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At least 613 records · Page 34Linked to original sources
PubMed2004

Clinical course of lung cancer in patients with chronic kidney disease.

Co-morbidity has a major impact on survival in early and late-stage lung carcinoma. Patients maintained on dialysis are potentially at increased risk of cancer. However, since very few studies have examined the clinical course of lung cancer in patients with chronic kidney disease (CKD), we felt it was important to study the course of non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) in this patient population. We performed a retrospective chart review of patients diagnosed with lung cancer and co-existent CKD. 107 patients (101 males and six females), with a mean age at diagnosis of 69 years (range: 39-86 years) were included in our study. Of these, 17 (15.9%) patients had SCLC while 87 (81.3%) had NSCLC. Dyspnea, weight loss, and chest pain were the most common symptoms at presentation in our patient population occurring in 25, 20, and 15% of patients, respectively. The median survival of all the patients in the study was 10 months (range: 0-116 months). Patients with SCLC had a median survival of 7 months. Patients with NSCLC had a median survival of 10 months. We found that the clinical course and survival in patients with lung cancer and CKD appear to be comparable to that of patients with lung cancer, but without kidney dysfunction. Hence though treatment of lung cancer does need to be individualized in the setting of CKD, it should not dissuade the clinician from treating the malignancy.

Adult↗
PubMed2026

Risk factors for loss of skeletal muscle mass in patients with chronic kidney disease on a low-protein diet.

OBJECTIVES: A low-protein diet (LPD) is recommended for patients with chronic kidney disease (CKD) to prevent a further decline in renal function. However, its impact on muscle mass in these patients remains unclear. This study investigated the risk factors for loss of muscle mass in patients with CKD on an LPD. METHODS: Eighty-four patients with predialysis CKD (59 men, mean age 61.9 &#xb1; 11.5 y) who participated in a multicenter randomized controlled trial initiated in 2014 were retrospectively reviewed. We collected data on baseline blood and urine tests, body composition, and dietary records at the start and end of the observation period. We evaluated muscle mass using the skeletal muscle index (SMI) and analyzed risk factors for a decrease in SMI during the 24-wk observation period, using logistic regression analysis. Variables with an association (P < 0.1) in univariate analysis, as well as age, sex, use of low-protein rice, and changes in protein intake, were subjected to multivariate analysis. RESULTS: SMI decreased in 50 patients (59.5%) during the observation period. Multivariate analysis identified significant associations of the SMI with serum albumin at baseline (odds ratio 0.11, 95% confidence interval 0.02-0.52, P = 0.004) and changes in energy intake while on the LPD (odds ratio 3.39, 95% confidence interval 1.00-11.43, P = 0.049). CONCLUSIONS: Risk factors for reduced SMI in patients with CKD on an LPD were malnutrition when initiating the LPD and reduced energy intake during its implementation. Clinicians should optimize nutritional status before initiation of an LPD and ensure adequate energy intake throughout treatment.

Humans↗
PubMed2005

Anemia and heart failure in chronic kidney disease.

Cardiovascular disease is mainly responsible for the poor long-term survival observed in chronic kidney disease (CKD) patients on dialytic treatment. Anemia is an early complication of CKD and, by inducing important cardiovascular alterations, first of all left ventricular hypertrophy, it does not only impair quality of life, but has also been shown to be an independent risk factor for adverse cardiovascular outcomes in CKD patients. Clinical studies, although with discordant results, have shown that cardiovascular benefits, mainly in terms of left ventricular hypertrophy regression, may be achieved by a partial correction of hemoglobin levels, however, it still is unclear whether starting anemia correction in a very early phase of CKD or aiming for complete normalization of hemoglobin levels higher than the targets recommended by current guidelines may provide further cardiovascular advantages. Results of ongoing, large-scale, prospective, randomized, clinical trials therefore are awaited with much interest to clarify better which practices of anemia correction may provide the best results on the improvement of cardiovascular status and thus of long-term survival of patients with renal disease.

Age Distribution↗
PubMed2006

Vascular calcification in uremic conditions: new insights into pathogenesis.

Chronic kidney disease (CKD) patients have an higher incidence of cardiovascular morbidity and mortality compared with the general population. In the past 10 years, several studies pointed out that vascular calcification is a major cause of cardiovascular disease in the dialysis population. In CKD patients, high levels of serum phosphate and parathyroid hormone play a critical role in the pathogenesis of cardiovascular events. Calcium- and aluminum-free phosphate binders provide a new and effective therapeutic tool in preventing cardiovascular calcifications in CKD in animal models and in hemodialysis patients. Moreover, the pathogenesis of vascular and soft-tissue calcification, which traditionally has been associated with a passive calcium-phosphate deposition, certainly also is related to an active, cell-mediated process. In fact, some bone regulatory proteins seem to be able to induce or inhibit mineral deposition in the vasculature. In particular, bone matrix protein 7, alpha2-HS glycoprotein, and matrix GLA protein may be regulatory keys in preventing extraskeletal calcification in uremic conditions. This review presents the current understanding of the pathogenesis of vascular calcification in CKD patients, focusing on these 3 proteins and their protective action on extraskeletal calcification.

Calcinosis↗
PubMed2006

Sleeping disorders in early chronic kidney disease.

Studies in patients on maintenance hemodialysis have disclosed a high prevalence of sleeping disorders, which have been linked to various factors including blood urea levels, creatinine levels, parathyroid hormone levels, anemia, systolic and diastolic blood pressure, quality of life, disease intrusiveness, and comorbidities. In contrast, few studies have been performed in patients with chronic kidney disease (CKD), who represent the target of the present study. A group of 52 CKD patients were enrolled after characterization of their renal function. Comorbidities were evaluated by means of the Charlson Comorbidity Index. Sleep disorders were evaluated by means of the Sleep Disorder Questionnaire (SDQ), a 26-item questionnaire providing a hierarchic classification for relevant insomnia, relevant hypersomnia, subclinical disorders, or absence of sleep complaints. Results indicate that, in the early stages of CKD, at a time the comorbidity index is low, sleep disorders are present in 80.7% of patients. This finding, which needs to be confirmed in a larger cohort of patients, indicates that sleep disorders affect the lives of CKD patients as soon a diagnosis of disease potentially progressing to end-stage renal disease was made.

Aged↗
PubMed2003

Analysis of long-term survival after revascularization in patients with chronic kidney disease presenting with acute coronary syndromes.

Ischemic heart disease is the most common cause of death in patients with chronic kidney disease (CKD). Patients with CKD who develop an acute coronary syndrome (ACS) have a poor prognosis, with >70% mortality at 2 years. Despite this heavy burden of disease, the optimal management of ACS in this patient population is unknown. Our goal was to compare the effect of coronary revascularization or medical therapy alone on the long-term survival of patients with CKD presenting with ACS. From 1990 to 1998, data were prospectively collected on 4,758 patients admitted to a coronary care unit with the diagnosis of ACS. Of these, 3,104 had preserved renal function, and 1,654 had significant renal dysfunction, as defined by the National Kidney Foundation in the Kidney Disease Outcomes Quality Initiative classification of kidney function as an estimated glomerular filtration rate of <60 ml/min/1.73 m(2). Long-term survival was assessed and outcomes were compared according to whether patients were treated with medical therapy alone or if they underwent a percutaneous or surgical revascularization procedure. Follow-up information was available in 99% of the patients up to 8 years after the index hospitalization. Of the 1,654 patients with significant renal dysfunction, 64 underwent coronary artery bypass surgery, 232 underwent percutaneous coronary revascularization, 280 underwent a diagnostic cardiac catheterization and were subsequently treated medically, whereas 1,078 were treated with medical therapy alone. Percutaneous coronary revascularization was associated with superior long-term survival. In conclusion, patients with severe CKD and ACS had improved long-term survival when treated with percutaneous coronary revascularization.

Aged↗
PubMed2003

Circulating endothelial cells as potential markers of the state of the endothelium in hemodialysis patients.

BACKGROUND: Patients with chronic kidney disease (CKD) are at high risk for atherosclerotic cardiovascular disease (ACVD). In addition to the same epidemiological risk factors of the general population, factors unique or secondary to the uremic milieu may contribute to excess cardiovascular morbidity and mortality. Recent studies suggest the endothelium has a key role in the development of atherosclerosis. Circulating endothelial cells (CECs) may be a tool to study the state of the endothelium, with their number markedly increased in conditions associated with a high degree of endothelial cell activation and/or injury. Our hypothesis is that CEC number increases in diseases that commonly progress to stage 5 CKD, as well as in patients on hemodialysis (HD) therapy, reflecting ongoing endothelial cell activation and/or injury. METHODS: The study population consisted of 22 healthy nonsmoking individuals, 29 individuals undergoing long-term HD treatment, 10 individuals with the diagnosis of diabetes mellitus and stage 1 or 2 CKD, and 7 individuals with hypertension and stage 1 or 2 CKD. The number of CECs was enumerated in all study groups. RESULTS: We found that CEC number was increased in HD patients, hypertensive patients, and patients with diabetes compared with healthy individuals. In addition, although CEC number did not accurately reflect the presence of ACVD, the number was increased significantly in a group of HD patients with active ACVD, whereas it was decreased significantly in a group of HD patients with stable ACVD. CONCLUSION: Our results suggest that CEC number may reflect ACVD activity in HD patients, independent of the presence of ACVD.

Adult↗
PubMed2004

Calcium channel blockers and the kidney.

Although end-stage renal disease (ESRD) currently affects only a small percentage (<0.2%) of the US population, its precursor, the mild and moderate forms of chronic kidney disease (CKD), affects 11% of the population, with significant growth in both ESRD and CKD anticipated in the rapidly aging US population. The primary diagnoses in the majority of ESRD patients are diabetes and hypertension. Results of clinical studies demonstrate that the level of proteinuria and sympathetic activation contribute to the progression of CKD to ESRD. There are sufficient clinical data to demonstrate that the dihydropyridine calcium channel blocker (DHP CCB) class of antihypertensives such as amlodipine and nifedipine, although effective in reducing systemic hypertension, lack activity in reducing proteinuria or attenuating sympathetic activity. Experimental studies and a limited number of clinical studies suggest that non-DHP CCBs, including verapamil and diltiazem, have a mechanism of action that differs from DHP CCBs. Non-DHP CCBs could potentially attenuate sympathetic activity and reduce protein excretion in patients with CKD.

Black or African American↗
PubMed2005

The renoprotective potential of pentoxifylline in chronic kidney disease.

Current interventions with proven efficacy, such as glycemic and blood pressure control, dietary protein restriction, and angiotensin II blockade, slow the progression of chronic kidney disease (CKD); however, whether long-term cessation of CKD progression is possible remains unclear. Because of the pathogenetic complexity of this condition, multidrug interventions with the least adverse effects should be investigated as the next step in attempts to stop CKD progression. Pentoxifylline, a non-selective phosphodiesterase inhibitor with indiscernible toxicity, exerts potent inhibitory effects against cell proliferation, inflammation, and extracellular matrix accumulation, all of which play important roles in CKD progression. Pentoxifylline monotherapy markedly reduces proteinuria in patients with membranous nephropathy. Moreover, limited human studies have proven pentoxifylline efficacy in reducing proteinuria in patients with diabetes receiving angiotensin-converting enzyme inhibitors, and in patients with nephrotic syndrome secondary to lupus nephritis despite immunosuppressive therapy. Further clinical trials are necessary to examine whether pentoxifylline can improve renal outcomes in patients receiving interventions of proven efficacy.

Cell Proliferation↗
PubMed1997

Cis-autophosphorylation of juxtamembrane tyrosines in the insulin receptor kinase domain.

Receptor tyrosine kinases undergo ligand-induced dimerization that promotes kinase domain trans-autophosphorylation. However, the kinase domains of the insulin receptor are effectively dimerized because of the covalent alpha2beta2 holomeric structure. This fact has made it difficult to determine the molecular mechanism of intraholomeric autophosphorylation, but there is evidence for both cis- and trans-autophosphorylation in the absence and presence of insulin. Here, using the cytoplasmic kinase domain (CKD) of the human insulin receptor, we demonstrate that autophosphorylation in the juxtamembrane (JM) subdomain follows a cis-reaction pathway. JM autophosphorylation was independent of CKD concentration over the range 6 nM-3 microM and was characterized kinetically: Half-saturation (K(ATP)) was observed at 75 microM ATP [5 mM Mn(CH3CO2)2] with a maximal rate of 0.24 mol of PO4 (mol of CKD)(-1) min(-1). Pairwise substitutions of Phe for Tyr in the other two autophosphorylation subdomains, generated by site-directed mutagenesis, altered the kinetics of JM autophosphorylation but did not change the pathway from a cis-reaction. Tyr(1328,1334) to Phe (in the carboxy-terminal subdomain) yielded <2-fold increase in the efficiency of JM autophosphorylation, whereas Tyr(1162,1163) to Phe (in the activation loop subdomain) yielded approximately 38-fold increased efficiency of JM autophosphorylation, due predominantly to a 23-fold decreased K(ATP). These findings demonstrate basal state binding of ATP to the CKD leading to cis-autophosphorylation and novel basal state regulatory interactions among the subdomains of the insulin receptor kinase. On the basis of these results and the crystal structure of the conserved catalytic core of this kinase [Hubbard, S. R., et al. (1994) Nature 372, 746], a model is proposed which reconciles the JM cis-reaction and the activation loop cis-inhibition/trans-reaction with the complex kinetics of insulin receptor autophosphorylation [Kohanski, R. A. (1993) Biochemistry 32, 5766].

Adenosine Triphosphate↗
PubMed2005

Therapy insight: congestive heart failure, chronic kidney disease and anemia, the cardio-renal-anemia syndrome.

Congestive heart failure (CHF) and chronic kidney disease (CKD) often progress to end stage even with optimum medical therapy. One factor that is common to both conditions is anemia, which is present in about a third of CHF patients. CHF can cause or worsen both anemia and CKD, and CKD can cause or worsen both anemia and CHF. Thus, a vicious circle exists between these three conditions, with each causing or worsening the other. We have called this condition the cardio-renal-anemia syndrome. Anemia in CHF is associated with increased mortality and hospitalization, reduced cardiac function and evidence of more severe CHF and CKD than in nonanemic patients. Intervention studies in anemic CHF patients have shown that optimum medical treatment of CHF and the correction of the associated anemia with subcutaneous erythropoietin and oral iron or intravenous iron sucrose can improve cardiac function, patients' functional status, renal function and quality of life, and reduce the frequency of hospitalization and the dose of diuretics required.

Anemia↗
PubMed2006

Arginine, arginine analogs and nitric oxide production in chronic kidney disease.

Nitric oxide (NO) production is reduced in renal disease, partially due to decreased endothelial NO production. Evidence indicates that NO deficiency contributes to cardiovascular events and progression of kidney damage. Two possible causes of NO deficiency are substrate (L-arginine) limitation and increased levels of circulating endogenous inhibitors of NO synthase (particularly asymmetric dimethylarginine [ADMA]). Decreased L-arginine availability in chronic kidney disease (CKD) is due to perturbed renal biosynthesis of this amino acid. In addition, inhibition of transport of L-arginine into endothelial cells and shunting of L-arginine into other metabolic pathways (e.g. those involving arginase) might also decrease availability. Elevated plasma and tissue levels of ADMA in CKD are functions of both reduced renal excretion and reduced catabolism by dimethylarginine dimethylaminohydrolase (DDAH). The latter might be associated with loss-of-function polymorphisms of a DDAH gene, functional inhibition of the enzyme by oxidative stress in CKD and end-stage renal disease, or both. These findings provide the rationale for novel therapies, including supplementation of dietary L-arginine or its precursor L-citrulline, inhibition of non-NO-producing pathways of L-arginine utilization, or both. Because an increase in ADMA has emerged as a major independent risk factor in end-stage renal disease (and probably also in CKD), lowering ADMA concentration is a major therapeutic goal; interventions that enhance the activity of the ADMA-hydrolyzing enzyme DDAH are under investigation.

Absorption↗
PubMed2006

Vitamin D in chronic kidney disease: a systemic role for selective vitamin D receptor activation.

Hyperparathyroidism occurs in most patients during the progression of chronic kidney disease (CKD) and one of its initiating events, reduced serum levels of 1,25-dihydroxyvitamin D, results from a decrease in renal 1alpha hydroxylase activity, which converts 25-hydroxyvitamin D to its activated form. The combination of persistently high parathyroid hormone (PTH) and low 1,25-dihydroxyvitamin D is associated with bone loss, cardiovascular disease, immune suppression and increased mortality in patients with end-stage kidney failure. Recent studies in dialysis patients suggest that paricalcitol, a selective activator of the vitamin D receptor (VDR), is associated with a more favorable efficacy to side effect profile than calcitriol, with less morbidity and better survival. One hypothesis derived from such studies suggests that systemic activation of VDRs may have direct effects on the cardiovascular system to decrease mortality in CKD. Although current guidelines for regulating serum calcium, phosphate and PTH recommend specific interventions at the various stages of CKD to prevent or postpone irreversible parathyroid disease and decrease cardiovascular morbidity and mortality, emerging data suggest that vitamin D therapy may prolong survival in this patient population by mechanisms that are independent of calcium, phosphate and PTH. It is suggested that a re-evaluation of current treatment recommendations is needed and that future research should focus on mechanisms that distinguish potential tissue specific benefits of selective VDR activators in patients with CKD.

Animals↗
PubMed2006

The progression of chronic kidney disease: a 10-year population-based study of the effects of gender and age.

The increase in demand for renal replacement therapy makes it important to investigate the prognosis of the earlier stages of chronic kidney disease (CKD). We examined the change in glomerular filtration rate (GFR), and patient and renal survival in CKD stage 3 in the municipality of Tromsø, a well-defined European community with a population of 58,000. All patients with estimated GFR between 30 and 59 ml/min/1.73 m(2) for more than 3 months during a 10-year study period were identified from a complete database of all 248 560 measurements of serum creatinine made in the community in the study period. Change in GFR was estimated for each patient using a multilevel model. A complete follow-up with respect to patient and renal survival was obtained from hospital databases. A total of 3047 patients was included. The median number of measurements of creatinine for each patient was 9, and the median observation time was 44 months. Mean estimated change in GFR was--1.03 ml/min/1.73 m(2)/year. Seventy-three percent of the patients experienced a decline in GFR. The 10-year cumulative incidence of renal failure was 0.04 (95% CI 0.03-0.06) and mortality 0.51 (95% CI 0.48-0.55). Female gender was associated with slower decline in GFR and better patient and renal survival. In this population-based study, the decline in GFR in CKD was slower than in previously studied selected patient groups. A high mortality pre-empted the development of renal failure in many patients. The prognosis of CKD depended strongly on gender.

Adult↗
PubMed2006

Prognostic importance of clinic and home blood pressure recordings in patients with chronic kidney disease.

Blood pressure (BP) measured only in the clinic substantially misclassifies hypertension in patients with chronic kidney disease (CKD). The role of out-of-clinic recordings of BP in predicting end-stage renal disease (ESRD) and death in patients with CKD is unknown. A prospective cohort study was conducted in 217 Veterans with CKD. BP was measured at home and in the clinic by 'routine' and standardized methods. Patients were followed over a median of 3.5 years to assess the end points of total mortality, ESRD or the composite outcome of ESRD or death. Home BP was 147.0+/-21.4/78.3+/-11.6 mmHg and clinic BPs were 155.2+/-25.6/84.7+/-14.2 mmHg by standardized method and 144.5+/-24.2/75.4+/-14.7 mmHg by the 'routine' method. The composite renal end point occurred in 75 patients (34.5%), death in 52 patients (24.0%), and ESRD in 36/178 patients (20.2%). One standard deviation (s.d.) increase in systolic BP increased the risk of renal end point by 1.27 (95% confidence interval (CI) 1.01-1.60) for routine clinic measurement, by 1.69 (95% CI 1.32-2.17) for standardized clinic measurement and by 1.84 (95% CI 1.46-2.32) for home BP recording. One s.d. increase in home systolic BP increased the risk of ESRD by 1.74 (95% CI 1.04-2.93) when adjusted for standardized clinic systolic BP, proteinuria, estimated glomerular filtration rate, and other risk factors. In patients with CKD, BPs obtained at home are a stronger predictor of ESRD or death compared to BPs obtained in the clinic. Systolic home BP is an independent predictor for ESRD.

Adult↗
PubMed2006

Association of anemia with outcomes in men with moderate and severe chronic kidney disease.

Anemia is a common complication of chronic kidney disease (CKD), but the outcomes associated with lower hemoglobin (Hgb) levels in patients with CKD not yet on dialysis are not well characterized. Analyses exploring outcomes associated with a single baseline Hgb value also do not account for the longitudinal variation of this measure. After collecting all Hgb measurements (N=17 194, median (range): 12 (1-168)) over a median follow-up period of 2.1 years in a historical prospective cohort of 853 male US veterans with CKD Stages 3-5 not yet on dialysis, we examined the association of time-averaged Hgb levels with predialysis all-cause mortality, end-stage renal disease (ESRD), and a composite end point of both. Kaplan-Meier survival analysis and Cox models adjusted for age, race, body mass index, smoking status, blood pressure, diabetes mellitus, cardiovascular disease, categories of estimated glomerular filtration rate, serum concentrations of albumin and cholesterol, and proteinuria were examined. Lower time-averaged Hgb was associated with significantly higher hazard of the composite end point (hazard ratio (95% confidence interval) in the adjusted model for time-averaged Hgb of <110, 111-120 and 121-130, compared to >130 g/l: 2.57 (1.85-3.58), 1.97 (1.45-2.66), 1.19 (0.86-1.63), P(trend)<0.001). Lower time-averaged Hgb was associated with both significantly higher pre-dialysis mortality and higher risk of ESRD, when analyzed separately. Anemia (especially time-averaged Hgb <120 g/l) is associated with both higher mortality and increased risk of ESRD in male patients with CKD not yet on dialysis.

Aged↗
PubMed2006

Leptin and inflammation-associated cachexia in chronic kidney disease.

Leptin is an adipocyte-derived hormone that acts as a major regulator of food intake and energy homeostasis. It circulates both as a free and as a protein-bound entity. Leptin is released into the blood in proportion to the amount of body fat and exerts sustained inhibitory effects on food intake while increasing energy expenditure. The leptin receptor belongs to the class I cytokine receptor superfamily and possesses strong homology to the signal-transducing subunits of the IL-6 receptor. The hypothalamic melanocortin system, and specifically the melanocortin-4 receptor (MC-4R), is critical in mediating leptin's effect on appetite and metabolism. Serum leptin concentrations are elevated in patients with chronic kidney disease (CKD) and correlate with C-reactive protein levels suggesting that inflammation is an important factor that contributes to hyperleptinemia in CKD. Hyperleptinemia may be important in the pathogenesis of inflammation-associated cachexia in CKD. We showed that experimental uremic cachexia was attenuated in db/db mice, a model of leptin receptor deficiency. Nephrectomy in these animals did not result in any change in weight gain, body composition, resting metabolic rate, and efficiency of food consumption. Furthermore, experimental uremic cachexia could be ameliorated by blocking leptin signaling through the hypothalamic MC-4R. MC-4R knockout mice or mice administered the MC-4R and MC-3R antagonist, agouti-related peptide, resisted uremia-induced loss of lean body mass and maintained normal basal metabolic rates. Thus, melanocortin receptor antagonism may provide a novel therapeutic strategy for inflammation-associated cachexia in CKD.

Animals↗
PubMed2006

Safety of low-dose radiocontrast for interventional AV fistula salvage in stage 4 chronic kidney disease patients.

The Dialysis Outcomes Quality Initiative emphasizes increasing arteriovenous fistula prevalence, by promoting referral for fistula creation in patients with stage 4 chronic kidney disease (CKD). The aim is to provide an optimal access for initiation of dialysis, thus avoiding central venous catheter use. The endovascular management of nonmaturing fistulas is more complicated in these patients, where the expected benefit of catheter avoidance must be weighed against the risk of contrast induced nephropathy (CIN). This study reports on the safety of a low-dose radiocontrast regimen, used in performing endovascular fistula salvage procedures in patients with stage 4 CKD. All consecutive endovascular procedures performed over a 2-year period in patients with stage 4 CKD and nonmaturing access were identified. Data collected included the type of procedure, contrast volume per procedure, pre, 2- and 7-day creatinine, need for acute dialysis, and the type of access used to initiate dialysis. Total of 65 procedures were performed in 34 patients. The mean contrast volume was 7.8 ml per procedure. The incidence of CIN (25% increase in serum creatinine) was 4% at 2 days and 4.6% at 1 week. All values returned to baseline within 2 weeks, and no patient required acute dialysis. Among the 33 patients with nonmaturing fistulas, 20 initiated dialysis during the follow-up period, 15 (75%) using their fistula, and five (25%) using a catheter. This study demonstrates that in patients with advanced CKD, fistulas can be successfully salvaged using small contrast volumes with a low incidence of CIN.

Aged↗