Hypertensive End-stage Renal Disease Research Articles

End-stage renal disease incidence in a cohort of US firefighters from San Francisco, Chicago, and Philadelphia.

Firefighters perform strenuous work in hot environments, which may increase their risk of chronic kidney disease. The purpose of this study was to evaluate the risk of end-stage renal disease (ESRD) and types of ESRD among a cohort of US firefighters compared to the US general population, and to examine exposure-response relationships. ESRD from 1977 through 2014 was identified through linkage with Medicare data. ESRD incidence in the cohort compared to the US population was evaluated using life table analyses. Associations of all ESRD, systemic ESRD, hypertensive ESRD, and diabetic ESRD with exposure surrogates (exposed days, fire runs, and fire hours) were examined in Cox proportional hazards models adjusted for attained age (the time scale), race, birth date, fire department, and employment duration. The incidence of all ESRD was less than expected (standardized incidence ratio (SIR) = 0.79; 95% confidence interval = 0.69-0.89, observed = 247). SIRs for ESRD types were not significantly increased. Positive associations of all ESRD, systemic ESRD, and hypertensive ESRD with exposed days were observed: however, 95% confidence intervals included one. We found little evidence of increased risk of ESRD among this cohort of firefighters. Limitations included the inability to evaluate exposure-response relationships for some ESRD types due to small observed numbers, the limitations of the surrogates of exposure, and the lack of information on more sensitive outcome measures for potential kidney effects.

Genetic susceptibility of hypertension-induced kidney disease.

Hypertension is the second leading cause of end‐stage renal disease (ESRD) after diabetes mellitus. The significant differences in the incidence of hypertensive ESRD between different patient populations worldwide and patients with and without family history indicate that genetic determinants play an important role in the onset and progression of this disease. Recent studies have identified genetic variants and pathways that may contribute to the alteration of renal function. Mechanisms involved include affecting renal hemodynamics (the myogenic and tubuloglomerular feedback responses); increasing the production of reactive oxygen species in the tubules; altering immune cell function; changing the number, structure, and function of podocytes that directly cause glomerular damage. Studies with hypertensive animal models using substitution mapping and gene knockout strategies have identified multiple candidate genes associated with the development of hypertension and subsequent renal injury. Genome‐wide association studies have implicated genetic variants in UMOD, MYH9, APOL‐1, SHROOM3, RAB38, and DAB2 have a higher risk for ESRD in hypertensive patients. These findings provide genetic evidence of potential novel targets for drug development and gene therapy to design individualized treatment of hypertension and related renal injury.

SUN-250 INDIVIDUALISED COOL DIALYSIS ALTERS THE ET-1/NO RATIO AND IMPROVES INTRADIALYTIC HYPERTENSION

While hemodialysis lowers blood pressure in most hypertensive end-stage renal disease (ESRD) patients, some patients exhibit a paradoxical increase in blood pressure during hemodialysis. This adversely increases morbidity and mortality of hemodialysis patients. Aims: To study the effect of individualised cool dialysis [iCoolHD] on intradialytic hypertension [IDH]. To find if this is mediated by temperature mediated change in Endothelin-1[ET-1] and Nitric Oxide [NO] ratio. Objectives: To evaluate the incidence of intradialytic hypertension in patients on maintenance hemodialysis at 37°C[sHD] and iCoolHD. To evaluate the correlation between ET-1/NO ratio during sHD vs iCoolHD. Methods: All 48 dialysis patients had IDH. Each were dialysed at sHD and iCoolHD (i.e., dialysate temperature was adjusted to their basal body temperature as measured by Tympanic thermometer). For iCoolHD, the temperature of the dialysis was adjusted to the patients prevailing body temperature. The mean between group variation of 0.1-0.6°C was maintained throughout dialysis (fig1). The mean systolic blood pressure was 170.1±7 mmHg in sHD vs 166.8±6.6 mmHg in iCoolHD (fig2). Thirty four (71%) of the patients had mean systolic blood pressure higher during sHD (37C) in comparison to patients when dialyzed by iCoolHD. The difference was statistically significant in 18(37.5%) of patients. Only 2(4.1%) patients had higher mean systolic blood pressure at iCoolHD than sHD (fig3). The SN ratio of systolic blood pressure in sHD (variation in SN ratio of 11mmHg) and iCoolHD (variation in SN ratio of 4 mmHg) demonstrated better blood pressure stability during iCoolHD (fig4). During iCoolHD, all the patients had the ET-1/NO ratio < 1.0, whereas 36(75% ) of patients had ratio >0.92 (fig5). For the first time we show that individualised cool dialysis has a definite role in reducing the incidence of intra-dialytic hypertension. iCoolHD improved IDH in 38% of our cohort. ET1/NO ratio is affected by temperature modulation during dialysis. ET1/NO ratio is significantly reduced only at iCoolHD.

Protective effect of high levels of TGF-β1 cytokine and its corresponding allele at C-509T locus in Punjabi ESRD population

End Stage Renal Disease (ESRD) is a chronic inflammatory condition when the kidney function has diminished to <10% of its normal capacity. In contrast to most of the reports from the west, our earlier study on Punjabi population documented lower circulating levels of transforming growth factor-β1 (TGF-β1) in ESRD patients as compared to their age and sex matched healthy controls. This prompted us to investigate the correlation between circulating TGF-β1 protein levels and C-509 T promoter polymorphism (rs1800469) in Punjabi ESRD population. A total of 192 ESRD (77 diabetic ESRD and 115 hypertensive ESRD) and 130 normal healthy controls, participated in this study. Genotyping of C-509 T polymorphism was done with Amplification Refractory Mutation System Analysis (ARMS–PCR) and circulating TGF-β1 levels were measured with ELISA. Diabetic ESRD group revealed significantly different allele frequencies from normal population (χ2 = 4.615; p = .032). Also, levels of TGF-β1 cytokine were significantly depleted between diabetic (11.44 ± 7.79 ng/ml) as well as hypertensive (8.68 ± 6.54 ng/ml) ESRD patients as compared to their normal counterparts (26.09 ± 10.73 ng/ml). A comparison of mean TGF-β1 protein levels among individuals carrying CC, CT and TT genotypes within diabetic ESRD (p = .561) and hypertensive ESRD population (p = .221) did not present any association. We submit the first report on the correlation between TGF-β1 C-509 T polymorphism with its corresponding circulating levels in north India Punjabi population. Our results suggest a protective effect of T allele against developing ESRD within Punjabi diabetic population [odds ratio = 0.63 (CI = 0.41–0.96)]. It also suggests that TGF-β1 does not play its anticipated pro-fibrotic role but perhaps mediates an equally important anti-inflammatory function.

Changes in left ventricular filling parameters before and after dialysis in patients with end stage renal disease.

The aim of this study was to investigate the grading of diastolic dysfunction (DD) in relation to hemodialysis in patients with end stage renal disease (ESRD) on hemodialysis (HD) Cardiovascular disease is prevalent in patients with ESRD and accounts for significant morbidity and mortality. Left ventricular hypertrophy (LVH) is common in ESRD but little is known about the impact of HD on currently recommended grading schemes for DD. Comprehensive echocardiographic data was obtained in consecutive patients with ESRD before (n = 247) and immediately after (n = 239) standard HD regimen. Grading of DD was performed according to current recommendations both pre- and post HD. Prior to HD, DD was classified as present in 83 patients (34%), indeterminate in 51 patients (21%) and absent in 113 patients (45%). Patients with DD at baseline compared to those without were older [67.3 years (13.1) vs. 63.2 (14.3), p = 0.037], were more likely to have diabetic- or hypertensive ESRD (43.4% vs. 35.4%, p = ns) and LVMi was significantly higher [119g/cm2 (27.5) vs. 103g/cm2 (24.3), p < 0.001]. After HD [mean HD time = 221min (27.6), mean ultrafiltration volume = 2 L (1.1)], 39 patients (16%) exhibited sustained DD. These patients were older [69.4 years (14.5) vs. 65.0 years (13.9), p = 0.071], were more likely to have diabetic- or hypertensive ESRD (59% vs. 36%, p = 0.010). Myocardial adverse remodeling was more advanced with higher LVMi [127.4g/m2 (27.5) vs. 106.5g/m2 (25.3), p < 0.001], lower LVEF [44.7% (11.0) vs. 54.5% (8.7), p < 0.001] and more impaired GLS [- 13.4% (4.3) vs. - 15.8% (4.0), p = 0.006]. Echocardiographic evaluation of diastolic function in patients with ESRD on HD is critically dependent on timing relative to dialysis. The presence of sustained DD after volume unloading by HD identifies a population of patients with an adverse phenotype of blunted vascular response and severe cardiac remodeling.

Environmental impact on the onset of hypertension-induced end-stage renal disease

ABSTRACTThis study intends to assess the impact of environmental factors on the onset of hypertension-induced end-stage renal disease (ESRD) and to compare the level of oxidative stress with nonhypertensive diabetic ESRD.ESRD patients were evaluated along with healthy controls through questionnaire for demographic, nutritional and lifestyle variables. Oxidants were measured along with antioxidants. Multiple linear regression (MLR) models were applied to analyze association of studied variables with oxidants and antioxidants.Most of the hypertensive nephrosclerotic patients were residing in locality that was either closer to industrial belt or polluting water bodies, belonging to low socioeconomic status that invariably affected their lifestyle and nutritional status. Hypertensive ESRD patients showed more pronounced oxidative stress than diabetic ESRD. Several of the studied variables were significantly associated with oxidants and antioxidants.Demographic, nutritional and lifestyle variables appeared to have suggestive effect on the onset of hypertensive nephrosclerosis.

Renalase gene polymorphisms (rs2576178 and rs10887800) in Egyptian hypertensive end stage renal disease patients

BackgroundThe highly polymorphic gene encoding human renalase (RNLS) is a 311,000 bp gene located on chromosome 10. AimThis study aimed at studying the possible association of the two RNLS gene polymorphisms rs2576178 and rs10887800 with chronic kidney disease in general or specifically with hypertensive nephropathy in Egyptian end stage renal disease (ESRD) patients on maintenance hemodialysis. Subjects and methodThis case control study was conducted on two hundred and eighty one individuals, divided equally into two groups; an end stage renal disease patients on maintenance hemodialysis with/without hypertension and healthy matching individuals as a control group. Full clinical examination, Biochemical analysis and Molecular genetic testing were performed to detect single nucleotide polymorphism using restriction fraction length polymorphism (RFLP) for RNLS rs2576178 and rs1088780. ResultsThe results of this study demonstrated that the risk of developing ESRD was increased among carriers of AA genotype for the rs10887800 (3.05 times) p = 0.001, OR = 3.05, CI95% (1.558–5.971) and GG genotype for the rs2576178 p = 0.047, OR = 1.949, CI95% (1.028–3.694). ConclusionOur study revealed that the risk of developing end stage renal diseases was increased among carriers of AA genotype for the rs10887800 polymorphism and GG genotype for the rs2576178 polymorphism.

IgA nephropathy presenting as hypertensive emergency and end-stage renal disease in a child

IgA nephropathy (IgAN) is the most common noninfectious glomerulonephritis worldwide. Most of the children and young adults with IgAN present with macroscopic hematuria during an upper respiratory or gastrointestinal illness. However, various atypical presentations including overt nephrotic syndrome and rapidly progressive renal injury have been reported. Here, we present a case of IgAN that presented with hypertensive encephalopathy with features of end-stage renal disease as the initial presentation.

Impact of sodium profiling on ambulatory blood pressure in patients on maintenance hemodialysis

Introduction/Objective. Most patients with end-stage renal disease (ESRD) have hypertension. However, dialysis-related strategies to optimize blood pressure in these patients remain controversial. The current study aims to investigate the influence of dialysate sodium profiling on ambulatory blood pressure (ABP) in patients on maintenance hemodialysis, when there are no adequate dialytic and economic resources or high patient compliance. Methods. This prospective, single-center study enrolled 60 hypertensive ESRD patients. Subjects received maintenance dialysis with regular dialysate sodium concentration (140 mmol/L) during the initial three months after the enrollment, and were randomly assigned to continue regular sodium dialysate (group A) or switch to sodium profiling (group B) for duration of three months. ABP, heart rate (HR), pre-/postdialysis serum sodium levels, antihypertensive treatment dosages, and interdialytic weight gain (IDWG) etc. were recorded after treatment assignment. Results. Thirty patients each were enrolled in groups A and B. The characteristics at baseline were not significantly different between the two groups. Compared to patients in group A three months later, patients in group B had lower systolic ABP (p = 0.00), HR (p = 0.04), IDWG (p = 0.04), and antihypertensive medication dosages (p = 0.04). Throughout the treatment duration, no significant inter-group differences were observed for pre-/post-dialysis serum sodium and intradialytic complications. Additionally, no significant correlations were found between systolic or diastolic ABP and other variables studied in this study. Conclusion. In this study, we found that dialysate sodium profiling successfully ameliorated hypertension and reduced BP medications without altering natremic levels or increasing complications among patients on maintenance hemodialysis during the three months. Dialysate sodium profiling was relatively safe in this duration.

Effect of discontinuing morning dose of antihypertensive for renal transplant surgery on haemodynamic and early graft functioning: A prospective, double-blind, randomised study

Background and Aims:Antihypertensive drugs are continued until the day of renal transplant surgery. These are associated with increased incidence of hypotension and bradycardia. Hence, this study was designed to evaluate perioperative haemodynamic and early graft functioning in renal recipients with discontinuation of antihypertensive drugs on the morning of surgery.Methods:This prospective, randomised, double-blind study recruited 120 patients. Group 1 patients received placebo tablet while Group 2 patients received usual antihypertensive drugs on the day of surgery. Perioperative haemodynamics and time for reinstitution of antihypertensives were the primary outcome measures. The secondary outcome measures were need for inotropic support and graft function. Perioperative haemodynamics were analysed using ANOVA and Student's t-tests with Bonferroni correction. Fischer's exact test was used for analysis.Results:Systolic blood pressure (SBP) declined, which was more in Group 2. Forty-one patients developed significant hypotension; a correlation was found between the maximum observed hypotension and number of antihypertensive medications (P = 0.003). Four cases had slow graft function (one in Group 1 and three in Group 2). Twenty-eight patients in Group 2 required mephentermine boluses to maintain their SBP compared to 13 patients in Group 1 (P < 0.001). Two patients in Group 2 required dopamine to maintain SBP above 90 mmHg after the establishment of reperfusion as compared to none in Group 1.Conclusion:Single dose of long-acting antihypertensive drugs can be omitted on the morning of surgery without any haemodynamic fluctuations and graft function in controlled hypertensive end-stage renal disease renal transplant patients receiving a combined epidural and general anaesthesia.

Patterns of End-Stage Renal Disease Caused by Diabetes, Hypertension, and Glomerulonephritis in Live Kidney Donors.

Inferences about late risk of end-stage renal disease (ESRD) in live kidney donors have been extrapolated from studies averaging <10 years of follow-up. Because early (<10 years) and late (≥10 years) postdonation ESRD may differ by causal mechanism, it is possible that extrapolations are misleading. To better understand postdonation ESRD, we studied patterns of common etiologies including diabetes, hypertension and glomerulonephritis (GN; as reported by providers) using donor registry data linked to ESRD registry data. Overall, 125 427 donors were observed for a median of 11.0 years (interquartile range 5.3-15.7 years; maximum 25 years). The cumulative incidence of ESRD increased from 10 events per 10 000 at 10 years after donation to 85 events per 10 000 at 25 years after donation (late vs. early ESRD, adjusted for age, race and sex: incidence rate ratio [IRR] 1.3 1.72.3 [subscripts are 95% confidence intervals]). Early postdonation ESRD was predominantly reported as GN-ESRD; however, late postdonation ESRD was more frequently reported as diabetic ESRD and hypertensive ESRD (IRR 2.3 7.725.2 and 1.4 2.64.6 , respectively). These time-dependent patterns were not seen with GN-ESRD (IRR 0.4 0.71.2 ). Because ESRD in live kidney donors has traditionally been reported in studies averaging <10 years of follow-up, our findings suggest caution in extrapolating such results over much longer intervals.

Analytical Validation of a Personalized Medicine APOL1 Genotyping Assay for Nondiabetic Chronic Kidney Disease Risk Assessment

The incidence of chronic kidney disease (CKD) varies by ancestry, with African Americans (AA) having a threefold to fourfold higher rate than whites. Notably, two APOL1 alleles, termed G1 [c.(1072A>G; 1200T>G)] and G2 (c.1212_1217del6), are strongly associated with higher rates of nondiabetic CKD and an increased risk for hypertensive end-stage renal disease. This has prompted the opportunity to implement APOL1 testing to identify at-risk patients and modify other risk factors to reduce the progression of CKD to end-stage renal disease. We developed an APOL1 genotyping assay using multiplex allele-specific primer extension, and validated using 58 positive and negative controls. Genotyping results were completely concordant with Sanger sequencing, and both triplicate interrun and intrarun genotyping results were completely concordant. Multiethnic APOL1 allele frequencies were also determined by genotyping 7059 AA, Hispanic, and Asian individuals from the New York City metropolitan area. The AA, Hispanic, and Asian APOL1 G1 and G2 allele frequencies were 0.22 and 0.13, 0.037 and 0.025, and 0.013 and 0.004, respectively. Notably, approximately 14% of the AA population carried two risk alleles and are at increased risk for CKD, compared with <1% of the Hispanic and Asian populations. This novel APOL1 genotyping assay is robust and highly accurate, and represents one of the first personalized medicine clinical genetic tests for disease risk prediction.

Coagulation factor XIIa-kinin-mediated contribution to hypertension of chronic kidney disease.

Activated coagulation Factor XII (FXIIa) infusion increases peripheral resistance (TPR) and mean arterial pressure (MAP) of Brown Norway but not plasma kininogen deficient Brown Norway Katholiek (BNK) rats. FXIIa concentrations are elevated in hypertensive end-stage renal disease patients receiving conventional haemodialysis (CHD). Conversion to nocturnal haemodialysis (NHD) lowers peripheral resistance and MAP. To determine whether the plasma coagulation FXIIa-kallikrein-kinin axis contributes to the hypertension of chronic kidney disease (CKD). Plasma FXIIa and haemodynamic data were acquired in 11 CHD patients before and after 2 months of NHD. Cardiac and systemic haemodynamics of Brown Norway and BNK rats rendered hypertensive and uremic by 5/6 nephrectomy (NX) were determined before and after acute FXIIa inhibition. FXIIa was increased three-fold in CHD patients relative to control plasma (P < 0.05). After conversion to NHD, both ΔMAP and ΔTPR correlated with ΔFXIIa. In rats, plasma FXIIa was three-fold higher in both NX groups than respective SHAM controls (all P < 0.05), but MAP (147 ± 4 vs. 133 ± 2 mmHg; P < 0.05) and TPR (2.8 ± 0.2 vs. 2.3 ± 0.2 units; P < 0.05) were greater in Brown Norway NX (n = 16) than in BNK (n = 15) NX rats. FXIIa correlated with MAP only in Brown Norway NX, and plasma catecholamines were increased relative to SHAM only in Brown Norway NX (P < 0.05). In Brown Norway NX rats, FXIIa inhibitor infusion decreased MAP (-12 mmHg) and TPR (-0.5 Units) (both P < 0.05), and halved catecholamines (P < 0.05). No such changes occurred in BNK NX rats. FXIIa-kininogen mediated vasoconstriction contributes significantly to CKD hypertension in Brown Norway rats; this novel mechanism may be active in humans with CKD.

Association of E-Selectin Gene Polymorphism and Serum PAPP-A with Carotid Atherosclerosis in End-Stage Renal Disease

Atherosclerotic vascular disease represents a significant cause of morbidity and mortality in patients with end-stage renal disease (ESRD). The endothelium plays a crucial role in vascular inflammation. E-selectin is exclusively expressed on activated endothelial cells and is upregulated following an inflammatory response and oxidative stress, while serum pregnancy-associated plasma protein-A (PAPP-A) concentrations are related to the presence and stability of carotid atherosclerotic plaques. The aim of this study was to investigate whether there is an association between SELE rs5355C>T gene polymorphism, serum PAPP-A level and the presence of carotid atherosclerosis in ESRD patients. Seventy subjects were recruited into this study; 40 ESRD patients [age (mean±SD) 43.42±13.94years] and 30 age- and gender-matched healthy individuals assigned to the control group. Polymerase chain reaction-restriction fragment length polymorphism was performed for the analysis of SELE rs5355C>T gene polymorphism, while serum PAPP-A concentrations were measured using electro-chemiluminescence immunoassay. Routine laboratory tests were measured on an automated chemistry analyzer. Carotid ultrasonographic studies were performed by a bilateral high-resolution B-mode ultrasound. There was no significant relationship between the SELE rs5355C>T gene polymorphism and ESRD incidence. Serum PAPP-A levels were significantly higher in ESRD patients compared with controls [median (interquartile range) 5.8 (5.1-11.6) and 5.1 (4.1-6.7), respectively; p=0.005]. Serum PAPP-A correlated positively with urea, creatinine, systolic and diastolic blood pressure (DBP). Serum PAPP-A showed a statistically significant increase in SELE rs5355TT versus CC in both patients and controls. There was no association on comparing right intima-media thickness (IMT), left IMT, right cross-sectional area (CSA) and left CSA with the CC, CT and TT genotypes of SELE rs5355C>T. No correlation between serum PAPP-A with each of the above-mentioned carotid doppler findings was observed. There was a statistically significant increase in DBP in TT genotype carriers when compared with CC genotype carriers (p=0.009). Serum PAPP-A levels were higher in hypertensive ESRD patients when compared with normotensive ESRD patients. There was a statistically significant decrease in high-density lipoprotein cholesterol (HDL-C) in TT genotype carriers when compared with CT genotype carriers in the whole study group (p=0.003). Serum PAPP-A correlated negatively with HDL-C. The lack of a direct association between SELE rs5355C>T gene polymorphism, serum PAPP-A level and IMT suggests that their hypothesized association with carotid atherosclerosis might reflect an indirect mechanism of SELE rs5355C>T gene polymorphism and serum PAPP-A with cardiovascular risk factors such as blood pressure and HDL-C rather than a direct effect on the vasculature.

Adrenergic Genetic Mechanisms in Hypertension and Hypertensive Kidney Disease

Catecholamine secretory traits were significantly heritable, as were stress-induced blood pressure changes. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine biosynthesis. In the tyrosine hyroxylase promoter, significant associations were found for urinary catecholamine excretion and for blood pressure response to stress. TH promoter haplotype 2 (TGGG) showed pleiotropy, increasing both norepinephrine excretion and blood pressure during stress. In hypertension, 2 independent case-control studies (1,266 subjects with 53% women and 927 subjects with 24% women) replicated the effect of C-824T in the determination of blood pressure. Chromogranin A (CHGA) plays a fundamental role in the biogenesis of catecholamine secretory granules. Changes in the storage and release of CHGA in clinical and experimental hypertension prompted us to study whether genetic variation at the CHGA locus might contribute to alterations in autonomic function, and hence hypertension and its target organ consequences such as hypertensive kidney disease (nephrosclerosis). Systematic polymorphism discovery across the human CHGA locus revealed such regulatory regions as the proximal promoter and 3'-UTR. In chromaffin cell-transfected CHGA 3'-UTR and promoter/luciferase reporter plasmids, the functional consequences of the regulatory/non-coding allelic variants were documented. Variants in both the proximal promoter and the 3'-UTR displayed statistical associations with hypertension and hypertensive end stage renal disease. Therefore, I would like to review the common genetic variation in TH and CHGA as a cause of inter-individual variation in sympathetic activity, and ultimately blood pressure and hypertensive kidney disease.

Full Calcified Jacket of Saphenous Vein Graft

A 57-year-old male visited our clinic with chief complaint of exertional chest pain. He had been on anti-hypertensive medication for 15 years. In 1999, he went through coronary artery bypass graft surgery for myocardial infarction, using an aorto-left anterior descending artery (LAD) bypass with the left internal mammary artery, and aorto-right coronary artery (RCA) bypass with saphenous vein. From 2005, he received peritoneal dialysis due to hypertensive end stage renal disease. The coronary angiography shows significant stenosis in mid-LAD, total occlusion in RCA (Fig. 1A, black arrowhead) and diffuse calcified silhouette of saphenous vein graft (SVG) (Fig. 1A, white arrow-head), which is patent with good flow (Fig. 1B). A Chest X-ray shows calcifications that encircle the aorta (Fig. 1C), which indicates calcifications burden of this patient. Coronary CT angiography reveals well diffuse calcified SVG (Fig. 1D). Finally, he received percutaneous coronary intervention at LAD. Fig. 1 It has been reported that several risk factors, such as smoking, diabetes, and long standing graft contribute to a graft calcification.1) In this particular case, low glomerular filtration rate and advanced glycation end products, occurring during peritoneal dialysis,2),3) might have contributed to the extensive graft calcification. Also, the fact that SVG calcifications occurred mainly within the wall, and not within the plaque, which suggest that SVG calcifications are not just results of lesion formation, but also of hemodynamic changes that are associated with arterializations of SVG.1) Increasing calcified plaques of coronary artery are associated to angiographically severe stenosis,4) but it's not apparent that SVG calcifications is related to stenosis in that the location of SVG calcium is more diffuse and concentric in the vessel wall. The images we included in this paper illustrate the process clearly.

Late-Onset Development of Renal Sinus Lipomatosis in a Transplant Patient on Sirolimus

Late-Onset Development of Renal Sinus Lipomatosis in a Transplant Patient on Sirolimus

Coiled catheter for recurrent migration.

Sir, Double-cuffed Tenckhoff’s catheters has been widely used for continuous ambulatory peritoneal dialysis (CAPD). Various techniques of insertion have been described with placement of catheter tip downwards into the pelvis for maximal drainage. One of the well-known complications of CAPD is migration of the catheter tip out of the pelvis which leads to inadequate drainage and dialysis. The incidence of this problem varies considerably from center to center (5–35%), depending on the surgical technique, the patient’s body habitus, the presence of adhesions from previous surgeries, excessive omentum and the type of the peritoneal dialysis catheter [1]. Swan-neck coiled catheters were found to have advantages of coiled intraperitoneal segments in reducing the probability of infusion or tip pressure pain [2]. But only one study demonstrated that the double-cuff, swan-neck coiled-end configuration was associated with a considerably lower incidence of migration [3]. In that study, there was catheter tip migration in three patients with the straight catheters compared to one patient with the swan-neck coiled catheter [3]. We present a 28-year-old non-diabetic gentleman with hypertensive end-stage renal disease, who was initiated on CAPD in January 2010. He had no history of previous abdominal surgery. He underwent double-cuff swan-neck curved CAPD catheter insertion by surgical technique. He was initiated on regular CAPD exchanges after a 2-week break-in period. After 1 month, he presented with catheter malfunction. Radiograph of the abdomen showed catheter migration to the right hypochondrium. He underwent catheter removal with repositioning of a new double-cuff swan-neck curved CAPD catheter into the pelvis by laparotomy. Within a month he had again recurrence of catheter migration with malfunction. This time the existing catheter was replaced with a double-cuff swan-neck catheter with coiled tip. After 1 month of follow-up, the catheter position was re-examined, and the coiled-tip catheter had also migrated to the right hypochondrium but there was no complaint of malfunction. The catheter position was checked once the following month. It remained in the same position in right hypochondrium but without malfunction. The plausible explanation for the proper functioning, despite its migration to right hypochondrium, would be that the opening of the catheter remained directed down. Data on the use of coiled-tip catheters are scarce and it is known that migrated catheters might still function. The utility of a coiled-tip catheter for prevention of migration should be further investigated, but it should be remembered that such a coiled catheter might still function even after migration.

Intraoperative Diagnosis of Stanford Type A Dissection by Transesophageal Echocardiogram in a Patient Presenting for Renal Transplantation

A 48-year-old patient with hypertensive end-stage renal disease presented for cadaveric renal transplantation. On physical exam, a previously undocumented diastolic murmur was heard loudest at the left lower sternal border. The patient had a history of pericardial effusions and reported “a feeling of chest fullness” when lying flat. As such, a transesophageal echocardiogram (TEE) was performed after induction of anesthesia to evaluate the pericardial space and possibly determine the etiology and severity of the new murmur. The TEE revealed a Stanford Type A aortic dissection. The renal transplant was cancelled (organ reassigned within region), and the patient underwent an urgent ascending and proximal hemiarch aortic replacement. This case demonstrates the importance of a thorough physical exam and highlights the utility of TEE for noncardiac surgical cases.

Mortality and end-stage renal disease incidence among dry cleaning workers

ObjectivePerchloroethylene (PCE) is a known animal carcinogen and probable human carcinogen. Dry cleaning exposures, particularly PCE, are also associated with renal toxicity. The objective was to follow-up a cohort of...