Renal Artery Resistance Research Articles

The Effect of Exercise Training on the Responsiveness of Renal Resistance Arteries in Rats

Blood flow to several tissues changes during an acute bout of exercise. The kidney is one of the organs that are most affected by exercise-induced blood redistribution. The aim of the present study was to investigate possible exercise-induced vascular reactivity changes in renal resistance arteries in rats. Renal resistance arteries were isolated from rats that underwent 8 weeks of swimming and sedentary control rats, and the arteries were evaluated using wire myography. Similar dilation responses to acetylcholine, bradykinin, adenosine, isoproterenol, and sodium nitroprusside were observed in both groups. The vasoconstrictive agents vasopressin, endothelin-1, potassium chloride, and thromboxane A2 also induced similar responses in both groups; however, the trained group had an increased constrictive response to norepinephrine compared to the control rats. The results of our study show that renal resistance arteries of trained rats behave differently than conduit-type renal arteries and exhibit an increased contractile response to sympathetic agonists. This finding provides supporting evidence that renal blood flow markedly decreases during exercise in trained individuals.

Heme oxygenase regulates renal arterial resistance and sodium excretion in cirrhotic rats

Heme oxygenase (HO) catabolizes heme into biliverdin, carbon monoxide (CO), and free iron. CO generated in endothelial and smooth muscle layers of blood vessels modulates vascular tone by inducing relaxation of vascular smooth muscle cells. The aim of this study was to verify the role played by HO in regulating renal arterial resistance and Na(+) excretion in cirrhosis. Twenty control rats and 20 rats with CCl(4)(-) induced cirrhosis, 10 of which were chronically treated with the HO inducer cobalt-protoporphyrin (CoPP), were studied. Pressurized renal interlobar arteries were challenged with increasing doses of phenylephrine (PE) and acetylcholine (ACh). Dose-response curves were evaluated under basal conditions and after inhibition of HO with chromium-mesoporphyrin (CrMP). HO-1 (inducible form) and HO-2 (constitutive form) expression was measured in the main and interlobar renal arteries. Serum and urinary levels of Na(+) and creatinine were also evaluated. In renal interlobar arteries from cirrhotic rats, the response to PE was increased, while that to ACh was blunted. After HO inhibition, the responsiveness to these vasoactive substances was comparable in the two groups. In cirrhotic rats, HO-1 expression was impaired in the main and the interlobar renal arteries. Chronic HO induction normalized the response to the vasoconstrictor, but not to the vasodilator. Cirrhotic rats treated with CoPP showed higher urinary Na(+) concentration and fractional Na(+) excretion, compared to both untreated cirrhotic and control rats. In cirrhotic rats, an impaired HO-1 expression promotes vasoconstriction of renal interlobar arteries. Chronic HO induction normalizes the sensitivity to PE and promotes Na(+) excretion.

Significant Increase in 1-Year Posttransplant Renal Arterial Index Predicts Graft Loss

Conflicting data have been reported concerning the use of kidney graft arterial resistance index (RI) measured by Doppler to predict death-censored graft loss. We hypothesized that changes in RI values could carry better information than a single measure of RI. Four hundred twenty-five renal transplant recipients were included in the study. We tested whether changes in renal arterial resistance index between 4 and 12 months after transplant (ΔRI(4→12)) were predictive of graft loss. Neither 4-month nor 1-year RI predicted graft loss. The area under the receiver operating characteristics curve of ΔRI(4→12) for graft loss was 0.75. A ΔRI(4→12) ≥10% had the best sensitivity and specificity. One year after transplant, 22% of the study population had ΔRI(4→12) ≥10%. Fifty-five patients (12.9%) experienced graft loss during follow-up. The annual incidence of graft loss was higher in patients with ΔRI(4→12) ≥10% (3.5 versus 1.3%; P = 0.009). In multivariate analysis, patients with ΔRI(4→12) ≥10% had an increased risk of graft loss (hazard ratio, 6.21; 95% confidence interval, 1.99 to 22.15; P = 0.002). A variation in RI ≥10% in the first year after transplant is an independent risk factor for death-censored graft loss in renal transplant recipients.

Purinoreceptor-mediated current in myocytes from renal resistance arteries.

Ionotropic purinoreceptors (P2X) in renal vascular smooth muscle cells (RVSMCs) are involved in mediating the sympathetic control and paracrine regulation of renal blood flow (RBF). Activation of P2X receptors elevates [Ca(2+)](i) in RVSMCs triggering their contraction, leading to renal vasoconstriction and decrease of RBF. The goal of the present work was to characterize the P2X receptor-mediated ionic current (I(P2X)) and to identify the types of P2X receptors expressed in myocytes isolated from interlobar and arcuate arteries of rat kidney. The expression of P2X receptors in isolated RVSMCs was analysed by reverse transcription (RT)-PCR. I(P2X) and membrane potential were recorded using the amphotericin B-perforated patch method. RT-PCR analysis on single RVSMCs showed the presence of genes encoding P2X1 and P2X4 receptors. Under voltage clamp conditions, the selective P2X receptor agonist alphabeta-methylene ATP (alphabeta-meATP) evoked I(P2X) similar to that induced by ATP. Under current clamp conditions, both ATP and alphabeta-meATP evoked a spike-like membrane depolarization followed by a sustained depolarization, linking P2X receptors in RVSMCs to sympathetic control of renal vascular tone. A selective antagonist of P2X1 receptors, NF279, reduced I(P2X) amplitude by approximately 65% concentration-dependently manner within the nanomolar to sub-micromolar range. The residual current was resistant to micromolar concentrations of NF279, but was inhibited by sub-millimolar to millimolar concentrations of NF279. Two types of functional P2X receptors, monomeric P2X1 and heteromeric P2X1/4 receptors, are expressed in RVSMCs. Our study has identified important targets for possible pharmacological intervention in the sympathetic control of renal circulation.

Developmental effect of antenatal exposure to betamethasone on renal angiotensin II activity in the young adult sheep

Antenatal corticosteroids may have long-term effects on renal development which have not been clearly defined. Our objective was to compare the responses to intrarenal infusions of ANG II in two groups of year-old, male sheep: one group exposed to a clinically relevant dose of betamethasone before birth and one not exposed. We wished to test the hypothesis that antenatal steroid exposure would enhance renal responses to ANG II in adult life. Six pairs of male sheep underwent unilateral nephrectomy and renal artery catheter placement. The sheep were infused for 24 h with ANG II or with ANG II accompanied by blockade of the angiotensin type 1 (AT(1)) or type 2 (AT(2)) receptor. Baseline mean arterial blood pressure among betamethasone-exposed sheep was higher than in control animals (85.8 +/- 2.2 and 78.3 +/- 1.0 mmHg, respectively, P = 0.003). Intrarenal infusion of ANG II did not increase systemic blood pressure (P >/= 0.05) but significantly decreased effective renal plasma flow and increased renal artery resistance (P < 0.05). The decrease in flow and increase in resistance were significantly greater in betamethasone- compared with vehicle-exposed sheep (betamethasone P < 0.05, vehicle P >/= 0.05). This effect appeared to be mediated by a heightened sensitivity to the AT(1) receptor among betamethasone-exposed sheep. Sodium excretion initially decreased in both groups during ANG II infusion; however, a rebound was observed after 24 h. AT(1) blockade was followed by a significant rebound after 24 h in both groups. AT(2) blockade blunted the 24-h rebound effect among the vehicle-exposed sheep compared with the betamethasone-exposed sheep. In conclusion, antenatal corticosteroid exposure appears to modify renal responsiveness to ANG II by increasing AT(1)- and decreasing AT(2) receptor-mediated actions particularly as related to renal blood flow and sodium excretion.

Abstract 5562: Renal Resistive Index is Strongly Associated With Poor Outcome After Coronary Bypass Surgery: A Prospective Study

Backgound: The presence of peripheral artery disease and renal failure are known as poor prognostic markers in patients undergoing coronary revascularization. While the presence of renal artery stenosis (RAS) is frequent in patients with coronary artery disease, the prognostic value of this lesion has never been assessed in the setting of coronary revascularization. Hypothesis: We hypothesized that renal vascular disease is associated with poorer postoperative outcome after coronary bypass surgery (CABG), independent of renal function. Methods: We prospectively assessed by Duplex the renal arteries of 401 consecutive patients prior to CABG. We defined RAS by the presence of at least 2 out of the 3 following criteria: maximal velocity &gt;1.8 m/s, reno-aortic velocity ratio &gt;3.5, reno-renal velocity ratio &gt;2.7. Additionally we defined high renal arterial resistance (HRAR) in case of resistive index &gt;0.80. The 30-days post-operative outcome was composite, combining death, stroke or myocardial infarction. Logistic regression models were used to assess associations. Results: Among the 68 women and 333 men enrolled (age 67.6±10.7 years), RAS and HRAR were found in 33 (8.2%) and 45 (11.2%) cases, respectively. Adjusted for age, sex, glomerular filtration rate, CVD risk factors, treatments, the presence of peripheral artery disease, and the presence of chronic pulmonary disease, we did not find any significant association between RAS and the composite outcome (OR=0.90, 95%CI:0.28 –2.95, p=ns). Conversely, in the same model, HRAR was strongly associated with the primary composite outcome (OR=3.97, 95%CI:1.36 –11.02, p=0.01). Conclusion: Beyond the glomerular filtration rate and other usual prognostic markers, renal artery ultrasound provides additional prognostic information. While the presence of renal artery stenosis is not found of any post-operative prognostic value, a high renal arterial resistance is strongly and independently associated with short-term cardiovascular outcomes.

Targeting circulatory dysfunction in cirrhosis: Terlipressin and the hepatorenal syndrome

Hong Kong is adeveloped country with a relatively well-informed, highly literatesociety, so that levels of awareness regarding NAFLD are likely tobe much worse among less well-off populations with lower lit-eracy rates. This is worrying, given the magnitude of public healthproblems posed by NAFLD.NAFLD is one of the commonest, if not the commonest, liverdiseases in Western populations, affecting at least 24–42% ofadults.

Effects of terlipressin on systemic, hepatic and renal hemodynamics in patients with cirrhosis

Terlipressin has been shown to be effective in the management of hepatorenal syndrome. However, how terlipressin exerts its effect on the renal artery is unknown. The aim of the present study was to assess the effects of terlipressin on systemic, hepatic and renal hemodynamics in cirrhosis. Twenty-eight patients with cirrhosis and portal hypertension were studied. Systemic and hepatic hemodynamics, hepatic and renal arterial resistive indices and neurohumoral factors were measured prior to and 30 min after intravenous administration of 1 mg terlipressin (n = 19) or placebo (n = 9). After terlipressin, there were significant increases in both mean arterial pressure (P < 0.001) and systemic vascular resistance (P < 0.001), whereas heart rate (P < 0.001) and cardiac output (P < 0.001) decreased significantly. There was a significant decrease in the hepatic venous pressure gradient (P < 0.001). Portal venous blood flow also decreased significantly (P < 0.001). The mean hepatic arterial velocity increased significantly (P < 0.001). Although there was a significant decrease in the hepatic arterial resistive index (0.72 +/- 0.08 to 0.69 +/- 0.08, P < 0.001) and renal arterial resistive index (0.74 +/- 0.07 to 0.68 +/- 0.07, P < 0.001), portal vascular resistance was unchanged (P = 0.231). Plasma renin activity decreased significantly (P < 0.005), and there was a significant correlation between this decline and the decrease in renal arterial resistive index (r = 0.764, P < 0.005). The effects of terlipressin on systemic, hepatic and renal hemodynamics were observed similarly in patients with and without ascites. Placebo caused no significant effects. Terlipressin decreases hepatic and renal arterial resistance in patients with cirrhosis.

Intrarenal artery superoxide is mainly NADPH oxidase-derived and modulates endothelium-dependent dilation in elderly patients

The present study was performed to investigate the contribution of NADPH oxidases (Nox) to superoxide formation in human renal proximal resistance arteries and to test whether superoxide formation contributes to acute vasoconstrictor responses and endothelium-dependent vasodilation in these vessels. Arcuate and proximal interlobular artery segments were from patients who underwent nephrectomy because of a renal tumour. Vessels were dissected from tumour-free parts of the kidneys. Additional intrarenal arteries were obtained from rats. Superoxide formation was measured by lucigenin-enhanced chemiluminescence, expression of Nox isoforms was analysed by RT-PCR, and functional studies were performed by small vessel wire myography. Sixty per cent of superoxide formation in human arcuate and proximal interlobular arteries was due to Nox activity. mRNA expression analyses revealed the presence of Nox2 and Nox4 but not Nox1. Phenylephrine and endothelin-1 induced powerful concentration-dependent vasoconstrictions that were unaffected by superoxide scavengers. Vasopressin elicited small and variable vasoconstrictions with signs of tachyphylaxis. Endothelium-dependent vasodilation was blunted by tiron and Nomega-nitro-L-arginine methyl ester but not by superoxide dismutase or catalase. Exogenous hydrogen peroxide elicited vasoconstriction. Nox activity is the major source of superoxide formation in renal proximal resistance arteries from elderly patients. Acute vasoconstrictor responses to alpha1-adrenoreceptor activation and to endothelin-1 do not depend on superoxide formation, while endothelium-dependent vasodilation in intrarenal arteries is reactive oxygen species-dependent.

L-NIL prevents renal microvascular hypoxia and increase of renal oxygen consumption after ischemia-reperfusion in rats

Even though renal hypoxia is believed to play a pivotal role in the development of acute kidney injury, no study has specifically addressed the alterations in renal oxygenation in the early onset of renal ischemia-reperfusion (I/R). Renal oxygenation depends on a balance between oxygen supply and consumption, with the nitric oxide (NO) as a major regulator of microvascular oxygen supply and oxygen consumption. The aim of this study was to investigate whether I/R induces inducible NO synthase (iNOS)-dependent early changes in renal oxygenation and the potential benefit of iNOS inhibitors on such alterations. Anesthetized Sprague-Dawley rats underwent a 30-min suprarenal aortic clamping with or without either the nonselective NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) or the selective iNOS inhibitor L-N(6)-(1-iminoethyl)lysine hydrochloride (L-NIL). Cortical (CmicroPo(2)) and outer medullary (MmicroPo(2)) microvascular oxygen pressure (microPo(2)), renal oxygen delivery (Do(2ren)), renal oxygen consumption (Vo(2)(ren)), and renal oxygen extraction (O(2)ER) were measured by oxygen-dependent quenching phosphorescence techniques throughout 2 h of reperfusion. During reperfusion renal arterial resistance and oxygen shunting increased, whereas renal blood flow, CmicroPo(2), and MmicroPo(2) (-70, -42, and -42%, respectively, P < 0.05), Vo(2)(ren), and Do(2ren) (-70%, P < 0.0001, and -28%, P < 0.05) dropped. Whereas L-NAME further decreased Do(2ren), Vo(2)(ren), CmicroPo(2), and MmicroPo(2) and deteriorated renal function, L-NIL partially prevented the drop of Do(2ren) and microPo(2), increased O(2)ER, restored Vo(2)(ren) and metabolic efficiency, and prevented deterioration of renal function. Our results demonstrate that renal I/R induces early iNOS-dependent microvascular hypoxia in disrupting the balance between microvascular oxygen supply and Vo(2)(ren), whereas endothelial NO synthase activity is compulsory for the maintenance of this balance. L-NIL can prevent ischemic-induced renal microvascular hypoxia.

Fetal renal artery impedance as assessed by Doppler ultrasound in pregnancies complicated by intraamniotic inflammation and preterm birth

The objective of the study was to evaluate the fetal renal artery impedance in the context of inflammation-associated preterm birth. We conducted a prospective Doppler assessment of the fetal renal artery impedance in 70 singleton fetuses. The study group consisted of 56 premature fetuses (median, 28.1 [interquartile range, 25.3-30.6] weeks at enrollment). Gestational age (GA) reference ranges were generated based on fetuses with uncomplicated pregnancies (n = 14). Doppler studies included renal artery pulsatility index (PI), resistance index (RI), systolic/diastolic (S/D) ratio, and presence or absence of end-diastolic blood flow. Proteomic profiling (surface-enhanced laser desorption ionization time-of-flight) was used for assessment of intraamniotic inflammation and biomarker peak corresponding to beta2-microglubin. Data were interpreted in relationship to amniotic fluid index (AFI), cord blood interleukin (IL)-6 and erythropoietin (EPO) levels. The cardiovascular and metabolic profiles of the neonates were investigated in the first 24 hours of life. Fetuses delivered by mothers with intraamniotic inflammation had higher cord blood IL-6 but not EPO levels. Fetal inflammation did not affect either renal artery PI, RI, S/D ratio, or end-diastolic blood flow. Neonates delivered in the context of intraamniotic inflammation had higher serum blood urea nitrogen levels, which correlated significantly with AF IL-6 levels. The renal artery RI and SD ratio were inversely correlated with the AFI independent of GA, cord blood IL-6, and status of the membranes. The fetus is capable of sustaining normal renal artery impedance despite inflammation. Resistance in the renal vascular bed affects urine output independent of inflammation.

A central body fat distribution is related to increased renal arterial resistance index and renal function impairment in HIV-1 infected patients

Purpose of the study HIV-infected patients receiving antiretroviral therapy often develop changes in body fat distribution. Central fat accumulation is usually due to visceral as opposed to subcutaneous fat and this condition correlates with dyslipidemia, insulin resistance and increased cardiovascular risk. Recent studies conducted on obese patients have demonstrated a significative association between obesity and renal damage. The purpose of our study was to investigate if, in HIV-infected patients, central fat distribution may be associated with renal function abnormalities.

Peri-renal fat diameter is related to intima media thickness and renal arterial resistance index in HIV-1 infected patients

Peri-renal fat diameter is related to intima media thickness and renal arterial resistance index in HIV-1 infected patients

Performance of Doppler ultrasound in the prediction of severe portal hypertension in hepatitis C virus‐related chronic liver disease

To evaluate the correlation between hepatic vein pressure gradient measurement and Doppler ultrasonography (DUS) in patients with chronic liver disease (CLD). Sixty-six patients with fibrotic to cirrhotic hepatitis C virus-related CLD, were consecutively included upon referral to our haemodynamic laboratory. Superior mesenteric artery pulsatility index (SMA-PI), right interlobar renal and intraparenchymal splenic artery resistance indices, were determined, followed by hepatic venous pressure gradient (HVPG) measurement. A correlation was found between HVPG and intraparenchymal splenic artery resistance index (SA-RI) (r=0.50, P<0.0001), SMA-PI (r=-0,48, P<0.0001), right interlobar renal artery resistance index (RRA-RI) (r=0.51, P<0.0001) in the whole patient population. However, dividing patients according to the presence/absence of severe portal hypertension (i.e. HVPG > or =12 mmHg), a correlation between HVPG and intraparenchymal SA-RI (r=0.70, P<0.0001), SMA-PI (r=-0.49, P=0.02), RRA-RI (r=0.66, P=0.0002) was observed only for HVPG values <12 mmHg. HVPG but not DUS correlated with the presence of esophageal varices (P<0.0001). Superior mesenteric artery pulsatility index, intraparenchymal splenic and right interlobar renal artery resistance indices do not adequately predict severe portal hypertension.

Renal arterial resistance in septic shock: effects of increasing mean arterial pressure with norepinephrine on the renal resistive index assessed with Doppler ultrasonography

To determine the effects of increasing mean arterial pressure (MAP) on renal resistances assessed by Doppler ultrasonography in septic shock. Prospective, single-center, nonrandomized, open-label trial in the surgical intensive care unit in a university teaching hospital. 11 patients with septic shock who required fluid resuscitation and norepinephrine to increase and maintain MAP at or above 65 mmHg. Norepinephrine was titrated in 11 patients in septic shock during three consecutive not randomized periods of 2 h to achieve a MAP at successively 65, 75, and 85 mmHg. At the end of each period hemodynamic parameters and renal function variables (urinary output, creatinine, clearance) were measured, and Doppler ultrasonography was performed on interlobar arteries to assess the renal resistive index. When increasing MAP from 65 to 75 mmHg, urinary output increased significantly from 76 +/- 64 to 93 +/- 68 ml/h and the resistive index significantly decreased from 0.75 +/- 0.07 to 0.71 +/- 0.06. No difference was found between 75 and 85 mmHg. Doppler ultrasonography and resistive index measurements may help determine in each patient the optimal MAP for renal blood flow and may be a relevant end-point to titrate the hemodynamic treatment in septic shock.

The Predictive Value of Renal Vascular Resistance for Late Renal Allograft Loss

The renal artery resistance index (RI), assessed by Doppler ultrasonography, was recently identified as a new risk marker for late renal allograft loss. This finding requires confirmation since RI in that study was not measured at predetermined time points and ultrasonography is operator-dependent. We investigated the predictive value of renal vascular resistance (RVR), a less operator-dependent method as assessed by mean arterial pressure divided by renal blood flow, for the prediction of recipient mortality and death-censored graft loss. RVR was compared to commonly used risk markers such as creatinine clearance (CrCl), serum creatinine (SCreat) and proteinuria (UProt) in 793 first-time cadaveric renal transplant recipients at predetermined time points after transplantation using receiver operating characteristics (ROC) and Cox survival analyses. The present study showed that RVR is a prominent risk marker for recipient mortality and death-censored graft loss. However, the predictive value of RVR for recipient mortality owed mainly to the impact of mean arterial blood pressure. In contrast, RVR constituted more than the sum of its components for death-censored graft loss, but showed less predictive value than SCreat in univariate analysis. As the assessment of RVR is expensive and time-consuming, we believe that RVR holds no clinical merit for the follow-up of renal transplant recipients.

Long-term effects of percutaneous nephrolithotomy on renal morphology and arterial vascular resistance as evaluated by color Doppler ultrasonography: preliminary report

We evaluated the long-term effects of percutaneous nephrolithotomy (PNL) on renal morphology and vascular resistance. Parenchyma thickness, echogenicity and resistive index (RI) of upper, middle and lower poles of operated and contralateral kidneys of 41 patients with 82 renal units who underwent unilateral PNL with single pole access between 2000 and 2002 were examined separately by color Doppler ultrasonography. Mean patient age and duration between PNL and evaluation time were 38.29+/-11.53 years and 46.44+/-10.9 months, respectively. In operated kidney, mean RI, parenchyma thickness and echogenicity of the access pole were not statistically different than those of the adjacent two poles (0.608+/-0.053 vs. 0.608+/-0.052 for RI, P=0.895; 11.46+/-2.58 vs. 11.41+/-2.68 mm for parenchyma thickness, P=0.838; 0.049+/-0.31 vs. 0.073+/-0.33 for parenchyma echogenicity, P=0.160, respectively). Although mean RI and parenchyma thickness of access pole were statistically significantly different than the mean values of contralateral kidney (0.562+/-0.032 and 14.31+/-1.37 mm, respectively), no statistical difference was found between mean parenchyma echogenicities of both of them (echogenicity of contralateral kidney was 0, P=0.317). No significant difference was found between the average echogenicities of the three poles of the operated and contralateral kidneys (0.063+/-0.32 vs. 0, P=0.080). In 14 patients RI decreased from 0.694+/-0.058 to 0.602+/-0.056 in operated kidney (P=0.001) and from 0.604+/-0.06 to 0.559+/-0.031 in contralateral kidney (P=0.018) following PNL. It seems that PNL does not cause renal scarring, renal parenchymal loss or increase in renal vascular resistance in the long term. However, prospective studies must be performed for more definitive conclusions.

The effects of endothelin and L-NAME on plasma uric acid and urea concentration in Wistar rats

Effects of endothelins, which include vasoconstriction and vasodilatation are possible by different molecular mechanisms. Endothelins induce increased synthesis of nitric oxide which in turn inhibits the synthesis of endothelin. Changes in biochemical parameters connected with the increased and decreased synthesis of nitric oxide are not thoroughly examined yet. In a series of experiments we compared the effects of endothelin (ET-1) on the inhibition of nitric oxide synthase (NOS), as well as the effects of L-nitro arginin metal estar (L-NAME) on plasma urea and uric acid concentration. Experiments were performed on anesthetized female adult Wistar rats. The experimental groups received an i. v. bolus of ET-1, L-NAME or saline. All parameters, heamodynamic and biochemical, were measured before the animals were sacrificed. L-NAME increased the mean arterial pressure, decreased renal blood flow and increased vascular resistance in carotid and renal arteries and increased in plasma uric acid and urea concentrations. ET- 1 significantly decreased uric acid concentration in the plasma but did not effect plasma urea concentration compared to the control group. These differences show complex relations of nitric oxide with cellular signalization compared to the basic NO-cGMP pathway.

Renal Artery Resistance Index, Thyroid Hormones, and Thyroid Volume in the Early Kidney Transplants Recipients

Background Thyroid hormones could affect renal function, and, on the other hand, renal dysfunction may affect thyroid function. Disturbances of concentrations of thyroid hormones are often associated with thyroid gland enlargement. The aim of the study was to assess the function and morphology of the thyroid (volume and hormones concentration) and kidney function after transplantation (creatinine concentration and resistance index [RI] of transplant artery). Material and Methods The group included 13 females, 19 males; aged 19–69 years, mean 44.75 ± 14.8 years after transplantation with stable graft function. Thyroid volume, renal artery RI, creatinine concentration, and concentrations of T3, rT3, FT3, FT4, and TSH were estimated the day before surgery, and at 1, 3, 6, and 10 days after transplantation. Results The statistical analysis revealed a negative correlation between delta RI (difference between RI at 3 and 6 days after transplantation) and serum creatinine concentration, 10 days after transplantation ( r = −0.63; P < 0.01). We also observed a negative correlation between creatinine serum concentration at 10 days after transplantation and delta thyroid volume (Δ Vol; r = − 0.48; p < .05), a positive correlation between delta FT4 (Δ FT4) serum concentration, and delta creatinine (Δ Crea; r = 0.73; P < .001). Conclusions The dynamics of RI changes in the transplant kidney artery between 3 and 6 days after transplantation may predict graft function. Together with improved kidney function at 10 days after transplantation, we observed a regression of goiter.

Increased Renal Arterial Resistance Predicts the Course of Renal Function in Type 2 Diabetes With Microalbuminuria

Type 2 diabetic patients often die because of end-stage renal failure, but no definitive reliable factor predicting long-term renal outcome has been identified. We tested whether a renal arterial resistance index (R/I) > or =80, using Doppler ultrasound technique, was predictive of worsening renal function. The primary end points of the study were 1) the course of glomerular filtration rate (GFR) and 2) the albumin excretion rate in 157 microalbuminuric, hypertensive, type 2 diabetic patients after a 7.8-year follow-up period (range 7.1-9.2). Kaplan-Meier curves for the primary end point (decrease of GFR > or = -3.0 ml/min per 1.73 m(2) per year) was two to three times more frequently observed in patients with R/I > or =80. Four- to fivefold fewer patients showed a regression to normoalbuminuria during the follow-up period from baseline microalbuminuria in the cohort with R/I > or =80. Overt proteinuria did develop in 24% of patients with R/I > or =80 and in 5% of patients with R/I <80 (P < 0.01). In conclusion, intrarenal arterial resistance appears to play a nontrivial role in deteriorating renal function in type 2 diabetic patients. R/I is a noninvasive diagnostic procedure, which strongly predicts the outcome of renal function in type 2 diabetic patients, even when GFR patterns are still normal.