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Objectives: Cross-sectional studies have long suggested that renalfunction declines with age. However, there are limited longitudinalstudies with data on within individual changes in renal function withtime. The aim of our study was to assess the natural rate of declinein glomerular filtration rate with age in a longitudinal study both inhealthy subjects and in subjects with co-morbidities. Methods: Weretrospectively analyzed database of subjects attending a screeningcenter in Israel. Estimated glomerular filtration rate (eGFR) wasassessed consequently in subjects who had 5 visits or more, eachvisit at least one year apart. The Chronic Kidney Disease Epidemiol-ogy Collaboration (CKD-EPI) equation was used to assess eGFR. Onlysubjects with age range of 20–80 years and baseline line eGFR ofN90 mL/min/1.73 m2 were included. Results: Out of 23,223 subjects,2923 had a base line eGFR above 90 mL/min/1.73 m2 and visitedthe screening center five times or more each visit at least one yearapart. 2693 subjects were apparently healthy while 230 had differentco-morbidities. The mean (SD) follow up time was 7.8 years ± 2.2(range 4–12 years). The mean (±standard error) annual rate ofdecline in eGFR in healthy subjects was of 0.97 ± 0.02 mL/min/year/1.73 m2. The annual decline in eGFR at different age groups increasedsignificantly from 0.82 ± 0.22 at age group 20–30 years to 0.84 ±0.08, 1.07 ± 0.08 and 1.15 ± 0.12 mL/min/year/1.73 m2 in age groups31–40, 41–50 and 50 years and older respectively (p b 0.001). Therewas no correlation between the annual decline in eGFR and bodymassindex (BMI) category. In subjects with either hypertension, diabetesmellitus, impaired fasting glucose or combined co-morbidity thedecline in eGFR was 1.12 ± 0.12, 0.77 ± 0.16, 0.85 ± 0.17, 1.18 ±0.26 mL/min/year/1.73 m2 respectively. Discussion: The main resultof this large longitudinal study is to provide a better estimation ofthe annual decrease in eGFR with age in normal subjects, found tobe 0.97 ± 0.02 mL/min/year/1.73 m2. This value is higher than thecommon number referred to in the literature of 0.8 mL/min/year/1.73 m2. Moreover, we have demonstrated that the annual changein GFR increased significantly with age. Our study is unique forthe following: a large number of approximately 3000 subjects wereassessed; the latest and most accurate equation for estimating GFRwas used; subjects with a wide age range were included; the studywas not limited to subjects with impaired baseline GFR; five or morerepeated measurements of eGFR were performed throughout thefollowup period giving a powerful validation of the results.Conclusion:This large longitudinal study provides new data on the annual decreasein eGFR both in healthy subjects as well as in thosewith co-morbidities.Accurate prediction of the natural rate of GFR decline can distinguishbetween normally aging kidney and those with chronic kidneydisease avoiding unnecessary diagnostic procedures in the formerand providing appropriate treatment in the latter.

doi:10.1016/j.ejim.2013.08.159

ID: 100Hypertension in autosomal dominant polycystic kidney disease:A clinical study of 278 casesN. Mchirgui, S. Barbouch, K. Ben Abdelghani, F. Jaziri, A. Khedher

Internal Medicine A, Charles Nicolle Hospital, Tunis, Tunisia

Objective: Autosomal dominant polycystic kidney disease (ADPKD)is a frequent hereditary disease and hypertension (HT) is a commoncomplication of this disease. The aims of this study are to know theclinical features of ADPKD in our department, to assess the prevalenceof HT and to analyse the relationship between HT and ADPKD.Methods: It is a retrospective study including 278 patients affectedby ADPKD and hospitalised between 1965 and 2000. All patients were

assessed by genetic evaluation as well as complete clinical and lab-oratory exams. Statistic analyses were made with the chi-square testand student's test. Results: Patients were 141 males (50, 7%) and 137females (49, 3%) aged between 8 and 75 years (mean age 49, 6 ± 11,8 years). Molecular genetic studywas undertaken only in 8 families andshowed: 62, 5% of PKD1, 12,5% of PKD2 and 25% of no PKD1 no PKD2.The primary symptoms of ADPKD included renal failure (RF) in 155cases (55, 7%), lumbar pain in 138 cases (49, 6%), HT in 94 cases (33,8%)and hematuria in 86 cases (30,9%). Themain physical examination signswere large kidneys in 188 cases (66,7%) and HT in 152 cases (54,7%).Renal function was normal in 62 patients (50% hypertensives and 50%normotensives) while RF was observed in 216 patients (56% hyperten-sives and 44% normotensives). ADPKD was associated to hepatic cystsin 104 patients (37,4%). The prevalence of HT was the same betweenisolated ADPKD and the form associated to hepatic cysts (56,9% VS50,9%, p = 0,33). After a mean follow up of 12 months (min. 1 monthand max. 242 months), renal function was stable in 48,6% of patientsand impaired in 51,4% of them. This deterioration of renal function wasmore frequent in males and hypertensive patients. Conclusion: Thediagnosis of ADPKD was made often in patients with chronic renalfailure. It appeared that HT is an early event in the natural history ofADPKD, and has no influence on the onset of RF and contributes to therenal function damage.

doi:10.1016/j.ejim.2013.08.160

ID: 208Urinary GGT: A cheaper predictor of acute kidney injury?Kani Masarogullaria, Asuman Camyarb, Alev Garipb, Selahattin Bicakc,Cenk Gokalpd, Ender Hure, Banu Sarsikf, Eser Sozmeng, Soner Dumanb

aNephrology Department, Near East University, Nicosia, CyprusbInternal Medicine Department, Ege University Hospital, Izmir, TurkeycInternal Medicine, Sehitkamil State Hospital, Gaziantep, TurkeydNephrology Department, Ege University Hospital, Izmir, TurkeyeNephrology Department, Bulent Ecevit University, Zonguldak, TurkeyfPathology Department, Ege University Hospital, Izmir, TurkeygBiochemistry Department, Ege University Hospital, Izmir, Turkey

Objective: Acute kidney injury (AKI) is a common condition inintensive care units and is associated with increased mortality rates.As its reliability to show AKI with a GFR N 60 mL/min is questionable,alternative biomarkers apart from serum creatinine might providea more sensitive and rapid means of detecting AKI. The destructionof cell membrane due to acute injury, results in increased levels ofkidney enzymes in urine and these enzymes appear to be goodmarkers for AKI. This has been shown in aminoglycoside-inducedacute tubular necrosis in animal models and human studies. Theaim of this study was to investigate the correlation between theurinary neutrofil gelatinase-associated lipocalin (NGAL), gamma-glutamyl transpeptidase (GGT), glutathione (GSH), kidney injurymolecule-1 (KIM-1) levels and the total renal histologic score (TRHS)of the gentamicin-induced nephrotoxicity in rats to observe analternative low cost predictor of acute kidney injury. Methods:100 mg/kg/day dose of gentamicin has been administered intramus-cularly for 8 days to seventy eight non-uremic wistar albino ratsweighing 180–220 g. Renal tissues, blood and 24-hour urine sampleshave been collected at the end of the study. Albumin, creatinine,calcium and phosphorus levels in serum and NGAL, GGT, GSH andKIM-1 levels in 24-hour urine samples have been measured. Semi-quantitative assessment has been carried out by the same pathologist.TRHS has been determined according to tubular degeneration, necrosis,regeneration and tubulointerstitial inflammation. We analysed the

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results using Pearson Correlation Test, and P b 0.05 considered assignificant. Results: We observed a correlation between TRHS andurinaryGGT, NGAL, GSH andKIM-1 levels. UrinaryGGT has the ability topredict AKI besides GSH, NGAL and KIM-1 and the results that we haveobserved were statistically significant (P b 0.05). Conclusions: UrinaryGGT measurement is an easy, low cost and widely accessible test thatcan be used to predict AKI as an alternative method.

doi:10.1016/j.ejim.2013.08.161

ID: 243A case of hypercalcemia and renal failure after the overdose ofvitamin DN. Tezcana, H.T. Kania, S. Nalcacıb, S. Tuglularb, C. Ozenerb

aInternal Medicine, Marmara University Faculty of Medicine, Istanbul,TurkeybNephrology, Marmara University Faculty of Medicine, Istanbul, Turkey

Introduction: Given the proven benefits of vitamin D in fractureand fall risk reduction and the possible health benefits beyond theskeleton, there is an increased interest in vitamin D supplementa-tion. Vitamin D intoxication commonly results from the replacementby health care providers with high doses of Vitamin D without thediagnosis of the deficiency. We present a patient who admitted toour center with acute kidney injury with findings of hypercalcemiain renal biopsy and had a history of Vitamin D replacement therapyin toxic doses. Case: A 43-year-old female who had hypertension forthree years, had a skin eruption and her laboratory investigationrevealed a creatinine level of 2.0 mg/dl, calcium level of 13.4 mg/dland phosphorus level of 6.2 mg/dl. Her creatinine raised up to3.5 mg/dl in the follow-up. In the renal biopsy which was made forthe etiology of the renal failure, there was calcium deposits in tubules,50% glomerulosclerosis, and interstitial cell infiltration (Figure 1).Reevaluation of the specific drughistory disclosed the use of 6 ampoulesof Vitamin D containing 300,000 U every other day 5 months ago andmonthly for 5 months with the advice of a physical therapist. Her 25(OH)Vitamin D level was 132 ng/ml (30–80 ng/ml) and 1,25 (OH)2VitD level was 68 pg/ml (15–75 pg/ml). Hydrationwith isotonic saline andfurosemide therapy was started, there was no regression in creatinineand calcium levels and the patient was hemodialised for two days. Inthe next visit one month later her calcium was 12.1 mg/dl, creatininewas 2.1 mg/dl and 25 (OH)Vitamin D level was 113 ng/ml. Discussion:The tolerable upper limit of Vitamin D in adults is 4000 IU/day. Oneof the severe results of Vitamin D intoxication is acute and/or chronicrenal injury. Because Vitamin D is lipophilic and stored in fat, toxiceffects (hypercalcemia/hypercalciuria) remain even after the treatmentis stopped as in our patient. The patients who are on the Vitamin Dreplacement therapy should strictly be followed for the intoxication.

doi:10.1016/j.ejim.2013.08.162

ID: 322C reactive protein and the long-term risk for decreasedkidney functionE. Kuglera, E. Cohena,b, E. Goldberga,b, Y. Nardic, M. Gartyb,d, I. Krausea,b

aDepartment of Medicine F — Recanati, Rabin Medical Center(Beilinson Campus), Petah Tikva, IsraelbSackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel

cFaculty of Industrial Engineering and Management, Technion — IsraelInstitute of Technology, Haifa, IsraeldRecanati Center for Preventive Medicine, Rabin Medical Center(Beilinson Campus), Petah Tikva, Israel

Objectives: Among apparently healthy individuals, the baselinelevel of high sensitive C reactive protein (CRP) predicts the long-term risk of a first myocardial infarction (MI), ischemic stroke,peripheral vascular disease, and all-cause mortality. The role of CRPin predicting the long-term risk for chronic kidney disease (CKD) hasnot yet been thoroughly investigated. The aim of our study was toassess whether elevated levels of CRP in subjects without apparentkidney disease is associated with the development of CKD. Methods:We conducted a retrospective analysis on a prospectively collecteddata from a large screening center in Israel. All participants who hada follow up interval of more than 5 years in the screening center,and presented with an estimated glomerular filtration rate (eGFR)above 60 ml/min at baseline were included. High sensitive C reactiveprotein levels at baseline and mean CRP levels on subsequent visitswere calculated. Two groups of CRP levels were defined as low andhigh (below and above 1 mg/dl respectively). Risk for CKD at endof follow up (defined as eGFR b 60 ml/min) was assessed in relationto mean CRP levels. In addition, the confounding effects of otherpredictors of CKD such as diabetes mellitus, hypertension, age andcholesterol levels were examined. Results: Our data consist of 25,948repeated measurements of 4345 subjects between the years 2000and 2012 (26% females). Out of 4345, 1% of patients developed CKDin a mean follow up of 7.6 ±2 years. High CRP levels were associatedwith greater risk for CKD (OR 4.2, 95% CI 1.5 to 12). In a multivariateanalysis that include diabetes mellitus, hypertension, BMI, age,gender, total cholesterol, HDL cholesterol and current smoking, highCRP levels remained significantly associated with greater risk forCKD. In addition, when applying logistic regression models treatingCRP as a continuous variable together with diabetes mellitus andhypertension (separately), these two predictors were highly signif-icant as well (P b 0.001 for both). Conclusion: C reactive proteinlevels at baseline in subject with no apparent kidney disease may beused to predict the risk for CKD. For subjects with high CRP levelsand hypertension or diabetes mellitus the risk is increased. The riskis not associated with gender.

doi:10.1016/j.ejim.2013.08.163

ID: 334Microinflammation and cardiovascular mortality inhemodialysis patientsS. Bevc, T. Zorman, R. Ekart, R. Hojs

Clinic of Internal Medicine, Department of Nephrology and Dialysis,University Medical Centre Maribor, Maribor, Slovenia

Objective: Risk for coronary heart disease is higher among patientson hemodialysis (HD) than in the general population. However, thisexcess risk for coronary heart disease is not entirely explained bytraditional risk factors for cardiovascular (CV) disease. The aim of ourstudy was to determine the impact of some inflammatory mediatorson CV mortality in HD patients. Methods: 71 HD patients (mean age59 years, ranged from 22 to 78 years) were enrolled in our study, 32(45%) were women and 39 (55%) were men. In follow up period 26(36.6%) patients died, in 16 (22.5%) patients CV death was confirmed.Inflammatory mediators high sensitive C-reactive protein (hs-CRP),

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