, the cardiovascular system, leads to diminished cardiac function that affects patients' functional capacity and physical activity levels, reducing survival and increasing all-cause mortality. Systematic exercise training ameliorates uremia induced body deficits and significantly improves the survival of CKD patients. Intradialytic exercise training has been recommended as a complementary therapeutic modality equally important to hemodialysis. The aim of this systematic review is to provide an update on recent advances in our understanding of how exercise training improves functionality of the cardiovascular system through the hemodynamic changes induced by habitual or intradialytic and/or home-based exercise training programs. Systematic exercise training induces beneficial adaptive responses and influences many sensitive physiological biomarkers, such as oxidative stress biomarkers that are implicated in the development of atherosclerosis. Additionally, exercise training decreases the cardiovascular risk by improving the autonomic nervous system activity and the left ventricular function and by reducing nontraditional risk factors such as epicardial adipose tissue. It seems that all these central and peripheral adaptations to exercise training significantly contribute to improvements in functional capacity and exercise tolerance among CKD patients and result in the risk reduction of CKD-associated disorders. Exercise training could serve as a complimentary therapeutic strategy in CKD patients while health care providers should motivate patients to engage in any type of exercise training programs.

Septic related acute kidney injury

Sepsis is the leading cause of acute kidney injury (AKI) in pediatric intensive care unit.Development of AKI during sepsis increased patient morbidity,predicts higher mortality and days of stay in the intensive care unit.The mechanisms behind AKI in sepsis remain controversial but were believed to be complex and multi-factorial.The pathophysiology of AKI in sepsis involved intrarenal hemodynamic changes,endothelial dysfunction,infiltration of inflammatory cytokines.The new markers of neutrophil gelatinase-associated lipocalin as the representative is helpful for early diagnosis of AKI.Renal replacement therapy (RRT)is the main treatment of sepsis related AKI.At present,the model,dose and exact timing of RRT is not well defined.A widely accepted viewpoint is that the injury stage of RIFLE diagnostic criteria and fluid overload up to 10％ ～ 20％ is the beginning of the most appropriate chance of RRT. Key words: Acute kidney injury; Sepsis; Renal replacement therapy; Children

Changes in Renal Doppler Ultrasonographic Parameters in Patients Managed with Rigid Ureteroscopy

There has been no study evaluating the intrarenal hemodynamic changes after ureteroscopy in the published literature. To determine preoperative and postoperative intrarenal vascular parameters such as resistive index (RI), pulsatility index (PI), peak systolic velocity (PSV), end-diastolic velocity (EDV), measure changes on these values (ΔRI, ΔPI, ΔPSV, ΔEDV) after ureteroscopy (URS) and compare the outcomes with the results of normal contralateral kidneys, and finally investigate possible parameters that would affect renal vascular resistance changes. We prospectively studied 47 patients who underwent rigid URS. Preoperative gray-scale and Doppler ultrasonography (CDUS) measurements were obtained 24 h before URS. Similarly, postoperative CDUS measurements were done 24 h after the operation. The degree of hydronephrosis and location of stones in the obstructed kidneys, diameters of both kidneys, and thickness of renal parenchyma were evaluated with gray-scale US followed by CDUS with calculation of the intrarenal RI, PI, PSV, and EDV values for each kidney. For the operated kidneys, statistically significant P values were noticed when RI and PI values were considered (P < 0.001). ΔRI and ΔPI of the operated kidneys were also significantly greater than the values for non-operated kidneys (P < 0.001). However, it was not the case for ΔPSV and ΔEDV values. In Spearman correlation coefficient analysis, ΔRI was found to be correlated with the parameters: "operative time" and "irrigation fluid volume". No significant relation was documented between ΔRI and the other parameters: age, gender, side of ureteroscopy, stone location, and degree of hydronephrosis. Significant changes in RI and PI values in patients treated with URS reveal that URS can cause a significant increase in renal vascular resistance. With the increase in operative time and irrigation fluid volume used during the operation, RI seems to be significantly increased.

Moderate Intrarenal Vasoconstriction after High Pressor Doses of Norepinephrine in the Rat: Comparison with Effects of Angiotensin II

Aims: Treatment of arterial hypotension with norepinephrine (NE) is associated with renal vasoconstriction and may lead to ischemic kidney injury; the risk involved is still a matter of debate. Methods: In anesthetized, acutely uninephrectomized rats, we examined changes in intrarenal hemodynamics induced by intravenous infusion of NE and angiotensin II (Ang II), at doses that increased arterial pressure by ∼25 mm Hg (20%). Renal blood flow (RBF) was determined using a Transonic probe, and superficial cortical, outer and inner medullary flows (CBF, OMBF, IMBF) as laser-Doppler fluxes. Results: NE decreased regional intrarenal perfusion similarly, by 16, 15 and 16% for RBF, OMBF and IMBF, respectively (all changes significant). The respective decreases after Ang II were significantly greater and clearly differentiated: 45, 32 and 22%, respectively. The renal vascular resistance increased 47 ± 4% after NE and 131 ± 11% after Ang II, indicating that the latter drug induces much more pronounced renal vasoconstriction. Conclusion: An ∼15% decrease of renal perfusion may be taken as an indication of an impairment of renal circulation during antihypotensive NE therapy. While superiority of NE over Ang II is obvious, a further search for drugs even less harmful to renal perfusion and function is desirable.

Renal Hemodynamics and Renoprotection

Background: Angiotensin II (AII) is the well-known determinant of kidney damage increasing intraglomerular pressure, matrix expansion and fibroblast proliferation. Renin-angiotensin system (RAS) inhibition, limiting the hemodynamic effects of AII, reduces proteinuria and is renoprotective in the long term. Methods: We studied 15 chronic proteinuric patients by Doppler ultrasonography to clarify the intrarenal hemodynamic changes during RAS blockade by Benazepril (10–20 mg/day) alone and combined with Valsartan (80–160 mg/day). We also investigated the correlation between hemodynamic indices, RAS components and antiproteinuric effect. Results: After 1 month of Benazepril proteinuria, resistive index (RI) and pulsatility index (PI) significantly decreased and proteinuria reduction was directly correlated to decrease in RI (r = 0.55, p = 0.03). Contrarily, after 1 month of combined therapy, RI and PI restored to baseline and progressively increased in the following 3 months, while proteinuria decreased. Increase in RI was directly correlated to concomitant increase in plasma renin activity (r = 0.65, p = 0.01) suggesting a direct role of renin in restoring intrarenal resistances. Conclusion: The hemodynamic changes caused by RAS inhibitors partially contribute to the antiproteinuric effect. Other RAS components, such as renin, may contribute to renal vasoconstriction and could be a further determinant of kidney damage besides a promising target for renoprotection.

Whole-Body Volume Regulation and Escape from Antidiuresis

Both individual cells and organs regulate their volume in response to sustained hypo-osmolality via solute and water losses. Similar processes occur in the whole body to regulate the volumes of extracellular fluid (ECF) and intravascular spaces toward normal levels. Body water losses occur via the phenomena “escape from antidiuresis”; solute losses occur through the secondary natriuresis induced by water retention. As a result of resistance to arginine vasopressin (AVP) signaling, escape from antidiuresis is caused by downregulation of kidney aquaporin-2 expression despite high AVP plasma levels. Recent data have implicated downregulation of vasopressin V 2R as a potential mechanism of resistance, and suggest that this may be a result of decreased intrarenal angiotensin II signaling in combination with increased intrarenal nitric oxide and prostaglandin E 2 signaling. The natriuresis that results in volume regulation of the ECF and vascular spaces is the result of intrarenal hemodynamic changes produced by volume expansion, but the degree to which these effects are modulated by aldosterone secretion and the activity of distal sodium cotransporters and channels remains to be elucidated. The clinical implication of these volume-regulatory processes is that the chronic hyponatremic state is one of water retention and solute losses from intracellular fluid and ECF compartments. The degree to which solute losses versus water retention contribute to hyponatremia will vary in association with many factors, including the etiology of the hyponatremia, the rapidity of development of the hyponatremia, the chronicity of the hyponatremia, the volume of daily water loading, and individual variability. Understanding these volume-regulatory processes allows a better understanding of many aspects of the conundrum of patients with “clinical euvolemia” and dilutional hyponatremia from AVP-induced water retention.

Presence of protein fragments in urine of critically ill patients with acute renal failure: a nephrologic enigma.

Predicting complications in intensive care units (ICUs) is an important step in the care of critically ill patients. Intensive care specialists have developed numerous prognostication tools for patients admitted to the ICU; however, although useful, many of these tools are not applicable in a clinical setting, and multiple severity-of-illness scores often underestimate hospital mortality in several conditions (1)(2). Many acute pathologic states, such as burns, trauma, bleeding, and sepsis, are associated with the induction of a “systemic inflammatory response”, which is characterized by the release of pro-inflammatory mediators and the activation of different types of cellular elements (3)(4)(5)(6). This response primarily involves endothelial cells and leukocytes (7)(8)(9). It is possible to use renal function as an early marker for systemic illness because kidney involvement is a recognized complication of several systemic diseases. Acute renal failure (ARF), usually attributable to intrarenal hemodynamic changes, often complicates the clinical course of critically ill patients (10)(11)(12). Microalbuminuria has been proposed as a marker of capillary leak severity in the ICU (13)(14). It has previously been demonstrated that urinary albumin degrades into multiple fragments in meningococcal sepsis and …

Role of NO and cytochrome P-450-derived eicosanoids in ET-1-induced changes in intrarenal hemodynamics in rats.

Endothelin-1 (ET-1) produces potent renal effects that we have previously shown to be dependent on cytochrome P-450 (CYP450) metabolites of aracidonic acid (24) This study evaluated the role of these metabolites in the effects produced by ET-1 on renal blood flow (RBF), cortical blood flow (CBF), medullary blood flow (MBF), and mean arterial blood pressure (MBP). ET-1 (20-200 pmol/kg) increased MBP, renal vascular resistance (RVR), and MBF but reduced CBF and RBF in a dose-dependent manner. The decreases in CBF and RBF, and increases in MBP and RVR were blunted by BMS-182874, an ET(A) receptor antagonist or BQ-788, an ET(B) receptor antagonist. Similarly, indomethacin, an inhibitor of cyclooxygenase activity, or 12,12-dibromododecenoic acid (DBDD), a CYP450-dependent inhibitor of production of 20-hydroxyeicosatetraenoic acid (20-HETE), blunted these effects. ET-3 elicited dose-related reduction in CBF and increase in MBF. Indomethacin accentuated the reduction in CBF and attenuated the increase in MBF, as did DBDD. ET-1-induced increase in MBF was attenuated by BQ-788, N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, indomethacin, or DBDD. DBDD inhibited the hemodynamic effects of L-NAME. Miconazole, the inhibitor of CYP450-dependent epoxygenase activity, was without effect. These results indicate that hemodynamic changes produced by ET-1 are mediated by vasoconstrictor prostanoids and/or prostanoid-like substances, possibly, 20-HETE via activation of ET(A) and ET(B) receptors. However, the increase in MBF is mediated by vasodilator prostanoids or by NO via ET(B) receptor activation.

Atherosclerosis profile and microalbuminuria in essential hypertension.

Whether microalbuminuria (MA) is the result of intrarenal hemodynamic changes induced by increased systemic blood pressure (BP) or a marker of capillary leakiness at the glomerular level that reflects more generalized atherosclerotic vascular damage is still debated. To address this question, 319 patients without diabetes, 154 men and 165 women aged 57 +/- 8.6 years (range, 37 to 73 years), but with essential hypertension (EH) never treated with drugs were enrolled onto the study. Using a multiple linear regression analysis, we analyzed the prevalence of MA and its relationship with BP level as well as with other risk factors for the development of atherosclerosis. MA was present in 40% of the population studied. A univariable analysis of ambulatory BP monitoring measurements showed that only 24-hour systolic BP (P = 0.04), daytime systolic BP (P = 0. 02), and 24-hour daytime and nighttime systolic BP load (P < 0.01) predicted the presence of MA, whereas all BP variability parameters significantly predicted it. Multivariable analysis showed that only a positive family history of hypertension (P < 0.001), BMI (P < 0. 001), glucose (P < 0.001), and 24-hour systolic BP coefficient of variation (P < 0.001) independently predicted MA. In summary, the prevalence of MA in our group of patients with EH was high, presumably as a consequence of the older mean age of the population and the selection criteria. Besides being a marker of concomitant cardiovascular damage, MA was associated with a worse pattern of atherosclerotic risk factors. Although its pathophysiological meaning remains to be completely clarified, MA seems to be more related to other atherosclerosis risk factors and presumably reflects a more diffuse vascular injury.

Albuminuria and Transferrinuria in Essential HypertensionEffects of Antihypertensive Therapy

The objectives of this study were to evaluate the effects of an ACE inhibitor (fosinopril) and a calcium antagonist (amlodipine) on the urinary albumin and transferrin excretion and their relationship to the blood pressure in essential hypertension. Twenty-four never-treated patients (mean age, 46.4 +/- 8.9 years) with a diastolic blood pressure between 90 and 114 mm Hg and normal renal function, randomly received amlodipine or fosinopril and, if the diastolic blood pressure was not normalized, doxazosin was added to the therapy. Twenty-four-hour ambulatory blood pressure monitoring and 24-h urine collection for albumin and transferrin measurements were performed before and after 3 and 6 months of therapy. Diastolic blood pressure was normalized in 23 patients (96%). Before treatment, microalbuminuria was present in 50% of patients. In the amlodipine and fosinopril group, antihypertensive therapy significantly decreased blood pressure and, only in the fosinopril group, albuminuria. Transferrinuria did not change significantly in both groups. Fosinopril lowered albuminuria in all patients, whereas amlodipine only in half of patients. Albuminuria, but not transferrinuria, was significantly correlated to the ambulatory blood pressure. This correlation was more pronounced for systolic than for diastolic pressure. In essential hypertensive patients with normal renal function, a high prevalence of microalbuminuria can be observed. Albuminuria appears to correlate with ambulatory blood pressure, particularly with systolic pressure. Intrarenal hemodynamic changes seem to play a more important role than systemic blood pressure decrease in the reduction of albuminuria. Transferrinuria does not seem a useful marker to follow-up nondiabetic hypertensive patients with early signs of glomerular dysfunction.

Effects of neuropeptide Y on intrarenal hemodynamics, plasma renin activity and urinary sodium excretion in rats.

Neuropeptide Y (NPY) is a vasoconstrictor peptide possibly involved in the regulation of renal sodium handling and renin release. This investigation was undertaken to assess in conscious normotensive rats the acute effects of a non-pressor dose of NPY on renal plasma flow, glomerular filtration rate, sodium excretion and plasma renin activity. Experiments were also performed during concomitant beta-adrenoceptor stimulation with isoproterenol. NPY per se had no effect on the studied parameters. Renal plasma flow was increased by isoproterenol and was significantly higher when the beta-adrenoceptor stimulant was infused alone (13.4 +/- 2.1 ml/min, p < 0.05, mean +/- SEM) that when administered together with NPY (7.2 +/- 2.0 ml/min). This was also true for glomerular filtration rate (3.3 +/- 0.3 vs. 1.8 +/- 0.3 ml/min, p < 0.01) and plasma renin activity (6.3 +/- 1.7 vs. 2.1 +/- 0.4 ng Ang I/ml/h, p < 0.05). Our data however do not allow to deduce whether the inhibitory effect of NPY on isoproterenol-induced renin release is mediated by changes in intrarenal hemodynamics or a direct effect on juxtaglomerular cells.

Renal hemodynamics in patients with obstructive uropathy evaluated by color Doppler sonography.

Prior animal studies have shown through direct pressure measurements that there is a definite rise in the renal vascular resistance in obstruction. Therefore intrarenal hemodynamic changes can be determined by the vascular impedance expressed as pulsatility and resistive indexes (PI and RI) obtained from the Doppler waveforms of intrarenal arteries. We investigated whether various degrees of obstruction result in different hemodynamic responses according to color Doppler sonography. 22 kidneys with varied degrees of hydronephrosis and 19 normal kidneys were examined. The pulsatility and resistive index of Doppler waveforms from interlobar arteries were obtained. The grade of hydronephrosis was based upon the width of parenchyma. The mean resistive index in the study and controls were 0.70 +/- 0.07 and 0.60 +/- 0.03, respectively. The difference was significant (p < 0.001). Pulsatility indexes in the study and controls were 1.07 +/- 0.34 and 0.98 +/- 0.23, respectively. The difference was not significant (p > 0.005). Significant difference was also noticed in the parenchymal widths between both groups (p < 0.001). It appeared that intrarenal color Doppler sonography can provide physiologic information reflecting renal vascular resistance status by means of an easily obtained parameter: resistive index.