scholarly journals Role of Contrast-Enhanced Ultrasound (CEUS) in Native Kidney Pathology: Limits and Fields of Action

Diagnostics ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1058
Author(s):  
Antonio Granata ◽  
Irene Campo ◽  
Paolo Lentini ◽  
Francesco Pesce ◽  
Loreto Gesualdo ◽  
...  

Gray scale ultrasound has an important diagnostic role in native kidney disease. Low cost, absence of ionizing radiation and nephrotoxicity, short performance time, and repeatability even at the bedside, are the major advantages of this technique. The introduction of contrast enhancement ultrasound (CEUS) in daily clinical practice has significantly reduced the use of contrast enhancement computed tomography (CECT) and contrast enhancement magnetic resonance (CEMR), especially in patients with renal disease. Although there are many situations in which CECT and CEMRI are primarily indicated, their use may be limited by the administration of the contrast medium, which may involve a risk of renal function impairment, especially in the elderly, and in patients with acute kidney injury (AKI) and moderate to severe chronic kidney disease (CKD). In these cases, CEUS can be a valid diagnostic choice. To date, numerous publications have highlighted the role of CEUS in the study of parenchymal micro-vascularization and renal pathology by full integration with second level imaging methods (CECT and CEMRI) both in patients with normal renal function and with diseased kidneys. The aim of this review is to offer an updated overview of the limitations and potential applications of CEUS in native kidney disease.

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
M. Tesauro ◽  
A. Mascali ◽  
O. Franzese ◽  
S. Cipriani ◽  
C. Cardillo ◽  
...  

Chronic kidney disease is a major public health problem and characterized by a progressive loss in renal function over a period of months or years as defined by structural or functional abnormalities of the kidney. Several elements contribute to determine a progression of the kidney injury, inducing a worsening of renal damage and accelerating the decline of renal function: obesity and hypertension are two known factors of kidney progression. Remarkable improvements have been recently achieved in the study of the endocrine features of the adipose tissue and have been able to produce hormone-like peptides named adipokines or adipocytokines. Among these adipocytokines, which represent a link between obesity, hypertension, and chronic nephropathy, leptins and adiponectin appear to play an important role. Leptin not only is a prohypertension element (renal progression factor) through the activation sympathetic nervous, but also is able to induce prosclerotic effects directly on the kidney. In contrast, a decline of adiponectin levels has been shown to be related to a picture of hypertension: an endothelial dysfunction has been described as the main pathogenic mechanism responsible for this phenomenon.


2020 ◽  
Vol 4 (4) ◽  
pp. 108-112
Author(s):  
Konstantina Papakonstantinopoulou ◽  
Ioannis Sofianos

World’s population is aging. The elderly are at high risk for both chronic kidney disease (CKD) and hip fractures. Severe chronic kidney disease is a well-known risk factor for fractures and death especially in the elderly. Mild and moderate stages of kidney disease are often undiagnosed and/or untreated, thus their effect on fracture risk is not well established. Many ways of estimating glomerular filtration rate (GFR) have been developed but there are very few studies recommending the best and most valuable method for estimated GFR (eGFR) calculation that could correlate with fracture risk. In this mini- review we searched the literature concerning the use of cystatin C in the estimation of GFR related to the risk of hip fractures in the elderly. Our goal was to review the most important recent evidence on whether cystatin C could become a useful biomarker for the prediction of fracture risk. We concluded that there is evidence to support the use of cystatin C in hip fracture risk prediction in elder patients with chronic kidney disease.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Feyza Bora ◽  
Emine Asar ◽  
Fatih Yılmaz ◽  
Ümit Çakmak ◽  
Fevzi F Ersoy ◽  
...  

Abstract Background and Aims It is evident that Chronic Kidney Disease (CKD) influences the risk of developing AKI (Acute Kidney Injury) and recent studies suggest that CKD patients who experienced an episode of AKI are more likely to progress to end stage renal disease (ESRD) than patients without CKD. AKI-CKD association might originate from common comorbidities associated with both AKI and CKD, such as diabetes and/or hypertension, and concurrent increase in interventions leading to frequent exposure to various nephrotoxins. AKI in the elderly has been shown to increase the risk of progression to CKD to ESRD. AKI is common in critically ill patients, and those patients with the most severe form of AKI, requiring RRT, have a mortality rate of 50–80 %. Patients with an eGFR <45 ml/min per 1.73m2 who experienced an episode of dialysis-requiring AKI were at very high risk for impaired recovery of renal function. Our aim was to determine the reasons that initiate hemodialysis (renal decompensation) in patients with regular follow-up in the low clearance polyclinic without renal replacement treatment (RRT). Method The retrospective study included predialysis CKD patients who had followed up regularly and had undergone RRT in recent 4 years. Data on baseline characteristics and medical history were obtained from patient hospital records. Results Of the 228 patients, 155 (68%) were male and 73 (32%) were female. The mean age was 58 years (45-66). Diabetes Mellitus was the first in the etiology of CKD (26,3 %), the second was unknown (12,7 %), the third was hypertension (11,8 %). 145 patients (63,6%) underwent regular hemodialysis (HD) (62 years, 55-69), 25 patients (11%) began peritoneal dialysis (PD), 58 patients (25%) had renal transplantation. 52 patients underwent HD with renal decompensation, 22 (%42,3) had working arteriovenous fistula (AVF). There was no decompensation in patients with PD or transplantation plan. 34 patients started HD because of infections (65%), 8 patients (15%) after operations (4 was Coronary Artery Bypass Grafting-CABG), 6 patients (%11,5) after coronary angiography, 4 patients (7,5%) with cardiac decompensation. 2 patients died during the hospitalisation for infections. Of 145 HD patients, 89 (%61,4) had AVF. The patients who had renal decompensation were more older 63 (58-70), have lower Hgb 9,7 g/L (9,1-10,7) and albumin 3,5 g/L (3,2-3,9) level (p<0,05). There was no difference in eGFR at the beginning of HD between renal decompensation and other HD patients. 42 patients did not undergo HD at the time we suggested during visits. Of them 9 patients (%21) had renal decompensation (6 infections,3 CABG), 17 patients (%40) had AVF. 3 of them died. The others underwent HD for uremic complications. Conclusion We have shown that infections are as the leading cause of renal decompensation. Most of our patients who started to RRT from our low clearance outpatient clinic have chosen HD for RRT. Prevention of infections via vaccination programs or early diagnosis at regular policlinic or telephone visits, and informing patients adequately about nephrotoxic drugs or the conditions that may cause renal decompensation are among the first tasks of the predialysis outpatient clinic. Transition of CKD patients to RRTs, with proper preparation, neither late nor early- at the most appropriate time- should be among in our goals. This may reduce the cost of ESRD patients.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ashlyn C Harmon ◽  
Ashley C Johnson ◽  
Santosh Atanur ◽  
Klio Maratou ◽  
Tim Aitman ◽  
...  

Hypertension, diabetes and obesity, along with genetic predisposition, contribute to the growing number of chronic kidney disease patients. Our novel congenic model [S.SHR(11)] was developed through genetic modification of the Dahl salt-sensitive (S) rat, a model of hypertension related renal disease. The S.SHR(11) strain exhibits accelerated kidney injury compared to the already highly susceptible S rat. On either a low or high-salt diet, the S.SHR(11) model predominately exhibited more tubulointerstitial fibrosis compared to the S rat (17.1±1.29% vs. 12.9±1.22%). Increased α-SMA and macrophage infiltration was also observed. The S and S.SHR(11) had similar blood pressure (week 12), despite an early reduction in renal function in the S.SHR(11); however at an advanced age the S.SHR(11) demonstrated significantly higher blood pressure than the S (215±6.6 mm Hg vs. 183±5.9, respectively). This suggests that increased kidney injury is driving the development of hypertension later in life. Since these two animal models are identical with exception of chromosome 11, the causative genetic variants contributing to decreased renal function must reside within this region. The Dahl S and SHR genomes have been sequenced; this data provides a catalog of all the genetic variants between the two models. The 95% confidence interval of the genomic locus contains 28 non-synonymous SNP, with 15 of these SNP occurring within only three genes: Retnlg , Trat1 and Myh15. Two of these genes, Retnlg and Trat1, are known to play a role in immune response leading to our hypothesis that genetic variants in these genes alter protein function and lead to an increased immune response. Bone marrow transplant studies have been initiated to test our hypothesis and preliminary data shows that S rats who receive S.SHR(11) bone marrow have kidney function measurements similar to the S.SHR(11). The sequencing information has also lead to the development of nine new, more refined congenic strains. Through functional analysis of these new congenic animals, identification of the causative genetic variations will be expedited. In summary, we are employing a model of accelerated kidney disease to identify genes or genetic variants responsible for reduced kidney function and hypertension.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Mouna Malki abidi ◽  
Rajaa Aoudia ◽  
Soumaya Chargui ◽  
Imen Gorsane ◽  
Mouna Jerbi ◽  
...  

Abstract Background and Aims Acute kidney injury (AKI) is common in the elderly due to physiologic renal aging and underlying pathologies. Few studies focused on AKI in Tunisian elderly. The aim of our study was to highlight the epidemiological, clinical, etiological, therapeutic, and progressive characteristics of AKI in elderly. Method We conducted a descriptive retrospective study of AKI in patients admitted to our department over a period of 04 years from 01/01/2014 to 31/12/2017. Results We collected 40 patients including 25 women and 15 men with a sex ratio of 1.66. The mean age was 74 [65-87] years. We noted the presence of pre-existing chronic kidney disease in 58% of cases, diabetes in 50% of cases and hypertension in 73% of cases. Polypharmacy was found in 40% of cases. AKI was symptomatic in 80% of cases and found on a routine check-up in 20% of cases. Mean creatinine was 612+/-334 µmol/l. AKI was pre-renal in 37% and parenchymal in 63% of cases. Iatrogenic origin was found in 33% of cases. Renal biopsy was performed for diagnostic purposes in 6 cases. Haemodialysis was necessary in 50% of cases. Etiopathogenic treatment was initiated in 73% of cases. Intra-hospital mortality was 10%, recovery of renal function (RF) was partial in 40 % of cases and total in 20 % of cases. Follow-up time was 16 +/- 23.2 months. And at the last news, recovery of renal function (RF) was partial in 7 cases and total in 10 cases, 6 patients kept a chronic renal failure (CRF), among them 3 cases had and end-stage of CRF. Conclusion AKI is a frequent pathology in the elderly and its severity is linked to mortality and the transition to chronicity. Iatrogenic causes are frequent and preventable in this population, hence the major interest of prevention.


2016 ◽  
Vol 21 (4) ◽  
pp. 344-352 ◽  
Author(s):  
Yusuke Sata ◽  
Markus P. Schlaich

Sympathetic activation is a hallmark of chronic and end-stage renal disease and adversely affects cardiovascular prognosis. Hypertension is present in the vast majority of these patients and plays a key role in the progressive deterioration of renal function and the high rate of cardiovascular events in this patient cohort. Augmentation of renin release, tubular sodium reabsorption, and renal vascular resistance are direct consequences of efferent renal sympathetic nerve stimulation and the major components of neural regulation of renal function. Renal afferent nerve activity directly influences sympathetic outflow to the kidneys and other highly innervated organs involved in blood pressure control via hypothalamic integration. Renal denervation of the kidney has been shown to reduce blood pressure in many experimental models of hypertension. Targeting the renal nerves directly may therefore be specifically useful in patients with chronic and end-stage renal disease. In this review, we will discuss the potential role of catheter-based renal denervation in patients with impaired kidney function and also reflect on the potential impact on other cardiovascular conditions commonly associated with chronic kidney disease such as heart failure and arrhythmias.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S563-S563
Author(s):  
Mark Murphy ◽  
Sonya Tang-Girdwood ◽  
Peter Tang ◽  
Brady C Rebecca ◽  
Tomoyuki Mizuno ◽  
...  

Abstract Background Options for the treatment of infections caused by resistant gram-positive bacteria are limited in children with kidney disease. Ceftaroline (CFD) may be an attractive option but dosing recommendations are not available for children with renal dysfunction. We present a case of pharmacokinetics (PK) model-based individualization of CFD in an infant with kidney disease and mediastinitis. A 5-week-old infant with a hypoplastic left side of the heart developed mediastinitis following a Norwood and BT shunt. Blood and chest washout cultures grew S. epidermidis. Vancomycin therapy led to acute kidney injury (AKI) (eGFR ~15mL/minute) and therefore, CFD was initiated at 8 mg/kg every 12 hours. The model-based clinical service was consulted to assist with dosing. Methods Plasma levels were drawn on day 2 and 10 of CFD. CFD concentrations were determined by HPLC. The pharmacodynamic (PD) target used the MIC of the isolate, 1 µg/mL, and assumed drug diffusion into the mediastinum at 20% of plasma. The PD target was ƒT>MIC at 100%. Individual PK parameters were estimated using Bayesian estimation with MWPharm++ (Mediware, the Netherlands). Results CFD dosing of 8 mg/kg every 12 hours resulted in concentrations well above the target. The trough level was 10 times higher than levels seen in clinical trials. Repeat levels were checked on day 10 due to improved renal function (eGFR 30 mL/minute) and changes in volume status. Changes in both clearance and volume were noted. ƒT>MIC was maintained 100% during dosing intervals. We dose optimized CFD to achieve the target while minimizing potential toxicity with long-term use. A new dosing regimen, 5.4 mg/kg every 8 hours, was started on day 12 and continued for 6 weeks. Conclusion This is the first case report of CFD use in a child with AKI. Though initial dosing resulted in high concentrations, no adverse effects were noted. Successful treatment was completed with a final dosing regimen of 5.3 mg/kg every 8 hours, below the recommended 8 mg/kg every 8 hours. Lower dosing was needed to decrease high drug exposure due to the decreased clearance. This case also demonstrated the feasibility of PK model-based precision dosing within 48 hours, and documented utility in the setting of changes in renal function. Further PK/PD studies are needed in children with renal dysfunction. Disclosures All authors: No reported disclosures.


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