Cardiac Risk Assessment in Kidney Transplant Candidates: Clinical Usefulness of Different Guidelines.

Although cardiovascular (CV) assessment is recommended to minimize perioperative risk in all potential kidney transplant recipients, the utility and reliability of various assessment methods are not well established. In this study, we investigated the CV evaluations and outcomes of standardized CV assessment protocols (Lisbon and American Society of Transplantation [AST]) in potential kidney transplant recipients. Data were analyzed for 266 end-stage renal disease patients (mean age 45.4 ± 13 years, female-to-male ratio 126:140) accepted for kidney transplantation wait-listing. Patients were classified as low and high cardiac risk according to their first cardiac evaluation. Major cardiovascular events (CVEs) and deaths were recorded. At the end of follow-up (median 639 days), 72 (27.1%) patients underwent kidney transplantation. A total of 49 patients (18.4%) had CVEs and 42 (15.8%) patients died. Being over 45 years of age and having dialysis vintage over 1 year were found to be independent risk factors for CVEs. Forty-eight out of 60 high-risk patients evaluated with noninvasive tests had negative results. Twelve out of these 48 patients had a CVE in due course. Among 10 patients who underwent coronary angiography, 1 had a CVE and 1 died. The sensitivity and specificity of the AST guidelines (area under the curve = 0.647, P = .005, sensitivity 83%, specificity 54%) were higher than Lisbon. In conclusion, the predictive risk factors for CVEs were age over 45 years and dialysis vintage over a year. Our results also suggest that exercise electrocardiography and myocardial perfusion scintigraphy for cardiac evaluation are less sensitive in CVE prediction. We recommend clinicians to use the AST guidelines and to prioritize coronary angiography in pretransplant CV assessment.

Association of BK Virus Titers With Lymphocyte Count in Renal Transplant Patients.

OBJECTIVES: Regular screening for the BK virus (BKV) is recommended for early intervention in renal transplant patients. Identification of predictors for the development of BK viremia would improve their monitoring. We performed a retrospective study investigating whether the lymphocyte count may be a predictor of BKV development in renal transplant patients. PATIENTS AND METHODS: We retrospectively analyzed 268 renal transplant patients who were followed in our clinic from January 2011 to August 2014. The viral loads of BKV in blood detected by quantitative real-time polymerase chain reaction test were performed according to relevant guidelines. We also retrospectively monitored lymphocyte count, creatinine, immunosuppressive drug doses, and tacrolimus/cyclosporine/mTor inhibitors levels during the same time as BKV screening. Demographic and other clinical data were extracted from patients' files. The calculation of correlation coefficients and receiver operating characteristics (ROC) curve analysis were performed. RESULTS: Overall, 16 patients (5.9%) who experienced BKV-DNA positivity were included the study. Mean age of patients was 38.2 ± 12.8 years. All patients received steroid and calcineurin inhibitors (CNIs). Mycophenolate mofetil/mycophenolic acid (MMF/MPA) was administered to 14 patients. BKV-DNA was found in 64 of the 88 (72.7%) plasma samples. The lymphocyte count on the first day of positive BKV-DNA test was significantly lower than in those with negative BKV-DNA results (1700/µl vs 2400/µl, respectively; P = .009). Its AUC of the ROC curve was 0.77 (P = .012). The optimal cutoff point for lymphocyte count was 1900/µl, and sensitivity and specificity for predict BKV positivity were 75% and 78.57%, respectively. We also found that lymphocyte count negatively correlated with the first detectable BKV titers (r = -0.438; P = .015). However, there is no relation between CNI/mTOR inhibitor levels, MMF/MPA doses, lymphocyte count, and all BKV-titers. CONCLUSIONS: Decreased lymphocyte count may be a predictor for preceding BKV viremia. Clinicians should be more careful in terms of the decreased lymphocyte count in case of BKV replication in renal transplant patients.

Fibroblast growth factor-23 levels are associated with uric acid but not carotid intima media thickness in renal transplant recipients.

INTRODUCTION: Cardiovascular disease (CVD) is the leading cause of mortality in chronic kidney disease (CKD) patients. Fibroblast growth factor-23 (FGF-23) is associated with atherosclerosis and cardiovascular mortality in CKD patients and healthy subjects. However, data in renal transplant recipients (RTR) are scarce. We aimed to determine factors associated with FGF-23 and to explore its relationship to atherosclerosis. METHODS: Forty-six patients and 44 controls were included. FGF-23 was measured from plasma. Carotid intima media thickness (CIMT) was evaluated ultrasonographically. RESULTS: Patients had higher waist circumference (WC; 92.2 ± 14.9 vs 85.3 ± 11.0 cm; P < .05), glucose (99.8 ± 17.2 vs 90.3 ± 6.5 mg/dL; P < .01), creatinine (1.43 ± 0.6 vs 0.86 ± 0.1 mg/dL; P < .01), triglyceride (160.4 ± 58.9 vs 135.6 ± 59.8 mg/dL; P < .05), white blood cells (WBC; 7938.6 ± 2105.2 vs 6715.7 ± 1807.5 WBC/mm(3); P < .01), ferritin (217.0 ± 255.8 vs 108.3 ± 142.4 ng/mL; P < .05), uric acid (6.5 ± 1.6 vs 4.7 ± 1.3 mg/dL; P < .01), C-reactive protein (CRP; 8.2 ± 18.2 vs 5.3 ± 7.9 mg/L; P < .01), parathyroid hormone (PTH; 89.7 ± 59.2 vs 44.1 ± 16.7 pg/mL; P < .01), and alkaline phosphatase (ALP; 162.5 ± 86.6 vs 74.2 ± 21.9 U/L; P < .01). FGF-23 was higher in patients (11.7 ± 7.2 vs 9.6 ± 6.8 pg/mL; P < .05). CIMT was similar (0.58 ± 0.09 vs 0.57 ± 0.1 mm; P > .05). WC, creatinine, and uric acid were positively correlated with FGF-23, whereas albumin showed negative correlation. On multivariate analysis only creatinine and uric acid were determinants of FGF-23. CONCLUSION: FGF-23 levels are associated with uric acid in RTR. Larger studies are needed to confirm this finding.

Phosphorus control in peritoneal dialysis patients.

Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean+/-s.d. age of 55+/-16 years and mean duration of PD of 33+/-25 months. Serum calcium (Ca(2+)), ionized Ca(2+), phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D(3), 1,25-dihydroxy vitamin D(3), total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3+/-0.65, weekly creatinine clearance 78.5+/-76.6 l, and daily urine output 550+/-603 ml day(-1). Fifty-five percent of patients had a urine volume of <400 ml day(-1). Mean serum phosphorus level was 4.9+/-1.3 mg per 100 ml, serum Ca(2+) 9.4+/-1.07 mg per 100 ml, iPTH 267+/-356 pg ml(-1), ionized Ca(2+) 1.08+/-0.32 mg per 100 ml, calcium phosphorus (Ca x P) product 39+/-19 mg(2)dl(-2), 25(OH)D(3) 8.3+/-9.3 ng ml(-1), 1,25(OH)(2)D(3) 9.7+/-6.7 pg ml(-1), total alkaline phosphatase 170+/-178 U l(-1), and bone alkaline phosphatase 71+/-108 U l(-1). While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca(2+) level was > or =9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca x P product was >55 mg(2)dl(-2) in 136 patients (26%) and lower than 55 mg(2)dl(-2) in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1+/-1.4 and 4.5+/-1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca x P in 73%, serum Ca(2+) in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosphorus control in the majority of patients.

Effects of spironolactone in an experimental model of chronic cyclosporine nephrotoxicity.

BACKGROUND: Cyclosporine (CsA)-associated nephrotoxicity is a long-term complication in transplant patients. Chronic CsA nephrotoxicity is associated with renal fibrosis and hyaline arteriolopathy. The aim of this study was to investigate the effect of spironolactone on functional and structural alterations as well as on platelet-derived growth factor B (PDGF-B) and transforming growth factor (TGF) beta expression induced by CsA in a rat model of chronic CsA nephrotoxicity. MATERIALS AND METHODS: Twenty-four rats were divided into 3 groups. Group 1 (G1) received vehicle only (V); G2, CsA (15 mg/kg/d; CsA) by intraperitoneal (IP) injection; and G3, a similar CsA dosage + spironolactone (20 mg/kg/d; CsA + Ald.) by the oral route. At the end of 28 days, glomerular filtration rate (GFR) and blood CsA levels were measured as well as histopathological and immunohistochemical analyses performed on renal tissue. RESULTS: Mean CsA trough levels in G2 and G3 were both above 2000 ng/mL. In G2, GFR was lower than G1 and G3 (0.35 +/- 0.05, 1.64 +/- 0.24, and 1.20 +/- 0.25 mL/min, respectively; P < .001). There was a significantly increased number of arteriolopathic changes in G2 and G3 vs G1 (16% +/- 3.7%, 15% +/- 6.8%, 3% +/- 1.2%, respectively; P < .001). Interstitial fibrosis was significantly increased in G2 vs G1 and G3 (52%, 0%, 27%, respectively; P < .05). Marked by up-regulated PDGF-B and TGF beta expressions were observed in G2 vs G1 or G3: 100%, 0%, 37.5%, respectively, for PDGF-B (P < .001) and 87.5%, 0%, 12.5%, respectively, for TGF beta (P < .001). CONCLUSION: Our results suggested that chronic CsA nephrotoxicity may be mitigated by aldosterone receptor blockade which seemed to be associated with down-regulation of PDGF-B and TGF beta expression.

Renal protective effects of leukotriene receptor blockers in an experimental model of cyclosporine nephrotoxicity.

BACKGROUND: Chronic cyclosporine (CsA) nephrotoxicity is associated with renal fibrosis and hyaline arteriolopathy. Fibrogenic cytokines, such as transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF), play a pivotal role in CsA nephrotoxicity. Previous studies have demonstrated the possible role of leukotrienes (LT) in chronic CsA nephrotoxicity. The aim of this study was to examine the possible beneficial effects of LT blockers in attenuating the morphological and histochemical effects induced by CsA in a rat model of CsA nephrotoxicity. MATERIALS AND METHODS: Twenty-four male Wistar rats were divided into 3 groups (n = 8). The first group (G1) was treated with vehicle intraperitoneally (IP) for 60 days. The second group (G2) was treated with 15 mg/kg CsA IP for 60 days. The third group (G3) was treated with the same dose of CsA plus 4 mg/kg montelukast administered by oral gavage for 60 days. RESULTS: There was a statistically significant decrease in glomerular filtration rate (GFR) among G2 compared with G1 animals: 0.41 +/- 0.03 vs 1.63 +/- 0.12 mL/min (P < .001), or G3 hosts: 0.41 +/- 0.03 vs 0.95 +/- 0.05 mL/min (P < .005), respectively. The percentage of hyaline arteriolopathic changes was higher in G2 than G1 or G3: 81.66% +/- 8.2% vs 11.83% +/- 0.87% (P < .01) or 37.0% +/- 8.8% (P < .01), respectively. Fibrosis score was higher in G2 compared with G1 or G3: 1.5 +/- 0.04 vs 0.16 +/- 0.02 (P < .001) and 1.0 +/- 0.05 (P < .05), respectively. TGF-beta and VEGF immunoexpression were significantly increased in G2 compared with G1 (P < .05) or G3 (P < .05). CONCLUSIONS: Our study suggested that LT may play a critical role in the pathogenesis of chronic CsA nephrotoxicity; the administration of montelukast, a LT receptor blocker, may prevent CsA-induced nephrotoxicity.

Severe vitamin D deficiency in chronic renal failure patients on peritoneal dialysis.

UNLABELLED: The aim of this study was to evaluate the prevalence of vitamin D deficiency in chronic renal failure (CRF) patients on peritoneal dialysis (PD) and to correlate the findings with various demographic and renal osteodystrophy markers. METHOD: This cross-sectional, multicenter study was carried out in 273 PD patients with a mean age of 61.7 +/- 10.9 years and mean duration of PD 3.3 +/- 2.2 years. It included 123 female and 150 male patients from 20 centers in Greece and Turkey, countries that are on the same latitude, namely, 36-42 degrees north. We measured 25(OH)D3 and 1.25(OH)2D3 levels and some other clinical and laboratory indices of bone mineral metabolism. RESULTS: Of these 273 patients 92% (251 patients) had vitamin D deficiency i.e. serum 25(OH)D3 levels less than 15 ng/ml, 119 (43.6%) had severe vitamin D deficiency i.e., serum 25(OH)D3 levels, less than 5 ng/ml, 132 (48.4%) had moderate vitamin D deficiency i.e., serum 25(OH)D3 levels, 5-15 ng/ml, 12 (4.4%) vitamin D insufficiency i.e., serum 25(OH)D3 levels 15 - 30 ng/ml and only 10 (3.6%) had adequate vitamin D stores. We found no correlation between 25(OH)D3 levels and PTH, serum albumin, bone alkaline phosphatase, P, and Ca x P. In multiple regression analyses, the independent predictors of 25(OH)D3 were age, presence of diabetes (DM-CRF), levels of serum calcium and serum 1.25(OH)2D3. CONCLUSION: We found a high prevalence (92%) of vitamin D deficiency in these 273 PD patients, nearly one half of whom had severe vitamin D deficiency. Vitamin D deficiency is more common in DM-CRF patients than in non-DM-CRF patients. Our findings suggest that these patients should be considered for vitamin D supplementation.

Inhibition of the renin angiotensin system decreases fibrogenic cytokine expression in tacrolimus nephrotoxicity in rats.

The aim of our study was to investigate the influence of angiotensin-converting enzyme (ACE) inhibition and angiotensin II receptor blockage on the renal function by light microscopic and immunohistochemical findings in a rat model of tacrolimus nephrotoxicity. Thirty-two male Wistar rats were divided into four groups of eight: G1 = control group; G2-G3, G4 = Tacrolimus (Tac) 1 mg/kg/d intraperitoneally (ip); G3 (Tac + Q) = ip Tac and peroral quinapril 10 mg/kg; and G4 (Tac + V) = Tac and valsartan 40 mg/d. Serum blood urea nitrogen (BUN), creatinine, and creatinine clearance were measured before and at the end of the study period. Renal tissues were assessed for light microscopic findings of tacrolimus toxicity. Transforming growth factor-beta, VEGF, PDGF, BMP-7, and interleukin-6 (IL-6) expression were semiquantitatively scored after immunohistochemical staining. At the end of the study period serum BUN and creatinine levels were increased in all groups, but creatinine clearance was not significantly changed between the groups. Afferent arteriolopathy was significantly less pronounced in G3 versus G2 and G4. Interstial fibrosis was significantly less pronounced in G3 and G4 versus G2. TGF-beta, PDGF, and IL-6 expression were significantly increased in G2, G3, and G4 compared to G1, and in G2 compared to G3 and G4. BMP-7 expression was significantly decreased in G2, G3, and G4 compared to G1, whereas the differences between G2, G3, and G4 failed to reach statistical significance. In conclusion, the results of our study suggested that renin angiotensin inhibition down-regulates fibrogenic cytokine expression in rats displaying tacrolimus nephrotoxicity.

Transforming growth factor-beta1, vascular endothelial growth factor, and bone morphogenic protein-7 expression in tacrolimus-induced nephrotoxicity in rats.

The aim of our study was to investigate transforming growth factor (TGF)-beta1, vascular endothelial growth factor (VEGF), and bone morphogenic protein-7 (BMP-7) expression in the rat model of chronic tacrolimus (TAC) toxicity compared to healthy controls. Seventeen male Wistar rats were divided into two groups: group 1 animals were healthy controls and Group 2 animals were treated with TAC (1 mg/kg per day intraperitoneally for 8 weeks). At the end of the study period the animals were sacrificed following renal function studies including blood urea nitrogen (BUN), serum creatinine, and creatinine clearance, and renal tissues were examined by light microscopy for the findings of tacrolimus toxicity, specifically for afferent arteriolopathy and interstitial fibrosis. TGF-beta1, VEGF, and BMP-7 expression were assessed by semiquantitative scoring of the immunohistochemically stained specimens. Mean TAC levels were 5.53 +/- 2.38 ng/mL in group 2. BUN, creatinine levels, and creatinine clearance were 57.99 +/- 11.13 vs 39.49 +/- 5.64 mg/dL; 0.60 +/- 0.16 vs 0.65 +/- 0.09 mg/dL; 0.97 +/- 0.39 vs 1.17 +/- 0.32 mL/min in group 2 versus group 1. Only the BUN level was significantly higher in group 2 compared to group 1. Afferent arteriolopathy and interstitial fibrosis were significantly increased in group 2 compared to group 1. TGF-beta1 and VEGF expression was significantly increased while BMP-7 expression was significantly decreased in group 2 versus group 1. In conclusion, our findings suggest that TAC-induced nephrotoxicity is associated with increased TGF-beta1 and VEGF and decreased BMP-7 expression.

Cyclosporine-A induced nephrotoxicity is associated with decreased renal bone morphogenetic protein-7 expression in rats.

The aim of our study was to investigate bone morphogenetic protein-7 (BMP-7) expression in a rat model of chronic cyclosporine (CsA) toxicity compare with healthy controls, as well as the influence of treatment with the angiotensin-converting enzyme inhibitor (ACEI) quinapril. Twenty-four male Wistar rats were divided into groups of eight animals treated with CsA (15 mg/kg intraperitoneally) for 8 weeks (CsA group) without or with quinapril (10 mg/kg per day in the drinking water: CsA group + Q) for comparison with healthy controls (H group). The renal tissues were examined by light microscopy for CsA toxicity; specifically, tubulointerstitial damage and afferent arteriolopathy as well as BMP-7 expression were semiquantitatively scored by immunohistochemical staining. Mean CsA levels were 1982 ng/mL and 1968 ng/mL for the CsA and CsA + Q groups, respectively. At the end of the study period, the mean serum creatinine levels were 0.8 +/- 0.2 mg/dL, 1.6 +/- 0.8 mg/dL, and 1.4 +/- 0.8 mg/dL for the H, CsA, and CsA + Q groups, respectively. Interstitial fibrosis, tubular atrophy, and afferent arteriolar hyalinization were present in the CsA group and, to a lesser degree, in the CsA + Q group, compared with the H group. CsA-treated rats displayed significantly decreased BMP-7 expression compared with healthy controls (P <.0005). BMP-7 expression was higher among the CsA + Q group than the the group CsA group. In a rat model histologic changes characteristic of CsA-induced nephrotoxicity are associated with decreased expression of BMP-7, which seems to be at least partially restored by ACE inhibition.

Angiotension converting enzyme inhibition and calcium channel blockage improves cyclosporine induced glucose intolerance in rats.

The aim of this study was to evaluate the effects of quinapril, valsartan, and amlodipin on glucose tolerance in cyclosporine (CsA)-toxic rats. Among 40 male Wistar rats 32 were administered cyclosporine (CsA) (15 mg/kg) intraperitoneally for 6 weeks. Quinapril (10 mg/kg per day) (group Q), valsartan (40 mg/kg per day) (group V), and amlodipine (10mg/kg per day) (group A) were administered to individual sets of eight CsA-treated animals via the drinking water with the remaining untreated hosts followed as a control group (group C) and 8 healthy controls (group H). A Glucose-tolerance test was performed by administering oral glucose (2 g/kg) followed by blood samples obtained from the tail vein at baseline as well as 30,60,90, and 120 minutes after the glucose load. Glucose area under the curve (AUC) was calculated according to the trapezoidal rule. CsA levels were determined using an immunofluorescence method. Kruskal Wallis ANOVA test was used for statistical analysis. Median CsA levels were 1968 ng/mL, 1982 ng/mL, 1580 ng/mL, 1600 ng/mL; and glucose AUC, 232.4 +/- 130 mg/min per dL, 63.1 +/- 25 mg/min per dL, 115.0 +/- 90 mg/min per dL, 47.4 +/- 34 mg/min per dL 53.4 +/- 38 mg/min per dL for groups C,Q,V,A and H, respectively. Quinapril-treated and amilodipine-treated rats displayed a lower glucose AUC than group C (P <.01), which had higher glucose levels than healthy controls (P <.001). In summary, CsA treated rats show impaired glucose tolerance, which is improved by quinapril or amlodipine treatment. Angiotensin converting enzymes inhibitors and calcium channel blockers affect beta cell function rather than insulin sensitivity.

QT dispersion in hemodialysis and CAPD patients.

Prolongation of repolarization dispersion (QT interval dispersion) measured from the 12-lead surface ECG has been associated with sudden cardiac death and ventricular tachyarrhythmias in a variety of cardiac disorders. The aim of our study was to assess the effects of hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) on QT dispersion in end-stage renal disease patients. 20 chronic HD patients (mean age 57.75 +/- 13.79 years) and 20 CAPD patients (mean age 50.79 +/- 14.94 years) who had no complaints and symptoms of cardiac arrhythmias as well as 20 healthy volunteers (mean age 48.74 +/- 10.88 years) underwent ECG testing. All HD patients were on bicarbonate three times weekly with cuprophane capillaries. 12-lead ECGs were recorded on the day after HD. The CAPD patients were on a standard CAPD program (four times daily with 2,000 cm(3) peritoneal fluid). ECGs were recorded when the patients were receiving their regular standard CAPD program. All ECGs were analyzed manually by one observer. There were no statistically significant differences in dialysis duration, blood urea nitrogen, creatinine, sodium, calcium, and parathormone values between the HD and CAPD patients. The serum potassium values were significantly higher in HD patients when compared to CAPD patients. There was no difference in the mean of maximal QT among all three groups. The rate of QT interval dispersions was significantly higher in HD and CAPD patients as compared with healthy controls (p < 0.05). There was no statistically significant difference in the QT dispersion rates between HD and CAPD patients. In conclusion, there is a tendency to cardiac arrhythmias in HD patients during the postdialysis period. Although CAPD patients are receiving dialysis daily, they also have higher rates of QT dispersions and accordingly a tendency to arrhythmias.

Causes of late leaks in peritoneal dialysis patients.

BACKGROUND/AIMS: Late dialysis leakage is an important complication of peritoneal dialysis. The aim of our study was to investigate the causes of late leaks in patients on peritoneal dialysis. METHODS: 25 patients (19 F: 6 M; mean age: 56 +/- 14) with and 25 patients (10 F : 15 M; mean age: 57 +/- 12) without dialysis leakage on maintenance peritoneal dialysis treatment were included in the study. Data on demographic characteristics including age, sex, body mass index, body surface area, primary renal disease and peritoneal dialysis characteristics including implantation technique of the catheter, site of the catheter, time from catheter implantation to initiation of peritoneal dialysis, daily total filling volumes, use of hypertonic solutions, membrane transport properties and total and peritoneal creatinine clearances were retrospectively collected for both groups. RESULTS: The number of female vs. male patients (76% vs. 40%, p < 0.05) and patients on CAPD vs. APD (68% vs. 56%, p < 0.05) were significantly higher in the group with dialysis leakage. Patients with leakage also had lower average transport properties (p < 0.05) and lower total creatinine clearances (p < 0.05). Other demographic and peritoneal dialysis characteristics were similar in both groups. CONCLUSIONS: Female gender and CAPD as opposed to male gender and APD are the risk factors involved in the development of late dialysis leaks. Peritoneal membrane transport characteristics as well as total creatinine clearance also seems to influence the development of complications.

The impact of the earthquake in northwestern Turkey on the continuous ambulatory peritoneal dialysis patients who were living in the earthquake zone.

In August 1999, an earthquake of magnitude 7.8 on the Richter scale hit northwestern Turkey. The epicenter was in Izmit, an industrial town about 60 km from Istanbul. This paper presents data about the fate of CAPD patients who were living in that region at the time of the earthquake. A total of 42 continuous ambulatory peritoneal dialysis (CAPD) patients (14 females, 28 males; 37 adult patients, 5 pediatric patients) were permanent residents of the earthquake region. They were followed in the CAPD units of Marmara University Hospital (n = 6), Gata Military Hospital (n = 2), and Goztepe SSK Hospital (n = 10, including the 5 pediatric patients) in Istanbul, and in Uludag University Hospital in Bursa (n = 6) and Kocaeli University Hospital in Izmit (n = 18). Two CAPD patients, together with their families, died under the rubble in the city of Golcuk. One CAPD nurse from Kocaeli University Hospital in Izmit also died a victim of the earthquake. One patient who lived in Golcuk was under the rubble for 3 hours; she was rescued with no crush injuries and was able to continue with CAPD 24 hours after her rescue. Eight patients reported that their homes were completely destroyed during the earthquake, while nine patients reported serious damage to their houses. Ten patients had to move to other towns to live with relatives because their homes were no longer suitable for habitation, and twelve patients had to stay permanently in tents provided by the Red Cross. All of the patients were able to continue their CAPD therapy and had no interruption in the supply of their CAPD solutions. Four patients on continuous cycling peritoneal dialysis (CCPD) therapy continued to use their HomeChoice machines (Baxter Healthcare Corporation, Deerfield, IL, U.S.A.) even while living in a tent. CAPD patients from the Kocaeli University Hospital had to be temporarily referred to other CAPD centers in Istanbul and Bursa because the Kocaeli University Hospital was seriously damaged in the earthquake. We expect that these major changes in quality of life circumstances will have an important impact on the morbidity of these patients, especially in regard to the rate of peritonitis and the adequacy of dialysis.

Severe hyperkalemia in two renal transplant recipients treated with standard dose of trimethoprim-sulfamethoxazole.

Hyperkalemia is a serious electrolyte disorder and is a frequent finding in renal transplant recipients. Trimethoprim-induced hyperkalemia has been increasingly reported in recent years. We describe two renal transplant recipients who developed end-stage renal disease secondary to familial Mediterranean fever and presented with severe hyperkalemia secondary to the use of standard dose of trimethoprim. One of the patients had potential underlying adrenal insufficiency, which might be a contributing factor for the development of hyperkalemia. We concluded that renal transplant patients receiving even the standard dose of trimethoprim should be monitored closely for the development of hyperkalemia. They should be recognized as a group with increased risk in regard to their concurrent renal insufficiency, concomitant use of cyclosporine, and associated tubulointerstitial disease. Patients with secondary amyloidosis are at even greater risk, and subclinical adrenal insufficiency may be an underlying risk factor for the development of severe, life-threatening hyperkalemia among this group of patients.

Association between salt sensitivity and target organ damage in essential hypertension.

Cardiovascular events occur more frequently in sodium-sensitive patients with essential hypertension; recently, sodium sensitivity was shown to be a cardiovascular risk factor independently of other classic factors such as blood pressure and cigarette smoking This study examined the relationship between salt sensitivity status and target organ damage in hypertensive patients. Ninety-six patients (35 men, 61 women) with moderate essential hypertension were studied for salt sensitivity status and the presence of target organ damage, including hypertensive retinopathy, serum creatinine, creatinine clearance, and urinary albumin excretion (UAE). Four different patterns of left ventricular anatomic adaptation were identified by categorizing patients according to the values of left ventricular mass index and relative wall thickness by the means of echocardiography. Forty-five (47%) patients were shown to be salt-sensitive, in contrast to 51 (53%) salt-resistant subjects. Serum creatinine and UAE were significantly higher in the group of salt-sensitive hypertensives (P < .05 and P < .001, respectively). Left ventricular mass index (LVMI), relative wall thickness (RWT), and left atrial index (LAI) were all significantly higher in the group of salt-sensitive hypertensive patients. Concentric hypertrophy was significantly more prevalent in the salt-sensitive group (37.8% v 11.8%; P < .01). The prevalence of hypertensive retinopathy in the salt-sensitive group was 84.4%, in contrast to 59.6% in the salt-resistant group (P < .01). Multivariate regression analysis revealed salt sensitivity as a significant predictor of LVMI, RWT, and UAE, independently of age, body mass index, and mean blood pressure. In conclusion, salt-sensitive hypertensive patients are more prone to develop severe hypertensive target organ damage that may enhance their risk of renal and cardiovascular morbidity.

Tetracycline-induced acute interstitial nephritis as a cause of acute renal failure.

Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.