Left ventricular remodeling and arterial remodeling in patients with chronic kidney disease stage 1–3

Abstract

Introduction: Chronic kidney disease (CKD) is an independent factor for cardiovascular system complications, such as arterial hypertension, left ventricular hypertrophy (LVH), heart failure or accelerated atherosclerosis progression. The aim of the paper was to analyze left ventricular and arterial remodeling in patients with CKD stages 1–3 to identify the subclinical marker of cardiovascular system damage which changes first in the course of CKD. Methods: The examined group consisted of 90 patients with CKD stage 1–3 and 30 subjects constituting the control group. Left ventricular mass index (LVMI), left ventricular relative wall thickness (RWT) and ejection fraction (EF) were determined by echocardiographic examination. Pulse wave velocity (PWV) between the carotid and femoral arteries as well as common carotid artery intima–media thickness (IMT) was measured. 24-h ambulatory blood pressure monitoring was performed in all subjects. Results: No differences were found between blood pressure values in the examined groups of patients with CKD1, CKD2 and CKD3. Concentric remodeling was found in 20.0%, concentric hypertrophy in 22.2% and eccentric hypertrophy in 18.9% of patients. LVMI values in patients with CKD2 and 3 were higher than in the control group. IMT values in patients with CKD3 were higher than in patients with CKD2. PWV in patients with stage 3 CKD was significantly higher than in the control group (p?<?0.05). Conclusions: In the course of CKD, the left ventricle undergoes remodeling earlier than large arterial vessels. Echocardiographic assessment of LVH in early stages of CKD may identify patients at increased cardiovascular risk.     

Serum cystatin C and left ventricular diastolic dysfunction in children with chronic kidney disease

Previous studies indicate that serum cystatin C predicts incident heart failure in older adults. Children with chronic kidney disease (CKD) develop left ventricular (LV) diastolic dysfunction, often the initial abnormality of cardiac function. We hypothesized that cystatin C might predict LV diastolic dysfunction in children with CKD. Fifty-seven subjects, aged 6–21 years, with stage 2–4 CKD underwent echocardiography. Diastole was assessed from transmitral Doppler [maximum early (E wave) and late (A wave) diastolic flow velocities (E/A ratio)] and from tissue Doppler [septal mitral annular peak velocities (E′)]. LV filling pressures were determined, using a ratio of E/E′. Fourteen (25%) patients had low E′ and 15 (26%) had high E/E′. Children with abnormal E′ or E/E′ had significantly higher cystatin C levels than children with normal indices (P<0.05). Neither serum creatinine nor measured glomerular filtration rate (GFR) significantly correlated with E’ or E/E’. Stepwise multiple regression analysis showed that cystatin C (β=−0.825, P=0.023) and left ventricular mass (LVM) index (β=0.099, P=0.006) independently predicted E′; LVM index independently predicted E/E′ (β=0.0173, P=0.01). We conclude that, in contrast to measured GFR or serum creatinine level, elevated serum cystatin C might be associated with diastolic dysfunction in children with CKD.     

How to define anemia in children with chronic kidney disease?

In a cross-sectional study, we compared the prevalence of anemia based on age- and gender-specific reference intervals for hemoglobin (Hgb) and hematocrit (Hct) with the Kidney Disease Outcomes Quality Initiative (KDOQI) anemia definition (Hgb < 110 g/L) in 351 children with chronic kidney disease (CKD) stages I–V. Cystatin C-based GFRs were 122 ± 36 mL/min/1.73 m² in patients with stage I CKD (n = 196), 76 ± 8 mL/min/1.73 m² for stage II (n = 104), 45 ± 9 mL/min/1.73 m² for stage III (n = 36), and 22 ± 5 mL/min/1.73 m² in patients with stage IV+V CKD (n = 15). Fifty-nine patients received iron therapy and 32 patients were treated with Darbepoetin. For Hgb, a total of 90 patients fit the age and gender derived criteria, compared to only 54 patients identified by the KDOQI guidelines (p = 0.0010). Similarly, for Hct, a total of 78 patients fit the age and gender derived criteria, which was a significantly higher proportion than the 56 identified by the KDOQI guidelines (r = 0.22, p = 0.0435). There was a significant correlation between the GFR and both the Hgb Z-score (p = 0.0068) and the Hct Z-score (p = 0.0128). There was poor agreement between conventional and KDOQI definitions of anemia in children with CKD.     

Determinants of the intima–media thickness in children and adolescents with chronic kidney disease

The aim of the study was to evaluate changes in the arterial wall in children with chronic kidney disease (CKD). We studied 60 patients: 32 with stages 2–4 CKD [chronic renal failure (CRF)], 28 with stage 5 CKD [end-stage renal disease (ESRD)], and 43 controls (C). The evaluated parameters included intima–media thickness (IMT) of the carotid arteries, bone mineral density (BMD), serum lipid levels, and parameters of the calcium–phosphorus metabolism. Patients were divided into two groups: group 1 with normal arteries, and group 2 with arterial changes. The highest serum fetuin A level was found in group 1 compared with groups 2 and C. A negative correlation between IMT and fetuin A level was found. In patients with ESRD, a positive correlation of IMT with phosphorus level and age and a negative correlation with cyclase-activating parathyroid hormone and cyclase inhibiting parathyroid hormone (CAP/CIP) ratio was observed. Multiple linear regression showed that lower fetuin-A and alkaline phosphatase (AP) levels and higher lumbar spine BMD independently predicted higher IMT. Arterial wall changes in children with CKD were related to lower fetuin A and AP level and higher BMD. Low CAP/CIP and high phosphorus level may also be significant factors for arterial changes in patients with ESRD.     

Classification of metaphyseal change with magnetic resonance imaging in Legg-Calvé-Perthes disease

Seventy-eight patients (85 affected hips and 71 unaffected hips) with Legg-Calvé-Perthes disease were included in this study to evaluate the metaphyseal change in radiographs and magnetic resonance imaging (MRI) and to define the type of the metaphyseal cyst according to presence or absence of the epiphyseal involvement. The content of the metaphyseal cyst was evaluated by using T1,T2, proton, and gadolinium-enhanced T1-weighted MRI scans. Among 85 hips, there were no changes in 32 hips, marrow edema in 13 hips, false cyst with epiphyseal involvement in 28 hips, and true cyst without epiphyseal involvement in 12 hips. Granulation tissue was found in the false cysts and water-rich fibrotic tissue was found in the true cysts based on the MRI scans. The metaphyseal change in MRI scans was shown in 71% of groups 3 and 4 and in 35% of groups 1 and 2 according to the Catterall classification, and 52% of group A, 56% of group B, and 86% of group C according to the Herring classification. Of the 30 hips at the avascular stage, 33% showed metaphyseal cyst in MRI scans. Of the 53 hips at the fragmentation stage, 60% showed the metaphyseal cyst.     

Uraemic vasculopathy in children with chronic kidney disease: prevention or damage limitation?

Since the inception of pediatric dialysis programmes nearly 50 years ago, there have been vast improvements in both the technology and expertise in the care of children with chronic kidney disease (CKD). Nevertheless, children on dialysis continue to have a significantly higher mortality than their healthy peers and cardiovascular disease (CVD) is the most common cause of death in this group. Chronic kidney disease is described as the “perfect storm” of risk factors for CVD development, and vascular calcification is a highly regulated cell-mediated process with several promoters and inhibitors of calcification. CVD begins early in the course of CKD and there is an independent and graded association between cardiovascular morbidity and renal decline. Also, it is shown that once vascular damage and calcification begin, they progress inexorably in the uraemic milieu and may only be partially reversed after successful transplantation. Thus, preventing the development of CVD is key, and early identification and management of specific CVD-related risk factors should begin from the early stages of CKD. While the vasculopathy of childhood CKD is clearly multifactorial, clinical, epidemiological and cell biology studies provide converging evidence pointing to the role of dysregulated mineral metabolism as an important modifiable risk factor in the development of vascular calcification. In this review we focus on the role of calcium, phosphate, parathyroid hormone and vitamin D in ectopic vascular calcification, and discuss the role of screening, early intervention and management of established vascular calcification.     

Clinical characteristics and outcomes of children with stage 3–5 chronic kidney disease

The aim of this study was to report on the clinical characteristics and outcomes of Belgian children with chronic kidney disease (CKD). Between 2001 and 2005, we followed 143 new successive patients younger than 20 years of age with a glomerular filtration rate of <60 ml/min/1.73 m² prospectively in a Belgian department of pediatric nephrology. The incidence of diagnosed CKD was 11.9 per million child population (pmcp), and the incidence of renal replacement therapy was 6.2 pmcp. There were 67% patients in CKD stage 3, 19% in CKD stage 4 and 14% in CKD stage 5. Patients with congenital anomalies of the kidney and urinary tract (CAKUTs), hereditary diseases and glomerular diseases were diagnosed at a median age of 1, 2 and 10 years, respectively. CAKUTs were the main causes of CKD, accounting for 59% of all cases. After 3, 4 and 5 years of follow-up, 27, 31 and 38% of patients treated conservatively, respectively, reached end-stage renal failure (ESRF). The progression rate to ESRF was eightfold higher in patients with CKD stage 4 than in those with CKD stage 3. Among our patient group, hereditary diseases progressed more rapidly to ESRF than CAKUTs. Transplantation was performed preemptively in 22% of these children. Infections and cardiovascular diseases were the main causes of death.     

Diagnostic in chronic pancreatitis： imaging and function tests

慢性胰腺炎在组织病理学领域，是一种已经具有详细定义的疾病，但对于临床诊断来说，绝大多数病人并无组织切片。因此对于临床病史可疑的病人，影像学检查程序及补充性胰腺功能试验成为主要的诊断方法。正确诊断慢性胰腺炎对于晚期病人十分容易，但对于早期病人则较为困难。在该疾病早期病人中，内窥镜逆行性胰管造影(ERP)、及内镜超声(EUS)均是准确可靠的诊断方法。是否EUS优于ERP必须通过进一步研究证实。由于常规的非插管性功能试验，对于轻度及中度胰腺外分泌功能不足诊断准确率不满意，所以胰腺外分泌功能评估仅仅是形态学评估的补充。     

Renal PPARγ mRNA expression increases with impairment of renal function in patients with chronic kidney disease

Aim: Peroxisome proliferator‐activated receptor gamma (PPARγ) is generally accepted as renoprotective factor in type 2 diabetes mellitus, and PPARγ agonists have been reported to reduce albuminuria. However, little is known about renal PPARγ expression in chronic kidney disease, and especially human data are scarce. We hypothesized that renal PPARγ expression is associated with extent of proteinuria, kidney function, histological diagnosis and inflammatory mediators. Therefore, we investigated PPARγ mRNA expression in human kidney biopsies. Methods: We quantified PPARγ mRNA as well as the expression of macrophage chemoattractant protein‐1, transforming growth factor beta‐1 and interleukin‐6 in 64 human kidney biopsies from patients with chronic kidney disease and mild‐to‐marked proteinuria of diverse aetiology. We measured renal function, and macrophage invasion was quantified by CD68 and vascularization by CD34 immunostaining. Results: PPARγ mRNA expression correlated inversely with renal function. Higher blood pressure levels were associated with higher PPARγ expression levels. PPARγ mRNA expression correlated significantly (P < 0.001) with macrophage chemoattractant protein‐1 mRNA expression and showed a negative trend with transforming growth factor beta‐1 mRNA expression. No differences in PPARγ expression were detected with regard to extent of proteinuria, histological diagnosis, macrophage invasion, interleukin‐6 expression, and age or body mass index. Conclusions: PPARγ expression increases with loss of renal function and may be an important factor in maintaining normal renal function serving as a key protective mechanism to renal injury.     

Can bisphosphonates play a role in the treatment of children with chronic kidney disease?

In patients with chronic kidney disease (CKD) renal osteodystrophy, in the form of either low- or high-turnover bone disease, is quite common. While renal transplantation is expected to reverse renal osteodystrophy, long-term treatment with glucocorticoids before and/or after transplantation may lead to osteoporosis instead. Osteoporosis is defined as a skeletal disease with low bone mineral density, microarchitectural deterioration, and concomitant fragility. In adults, bisphosphonates are widely used to treat osteoporosis and other diseases associated with excessive bone resorption. In pediatric CKD patients the efficacy and safety of these drugs have not yet been addressed adequately and thus no evidence-based recommendations regarding the optimal type of bisphosphonate, dosage, or duration of therapy are available. Furthermore, while in adults the determination of areal bone mineral density is sufficient to diagnose osteoporosis, this is not the case in children. Instead, in pediatric patients, careful morphological assessment of bone structure and formation is required. Indeed, data from studies with uremic rats indicated that bisphosphonates, via a deceleration of bone turnover, have the potential not only to aggravate pre-existing adynamic bone disease, but also to impair longitudinal growth. Thus, the widespread use of bisphosphonates in children with CKD should be discouraged until the risks and benefits have been carefully elucidated in clinical trials.     

Physical activity in patients with pre‑dialysis chronic kidney disease is associated with decreased renal function

Clinical and Experimental Nephrology -     

Imaging of the intrahepatic portal vein in children with extrahepatic portal vein thrombosis — Comparison of magnetic resonance imaging and retrograde portography

PurposeExtrahepatic portal vein thrombosis (EPVT) is one major cause of portal hypertension in children. Surgical reinstallation of portal venous flow can be achieved in patients with patent intrahepatic portal venous system/Rex recess. Our study aimed to compare the ability of magnetic resonance imaging (MRI) and retrograde portography (RP) to assess patency of the intrahepatic portal venous system in children with EPVT.MethodsAll pediatric patients with EPVT who were examined with contrast enhanced MRI (1.5 T) and invasive RP between 2013 and 2017 were included in this retrospective study. Medical records were reviewed for demographic, biochemical and clinical data. Patency of the Rex recess as detected by MRI and RP was retrospectively reviewed.ResultsSixteen children (7.6 ± 5.0 years) with EPVT were included. Sensitivity, specificity, positive and negative predictive value for the detection of patent Rex recess by MRI compared to RP were 55%, 57%, 63% and 50%. Diagnostic accuracy was 56%. Diagnostic failure of MRI compared to RP was explained by the following: I. Problems differentiating collaterals from portal venous vessels II. Incapability showing dynamic blood flow in compromised portal venous flow III. Poor spatial resolution, especially in small children.ConclusionRP is a reliable method for the visualization of the Rex recess and the intrahepatic portal venous system in children with EPVT, whereas MRI has shown to be unsuitable for the assessment of the intrahepatic portal vein in these patients. In the preoperative setup, we recommend both procedures, RP and MRI for the visualization of the intrahepatic portal venous system, and the extrahepatic vessels, respectively.Level of evidenceLevel III.     

Does magnetic resonance imaging accurately predict residual disease in breast cancer?

Background

The accuracy of magnetic resonance imaging (MRI) in identifying residual disease after breast conservation therapy (BCT) is unclear.

Method

Review of an institutional database identified patients with positive or close (≤2 mm) margins undergoing MRI before re-excision. Histopathologic correlation was performed.

Results

Forty-three women underwent MRI after BCT. MRI suggested residual disease in 29 patients, of whom 20 (69%) had residual carcinoma pathologically. Nine patients had false-positive MRI as seen by benign pathology findings. Fourteen MRIs indicated no residual disease, of which 6 had residual disease pathologically. The sensitivity and positive predictive value of MRI was 77% and 69%, respectively. MRI conducted within 28 days of the original surgery was 85% sensitive. MRI performed after 28 days was 69% sensitive.

Conclusions

MRI is able to detect residual disease among most patients undergoing re-excision. False-positive results may be caused by inflammatory processes that resemble residual disease.