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Highlights: [•] Malnutrition during periods in development may have long-term effects in the adult. [•] We examine parasitological behavior and histopathological. [•] For the first time, this study describes the changes of the renal parenchyma. [•] Induced by postnatal malnutrition associated with infection caused by Schistosoma mansoni. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the diagnostic value of acoustic radiation force impulse (ARFI) to test the elasticity of renal parenchyma by measuring the shear wave velocity (SWV) which might be used to detect chronic kidney disease (CKD). Methods: 327 healthy volunteers and 64 CKD patients were enrolled in the study. The potential influencing factors and measurement reproducibility were evaluated in the healthy volunteers. Correlations between SWV and laboratory tests were analyzed in CKD patients.?Receiver-operating characteristic curve (ROC) analyses were performed to assess the diagnostic performance of ARFI. Results: The SWV of healthy volunteers correlated significantly to age (r = −0.22, P<0.001, n = 327) and differed significantly between men and women (2.06±0.48 m/s vs. 2.2±0.52 m/s, P = 0.018, n = 327). However, it did not correlate significantly to height, weight, body mass index, waistline, kidney dimension and the depth for SWV measurement (n = 30). Inter- and intraobserver agreement expressed as intraclass coefficient correlation were 0.64 (95% CI: 0.13 to 0.82, P = 0.011) and 0.6 (95% CI: 0.31 to 0.81, P = 0.001) (n = 40). The mean SWV in healthy volunteers was 2.15±0.51 m/s, while was 1.81±0.43 m/s, 1.79±0.29 m/s, 1.81±0.44 m/s, 1.64±0.55 m/s, and 1.36±0.17 m/s for stage 1, 2, 3, 4 and 5 in CKD patients respectively. The SWV was significantly higher for healthy volunteers compared with each stage in CKD patients. ARFI could not predict the different stages of CKD except stage 5. In CKD patients, SWV correlated to e-GFR (r = 0.3, P = 0.018), to urea nitrogen (r =  −0.3, P = 0.016), and to creatinine (r =  −0.41, P = 0.001). ROC analyses indicated that the area under the ROC curve was 0.752 (95% CI: 0.704 to 0.797) (P<0.001). The cut-off value for predicting CKD was 1.88 m/s (sensitivity 71.87% and specificity 69.69%). Conclusion: ARFI may be a potentially useful tool in detecting CKD. [ABSTRACT FROM AUTHOR]

Polycystic kidney disease (PKD), the most common genetic cause of chronic kidney failure, is characterized by the presence of numerous, progressively enlarging fluid-filled cysts in the renal parenchyma. The cysts arise from renal tubules and are lined by abnormally functioning and hyperproliferative epithelial cells. Despite recent progress, no Food and Drug Administration-approved therapy is available to retard cyst growth. MicroRNAs (miRNAs) are short noncoding RNAs that inhibit posttranscriptional gene expression. Dysregulated miRNA expression is observed in PKD, but whether miRNAs are directly involved in kidney cyst formation and growth is not known. Here, we show that miR-17~92, an oncogenic miRNA cluster, is up-regulated in mouse models of PKD. Kidney-specific transgenic overexpression of miR-17~92 produces kidney cysts in mice. Conversely, kidney-specific inactivation of miR-17~92 in a mouse model of PKD retards kidney cyst growth, improves renal function, and prolongs survival. miR-17~92 may mediate these effects by promoting proliferation and through posttranscriptional repression of PKD genes Pkd1, Pkd2, and hepatocyte nuclear factor-1β. These studies demonstrate a pathogenic role of miRNAs in mouse models of PKD and identify miR-17~92 as a therapeutic target in PKD. Our results also provide a unique hypothesis for disease progression in PKD involving miRNAs and regulation of PKD gene dosage. [ABSTRACT FROM AUTHOR]

The pathogenesis of fibromuscular dysplasia (FMD) remains unclear, but tobacco use is thought to be involved. This retrospective cross-sectional study aimed to evaluate smoking first as a risk factor for renal artery FMD diagnosis and second as a modifier of the clinical and radiological phenotype of this disease. We retrieved 337 adult patients diagnosed with FMD in a referral center for hypertension management, who were first individually matched to controls with essential hypertension for sex, age, systolic blood pressure, number of antihypertensive drugs, and year of visit. Smoking status and other relevant data were collected at first visit. The proportion of current smokers was higher for patients with FMD than for the controls (30% and 18%, respectively, P<0.001; odds ratio, 2.5 [95% confidence interval, 1.6-3.9]). Second, characteristics of FMD were compared between current smokers and other patients. Among patients with multifocal FMD, current smokers experienced an earlier diagnosis of hypertension (36 versus 42 years, respectively; P<0.001) and FMD (43 versus 51 years; P<0.001) than other patients, and a greater likelihood of renal artery interventions (57% versus 31%; P<0.001) and of kidney asymmetry (21% versus 4%; P=0.001). In conclusion, current smoking is associated with a higher likelihood of renal artery FMD diagnosis. Rather than a higher incidence of FMD, this may reflect a more aggressive course in smokers, who have earlier hypertension leading to increased and earlier recognition of the disease. Smoking cessation should be strongly encouraged in patients with FMD. [ABSTRACT FROM AUTHOR]

Historically, the evaluation of renovascular hypertension has been accomplished by US, renal scintigraphy and digital subtraction angiography. Based on its high accuracy reported in adults renal CT angiography (CTA) with pediatric-appropriate low radiation dose techniques has become an important tool in the workup of renovascular hypertension in children. Renal CTA has several advantages over more conventional imaging modalities, including rapid and non-invasive acquisition, high resolution and easy reproducibility. Additionally, in our experience high-quality renal CTA can be performed using low-dose radiation exposures and can be acquired without sedation in most instances. This article illustrates by examples the usefulness of renal CTA for diagnosis of childhood renovascular hypertension and provides an overview of renal CTA findings in the most common childhood renovascular diseases. [ABSTRACT FROM AUTHOR]

Previous studies show that neuropeptide Y1-36 (NPY1-36) and peptide YY1-36 (PYY1-36), by engaging Y1 receptors, stimulate proliferation of spontaneous hypertensive rat (SHR) preglomerular vascular smooth muscle cells (PGVSMCs). In contrast, these peptides have little effect on proliferation of Wistar-Kyoto (WKY) PGVSMCs. Why SHR and WKY PGVSMCs differ in this regard is unknown. Because receptor for activated C kinase 1 (RACK1) can modulate cell proliferation, we tested the hypothesis that differences in RACK1 levels/ localization may explain the differential response of SHR vs. WKY PGVSMCs to NPY1-36 and PYY1-36. Western blotting for RACK1 in subcellular fractions of cultured SHR and WKY PGVSMCs demonstrated increased levels of RACK1 in the membrane and cytoskeletal subcellular fractions of SHR vs. WKY PGVSMCs. NPY1-36 and PYY1-36 stimulated proliferation of SHR PGVSMCs, and siRNA knockdown of RACK1 abrogated this effect. Neither NPY1-36 nor PYY1-36 stimulated the proliferation of WKY PGVSMCs. However, in WKY PGVSMCs treated with a RACK1 plasmid, both NPY1-36 and PYY1-36 stimulated proliferation. In SHR PGVSMCs, inhibitors of the Gi/phospholipase C/PKC pathway (a pathway known to be organized by RACK1) attenuated the ability of NPY1-36 to stimulate the proliferation of SHR PGVSMCs. Our results suggest that RACK1 modulates the ability of PGVSMCs to respond to the proliferative actions of NPY1-36 and PYY1-36 and differences in RACK1 levels/ localization account for, in part, differential proliferative responses to NPY1-36 and PYY1-36 in SHR vs. WKY PGVSMCs. Because dipeptidyl peptidase IV inhibitors increase NPY1-36 and PYY1-36 levels, our findings have implications for the use of such drugs in diabetic patients. [ABSTRACT FROM AUTHOR]

Autoregulation is critical for protecting the kidney against arterial pressure elevation and is compromised in some forms of hypertension. Evidence indicates that activated lymphocytes contribute importantly to cardiovascular injury in hypertension. We hypothesized that activated lymphocytes contribute to renal vascular dysfunction by impairing autoregulation and P2X1 receptor signaling in ANG II-infused hypertensive rats. Male Sprague-Dawley rats receiving ANG II infusion were treated with a lymphocyte proliferation inhibitor, mycophenolate mofetil (MMF) for 2 wk. Autoregulation was assessed in vitro and in vivo using the blood-perfused juxtamedullary nephron preparation and anesthetized rats, respectively. ANG II-treated rats exhibited impaired autoregulation. At the single vessel level, pressure-mediated afferent arteriolar vasoconstriction was significantly blunted (P < 0.05 vs. control rats). At the whole kidney level, renal blood flow passively decreased as renal perfusion pressure was reduced. MMF treatment did not alter the ANG II-induced hypertensive state; however, MMF did preserve autoregulation. The autoregulatory profiles in both in vitro or in vivo settings were similar to the responses from control rats despite persistent hypertension. Autoregulatory responses are linked to P2X1 receptor activation. Accordingly, afferent arteriolar responses to ATP and the P2X1 receptor agonist β,γ-methylene ATP were assessed. ATP- or β,γ-methylene ATP-induced vasoconstriction was significantly attenuated in ANG II-infused hypertensive rats but was normalized by MMF treatment. Moreover, MMF prevented elevation of plasma transforming growth factor-β1 concentration and lymphocyte and macrophage infiltration in ANG II-infused kidneys. These results suggest that anti-inflammatory treatment with MMF prevents lymphocyte infiltration and preserves autoregulation in ANG II-infused hypertensive rats, likely by normalizing P2X1 receptor activation. [ABSTRACT FROM AUTHOR]

Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats (n = 7/group) were studied during 8 wk: water vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose. [ABSTRACT FROM AUTHOR]

The role of the kidney in the pathogenesis of elderly hypertension is bidirectional, as the kidney is responsible for producing hypertension as well as a victim of high blood pressure values (BPV). Objectives. The study of kidney microvascularization features and renal haemodynamics in the elderly by measuring the renal resistive index (RRI). Materials and methods. We study on a group of elderly with hypertension which have been separated into two subgroups: patients with normal renal function and with chronic kidney disease (CKD). We analyzed: mean values of the RRI and its correlation with creatinine, proteinuria, BPV. Conclusions. Correlation between the RRI and creatinine/proteinuria/BPV showed that RRI could be used for quantification of renal injury. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to evaluate whether cortical scars can be detected using the summed images of 99mTechnetium-mercaptoacetyltriglycine (99mTc-MAG3) renal dynamic scans, and to compare the results with 99mTechnetium-dimer-captosuccinic acid (99mTc-DMSA) scans. Materials and Methods: We evaluated a total of 135 renal units from 68 patients (12 boys and 56 girls, with a mean age of 9 years old; range 3-1 6 years old) who had 99mTc-MAG-3 and 99mTc-DMSA scintigraphy within a period of two weeks. Differential renal function (DRF) values and parenchymal function parameters obtained from the two studies were compared with semiquantitative scoring and grading systems. Results: The correlation between 99mTc-MAG-3 and 99mTc-DMSA cortical scintigraphy, according to the semiquantitative scoring and grading systems, was perfect (rk tau-b=0.833). The sensitivity, specificity, and accuracy of 99mTc-MAG-3 scintigraphy were 92.6%, 96.8%, and 95.5%, respectively. There was no significant difference between two methods in detecting renal scars (p>0.05). Conclusion: Most parenchymal lesions detected on 99mTc-DMSA scans were also identified on 99mTc-MAG-3 parenchymal scans. By lowering the radiation exposure, 99m-Tc MAG-3 scintigraphy can provide simultaneous information on renal perfusion, concentration, drainage, parencymal functions, and DRF without the need for additional imaging methods. The reliability of renal parenchyma evaluation was increased by using scoring and grading systems to compare the two methods. [ABSTRACT FROM AUTHOR]

Abstract: Background: The treatment of immunoglobulin A (IgA) nephropathy with normal renal function and minimal proteinuria is unknown. Methods: We randomly assigned 60 patients with IgA nephropathy, proteinuria <0.5 g/day, normal blood pressure and renal function to ramipril 2.5 mg daily or no treatment. Patients were followed for 5 years for the development of hypertension, proteinuria, or impaired renal function. Results: The blood pressure of the treatment group was marginally lower than the control group throughout the study period. At 60 months, the event-free survival was marginally higher for the treatment group as compared with the control group (81.1% vs 70.5%, P =.27). The proteinuria-free survival was similar at 82.9% and 79.3% for the treatment and control groups, respectively (P =.6); hypertension-free survival was 86.4% and 79.3% (P =.2). After 60 months of follow-up, the estimated glomerular filtration rate (GFR) was 108.1±29.0 mL/min/1.73 m2 for the treatment group and 105.7±17.7 mL/min/1.73 m2 for the control group (P =.7), but the difference was not statistically significant. None of the patients developed impaired renal function. The rate of GFR decline was similar between the treatment and control groups (−0.39±2.57 vs −0.59±1.63 mL/min/1.73 m2 per year, respectively, P =.7). In general, the study medication was well tolerated. Two patients needed to stop prematurely because of cough and dizziness. Conclusion: For early IgA nephropathy patients with minimal proteinuria, normal blood pressure, and normal renal function, treatment with 2.5 mg/daily of ramipril for 5 years does not offer any benefit. [Copyright &y& Elsevier]

Abstract: Aim: A prospective review of conservative management of primary non-refluxing megaureters (PM) was performed to determine the time taken for resolution (TTR) and complications. Material and Methods: Patient details were obtained from a prospectively maintained database from January 1, 2003, to December 31, 2011. The clinical features of USS and MAG3 findings were analyzed. All had annual USS and MAG 3 scans two yearly (and whenever necessary). Results: Fifty ureteric units (UU) in forty-four patients (six bilateral) were studied. There were thirty-three (75%) males. In the unilateral PM, 22/38 were left-sided. Children were classified according to the lower ureteric diameter (UD) into two groups: Group A (Gp A) UD <10mm (n=25, 26 UU), and Group B (Gp B) UD ≥10mm (n=19, 24 UU). Antenatal diagnosis was achieved in 21 (84%) UU in Gp A and 11 UU (58%) in Gp B. In Grp A, the median presenting UD was 6 (range 4–9)mm, and 76% resolved completely over a median duration of 60 (18–204)months. In Grp B, the median UD was 15 (10–27)mm, and 17% resolved completely over a median duration of 102 (42–210)months. Two developed ureteric calculi (removed ureteroscopically). Three with complications (obstructive drainage pattern in MAG 3 with decreasing function and debilitating infections) underwent ureteric tapering and reimplantation. An obstructed megaureter resolved after endoscopic dilatation. Another underwent temporary ureterostomy on developing hypertension. Conclusion: The exclusively conservative management of PM seems highly successful within Group A (i.e. UD <10mm). Complications (stones, decreasing renal function) were more common with higher UD. TTR seems to take over five years in both groups. [Copyright &y& Elsevier]

Abstract: Objective: Indications for pre-transplantation native nephrectomy (PTNN) include chronic renal parenchymal infection, proteinuria, intractable hypertension, polycystic kidneys and malignancy. Our aim was to establish the frequency and reasons for PTNN in children undergoing renal transplant at our center. Materials and methods: Children listed for renal transplant between 1998 and 2010 who underwent PTNN were analyzed. Etiology of established renal failure, indication for nephrectomy, stage of chronic kidney disease, laterality, complications, and timing of subsequent transplant were determined. Outcome of children, and that of preserved native kidneys following transplant, was reviewed. Results: 21/203 children listed for transplant (10.3%) underwent PTNN (32 nephrectomies). Indications were drug-resistant proteinuria (6 children), recurrent upper tract urosepsis (6), refractory hypertension (4), malignancy/malignant predisposition (4), concomitant procedure during ureterocystoplasty (1). Median age at nephrectomy was 3.3 years; 86% had impaired renal function at time of (first) nephrectomy. Median time until transplantation following bilateral nephrectomy was 1.7 years. 19/21 children have been transplanted; 17 reached stable graft function. Only 2 children who did not undergo PTNN required nephrectomy post-transplant. Conclusion: When malignancies were excluded, PTNN was performed in a minority (8.4%) of children, mainly for proteinuria. This adds great advantage by reducing morbidity. Resulting graft function seems favorable. [Copyright &y& Elsevier]

Summary: Urinary tract infections (UTIs) are one of the most common sources of bacterial infections among young febrile children. Accurate diagnosis of acute pyelonephritis (APN) and vesico-ureteral reflux (VUR) are important because of their association with renal scarring, sometimes leading to long-term complications. However, the gold standard examinations are either a DMSA scan for APN and scarring, or cystography for VUR, but both present limitations (feasibility, pain, cost, etc.). Procalcitonin, a reliable marker of bacterial infections, was demonstrated to be a good predictor of renal parenchymal involvement in the acute phase and in late renal scars, as well as of high-grade VUR. These findings need further broad validations and impact studies before being implemented into daily practice. However, procalcitonin may play a role in the complex and still debated picture of which examination should be performed after UTI in children. [Copyright &y& Elsevier]

Abstract: The role of arginine vasopressin (AVP) as a hypertensive hormone remains controversial. We have previously reported that intervention with a V1A receptor antagonist in 6-week-old prehypertensive spontaneously hypertensive rats (SHR) for 4 weeks attenuated the subsequent development of hypertension in adult SHR. This study assessed the age-dependent regulation of plasma AVP levels and kidney V1A and V2 receptor expression during the development of hypertension in SHR and in normotensive Sprague Dawley rats. Systolic blood pressure (SBP), plasma AVP, and plasma renin activity (PRA) and kidney V1A and V2 receptor expression were assessed. SHR were studied at three ages: prehypertensive (6 weeks), developed hypertension (10 weeks), and established hypertension (16 weeks). SBP increased with age in SHR (P < .01) and both plasma AVP (P < .01) and PRA (P < .05) were increased in 10-week-old SHR. Renal medulla V1A receptor gene expression decreased in 10-week and 16-week-old SHR (P < .01), with a reduction in V1A receptor protein in the inner medulla of 16-week-old SHR (P < .05) compared with young SHR. There was no change in V2 receptor expression during the development of hypertension. In normotensive rats, plasma AVP, PRA, and kidney V1A and V2 receptor expression were unchanged over time. These data suggest that in SHR, activation of plasma AVP and the renal V1A receptor occurs during developing hypertension, with downregulation when hypertension is established. The use of V1A receptor antagonists in prehypertension may provide a unique opportunity for the prevention of hypertension in high-risk individuals. [Copyright &y& Elsevier]

Abstract: Background: Ferulic acid (FA) is a naturally occurring nutritional compound. Although it has been shown to have antihypertensive effects, its effects on vascular function have not been intensively established. The aim of this study was to assess the vasoreactivity of FA in chronic two-kidney, one-clip (2K1C) renal hypertensive rats. Methods: Hypertension was induced in 2K1C rats by clipping the left renal artery and age-matched rats that received a sham treatment served as a control. Thoracic aortas were mounted in tissue baths to measure isometric tension. The effects of FA on vasodilatory responses were evaluated based on contractile responses induced by phenylephrine in the aortic rings obtained from both 2K1C and sham rats. Basal nitric oxide (NO) bioavailability in the aorta was determined by the contractile response induced by NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME). Results: FA induced concentration-dependent relaxation responses which were greater in 2K1C hypertensive rats than in sham-clipped control rats. This relaxation induced by FA was partially blocked by the removal of endothelium or by pretreating with l-NAME. l-NAME-induced contractile responses were augmented by FA in 2K1C rats, while no significant differences were noted in sham rats. FA improved acetylcholine-induced endothelium-dependent vasodilation in 2K1C rats, but not in sham rats. The simultaneous addition of hydroxyhydroquinone significantly inhibited the increase in acetylcholine-induced vasodilation by FA. Conclusion: These results suggest that FA restores endothelial function by altering the bioavailability of NO in 2K1C hypertensive rats. The results explain, in part, the mechanism underlying the vascular effects of FA in chronic renal hypertension. [Copyright &y& Elsevier]

Hypertensive renal disease occurs at increased frequency among the relatives of patients with this disease compared to individuals who lack a family history of disease. This suggests a heritable risk in which genetic variation may play a role. These observations have motivated a search for genetic variation contributing to this risk in both experimental animal models and in human populations. Studies of animal models indicate the capacity of natural genetic variants to contribute to disease risk and have produced a few insights into the disease mechanism. In its current phase, human population genetic studies have sought to associate genetic variation with disease in large populations by testing genotypes at a large number of common genetic variations in the genome, expecting that common genetic variants contributing to renal disease risk will be identified. These genome-wide association studies (GWAS) have been productive and are a clear technical success; they have also identified narrowly defined loci and genes containing variation contributing to disease risk. Further extension and refinement of these GWAS are likely to extend this success. However, it is also clear that few additional variants with substantial effects accounting for the greatest part of heritability will be uncovered by GWAS. This raises an interesting biological question regarding where the remaining unaccounted heritable risk may be located. At present, much consideration is being given to this question and to the challenge of testing hypotheses that lead from the various alternative mechanisms under consideration. One result of the progress of GWAS is likely to be a renewed interest in mechanisms by which related individuals can share and transmit traits independently of Mendelian inheritance. This paper reviews the current progress in this area and considers other mechanisms by which familial aggregation of risk for renal disease may arise. [ABSTRACT FROM AUTHOR]

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Renal medullary hypoxia-inducible factor ( HIF)-1α and its target genes, such as haem oxygenase and nitric oxide synthase, have been indicated to play an important role in the regulation of sodium excretion and blood pressure. HIF prolyl hydroxylase domain-containing proteins ( PHDs) are major enzymes to promote the degradation of HIF-1α. We recently reported that high salt intake suppressed the renal medullary PHD2 expression and thereby activated HIF-1α-mediated gene regulation in the renal medulla in response to high salt. To further define the functional role of renal medullary PHD2 in the regulation of renal adaptation to high salt intake and the longer term control of blood pressure, we transfected PHD2 expression plasmids into the renal medulla in uninephrectomized rats and determined its effects on pressure natriuresis, sodium excretion after salt overloading and the long-term control of arterial pressure after high salt challenge. It was shown that overexpression of PHD2 transgene increased PHD2 levels and decreased HIF-1α levels in the renal medulla, which blunted pressure natriuresis, attenuated sodium excretion, promoted sodium retention and produced salt sensitive hypertension after high salt challenge compared with rats treated with control plasmids. There was no blood pressure change in PHD2-treated rats that were maintained in low salt diet. These results suggested that renal medullary PHD2 is an important regulator in renal adaptation to high salt intake and a deficiency in PHD2-mediated molecular adaptation in response to high salt intake in the renal medulla may represent a pathogenic mechanism producing salt sensitive hypertension. [ABSTRACT FROM AUTHOR]

Summary: The posterior urethral valves (PUV) are the most common obstructive uropathy of the boy. It is a serious defect because that can lead to destruction of renal parenchyma and kidney failure. Aim: To clarify the clinical, radiological and outcome of this uropathy. Patients and methods: All children, managed for PUV during a period of 16 years (January 1996 to December 2011) in the paediatric surgery department “B”, of children''s hospital Bachir-Hamza of Tunis, were retrospectively studied. Results: A total of 38 boys were studied. Their age ranged from one day to 11 years. The diagnosis was made prenatally in ten cases and postnatally in the remaining cases during a urinary tract infection in 22 cases and voiding disorders in the remaining cases. All these children were investigated by renal ultrasound and retrograde cystourethrography (RCUG). Ultrasonography showed a bilateral uretero-hydronephrosis in 20 cases and unilateral in 11 patients with reduced renal parenchyma in 18 cases. The RCUG made the diagnosis of PUV in all cases, showing a dilated posterior urethra and distended bladder. Bladder diverticulum was seen in 25 cases and a vesicoureteral reflux (VUR) was present in 22 cases (bilateral in nine cases and unilateral in 13 cases). DMSA renal scintigraphy performed in 14 cases showed decreased uptake of cortical lesions in all cases with a non-functioning kidney in six cases. In addition to the correction of electrolyte disturbances and the appropriate antibiotics in case of urinary tract infections, treatment consisted of a first valve endoscopic section in 27 cases and a cystostomy in 11 cases. The immediate evolution was favourable in all cases, except two patients who died because of acute renal failure despite intensive resuscitation. In the long-term, ten patients progressed to end-stage renal failure (ESRF) and some of them are awaiting kidney transplant. Conclusion: Despite advances in diagnosis and management of posterior urethral valves, the prognosis of this uropathy remains subject to a significant risk of progression to ESRF. [Copyright &y& Elsevier]

The anatomical variations of the renal vein are uncommon and in the same time very important for the renal pathology. During a routine dissection on a 68-year old male cadaver we found a particular variation named retroaortic left renal vein (RA-LRV). Retroaortic left renal vein is characterized by the course of the left renal vein between the aorta and the vertebral column to drain into inferior vena cava. The clinical implications interest the cardiologists for renal hypertension, the surgeons operating for varicocele, renal transplantation and renal trauma. [ABSTRACT FROM AUTHOR]

Summary: Care of patients with type 1 diabetes (T1D) has changed during the past 30 years. Tools to control hyperglycemia have improved and it was shown that improvement in glycemic control diminished the risk of late diabetic complications, including nephropathy. Moreover, in patients with impaired renal function, aggressive treatment of hypertension and renoprotective blockade of the renin-angiotensin system were shown to postpone end-stage renal disease (ESRD), albeit for a short while. Despite these achievements, the incidence of ESRD caused by T1D in the US population has not decreased but rather has increased over the past 20 years, although it now occurs at slightly older ages. This state of affairs is a call to action. This should begin with adopting a new model of diabetic nephropathy in human beings. In that model, instead of microalbuminuria or proteinuria, the focus should be on diagnosis and treatment of progressive renal function decline that leads to ESRD. Such a model has received significant support in clinical and epidemiologic studies. Investigation of mechanisms of such progressive renal function decline should help in the identification of new therapeutic targets and the development of new interventions. To evaluate these interventions, accurate diagnostic algorithms are needed so T1D patients will be stratified according to time to onset to ESRD. Consistent with concepts of personalized medicine, the new interventions should be tailored to and evaluated in patients predicted to have rapid, moderate, or even slow progression to ESRD. [ABSTRACT FROM AUTHOR]

Recurrent urinary tract infection (UTI) raises a question mark regarding the anatomy and functionality of urinary apparatus of the child. Recurrent UTIs are common in children with renal malformations. Proper treatment can prevent or at least slow down the destruction of the renal parenchyma of the child until the renal abnormalities are, if possible, resolved. We will try to present a study on a small group of children with recurrent UTIs and secondary VUR, which releases secondary reflux, due to bladder diseases. Due to a study conducted over a period of 3 years, we found that bladder dysfunction of different causes may maintain VUR, and recurrent UTIs proper treatment helps maintain normal kidney function. Bladder dysfunction may be primary or secondary. Conclusion: Secondary VUR maintain recurrent urinary tract, and their correct treatment slows down the kidney destruction. [ABSTRACT FROM AUTHOR]

Abstract: We are reporting endovascular management of a renal artery aneurysm causing renal hypertension. The aneurysm by mass effect compressed the adjacent artery resulting in a hemodynamically significant stenosis. Endovascular management included embosphere embolization of the renal parenchyma distal to the stenosed segment and hydrocoil embolization of the aneurysm itself. [Copyright &y& Elsevier]

Despite the high rate of occurrence of both diabetes and hypertension in humans, the cardiovascular effects of the two conditions have not been investigated when they occur simultaneously. Thus this study examined the vascular effects of simultaneous type 2 diabetes and renal hypertension on endothelial function. Serum malondialdehyde and systolic blood pressure (SBP) were measured, glucose tolerance test (GTT) was performed, and concentration-response to phenylephrine (PE) in the absence and presence of nitro- l-arginine methyl ester ( l-NAME), acetylcholine and sodium nitroprusside were conducted on aortic rings from diabetic control, type 2 diabetes, sham-operated, renal hypertensive, and simultaneous type 2 diabetes plus hypertension rats respectively. Hypertension, diabetes, and simultaneous diabetes and hypertension were associated with either increased or decreased maximal responses ( Emax) of PE dependent on in the presence or absence of l-NAME. There was also increased serum malondialdehyde and decreased Emax of acetylcholine. Thus simultaneous hypertension and diabetes caused a greater decrease in Emax of acetylcholine compared to that seen with either diabetes or hypertension alone higher than that seen in hypertension. The blood glucose during GTT was lower than that seen in diabetes groups. Thus simultaneous type 2 diabetes and the SBP was renal hypertension is associated with improved glucose tolerance, but with further deterioration of endothelial dysfunction compared with either condition alone. [ABSTRACT FROM AUTHOR]

Hyperuricemia is particularly common in patients with arterial hypertension, metabolic syndrome, or kidney disease. Its role, however, as a risk factor for both renal and cardiovascular outcomes and in the context of the well-established interrelationship between cardiovascular disease and chronic kidney disease (CKD) is debated. For decades high serum uric acid levels were mainly considered the result of renal dysfunction and not a true mediator of renal disease development and progression. However, recent epidemiological studies suggest an independent association between asymptomatic hyperuricemia and increased risk of arterial hypertension, CKD, cardiovascular events, and mortality. Furthermore, data from experimental models of hyperuricemia have provided robust evidence in this direction. Hyperuricemia causes increased arterial pressure, proteinuria, renal dysfunction, and progressive renal and vascular disease in rats. The main pathophysiological mechanisms of these deleterious effects caused by uric acid are endothelial dysfunction, activation of local renin-angiotensin system, increased oxidative stress, and proinflammatory and proliferative actions. A small number of short-term, single-center clinical studies support the beneficial influence of pharmaceutical reduction of serum uric acid on total cardiovascular risk, as well as on renal disease development and progression. Hyperuricemia is probably related to the incidence of primary hypertension in children and adolescents, as serum uric acid lowering by allopurinol has an antihypertensive action in this group of patients. Finally, it is clear that adequately powered randomized controlled trials are urgently required to elucidate the role of uric acid in cardiovascular events and outcomes, as well as in the development and progression of CKD. [ABSTRACT FROM AUTHOR]

Reno-protective strategies are needed to improve renal outcomes in patients with atherosclerotic renal artery stenosis (ARAS). Adipose tissue-derived mesenchymal stem cells (MSCs) can promote renal regeneration, but their potential for attenuating cellular injury and restoring kidney repair in ARAS has not been explored. We hypothesized that replenishment of MSC as an adjunct to percutaneous transluminal renal angioplasty (PTRA) would restore renal cellular integrity and improve renal function in ARAS pigs. Four groups of pigs ( n = 7 each) were studied after 16 weeks of ARAS, ARAS 4 weeks after PTRA and stenting with or without adjunct intrarenal delivery of MSC (10 × 106 cells), and controls. Stenotic kidney blood flow (renal blood flow [RBF]) and glomerular filtration rate (GFR) were measured using multidetector computer tomography (CT). Renal microvascular architecture (micro-CT), fibrosis, inflammation, and oxidative stress were evaluated ex vivo. Four weeks after successful PTRA, mean arterial pressure fell to a similar level in all revascularized groups. Stenotic kidney GFR and RBF remained decreased in ARAS ( p = .01 and p = .02) and ARAS + PTRA ( p = .02 and p = .03) compared with normal but rose to normal levels in ARAS + PTRA + MSC ( p = .34 and p = .46 vs. normal). Interstitial fibrosis, inflammation, microvascular rarefaction, and oxidative stress were attenuated only in PTRA + MSC-treated pigs. A single intrarenal delivery of MSC in conjunction with renal revascularization restored renal hemodynamics and function and decreased inflammation, apoptosis, oxidative stress, microvascular loss, and fibrosis. This study suggests a unique and novel therapeutic potential for MSC in restoring renal function when combined with PTRA in chronic experimental renovascular disease. S TEM C ELLS 2012;30:1030-1041 [ABSTRACT FROM AUTHOR]

High blood pressure in children and adolescents is a growing health problem that is often overlooked by physicians. Normal blood pressure values for children and adolescents are based on age, sex, and height, and are available in standardized tables. Prehypertension is defined as a blood pressure in at least the 90th percentile, but less than the 95th percentile, for age, sex, and height, or a measurement of 120/80 mm Hg or greater. Hypertension is defined as blood pressure in the 95th percentile or greater. A secondary etiology of hypertension is much more likely in children than in adults, with renal parenchymal disease and renovascular disease being the most common. Overweight and obesity are strongly correlated with primary hypertension in children. A history and physical examination are needed for all children with newly diagnosed hypertension to help rule out underlying medical disorders. Children with hypertension should also be screened for other risk factors for cardiovascular disease, including diabetes mellitus and hyperlipidemia, and should be evaluated for target organ damage with a retinal examination and echocardiography. Hypertension in children is treated with lifestyle changes, including weight loss for those who are overweight or obese; a healthy, low-sodium diet; regular physical activity; and avoidance of tobacco and alcohol. Children with symptomatic hypertension, secondary hypertension, target organ damage, diabetes, or persistent hypertension despite nonpharmacologic measures should be treated with antihypertensive medications. Thiazide diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta blockers, and calcium channel blockers are safe, effective, and well tolerated in children. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the anatomical and functional renal alterations and the association with post-traumatic arterial hypertension. Methods: The studied population included patients who sustained high grades renal injury (grades III to V) successfully non-operative management after staging by computed tomography over a 16-year period. Beyond the review of medical records, these patients were invited to the following protocol: clinical and laboratory evaluation, abdominal computed tomography, magnetic resonance angiography, DMSA renal scintigraphy, and ambulatory blood pressure monitoring. The hypertensive patients also were submitted to dynamic renal scintigraphy (99mTc EC), using captopril stimulation to verify renal vascular etiology. Results: Of the 31 patients, there were thirteen grade III, sixteen grade IV (nine lacerations, and seven vascular lesions), and two grade V injuries. All the patients were asymptomatic and an average follow up post-injury of 6.4 years. None had abnormal BUN or seric creatinine. The percentage of renal volume reduction correlates with the severity as defined by OIS. There was no evidence of renal artery stenosis in Magnetic Resonance angiography (MRA). DMSA scanning demonstrated a decline in percentage of total renal function corresponding to injury severity (42.2 ± 5.5% for grade III, 35.3 ± 12.8% for grade IV, 13.5 ± 19.1 for grade V). Six patients (19.4%) had severe compromised function (< 30%). There was statistically significant difference in the decrease in renal function between parenchymal and vascular causes for grade IV injuries (p < 0.001). The 24-hour ambulatory blood pressure monitoring detected nine patients (29%) with post-traumatic hypertension. All the patients were male, mean 35.6 years, 77.8 % had a familial history of arterial hypertension, 66.7% had grade III renal injury, and average post-injury time was 7.8 years. Seven patients had negative captopril renography. Conclusions: Late results of renal function after conservative treatment of high grades renal injuries are favorable, except for patients with grades IV with vascular injuries and grade V renal injuries. Moreover, arterial hypertension does not correlate with the grade of renal injury or reduction of renal function. [ABSTRACT FROM AUTHOR]

Abstract: Acute kidney injury (AKI) is the most common nephrological emergency encountered in tropical countries. The reported incidence of AKI in different regions of the world is widely variable. In developed countries, the incidence of hospital-acquired AKI exceeds that of community-acquired AKI by 5–10 times. Poverty, poor sanitation, and climatic conditions aggravate renal disease in the tropics. Tropical infections can lead to AKI by direct invasion of the renal parenchyma with microbial agents, induction of an immune response leading to renal inflammation, or tubular necrosis due to haemodynamic disturbances and at times due to iatrogenic renal injury associated with treatment or prophylaxis against tropical infections. Clinical features may be due to systemic manifestations of the etiology responsible for AKI and the renal manifestations. The mortality due to AKI in tropics at a primary health center may reach up to 80% and it is reported to be between 20% and 30% in the referral hospitals. [Copyright &y& Elsevier]

Background and Purpose: Radiofrequency (RF) is an efficient, inexpensive, safe, and friendly option for the management of small renal tumors. The objective was to evaluate the ideal temperature for renal cell destruction in dogs by RF and to verify whether the injection of vasoactive drugs, such as prostaglandin E1 and adrenaline, can help to improve the results, compared with 'dry' RF ablation. Materials and Methods: The study was divided into three phases: Initially, 16 dogs of comparable weight underwent RF ablation of the renal parenchyma at temperatures of 80°C, 90°C, and 100°C. After that, seven other dogs received adrenaline (vasoconstrictor) and seven received prostaglandin E1 (vasodilator). Finally, the results from 14 animals were compared with those of the 16 (dry RF) dogs at the optimum temperature found. After 14 days, the animals underwent nephrectomy to evaluate the size of the lesions (width and depth), histology examination, and were then sacrificed. Results: There were no clinical or surgical complications in any of the dogs, and none died before the 14th day after the procedure. The optimum temperature was found to be 90°C. Prostaglandin E1 resulted in significantly larger lesions (in depth and width) than adrenaline, with lower impedance. Prostaglandin did not increase the lesions compared with dry RF. All the kidneys presented total coagulation necrosis, with no viable cells in the histologic analysis of the treated tissue. Conclusion: In the ablation of renal cells by RF, prostaglandin produced larger lesions (in depth and width) than the same procedure using adrenaline, and its performance was similar to that of RF without injection of drugs. [ABSTRACT FROM AUTHOR]

Abstract: The prevalence of hypertension in children is reported to be 1-3%. In recent years, the prevalence of hypertension in school-aged children appears to be increasing, perhaps as a result of the increased prevalence of obesity (Sorof JM, Lai D, Turner J, Poffenbarger T, Portman PJ. Overweight, ethnicity and the prevalence of hypertension in school-aged children. Pediatrics 2004;113:475-82.). The majority of these children have mild hypertension, most often primary. However, secondary causes of hypertension such as renal parenchymal diseases and renovascular disorders still remain the leading cause of paediatric hypertension, particularly in children < 12 years of age. Regardless of its cause, the significant elevation of blood pressure can lead to acute organ dysfunction, and hypertensive child almost always warrants a diagnostic evaluation. [Copyright &y& Elsevier]

Abstract: Objectives: To assess the predictive importance of ultrasonic grade 1 hyperechogenicity in potential live related kidney donors in the absence of urinary abnormalities and with perfect renal function. Subjects and methods: The study included 34 potential living related kidney donors with this abnormality; their mean (SD, range) age was 32.7 (8.45, 23–48) years. Ten matched healthy donors with normal ultrasonographic appearance of the kidneys were studied as controls. All cases were thoroughly investigated, including measuring glomerular filtration rate by isotopic scintigraphy. The renal reserve was estimated by dopamine and amino-acid infusion in all subjects (study and control groups). A percutaneous renal biopsy was taken from 17 subjects in the abnormal echogenicity group and open renal biopsy was taken from eight of the control subjects. Results: The renal reserve was comparable in both groups. Abnormal histopathological changes were found in seven subjects (41%) of the abnormal echogenicity group, i.e. partial glomerulosclerosis in one, mesangial thickening in two, interstitial fibrosis in one, focal tubular atrophy in one, immunoglobulin (Ig M) immune deposits in three and IgA in one. Only one subject in the control group showed mild mesangial thickening. Conclusion: Grade 1 echogenicity might be a sign of unrecognized kidney disease. Renal biopsy is mandatory when such related donors are the only available ones. Abnormal histopathology contraindicates donation. [Copyright &y& Elsevier]

We describe a new renal displacement technique using an 18-gauge needle to facilitate superior calix puncture and consequently to decrease intrathoracic morbidity. Initially, a lower or middle calix is punctured with an 18-gauge needle. Then, the proximal end of the needle is progressively pushed in the cephalic direction. Therefore, the kidney is pushed caudally by the lever maneuver. This technique has also been used to immobilize the kidney or to reorient complex and malrotated kidneys. [ABSTRACT FROM AUTHOR]

Abstract: Aims: To examine the vasodilatation induce by the NO donors, [Ru(terpy)(bdq)NO]3+ (TERPY) and sodium nitroprusside (SNP), and to compare their effects in aortic rings from hypertensive 2K-1C and normotensive 2K rats. Main methods: Vascular reactivity was performed in aortic rings pre-contracted with phenylephrine (Phe 100nM). We have analyzed the maximal relaxation (Emax) and potency (pD2) of NO donors. Key findings: Potency of SNP was greater than TERPY in both arterial groups. The vasodilatation induced by TERPY was greater in 2K than in 2K-1C, and it was inhibited by sGC inhibitor ODQ in 2K and in 2K-1C aortic rings. ODQ did not alter the efficacy to SNP, but it reduced its potency in 2K and 2K-1C. The blockade of K+ channels reduced the potency of TERPY only in aortic rings of 2K. On the other hand, the potency of SNP was reduced in both 2K and 2K-1C. The combination of ODQ and TEA reduced the relaxation induced by TERPY and SNP in 2K and reduced the efficacy to SNP in 2K-1C aortic rings but it had no additional effect on the TERPY relaxation in 2K-1C aortas. The production of cGMP induced by TERPY was greater than that produced by SNP, which was similarly increased in 2K and 2K-1C. Sarcoplasmic reticulum Ca-ATPase inhibition only impaired the relaxation induced by SNP in 2K aortic rings. Significance: Taken together, our results provide evidences that in this model of hypertension, impaired K+ channels activation by TERPY and SERCA activation by SNP may contribute to decreased vasodilatation. [Copyright &y& Elsevier]

The goals of postnatal management of congenital anomalies of the kidneys and the urinary tracts are two: The first to distinguish between patients (the minority) who are at risk for renal parenchyma damage, from neonates (the majority) who have not consequences to renal functionality; the second to avoid for healthy infant strenuous follow-up, painful diagnostic procedures, and unnecessary anxiety for their parents. [ABSTRACT FROM AUTHOR]

Hypertension is a chronic disorder which often entails debilitating cardiovascular and renal complications. Hypertension mostly arises as a complex quantitative trait that is affected by varying combinations of genetic and environmental factors. Secondary hypertension has been encountered with increasing frequency. The common causes of secondary hypertension include renal parenchymal disease, renal artery stenosis, primary aldosteronism, phaeochromocytoma, and Cushing's syndrome. The detection of a secondary cause is of the utmost importance because it provides an opportunity to convert an incurable disease into a potentially curable one. Early identification and treatment will provide a better opportunity for cure, prevent target organ damage, reduce socioeconomic burden and health expenditure associated with drug costs, and improve patients' quality of life. Hence, it is a condition not to be missed. [ABSTRACT FROM AUTHOR]

The brachial-ankle pulse wave velocity (baPWV) is a useful index of arterial stiffness. Mean platelet volume (MPV), an indicator of platelet activation, is associated with hypertension, stroke, and coronary artery disease, all of which may be caused by arteriosclerosis. However, little research has been conducted to investigate the relationship between MPV and arterial stiffness. In this cross-sectional study, we investigated the relationship between platelet count, MPV, and baPWV in 2645 apparently healthy Chinese participants (1676 men, 969 women) in a general health examination. Different metabolic parameters were compared across MPV quintiles (Q1: ≤≤8.1 fl, Q2: 8.2--8.5 fl, Q3: 8.6--9.6 fl, Q4: 9.7--10.7 fl, and Q5: ≥≥10.8 fl). Age-adjusted mean values of baPWV gradually increased with MPV quintiles (Q1 == 1124, Q2 == 1134, Q3 == 1199, Q4 == 1207, and Q5 == 1270 cm/s). Univariate analysis showed that age, sex, smoking status, body mass index (BMI), systolic blood pressure (SBP), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), total platelet count, and MPV were significantly associated with baPWV. In addition, age, sex, BMI, MPV, SBP, and FPG were significant factors in the multivariate model with baPWV. Notably, MPV was found to be a significant determinant for baPWV (ββ == 0.198; P < 0.001). The findings show that elevated MPV is positively correlated to arterial stiffness. [ABSTRACT FROM AUTHOR]

The present study evaluated pAKT, pmTOR, and PTEN expression in a tissue microarray of primary renal cell carcinomas (PRCCs), their metastases, and normal renal parenchyma (NRP) (N = 45) by means of immunohistochemistry. Metastases in most subcellular compartments showed comparable and stronger expression for pAKT, pmTOR, and PTEN than PRCC and NRP, which was even more pronounced in patients with high-risk Memorial Sloan-Kettering Cancer Center (MSKCC) score. Furthermore, most subcellular compartments showed no differences between lymphogenous, haematogenous, synchronous, and metachronous metastases, which is interesting with regard to sensitivity to mTOR inhibitor therapy in metastasized RCCs with alterations in the PI3K/AKT pathway. [ABSTRACT FROM AUTHOR]

Ask-Upmark kidney is a rare diagnosis of segmental hypoplasia in pediatric population clinically characterized by severe hypertension potentially treatable with partial to total nephrectomy. Although originally was described only as a congenital anomaly, recent data suggest to be caused by vesicoureteral reflux, either in utero or in early childhood and pyelonephritis. The case we reported indicates that Ask-Upmark kidney should be considered as potential cause of hypertension and renal failure both in children and adults. The renal biopsy is necessary for early diagnosis and may consent to normalize blood pressure with nephrectomy; however, if renal damage is severe and progressive with tubulointerstitial nephritis, surgical management is excluded and renal transplant should be considered. [ABSTRACT FROM AUTHOR]

ABSTRACT: Aim: To investigate whether the presence of multiple renal arteries in the remnant kidney has implications for lower renal function or increased incidence of hypertension. Methods: We reviewed the intraoperative and follow-up data of 101 live kidney donors who underwent nephrectomies at our institution. Sixty-nine donors (68.3%) had single artery in the remnant kidney (Group A), while 32 donors (31.7%) had multiple renal arteries in the remnant kidney (Group B). We compared the demographic and intraoperative data between the two groups. The follow-up data of donors in each group were divided into three subgroups based on the length of the follow-up period (12-24 months, 24-48 months and ≥48 months). Subgroups were created based on blood pressure and serum creatinine level. The δblood pressure (follow-up blood pressure minus preoperative blood pressure) and δserum creatinine (follow-up serum creatinine minus preoperative serum creatinine) in each subgroup in Group A were compared with the counterparts in Group B. Results: Renal arterial stenosis and calcification of renal arterial wall were not observed in all donors. There were no significant differences in the intraoperative characteristics (e.g. age, body mass index, operative duration and estimated blood loss) between the two groups. In addition, the blood pressure and serum creatinine level among subgroups within each group were similar. Furthermore, significant differences in δblood pressure and δserum creatinine were not observed between subgroups within the same follow-up period. Recipient survival rate and serum creatinine level were similar and acceptable in both groups. Conclusions: The presence of multiple renal arteries in the remnant kidney does not have additional negative influence on kidney donors after kidney donation. [ABSTRACT FROM AUTHOR]

Background: In patients with autosomal dominant polycystic kidney disease (ADPKD), renal cysts grow exponentially. Since remaining renal parenchyma has a capacity to compensate for the loss of glomerular filtration, the glomerular filtration rate (GFR) may be sustained until the disease progresses. The purpose of this study was to determine if renal volumetric indices and clinical parameters are associated with renal function in Japanese patients with ADPKD. Methods: In 73 ADPKD patients (28 men, 45 women), the associations of mean systolic blood pressure, mean diastolic blood pressure, estimated GFR (eGFR), the amount of proteinuria and albuminuria, body mass index (BMI), brachial-ankle pulse wave velocity (baPWV), ankle-brachial index, and total kidney volume (TKV) were retrospectively analyzed. Results: Multivariate linear regression analysis showed that eGFR was significantly and independently inversely correlated with patients' age and BMI. The median change in eGFR per year (ΔeGFR/y) was −2.8 ml/min/1.73 m/year. Multiple linear regression analysis showed that ΔeGFR/y was significantly and independently inversely correlated with the change in TKV per year (ΔTKV/y). Multiple linear regression analysis showed that ΔTKV/y was significantly related to initial TKV and the change in albuminuria per year. Conclusions: This study demonstrated a significant relationship between the change in renal function and the change in renal volume in Japanese ADPKD patients without renal insufficiency. It is possible that the volume measurements can be used as useful markers for disease progression in Japanese ADPKD patients. [ABSTRACT FROM AUTHOR]

The mesonephroi of two groups of Rana esculenta collected from two rice fields near Pavia, one relatively unpolluted and one polluted, were morphologically and histochemically investigated. Light and electron microscopy analyses were performed and certain enzyme activities studied (succinic dehydrogenase, SDH, alkaline phosphatase, AlkPase, acid phosphatase, AcPase, catalase, CAT, and NOS-related nicotinamide adenine dinucleotide phosphatase, NOS/NADPHd). The expression of the inducible NOS (iNOS) was evaluated through immunohistochemistry. In the renal parenchyma of the polluted group some structural modifications, mainly in the glomeruli and the proximal tubule epithelium, were observed. Peritubular inflammatory foci in most polluted samples were often found to be in combination with parasitic cysts. However, no necrotic processes were found in the renal parenchyma. Compared to controls, the histochemical studies on contaminated frogs evidenced an increase of the AcPase, NOS and CAT activities, and of the iNOS immunoexpression as well. All the results showed a good correspondence between the biomarkers responses and the environmental stress conditions. Overall, we can state that studying the sub-lethal effects of contamination in amphibians naturally exposed to toxicants has shown to be significant for the assessment of site-specific risk and potential hazards behind the phenomenon of progressive amphibian decline. [Copyright &y& Elsevier]

Abstract: The 2 kidney, 1-clip (2K, 1C) model of hypertension was used to investigate the potential antihypertensive effect of a standardized leaf extract of Ginkgo biloba (EGb 761). Clipping of the renal artery resulted in gradual elevation of the systolic blood pressure (SBP) reaching a plateau after 4 weeks of surgery. Treatment of hypertensive rats with EGb 761 (60, 90, 180mg/kg/day orally) was therefore started 4 weeks after surgery and continued for 3 weeks. This led to a dose-dependent reduction in SBP with no significant change in heart rate. Control hypertensive rats showed a significant elevation of total protein thiols (Pr-SHs level) in both clipped and non-clipped kidneys as well as in the serum. However, glutathione peroxidase (GSH-Px) activity was decreased in the clipped kidneys but elevated in the non-clipped ones and in the blood. The malondialdehyde (MDA) level was raised in clipped kidneys but not in non-clipped ones nor in the serum. Nitric oxide (NO level) and angiotensin converting enzyme (ACE) activity were increased in both clipped and non-clipped kidneys but not in the serum. Endothelium-dependent and -independent relaxation of aortic rings towards acetylcholine (Ach) and sodium nitroprusside (SNP) were impaired. Treatment with EGb 761 (180mg/kg/day for 3 weeks) was associated with recovery of GSH-Px activity in clipped kidneys, inhibition of ACE activity in both kidneys and a reduction in the elevated NO level of the non-clipped kidneys, decreased responsiveness to the vasoconstrictor NE and improvement of endothelial function as evidenced by restoration of endothelium-dependent vasorelaxation induced by Ach. The observed beneficial effects of the EGb 761 may be attributed to different factors, including ACE inhibition and maintenance of cellular antioxidant capacity as well as preserving vascular reactivity towards endothelium-dependent and -independent vasodilators while inhibiting responses to vasoconstrictors. [Copyright &y& Elsevier]

Percutaneous transluminal renal stenting (PTRS) does not consistently improve renal function in patients with atherosclerotic renovascular disease, but the mechanisms underlying irreversible kidney injury have not been fully elucidated. We hypothesized that renal dysfunction after PTRS is linked to ongoing renal microvascular (MV) remodeling. Pigs were studied after 10 wk of atherosclerosis and renal artery stenosis (ARAS), ARAS treated with PTRS 4 wk earlier, and normal controls (n = 10 each). Renal blood flow (RBF) and glomerular filtration rate (GFR) were studied using multidetector computer tomography. Renal microvascular architecture (micro-CT), angiogenic activity, oxidative stress, and fibrosis were evaluated ex vivo. Four weeks after PTRS, blood pressure was normalized. However, GFR and RBF remained similarly decreased in untreated ARAS and ARAS+PTRS (P < 0.05 vs. normal). MV rarefaction was unaltered after revascularization, and the spatial density of outer cortical microvessels correlated with residual GFR. Interstitial fibrosis and altered expression of proangiogenic and profibrotic factors persisted after PTRS. Tubulointerstitial injury in ARAS persisted 4 wk after mechanically successful PTRS, and vessel loss correlated with residual renal dysfunction. MV loss and fibrosis in swine ARAS might account for persistent renal dysfunction after PTRS and underscore the need to assess renal parenchymal disease before revascularization. [ABSTRACT FROM AUTHOR]

Heme oxygenase (HO) is an enzyme that is involved in numerous secondary actions. One of its products, CO, seems to have an important but unclear role in blood pressure regulation. CO exhibits a vasodilator action through the activation of soluble guanylate cyclase and the subsequent production of cyclic guanosine monophosphate (cGMP). The aim of the present study was to determine whether pathological and pharmacological HO-1 overexpression has any regulatory role on blood pressure in a renovascular model of hypertension. We examined the effect of zinc protoporyphyrin IX (ZnPP-IX) administration, an inhibitor of HO activity, on mean arterial pressure (MAP) and heart rate in sham-operated and aorta-coarcted (AC) rats and its interaction with the nitric oxide synthase (NOS) pathway. Inhibition of HO increased MAP in normotensive rats with and without hemin pretreatment but not in hypertensive rats. Pretreatment with NG-nitro-L-arginine methyl ester blocked the pressor response to ZnPP-IX, suggesting a key role of NOS in the cardiovascular action of HO inhibition. In the same way, AC rats, an experimental model of hypertension with impaired function and low expression of endothelial NOS (eNOS), did not show any cardiovascular response to inhibition or induction of HO. This finding suggests that eNOS was necessary for modulating the CO response in the hypertensive group. In conclusion, the present study suggests that HO regulates blood pressure through CO only when the NOS pathway is fully operative. In addition, chronic HO induction fails to attenuate the hypertensive stage induced by coarctation as a consequence of the impairment of the NOS pathway. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Nutcracker syndrome (NS) refers to compression of the left renal vein between the aorta and the superior mesenteric artery which results in left renal venous hypertension. The typical clinical presenting feature is hematuria. In this report we describe the case of patient with a single kidney who developed severe proteinuria due to NS. She was successfully treated with left renal vein transposition. This case clearly shows the relation between NS and severe proteinuria based on normal biopsy findings and the complete disappearance of proteinuria following surgery. [ABSTRACT FROM AUTHOR]

AbstractPurpose:To compare the effects of one-stage vsgradual dilation techniques during percutaneous nephrolithotomy (PCNL) on postoperative renal scar formation and overall renal function.Patients and Methods:Of 152 adult patients who underwent surgery during the study period, 48 were randomized into two groups. In group 1 (n=19), gradual tract dilation with Alken metallic dilators was used, and in group 2 (n=29), one-stage tract dilation was used. We compared patient demographics, intraoperative and preoperative parameters, postoperative overall renal function, and renal scar formation on the target renal pole.Results:Access time (P=0.001; 95% confidence interval [CI]: 3.19–6.30) and radiation exposure during access (P=0.03; 95% CI: 0.03–0.66) were significantly shorter in group 2. In group 1, the decrease in mean technetium-99m dimercaptosuccinic acid (99m-Tc DMSA) uptake from 44.1±20.1% to 43.4±19.6% 4 weeks postoperatively (–0.7%±0.5%; P=0.27; 95% CI: –0.56–1.93) was not significant. In group 2, however, there was a significant decrease in post-PCNL 99m-Tc DMSA uptake 2 (–2.4±0.3%, from 50.1±13.5% to 47.7±13.8%; P=0.001; 95% CI: 1.13–3.66). Four weeks after surgery, new scar formation or progression of the preoperative scar at the site of access were seen in 14 of 29 (48.3%) patients who were treated with one-stage dilation whereas only 2 of 19 (11.0%) patients who were treated with gradual dilation developed new scarring at the access site (P=0.007).Conclusion:Although the one-stage tract dilation technique reduced radiation exposure and access time, in the short term, it may cause more parenchymal damage than the gradual dilation technique. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: The aim of this retrospective study was to report the author’s experience of the surgical treatment of renovascular hypertension in children and to define the role of surgery in its treatment. Material and methods: This series includes 85 patients (50 girls, 35 boys), 28 months to 18 years of age (mean: 10.3) operated on from 1970 to 2005. All patients had arterial hypertension and underwent the investigations usually performed in hypertensive patients. Renal artery lesions were bilateral in 26 cases. Due to bilateral procedures and to secondary or late reoperations, the number of surgical procedures was 114 (15 nephrectomies and 99 arterial repairs). Results: Fibrodysplasia of the renal artery was the prevailing pathologic factor (71%). Associated vascular lesions were observed in 61% of the patients. There was no postoperative death in this series. Seven postoperative thromboses occurred (7% of the repairs). The complete cure of arterial hypertension was obtained in 82% of the patients. In young children, growth of the repairs was normal when age increased. Conclusion: Surgery still holds a prominent place in the treatment of renovascular hypertension in children. Its prognosis is favourable since atheroma or organ lesions are usually lacking. [Copyright &y& Elsevier]