Serum levels of galactose-deficient IgA are elevated in patients with IgA nephropathy but do not correlate to disease activity or progression.

INTRODUCTION: IgA nephropathy (IgAN) is the most common glomerulonephritis globally. Because of the heterogeneity of the disease prognostic biomarkers are highly needed. AIM: To investigate associations between galactose-deficient IgA1 (Gd-IgA1) concentrations in plasma and urine and disease activity and progression in patients with IgAN. METHODS: Serum and urine samples were collected at the time of kidney biopsy (baseline) in patients with IgAN (n = 40) and analysed for Gd-IgA1. Patients with chronic kidney disease (CKD) without IgAN (n = 21) and healthy controls (n = 19) were examined as controls. In 19 patients with IgAN, analyses of Gd-IgA1 were repeated after a median follow up time of approximately 10 years. RESULTS: Serum Gd-IgA1 and Gd-IgA1:IgA were significantly elevated at the time of kidney biopsy in patients with IgAN compared to patients with non-IgAN CKD and healthy controls (p < 0.001). Urinary Gd-IgA1:creatinine was significantly elevated in patients with IgAN compared to patients with non-IgAN CKD. Neither serum Gd-IgA1, nor serum Gd-IgA1:IgA, correlated significantly to estimated GFR, urine albumin:creatinine (UACR), or blood pressure, at baseline. Serum Gd-IgA1 and Gd-IgA1:IgA at time of biopsy did not correlate significantly to annual changes in eGFR or UACR during follow up. In patients with IgAN, serum Gd-IgA1 decreased significantly over time during approximately 10 years of follow up (Δ-20 ± 85%, p = 0.027). Urinary Gd-IgA1:creatinine showed a strong positive correlation to UACR in patients with IgAN and likely reflected unspecific glomerular barrier injury. CONCLUSION: Although serum Gd-IgA1 and the Gd-IgA1:IgA ratio were significantly elevated in patients with IgAN at the time of kidney biopsy they were not related to disease activity or progression in this patient cohort.

[The KDIGO guideline on blood pressure management in chronic kidney disease is based on weak evidence]. / Vi ifrågasätter blodtrycksmål vid diagnosen kronisk njursjukdom.

The recently published Kidney Disease Improving Global Outcomes (KDIGO) guideline on blood pressure (BP) management in chronic kidney disease (CKD) recommends a target systolic BP of <120 mm Hg in all adults with hypertension and CKD. This recommendation is controversial. It is based on weak evidence derived primarily from CKD subgroup analysis of a single randomized controlled trial. The Swedish Society of Nephrology recommends a BP target of <140/90 mm Hg in all patients and, provided that the treatment is well tolerated, a BP target of <130/80 mm Hg is recommended in most patients with CKD.

Performance of Dexcom G5 and FreeStyle Libre sensors tested simultaneously in people with type 1 or 2 diabetes and advanced chronic kidney disease.

BACKGROUND: Advanced chronic kidney disease (CKD) is a common complication for people with type 1 and 2 diabetes and can often lead to glucose instability. Continuous glucose monitoring (CGM) helps users monitor and stabilize their glucose levels. To date, CGM and intermittent scanning CGM are only approved for people with diabetes but not for those with advanced CKD. AIM: To compare the performance of Dexcom G5 and FreeStyle Libre sensors in adults with type 1 or 2 diabetes and advanced CKD. METHODS: This was a non-randomized clinical trial that took place in two outpatient clinics in western Sweden. All patients with type 1 or 2 diabetes and an estimated glomerular filtration rate (eGFR) of < 30 mL/min per 1.73 m2 were invited to participate. Forty patients (full analysis set = 33) carried the Dexcom G5 sensor for 7 d and FreeStyle Libre sensor for 14 d simultaneously. For referencing capillary blood glucose (SMBG) was measured with a high accuracy glucose meter (HemoCue®) during the study period. At the end of the study, all patients were asked to answer a questionnaire on their experience using the sensors. RESULTS: The mean age was 64.1 (range 41-77) years, hemoglobin A1c was 7.0% [standard deviation (SD) 3.2], and diabetes duration was 28.5 (SD 14.7) years. A total of 27.5% of the study population was on hemodialysis and 22.5% on peritoneal dialysis. The mean absolute relative difference for Dexcom G5 vs SMBG was significantly lower than that for FreeStyle Libre vs SMBG [15.2% (SD 12.2) vs 20.9% (SD 8.6)], with a mean difference of 5.72 [95% confidence interval (CI): 2.11-9.32; P = 0.0036]. The mean absolute difference was also significantly lower for Dexcom G5 than for FreeStyle Libre, 1.21 mmol/L (SD 0.78) and 1.76 mmol/L (SD 0.78), with a mean diffrenec of 0.55 (95%CI: 0.27-0.83; P = 0.0004).The mean difference (MD) was -0.107 mmol/L and -1.10 mmol/L (P = 0.0002), respectively. In all, 66% of FreeStyle Libre values were in the no risk zone on the surveillance error grid compared to 82% of Dexcom G5 values. CONCLUSION: Dexcom G5 produces more accurate sensor values than FreeStyle Libre in people with diabetes and advanced CKD and is likely safe to be used by those with advanced CKD.

Using Bioimpedance Spectroscopy for Diagnosis of Malnutrition in Chronic Kidney Disease Stage 5-Is It Useful?

OBJECTIVE: Malnutrition is common in chronic kidney disease stage 5 (CKD5) and has negative clinical impacts. The aim of the present study is to evaluate bioimpedance spectroscopy (BIS) in diagnosing malnutrition in CKD5 including hemodialysis and peritoneal dialysis patients (CKD5D) using cutoff values for fat-free mass index (FFMI) according to the Global Leadership Initiative on Malnutrition criteria. Dual-energy X-ray absorptiometry (DXA) was used as a reference method. DESIGN AND METHODS: We performed a single-center cross-sectional diagnostic study of 90 patients with CKD5 or CKD5D. RESULTS: BIS-derived FFMI estimates were significantly higher compared with those obtained by DXA (18.5 ± 2.6 vs.17.8 ± 2.0, P < .05). The mean difference in FFMI estimates between the methods (DXA-BIS) and Bland-Altman 95% limits of agreements is -0.38 (2.76, -3.52) kg/m2. Overhydration (B = 0.67, P < .001), age (B = 0.02, P = .037), and interactions between overhydration and CKD5 subgroups (P = .034) independently predicted bias in BIS-derived FFMI. BIS-derived FFMI showed poor sensitivity (64%) and positive predictive value (48%) in diagnosing malnutrition in the present study population. CONCLUSION: The present study showed a limited agreement between estimates of FFMI derived by BIS and DXA due to a large interindividual variation. Using BIS as a clinical tool for assessing FFMI has limited accuracy and poor sensitivity in diagnosing malnutrition in patients with CKD5 and CKD5D.

Patients with moderate chronic kidney disease without heart disease have reduced coronary flow velocity reserve.

AIMS: The overall aim was to identify sub-clinical cardiac abnormalities by echocardiography in patients with chronic kidney disease (CKD) stages 3 and 4 and to investigate underlying mechanisms. METHODS AND RESULTS: Ninety-one patients with CKD stages 3 and 4, without a diagnosis of heart disease, and 41 healthy matched controls were included in this cross-sectional study. Cardiac morphology and function were analysed with Doppler echocardiography and coronary flow velocity reserve (CFVR) in response to adenosine was measured in the left anterior descendent artery to detect coronary microvascular dysfunction (CMD). All study subjects had a left ventricular (LV) ejection fraction > 50%. Patients with CKD showed statistically significant increases in left atrial volume index and transmitral and pulmonary vein flow velocities during atrial contraction and prolonged LV isovolumetric relaxation time. Patients with CKD had significantly reduced CFVR vs. controls (2.74 ± 0.86 vs. 3.40 ± 0.89, P < 0.001), and 43% of patients were classified as having CMD compared with 9% of controls (P = 0.001). CONCLUSIONS: Patients with CKD stages 3 and 4, without a diagnosis of heart disease, showed early abnormalities in LV diastolic function that did not fulfil the criteria for LV dysfunction according to current guidelines. A large proportion of CKD patients had CMD, suggesting that microvascular abnormalities may have a pathogenic role in the development of heart failure in this patient group.

Impact of Abdominal Aortic Calcification on Central Haemodynamics and Decline of Glomerular Filtration Rate in Patients with Chronic Kidney Disease Stages 3 and 4.

BACKGROUND/AIM: Calcifications of large arteries are frequent in chronic kidney disease (CKD) and may contribute to the high cardiovascular risk in this population. The aim of this study was to examine whether abdominal aortic calcification volume (AACV) was a predictor of the rate of decline in glomerular filtration rate (GFR) in a cohort of patients with CKD stages 3 and 4. METHODS: Eighty-four patients with CKD stages 3 and 4 were enrolled in this prospective observational study. At study entry, and annually, GFR was measured by plasma 51Cr-EDTA clearance. At baseline, haemodynamics was assessed and AACV was determined by computer tomography. RESULTS: The mean follow-up time was 3.4 years and mean decline in GFR was -2.69 mL/min/1.73 m2 per year. At baseline, abdominal aortic calcification (AAC) was detected in 66 patients (79%). A binary logistic regression analysis revealed that age was the only statistically significant independent predictor of AAC. In patients with AAC, male gender (B = 0.413, p = 0.030), aortic diastolic blood pressure (B = -0.025, p = 0.001) and ankle-brachial index (B = -1.666, p = 0.002) were independently associated with AACV using a multiple linear regression analysis. Neither the presence nor the extent of AAC was significantly associated with the rate of change in GFR during follow-up. CONCLUSION: In this cohort of patients with CKD stages 3 and 4, only age was an independent predictor of the presence of AAC. AACV was not associated with the rate of decline in GFR.

Predictors and correlates of systolic blood pressure reduction with liraglutide treatment in patients with type 2 diabetes.

Liraglutide is associated with blood pressure reduction in patients with type 2 diabetes. However, it is not known whether this blood pressure reduction can be predicted prior to treatment initiation, and to what extent it correlates with weight loss and with improved glycemic control during follow-up. We analyzed data from a double-blind, placebo-controlled trial, in which 124 insulin-treated patients with type 2 diabetes were randomized to liraglutide or placebo. We evaluated various baseline variables as potential predictors of systolic blood pressure (SBP) reduction, and evaluated whether changes in SBP correlated with weight loss and with improved glycemic control. A greater reduction in SBP among liraglutide-treated patients was predicted by higher baseline values of SBP (P < 0.0001) and diastolic blood pressure (P = 0.012), and by lower baseline values of mean glucose measured by continuous glucose monitoring (CGM; P = 0.044), and serum fasting C-peptide (P = 0.015). The regression coefficients differed significantly between the liraglutide group and the placebo group only for diastolic blood pressure (P = 0.037) and mean CGM (P = 0.021). During the trial period, SBP reduction correlated directly with change in body weight and BMI, but not with change in HbA1c. We conclude that patients with lower mean CGM values at baseline responded to liraglutide with a larger reduction in SBP, and that improved HbA1c during follow-up was not associated with reductions of SBP. Our data suggest that some patients with type 2 diabetes may benefit from liraglutide in terms of weight and SBP reduction.

Adenine-Induced Chronic Renal Failure in Rats: A Model of Chronic Renocardiac Syndrome with Left Ventricular Diastolic Dysfunction but Preserved Ejection Fraction.

BACKGROUND/AIMS: Cardiovascular disease is the major cause of death in patients with chronic kidney disease (CKD). Rats with adenine-induced chronic renal failure (ACRF) develop severe renal insufficiency and metabolic abnormalities that closely resemble those in patients with uremia. The aim of the present study was to determine left ventricular (LV) morphology and function in rats with ACRF. METHODS: Male Sprague-Dawley rats received either chow containing adenine or were pair-fed an identical diet without adenine (controls, C). After 9-13 weeks animals were anesthetized with isoflurane and cardiac function was assessed both by echocardiography and by LV catheterization. RESULTS: Rats with ACRF showed increases in serum creatinine (323±107 vs. 33±5 µM, P< 0.05), mean arterial pressure (115±6 vs. 106±7 mmHg, P< 0.05) and LV weight (3.4±0.3 vs. 2.5±0.2 mg/kg, P< 0.05) vs. controls. Rats with ACRF had reduced early diastolic tissue Doppler velocities in the LV, enlarged left atrial diameter (4.8±0.8 vs. 3.5±0.4 mm, P< 0.05) and elevated LV end-diastolic pressure (15±5 vs. 8±1 mmHg, P< 0.01). Cardiac output was increased in ACRF rats (211±66 vs. 149±24 ml/min, P< 0.05) and systolic function preserved. In the LV of ACRF rats there were statistically significant (P< 0.05) increases in cardiomyocyte diameter, proliferation and apoptosis, while there was no difference between groups in fibrosis. CONCLUSION: Rats with ACRF develop LV hypertrophy and diastolic dysfunction while systolic performance was preserved. There was an increased hypertrophy and apoptosis of cardiomyocytes in the LV of ACRF rats. The cardiac abnormalities in ACRF rats resemble those in patients with CKD in which heart failure with preserved ejection fraction is common. Hence, this experimental model is well suited for studying pathophysiological mechanisms in chronic renocardiac syndromes.

Split renal function in patients with unilateral atherosclerotic renal artery stenosis-effect of renal angioplasty.

OBJECTIVE: To evaluate the effect of percutaneous transluminal renal angioplasty (PTRA) on split renal function (SRF) in patients with unilateral atherosclerotic renal artery stenosis (ARAS). METHODS: We performed a retrospective analysis of all consecutively examined patients at our centre with significant ARAS undergoing PTRA during 2002-07. A significant ARAS was defined as a lesion with a trans-stenotic mean arterial pressure gradient of at least 10 mmHg or a diameter stenosis >50% on angiography. Ambulatory (24 h) systolic and diastolic blood pressure (ASBP and ADBP, respectively) and calculated SRF using 99mTc-DTPA renal scintigraphy were evaluated before (baseline) and 4 weeks after PTRA. RESULTS: ASBP and ADBP were significantly lower 4 weeks after PTRA compared with baseline levels. Although total estimated glomerular filtration rate (eGFR; four-variable Modification of Diet in Renal Disease equation) had not changed by PTRA, analysis of SRF showed significantly increased eGFR in stenotic kidneys and a comparable reduction in eGFR in non-stenotic kidneys 4 weeks after PTRA. CONCLUSIONS: In patients with unilateral ARAS, PTRA significantly improved eGFR in stenotic kidneys and decreased filtration in contralateral, non-stenotic kidneys. These potentially beneficial effects may not be apparent when total renal function remains stable. The clinical significance of these findings needs to be evaluated further.

High-NaCl Diet Aggravates Cardiac Injury in Rats with Adenine-Induced Chronic Renal Failure and Increases Serum Troponin T Levels.

AIMS: To examine the effects of 2 weeks of high-NaCl diet on left ventricular (LV) morphology and serum levels of cardiac troponin T (cTnT) in rats with adenine-induced chronic renal failure (ACRF). METHODS: Male Sprague-Dawley rats either received chow containing adenine or were pair-fed an identical diet without adenine [controls (C)]. Approximately 10 weeks after the beginning of the study, the rats were randomized to either remain on a normal NaCl diet (NNa; 0.6%) or to be switched to high-NaCl chow (HNa; 4%) for 2 weeks, after which acute experiments were performed. RESULTS: Rats with ACRF showed statistically significant increases (p < 0.001) in arterial pressure (AP), LV weight and fibrosis, and serum cTnT levels compared to controls. Two weeks of high-NaCl intake augmented the increases in AP, LV weight and fibrosis, and serum cTnT concentrations only in ACRF rats (p < 0.05 for group × NaCl intake interaction). Compared to group C-NNa, cTnT levels were elevated approximately 6-fold in group ACRF-NNa and 24-fold in group ACRF-HNa. Focal LV injury with cardiomyocyte necrosis, scarring, and fibrinoid necrosis of small arteries were only detected in group ACRF-HNa. There was a strong correlation between the degree of LV fibrosis and serum cTnT levels in ACRF rats (r = 0.81, p < 0.01). CONCLUSION: Two weeks of high-NaCl diet in rats with ACRF produces LV injury and aggravates increases in serum cTnT levels, presumably by causing hypertension-induced small artery lesions leading to myocardial ischemia. This model may be suitable for studying pathophysiological mechanisms in chronic renicardiac syndromes.

High-NaCl diet impairs dynamic renal blood flow autoregulation in rats with adenine-induced chronic renal failure.

This study examined the effects of 2 wk of high-NaCl diet on kidney function and dynamic renal blood flow autoregulation (RBFA) in rats with adenine-induced chronic renal failure (ACRF). Male Sprague-Dawley rats received either chow containing adenine or were pair-fed an identical diet without adenine (controls). After 10 wk, rats were randomized to either remain on the same diet (0.6% NaCl) or to be switched to high 4% NaCl chow. Two weeks after randomization, renal clearance experiments were performed under isoflurane anesthesia and dynamic RBFA, baroreflex sensitivity (BRS), systolic arterial pressure variability (SAPV), and heart rate variability were assessed by spectral analytical techniques. Rats with ACRF showed marked reductions in glomerular filtration rate and renal blood flow (RBF), whereas mean arterial pressure and SAPV were significantly elevated. In addition, spontaneous BRS was reduced by ∼50% in ACRF animals. High-NaCl diet significantly increased transfer function fractional gain values between arterial pressure and RBF in the frequency range of the myogenic response (0.06-0.09 Hz) only in ACRF animals (0.3 ± 4.0 vs. -4.4 ± 3.8 dB; P < 0.05). Similarly, a high-NaCl diet significantly increased SAPV in the low-frequency range only in ACRF animals. To conclude, a 2-wk period of a high-NaCl diet in ACRF rats significantly impaired dynamic RBFA in the frequency range of the myogenic response and increased SAPV in the low-frequency range. These abnormalities may increase the susceptibility to hypertensive end-organ injury and progressive renal failure by facilitating pressure transmission to the microvasculature.

Brain natriuretic peptides in atherosclerotic renal artery stenosis and effects of renal angioplasty.

BACKGROUND: We hypothesized that plasma levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) would be elevated, and adiponectin concentrations reduced, in patients with atherosclerotic renal artery stenosis (ARAS) and that BNPs might be used to identify patients who would benefit from percutaneous transluminal renal angioplasty (PTRA). METHODS: Data were collected before renal angiography in 91 patients with hypertension and suspected ARAS (significant ARAS; n=47, and non-RAS; n=44) and in 20 healthy controls (C). In ARAS patients analyses were repeated four weeks after PTRA. RESULTS: Ambulatory systolic blood pressure (ASBP) was significantly elevated in the ARAS group vs. both C and non-RAS groups. Baseline plasma BNP and NT-proBNP levels were significantly elevated, and adiponectin concentrations reduced, in the ARAS group vs. C but not vs. the non-RAS group. One month after PTRA, ASBP was reduced vs. baseline (149±16 to 139±15 mm p<0.01). Brain natriuretic peptides were not significantly affected by PTRA. CONCLUSIONS: Patients with ARAS showed elevated of BNP and NT-proBNP concentrations, and reduced levels of adiponectin, compared to healthy controls but not vs. hypertensive individuals without RAS. Our data do no support the use of BNP analyses in the identification of ARAS patients who will have a beneficial blood pressure response to PTRA.

Effects of endothelin receptor antagonists on renal hemodynamics in angiotensin II-infused rats on high NaCl intake.

AIM: The aim was to investigate effects of selective endothelin (ET) receptor antagonists on renal hemodynamics and dynamic renal blood flow autoregulation (RBFA) in angiotensin II (Ang II)-infused rats on a high NaCl intake. METHODS: Sprague-Dawley rats received Ang II (250 ng/kg/min, s.c.) and an 8% NaCl diet for 14 days after which renal clearance experiments were performed. After baseline measurements animals were administered either: (a) saline vehicle; (b) ETA receptor antagonist BQ-123 (30 nmol/kg/min); (c) ETB receptor antagonist BQ-788 (30 nmol/kg/min); or (d) BQ-123 + BQ-788, for six consecutive 20-minute clearance periods. RESULTS: BQ-123 reduced arterial pressure (AP) and selectively increased outer medullary perfusion versus vehicle (p<0.05). These effects were attenuated or abolished by combined BQ-123 and BQ-788. BQ-788 reduced renal blood flow and increased renovascular resistance (p<0.05). Ang II-infused rats on high NaCl intake showed abnormalities in dynamic RBFA characterized by an impaired myogenic response that were not significantly affected by ET receptor antagonists. CONCLUSION: In hypertensive Ang II-infused rats on a high-NaCl intake selective ETA antagonism with BQ-123 reduced AP and specifically increased OM perfusion and these effects were dependent on intact ETB receptor stimulation. Furthermore, ET receptor antagonists did not attenuate abnormalities in dynamic RBFA.

Oxidative stress and inflammation in renal patients and healthy subjects.

The first goal of this study was to measure the oxidative stress (OS) and relate it to lipoprotein variables in 35 renal patients before dialysis (CKD), 37 on hemodialysis (HD) and 63 healthy subjects. The method for OS was based on the ratio of cholesteryl esters (CE) containing C18/C16 fatty acids (R2) measured by gas chromatography (GC) which is a simple, direct, rapid and reliable procedure. The second goal was to investigate and identify a triacylglycerol peak on GC, referred to as TG48 (48 represents the sum of the three fatty acids carbon chain lengths) which was markedly increased in renal patients compared to healthy controls. We measured TG48 in patients and controls. Mass spectrometry (MS) and MS twice in tandem were used to analyze the fatty acid composition of TG48. MS showed that TG48 was abundant in saturated fatty acids (SFAs) that were known for their pro-inflammatory property. TG48 was significantly and inversely correlated with OS. Renal patients were characterized by higher OS and inflammation than healthy subjects. Inflammation correlated strongly with TG, VLDL-cholesterol, apolipoprotein (apo) C-III and apoC-III bound to apoB-containing lipoproteins, but not with either total cholesterol or LDL-cholesterol.In conclusion, we have discovered a new inflammatory factor, TG48. It is characterized with TG rich in saturated fatty acids. Renal patients have increased TG48 than healthy controls.

Lipoprotein abnormalities in patients with atherosclerotic renovascular disease.

BACKGROUND: Patients with atherosclerotic renovascular disease (ARVD) have a high risk of cardiovascular death. The primary aim was to characterize abnormalities in apolipoprotein (Apo)-defined lipoprotein (Lp) subclasses in patients with ARVD. METHODS: Baseline measurements were performed on 42 patients with ARVD 4 weeks after renal angioplasty (PTRA). All patients were on statin treatment. Twenty age-matched healthy subjects without medications served as controls. Subsequently, patients were randomized to treatment with either candesartan (n = 21), or antihypertensive treatment without inhibitors of the renin-angiotensin-aldosterone system (n = 21) and followed for 11 months. RESULTS: At baseline, ApoC-III (12.7 ± 4.6 vs. 8.8 ± 2.6 (SD) mg/dl, p < 0.05), LpB:C:E (13.3 ± 5.4 vs. 8.4 ± 4.3 mg/dl, p < 0.05), and the sum of ApoC-III-containing lipoproteins, i.e. LpB:C + LpB:C:E + LpA-II:B:C:D:E (46 ± 15 vs. 37 ± 8 mg/dl, p < 0.05), were significantly elevated in ARVD patients versus healthy controls. Multiple regression analyses showed that only plasma renin activity was independently associated with ApoC-III levels at baseline (p < 0.05, r = 0.74). Treatment with candesartan did not correct abnormalities. CONCLUSIONS: Patients with ARVD treated with statins have an atherogenic lipoprotein profile characterized by elevated levels of ApoC-III-containing, triglyceride-rich lipoproteins that could accelerate atherosclerotic disease.

High-NaCl intake impairs dynamic autoregulation of renal blood flow in ANG II-infused rats.

The aim of this study was to investigate dynamic autoregulation of renal blood flow (RBF) in ANG II-infused rats and the influence of high-NaCl intake. Sprague-Dawley rats received ANG II (250 ng·kg(-1)·min(-1) sc) or saline vehicle (sham) for 14 days after which acute renal clearance experiments were performed during thiobutabarbital anesthesia. Rats (n = 8-10 per group) were either on a normal (NNa; 0.4% NaCl)- or high (HNa; 8% NaCl)-NaCl diet. Separate groups were treated with 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol; 1 M in drinking water). Transfer function analysis from arterial pressure to RBF in the frequency domain was used to examine the myogenic response (MR; 0.06-0.09 Hz) and the tubuloglomerular feedback mechanism (TGF; 0.03-0.06 Hz). MAP was elevated in ANG II-infused rats compared with sham groups (P < 0.05). RBF in ANG II HNa was reduced vs. sham NNa and sham HNa (6.0 ± 0.3 vs. 7.9 ± 0.3 and 9.1 ± 0.3 ml·min(-1)·g kidney wt(-1), P < 0.05). transfer function gain in ANG II HNa was significantly elevated in the frequency range of the MR (1.26 ± 0.50 dB, P < 0.05 vs. all other groups) and in the frequency range of the TGF (-0.02 ± 0.50 dB, P < 0.05 vs. sham NNa and sham HNa). Gain values in the frequency range of the MR and TGF were significantly reduced by tempol in ANG II-infused rats on HNa diet. In summary, the MR and TGF components of RBF autoregulation were impaired in ANG II HNa, and these abnormalities were attenuated by tempol, suggesting a pathogenetic role for superoxide in the impaired RBF autoregulatory response.

Accuracy of colour duplex sonography for the diagnosis of renal artery stenosis.

OBJECTIVE: To examine the diagnostic value of novel velocimetric colour duplex sonography indices in the screening of renal artery stenosis (RAS). METHODS: We performed a retrospective analysis of all consecutively studied patients at our centre with suspected RAS, and a colour duplex sonography carried out at less than 4 months (mean 34 days) before renal angiography during a 6-year period (2002-2007). A significant RAS was defined as an at least 60% stenosis on angiography or a transstenotic mean arterial pressure gradient of at least 10 mmHg or both. RESULTS: In a total of 169 patients, 111 stenotic and 206 nonstenotic kidneys were examined. The sensitivity and specificity for acceleration of blood flow in early systole (ACCmax) were 85 and 75%, respectively, and for the acceleration index (ACCmax/peak systolic velocity, AImax) 83 and 79%, respectively. Corresponding values in patients with estimated glomerular filtration rate of less than 30 ml/min/1.73 m2 were 90 and 73% (for ACCmax) and 74 and 88% (for AImax). In addition, the transstenotic mean arterial pressure gradient showed a significant, though weak, negative correlation to ACCmax (r = -0.26, P = 0.02) and AImax (r = -0.29, P = 0.01) in stenotic kidneys. CONCLUSION: ACCmax and AImax provide similar, good diagnostic accuracy in the detection of a haemodynamically significant RAS, even in patients with markedly reduced glomerular filtration rate. Presumably, the lack of superiority of the novel index AImax could be explained by a highly homogenous methodological approach in the present single-centre study.