Daily sodium intake in chronic kidney disease patients during nephrology clinic follow-up: an observational study with 24-hour urine sodium measurement.

OBJECTIVE: To determine daily sodium intake in 'real practice' in a large group of chronic kidney disease (CKD) patients who were under regular follow-up in a nephrology clinic. METHODS: A total of 373 consecutive outpatients with CKD stages 1-5 (not on dialysis; men: 52.3%, mean age: 51.6 ± 15.4 years) were included in the study. All patients had at least 3 or more nephrology visits and received information on reducing their sodium intake. Data for systolic and diastolic blood pressure, number of antihypertensive medications and 2 consecutive 24-hour urinary sodium levels were obtained from the patients' medical records. RESULTS: The mean 24-hour urinary sodium levels of 2 consecutive urine samples were 168.8 ± 70.3 and 169.3 ± 67.4 mEq/day (p > 0.05). Only 14.7% of the patients had a sodium excretion <100 mmol/day. There was no difference in daily sodium intake from stages 1 to 4, but it was significantly lower in stage 5 (126.6 ± 60.5 mEq/day, p < 0.05). No relation was found between 24-hour urinary sodium output, number of antihypertensives or thiazide use. CONCLUSIONS: This study showed that almost 85% of CKD patients under regular nephrologic care were consuming more sodium than the recommended level. More robust measures should be devised to increase patient and physician compliance with reducing sodium intake in CKD.

AA type renal amyloidosis secondary to FMF: a long-term follow-up in two patients.

Renal amyloidosis, which leads to renal failure, is the most important long-term complication of familial Mediterranean fever (FMF). Resolution of nephrotic syndrome secondary to amyloidosis in FMF following colchicine treatment has rarely been reported. We describe two patients with FMF and nephrotic syndrome. These patients were treated with colchicine 1.5 mg/day and had a complete remission of nephrotic syndrome with a stable clinical course over 30 years. To our knowledge, our patients have the longest follow-up time without proteinuria.

Copper deficiency with increased hematogones mimicking refractory anemia with excess blasts.

We describe a 19-year-old male patient with a previous diagnosis of familial Mediterranean fever (FMF), nephrotic syndrome and secondary amyloidosis, who presented with anemia and leukopenia. The bone marrow assessments showed dysplastic precursors including vacuolated myeloid and erythroid precursors and increased proportion of immature cells up to 19%. The patient received erythropoietin and G-CSF for myelodysplastic syndrome (MDS). No response was observed. During his evaluations copper deficiency was detected. One month after oral copper replacement, the peripheral blood counts and bone marrow findings became completely normalized. An evaluation to identify the cause of copper deficiency, revealed intestinal amyloidosis. Based on our experience we recommend serum copper determination in the diagnostic workup of MDS in patients with comorbidities.

A novel immunosuppressive agent, sirolimus, in the treatment of Kaposi's sarcoma in a renal transplant recipient.

Renal transplant recipients are susceptible to Kaposi's sarcoma (KS) because of treatment with immunosuppressive drugs. Sirolimus, a new immunosuppressive agent, has been successfully used for immune-suppression in kidney transplant recipients. Several studies have shown the potential role of sirolimus to inhibit progression of KS in kidney-transplant recipients. This report details a kidney-transplant recipient with cutaneous KS who had a complete remission in response to sirolimus therapy.

Association of mineral metabolism with an increase in cellular adhesion molecules: another link to cardiovascular risk in maintenance haemodialysis?

BACKGROUND: Abnormal mineral metabolism is associated with increased cardiovascular morbidity and mortality. The exact pathogenesis linking mineral metabolism to cardiovascular risk is unknown. This study was undertaken to investigate the association between serum phosphate and/or Ca x PO(4) product with serum levels of soluble E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 and the degree of carotid artery atherosclerosis in patients on haemodialysis. METHODS: Seventy-three patients (46 male, 27 female; mean age 48+/-13 years, on haemodialysis for 82+/-80 months) were included in the study. All patients were stable, had no evidence of vascular disease and/or active infection. Consecutive 6 months clinical and laboratory data were obtained for each patient from their medical records and mean values were used for analysis. Serum levels of soluble adhesion molecules were assayed by ELISA. All subjects underwent a detailed evaluation of the carotid arteries. RESULTS: The percentage of patients who met all three targets of NKF-K/DOQI for phosphate, calcium and Ca x PO(4) product was 27.1%, whereas those who did not achieve the target in one, two or three parameters was 28.1, 17.7 and 14.6%, respectively. The sICAM-1 levels were significantly higher in patients who had hyperphosphataemia (serum phosphate >5.5 mg/dl; P = 0.044) and hypercalcaemia (serum calcium >9.5 mg/dl; P = 0.014), both sE-selectin and sICAM-1 levels were significantly higher in patients with Ca x PO(4) product levels above 55 mg(2)/dl(2) (P = 0.002 and P = 0.000, respectively). Soluble E-selectin and sICAM levels demonstrated a near-linear increase in parallel to the degree of deviation from mineral metabolism targets. Soluble E-selectin and sICAM levels were correlated with serum phosphate and Ca x PO(4) product, but there were no correlations between adhesion molecules and carotid measurements. CONCLUSION: These findings suggest that in stable haemodialysis patients abnormal bone mineral metabolism was associated with increased soluble adhesion molecules. These alterations in adhesion molecules may favour the development of cardiovascular changes and contribute to high cardiovascular morbidity and mortality in patients with abnormal mineral metabolism.

The effects of maintenance recombinant human erythropoietin therapy on ambulatory blood pressure recordings: conventional, Doppler, and tissue Doppler echocardiographic parameters.

Cardiovascular disease is the major cause of mortality in maintenance hemodialysis patients. Left ventricular dysfunction is present in approximately 80% of these patients and is highly predictive of future ischemic heart disease, cardiac failure, and death. Anemia has been identified as one of several risk factors responsible for cardiac complications. The treatment of renal anemia with recombinant human erythropoietin (rHuEpo) and consequent improvement of cardiac performance may reverse pathological changes in left ventricular geometry. In this study, the acute and chronic effects of rHuEpo administration on 24-hour ambulatory blood pressure recordings and echocardiographic parameters in 30 rHuEpo-naïve maintenance hemodialysis patients were examined. Twenty-four-hour ambulatory blood pressure monitoring was performed prior to and after 1 week and 6 months of rHuEpo administration. The patients underwent echocardiographic examination prior to and after 6 months of rHuEpo administration. One week treatment with rHuEpo did not cause any significant change in 24-hour ambulatory blood pressure recordings. After 6 months of therapy, serum hemoglobin levels increased from 8.8 +/- 0.66 g/dL to 10.8 +/- 0.70 g/dL (P < 0.05). Echocardiographic examination revealed elevation in ejection fraction (62.26 +/- 6.84% vs. 69.90 +/- 8.98%, P < 0.05) with reductions in fractional shortening (36.70 +/- 4.96% vs. 35.96 +/- 6.32%, P < 0.05), interventricular septum thickness (1.21 +/- 0.16 vs. 1.00 +/- 0.16 cm, P < 0.05), and left ventricular mass index (148.2 +/- 46.5 g/m2 vs. 93.6 +/- 17.2 g/m2, P < 0.05). Doppler echocardiography and tissue Doppler imaging provided additional information in comparison with conventional echocardiography. Before treatment, mitral flow E wave (E, 0.64 +/- 0.27 vs. 0.82 +/- 0.17 cm/s), mitral flow A wave (A, 0.80 +/- 0.21 vs. 0.70 +/- 0.21 cm/s), early diastolic velocity of lateral wall (Lateral E', 11.2 +/- 2.8 vs. 12.4 +/- 2.3 cm/s), late diastolic velocity of lateral wall (Lateral A', 6.7 +/- 2.5 vs. 7.8 +/- 2.1 cm/s), early diastolic velocity of septal wall (Septal E', 9.7 +/- 2.9 vs. 11.3 +/- 1.1 cm/s), and late diastolic velocity of septal wall (Septal A', 6.4 +/- 2.1 vs. 7.8 +/- 2.0 cm/s) were significantly lower in patients than in the controls. Patients and controls have similar deceleration time of mitral flow E wave (E Dec, 186 +/- 57.8 vs. 192 +/- 62.4 ms), isovolumic left ventricular relaxation time (IVRT, 111.9 +/- 30.7 vs. 91.1 +/- 32 ms), systolic velocity of lateral wall (Lateral S', 7.8 +/- 2.3 vs. 8.1 +/- 2.0 cm/s), and systolic velocity of septal wall (Septal S', 7.5 +/- 1.9 vs. 7.7 +/- 1.4 cm/s) values. Therapy with rHuEpo did not cause significant changes in E (0.64 +/- 0.27 vs. 0.76 +/- 0.29 cm/s), A (0.80 +/- 0.21 vs. 0.79 +/- 0.23 cm/s), E Dec (186 +/- 57.8 vs. 165.8 +/- 60.1 ms), IVRT (111.9 +/- 30.7 vs. 101.6 +/- 36.2 ms), Lateral E' (11.2 +/- 2.8 vs. 11.5 +/- 4.4 cm/s), Lateral A' (6.7 +/- 2.5 vs. 7.4 +/- 2.1 cm/s), Lateral S' (7.8 +/- 2.3 vs. 8.1 +/- 2.0 cm/s), Septal E' (9.7 +/- 2.9 vs. 10.0 +/- 1.1 cm/s), Septal A' (6.4 +/- 2.1 vs. 6.6 +/- 2.0 cm/s), and Septal S' (7.5 +/- 1.9 vs. 7.9 +/- 1.4 cm/s) indicating persistence of diastolic dysfunction. In 6 months time, 24-hour ambulatory blood pressure recordings, however, tended to be higher (systolic: 125.16 +/- 21.02 mm Hg vs. 134.36 +/- 23.98 mm Hg; diastolic: 77.40 +/- 14.47 mm Hg vs. 83.26 +/- 14.89 mm Hg, P < 0.05). Correction of anemia with rHuEpo results in the elevation of blood pressure and reduction in left ventricular mass index. Myocardial contraction and relaxation velocities did not improve following regression of left ventricular hypertrophy, suggesting the persistance of diastolic dysfunction. Doppler echocardiography with tissue Doppler imaging reflects the real situation of diastolic function in patients on maintenance hemodialysis.

U-shaped association of body mass index with inflammation and atherosclerosis in hemodialysis patients.

OBJECTIVE: High body mass index (BMI) is associated with mortality in the general population, whereas obesity is suggested to confer a survival advantage in hemodialysis (HD) patients. However, underlying mechanisms are yet to be elucidated. We examined the cross-sectional association of BMI with inflammatory and nutritional markers and atherosclerosis in HD patients. DESIGN: Cross-sectional study. SETTING AND PARTICIPANTS: One hundred and nine maintenance HD patients in the Hacettepe University Hospital Haemodialysis Unit were studied. METHODS: Data on demographics, comorbidity, and anthropometry were obtained by patient interviews. Atherosclerosis was assessed by B-mode Doppler ultrasonography on common carotid artery. Serum markers of inflammation, nutrition, and lipid metabolism, including C-reactive protein (CRP), albumin, prealbumin, homocysteine and lipoproteins, were measured by standard methods. MAIN OUTCOME MEASURE: Distribution of inflammatory and nutritional markers and prevalence of atherosclerosis in underweight, normal, overweight, and obese HD patients. RESULTS: CRP levels were significantly higher in obese and underweight HD patients compared with normal and overweight patients (P < .05). The prevalence of atherosclerosis was significantly higher in underweight and obese patients (54.5% and 50%) compared with normal and overweight patients (25.7% and 33%) (P < .05). CONCLUSIONS: In the present study, obesity is associated with inflammation and atherosclerosis. An obesity-related survival advantage should be modified by other factors such as race, comorbid conditions, body composition, and nutritional status.

Impact of rHuEPO therapy initiation on soluble adhesion molecule levels in haemodialysis patients.

BACKGROUND: Increased levels of soluble adhesion molecules have been reported in haemodialysis (HD) patients. Recent studies have shown that recombinant human erythropoietin (rHuEPO) elicits proliferation and migration of endothelial cells and modifies endothelial function. The present study was design to explore the effects of rHuEPO on serum levels of soluble adhesion molecules in HD patients. METHODS: Soluble serum levels of E-selectin (sE-selectin), intracellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) were measured by ELISA in 29 rHuEPO naïve HD patients (20 males, 9 females) and 10 control subjects at baseline and second month. The HD patients with a haemoglobin level lower than 10.0 mg/dL (n = 19) were administered rHuEPO therapy and other HD patients (n = 10) were followed as a placebo group. RESULTS: Serum levels of soluble adhesion molecules were significantly higher in HD patients compared with the control group. A significant rise from the baseline in sE-selectin levels (77 +/- 70 vs 100 +/- 86 ng/mL, P < 0.05) was observed 2 months after rHuEPO initiation, while sICAM-1 and sVCAM-1 levels decreased (271 +/- 261 vs 197 +/- 89 and 1043 +/- 243 vs 990 +/- 236 ng/mL, respectively, P < 0.05). CONCLUSIONS: The present data indicate that rHuEPO could have an important action on serum levels of soluble adhesion molecules in HD patients. rHuEPO might modify the expression of adhesion molecules from endothelial cells either. However, the exact mechanism responsible for the serum elevation of these molecules in HD patients is yet to be fully elucidated.

Impact of cytokine gene polymorphism on cardiovascular risk in renal transplant recipients.

Cardiovascular events are the leading causes of morbidity and mortality in renal transplant recipients (RTR). Given the role of inflammation in atherosclerosis, the contribution of functional polymorphisms of cytokines to cardiovascular diseases (CVD) was assessed in RTR in this study. Polymorphisms of tumour necrosis factor alpha (TNF-alpha) gene [-308 (G-->A), -238 (G-->A)], interleukin-10 (IL-10) gene [-1082(A-->G), -819 (T-->C), -592 (A-->C)], transforming growth factor beta 1 (TGF-beta1) gene [codon 10 (T-->C), codon 25 (G-->C)], carotis intima media thickness (CIMT), left ventricular mass index (LVMI), 24-h ambulatory blood pressure and serum lipoprotein homocysteine level, erythrocyte sedimentation rate, serum C-reactive protein (CRP) and serum fibrinogen level of RTR were determined. Seventy-two RTR (26 cadaveric allograft, 46 living-related allograft, 43 male, 29 female) were included in this study. LVMI were similar in TNF-alpha, IL-10 and TGF-beta1 genotypes. Right and left CIMT were higher in TT genotype (n = 16) than CT (n = 46) and CC (n = 10) genotypes of TGF-beta1 codon 10 (T-->C) gene polymorphism (RCIMT, 7.7 +/- 2.2 mm vs. 7.0 +/- 1.4 mm vs. 5.9 +/- 1.4 mm, P = 0.025; LCIMT, 8.5 +/- 2.5 mm vs. 7.0 +/- 1.3 mm vs. 6.1 +/- 1.2 mm, P = 0.002). Lipoprotein (a) level of TT genotype (35.5 +/- 22.5 mg/dl) was higher than CC (4.1 +/- 2.8 mg/dl) and CT (20.4 +/- 11.2 mg/dl) genotypes of TGF-beta1 codon 10 (T-->C) gene polymorphism (P = 0.037). High producers of cytokine IL-10 -1082 [GG (n = 22) vs. AA + AG (n = 50)] and low producers of TGF-beta codon 25 [GC + CC (n = 17) vs. GG (n = 55)] had lower IMT of carotid artery but the difference did not reach statistical significance (P > 0.05). The CIMT of renal transplant patients was similar in IL-10 (-819, -592) and TNF-alpha (-308, -238) genotypes. No difference was observed in 24-h ambulatory blood pressure levels, serum lipoproteins, plasma homocysteine level, erythrocyte sedimentation rate, serum CRP, serum fibrinogen level in IL-10, TNF-alpha and TGF-beta1 genotypes. Besides the well-known factors, TGF-beta1 gene polymorphisms might play a role in CVD in RTR even at early stages of asymptomatic atherosclerosis.

Efficacy and safety of intravenous iron therapy for HCV-positive haemodialysis patients.

BACKGROUND: Iron supplementation is the cornerstone of anaemia management in haemodialysis (HD) patients. However, efficacy and safety of intravenous (IV) iron therapy in hepatitis C virus (HCV)-positive HD patients is yet to be elucidated. METHODS: Sixty-six maintenance HD patients with suboptimal response to recombinant human erythropoietin (rh-EPO) were administered IV iron. Each patient received 100 mg/session IV iron sucrose for ten consecutive HD sessions and then the dose was decreased to 50-100 mg weekly or biweekly. Patients were followed for haemoglobin (Hb), ferritin, rh-EPO dose requirements, transaminase levels, and adverse drug reactions. RESULTS: Baseline demographic and clinical characteristics, as well as Hb, ferritin, transaminase levels, rh-EPO and iron doses were similar between HCV-positive (n = 32) and HCV-negative patients (n = 29). After 5 months of follow-up, a significant increase in ferritin and Hb levels and decrease in rh-EPO doses were observed in both groups. The incidence of adverse drug reactions was not associated with HCV serology. Significant elevation in both alanine and aspartate aminotransferase levels were detected in HCV-positive patients. CONCLUSION: This study has shown that IV iron administration reverses suboptimal response to rh-EPO administration in HD patients regardless of HCV serology. There is however subtle increase of transaminase levels in HCV-positive patients. Further studies are warranted to reveal the impact of variation in serum transaminase levels during IV iron administration in HCV-positive HD patients.

TNF alpha-308 genotype and renin-angiotensin system in hemodialysis patients: an effect on inflammatory cytokine levels?

BACKGROUND: Renin-angiotensin system (RAS) was suggested to modulate inflammatory cytokine production. Angiotensin II was consistently shown to increase production of tumor necrosis factor alpha (TNF-alpha). However, inflammatory cytokines and RAS were modulated by genetic polymorphisms such as TNF-alpha-308 G > A and angiotensin-converting enzyme (ACE) I/D gene polymorphisms. The aim of this study was to investigate the effects of ACE and TNF-alpha genotypes on inflammatory cytokines in hemodialysis (HD) patients. METHODS: ACE I/D and TNF-alpha-308 G > A genotypes, pre- and postdialysis plasma renin activity (PRA), serum ACE, interleukin-1 beta (IL-1beta), and TNF-alpha levels were determined in 22 HD patients. RESULTS: Predialysis serum ACE activity is correlated with TNF-alpha (r = 0.63; P = 0.01), and PRA was correlated with IL-1beta levels (r = 0.49; P = 0.02). Pre/postdialysis IL-1beta and TNF-alpha were similar in DD and II/ID ACE genotypes. Predialysis TNF-alpha and IL-1beta (32.4 +/- 5; 35.1 +/- 4.2 vs. 28.1 +/- 3.7; 26.5 +/- 6.2 pg/mL; P < 0.05) and postdialysis TNF-alpha levels (30.4 +/- 1.4 vs. 28.4 +/- 0.82 pg/mL; P < 0.05) were significantly higher in TNF1/2 than TNF1/1 patients. CONCLUSION: ACE and TNF-alpha-308 G > A (1/2) gene polymorphisms may contribute to modulation of proinflammatory cytokine production and hence chronic inflammation in HD patients.

Angiotensinogen and plasminogen activator inhibitor-1 gene polymorphism in relation to chronic allograft dysfunction.

Chronic allograft dysfunction (CAD) is the most common cause of allograft failure in the long-term, and current immunologic strategies have little effect on this condition. The renin-angiotensin system (RAS) plays important roles progression of chronic renal disease. It is thought that plasminogen activator inhibitor-1 (PAI-1) functions in the RAS, in addition to involvement in thrombotic risk and fibrosis. This study investigated possible links between angiotensinogen (AGT) genotypes (M235T/MM, MT, TT) and PAI-1 genotypes (4G4G, 4G5G, 5G5G) and CAD assessments of both types of polymorphism were performed in 82 renal allograft recipients. One hundred healthy subjects were also investigated for AGT polymorphism, and 80 healthy subjects for PAI-1 polymorphism. Genotypes were determined using polymerase chain reaction (PCR) sequence-specific primers, and PCR followed by restriction fragment length polymorphism analysis. Kidney recipients with CAD had significantly lower frequencies of the MM genotype and the M allele than the recipients without CAD (p < 0.05 and <0.001). The transplant recipients with CAD also had significantly lower frequencies of the 5G5G genotype and the 5G allele than those without CAD (p < 0.001 and <0.05). Determination of AGT M235T and PAI-1 genotypes prior to transplantation may help identify patients who at risk for chronic renal transplant dysfunction.

Association between activated renin angiotensin system and bone formation in hemodialysis patients: is the bone mass genetically determined by ACE gene polymorphism?

BACKGROUND: Angiotensin II (ang II) receptor subtype I binding sites has been recently demonstrated on bone cell precursors. Ang II stimulates DNA and collagen synthesis in human adult bone cells. The aim of this study is to evaluate the role of renin angiotensin system in the bone metabolism and to address the genetic influence of angiotensin converting enzyme (ACE) gene polymorphism on bone mass in hemodialysis patients. METHODS: Forty-eight end-stage renal disease patients (28 male, 20 female mean age 42+/-13 years,) on maintenance hemodialysis were included in the study. Bone mineral density (BMD) was estimated at lumbar spine and T score worse than -1.5 were considered as osteopenia. Serum parathyroid hormone (iPTH) and osteocalcin (OC), bone alkaline phosphatase (bAP) and carboxy terminal propeptide type 1 collagen (PICP) levels were measured as markers of bone metabolism. Plasma renin activity (PRA), serum ACE activity and ACE gene polymorphism (II, ID, DD) were determined. RESULTS: Bone mineral density and T score of the hemodialysis patients were 0.92+/-0.17 g/cm2 and -1.36+/-1.50, respectively. Twenty-one patients (43,7%) were osteopenic (T score worse than -1.5) and mean T score of osteopenic patients was -2.72+/-0.72. T score of nonosteopenic group was -0.29+/-0.99. Serum calcium, serum, phosphorus, serum OC, serum bAP, serum PCIP, serum PTH levels were similar in osteopenics and nonosteopenics. No difference was observed in predialysis PRA and in both pre- and postdialysis serum ACE activity of patients in both groups. PRA after hemodialysis in nonosteopenic group was higher than osteopenics (p<0.05). Percent increment in PRA in hemodialysis patients was correlated with T score (R=0.48 p <0.05). Serum ACE activity was positively correlated with serum iPTH (R=0.29, p=0.02), serum OC (R=0.35, p=0.01), serum bAP (R=0.34, p=0.01), serum PCIP (R=0.36, p=0.01). T score (-0.7+/-1.5, vs -1.7+/-1.3 p <0.05) was higher in DD group (n=19) compared to II+ID group (n=29). CONCLUSIONS: Association of biochemical and radiological signs of increased bone formation with activated RAS in hemodialysis patients might be an evidence for the involvement of this system in the regulation of bone metabolism.

Apolipoprotein E gene polymorphism in renal transplant recipients: effects on lipid metabolism, atherosclerosis and allograft function.

INTRODUCTION: Atherosclerosis is a serious complication and leading cause of mortality in renal transplant recipients (RTRs). Hyperlipidemia may be associated with progression of renal disease and chronic allograft dysfunction. Similarities in the pathogenesis of glomerulosclerosis and atherosclerosis have been proposed. Apolipoprotein (apo) E gene code forms three major isoforms (E2, E3, and E4) with variable effects on lipid metabolism. PATIENTS AND METHODS: A total of 118 patients, at a mean age of 40 +/- 8 yr, were included in the study. Apo E genotyping was carried out on genomic DNA using polymerase chain reaction and restriction enzyme. Carotid artery intima media thickness and atherosclerotic plaques were evaluated by B-mode ultrasonography. The plasma levels of lipids and lipoproteins and acute phase reactants were also studied. Allograft function was evaluated by measuring serum creatinine and creatinine clearance values. RESULTS: The frequencies of E2, E3, and E4 alleles were 0.10, 0.78, and 0.12 respectively. Carotid artery atherosclerosis was found in 25% of E2 carriers, 30% of E3 carriers, and 57% of E4 carriers. Total cholesterol, total triglyceride, low-density lipoprotein, very low-density lipoprotein, apo B 100 levels were found to be higher in apo E4 carriers. Median apo A1 level was higher and allograft functions were better in apo E2 carriers (p < 0.05). Multiple regression analysis showed that allograft functions were negatively correlated with elevated acute phase reactants (p < 0.01) and only the age, but not the apo E genotypes, was an independent risk factor for atherosclerotic vascular disease (p < 0.01). DISCUSSION: The pathogenetic events linking lipid metabolism and allograft functions and development of atherosclerosis are complex and multifactorial in RTRs. Our results showed that apo E genotypes have influences on lipids, lipoproteins and allograft functions. The ultimate role of apo E4 gene polymorphism as a risk factor for development and progression of atherosclerosis in RTRs should be sought in further studies.

Increased incidence of carotid artery wall changes and associated variables in hemodialysis patients without symptomatic cardiovascular disease.

Cardiovascular disease (CVD) is still the major cause of the morbidity and mortality in hemodialysis (HD) patients. The characteristics of major arterial changes, atherosclerosis and related risk factors in HD patients remain unclear. We aimed to evaluate the atherosclerotic process in asymptomatic HD patients and healthy volunteers, and to determine the association between the risk factor(s) and the atherosclerotic process in these groups. 92 HD patients (female: 43, male: 49) and 62 age and sex matched healthy volunteers (female: 27, male: 35) were enrolled in this study. Diabetics, smokers, and patients with symptomatic CVD were excluded. The right and left carotid intima-media thicknesses (CIMTs) were measured and plaque structures were studied by B-mode ultrasound. The mean CIMT in patients and control group were 0.79 +/- 0.16 mm and 0.54 +/- 0.09 mm, respectively. Mean CIMT in HD patients was thicker (p < 0.001) and the presence ratio of plaque was higher in patients group (n=38, %61.2 vs n=9, %17.3) (p < 0.001). Calcified type of plaque was more frequent in HD patients than control group. Age (r=0.48, p < 0.001), left ventricular mass (r=0.42, p < 0.05), and homocysteine (r=0.46, p < 0.01), mean hematocrit (r=-0.36, p < 0.05), plasma CRP (r=0.50, p < 0.001), ESR (r=0.43, p < 0.01) and albumin (r= -0.34, p < 0.05) levels were correlated with the CIMT measurements and plaque presence, significantly. -CIMT as an atherosclerotic process indicator is thicker in asymptomatic HD patients than healthy subjects. We concluded that in addition to various classical risk factors, uremic environment may also contribute to acceleration of the atherosclerotic process.

Posterior leukoencephalopathy and nephrotic syndrome: just a coincidence?

Posterior leukoencephalopathy syndrome (PLES) is an acute neurological disorder. The most plausible hypothesis for the pathophysiology of PLES is the loss of autoregulation and consequent vasogenic edema. PLES is mostly attributed to severe or sudden elevations of arterial blood pressure. A number of reports, however, describe patients with PLES without severe hypertension. This report presents two patients with nephrotic syndrome who developed PLES without customarily severe hypertension. Proteinuria, low levels of serum albumin, or generalized increase in capillary permeability in nephrotic syndrome can initiate PLES with moderately high arterial blood pressure levels. PLES is increasingly recognized by neurologists, but it should also be remembered by internists when confronted with patients with nephrotic syndrome who present with neurological symptoms, whether or not they have severe hypertension.

The booster phenomenon in 2-step tuberculin skin testing of patients receiving long-term hemodialysis.

BACKGROUND: Tuberculosis remains a significant health problem for patients receiving long-term hemodialysis (HD). The tuberculin skin test (TST) is an important method for detecting Mycobacterium tuberculosis infection. This study examined the significance and frequency of the booster phenomenon in serial TST of HD patients. METHOD: Fifty-three outpatients in a hospital-based HD center in Turkey were screened for tuberculosis with the TST between August and October 1999. To determine the frequency of booster phenomenon, patients with less than 10 mm indurations to the initial TST were given a second test 7 days later. RESULTS: Nineteen (35.8%) of 53 patients had a significant tuberculin reaction (> or = 10 mm) on the initial TST. The booster effect was detected in 10 (29.4%) of 34 patients who had a negative reaction (< 10 mm) to the initial test. Overall, 29 (54.7%) patients showed a significant reaction on both tests. CONCLUSIONS: These results showed significant rates of TST positivity and the booster effect in this HD center.

Radiocontrast-induced nephrotoxicity and urinary alpha-glutathione S-transferase levels: effect of amlodipine administration.

AIMS: The exact pathogenesis and prophylaxis concerning radiocontrast-induced nephrotoxicity (RCIN) was unclear. Short-acting calcium antagonists were used to prevent RCIN. This study was designed to evaluate the role of a long-acting calcium antagonist (amlodipine) administration by determining serum creatinine (SCre) levels and 24 hour urinary excretion rates of glutathione S-transferase alpha (GST-alpha) which has a selective localization only to proximal tubular epithelium. METHODS: In a prospective trial, 29 outpatients (19 M, 10 F) undergoing coronary angiography were randomized and either amlodipine 10 mg/day (n = 15) or placebo (n = 14) were administered prior to angiography and continued thereafter. All patients had normal basal renal function and none of them had any risk factor for RCIN. A low osmolar, nonionic contrast media (iopamidol 76%) was administered to all patients. Creatinine clearance (CCre), SCre and 24-hour urinary GST-alpha levels were measured before, 24 hours and 7 days after angiography. RESULTS: SCre and 24 hour urinary GST-alpha values increased on 24th hour following the angiography in both groups (p < 0.017 and 0.001, respectively). Pretreatment with amlodipine created no difference in both variables (p > 0.05). CONCLUSIONS: A reversible tubular dysfunction occurs following radiocontrast administration which was manifested by an increase in urinary GST-alpha excretion rates. Pretreatment with a long acting calcium antagonist amlodipine has no effect on the course of enzyme excretion and alteration observed in SCre.