Cem Sungur
Hacettepe University
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Nephron | 1993
Arinsoy T; Tekin Akpolat; Ataman M; Nurol Arik; Cem Sungur; Ünal Yasavul; Cetin Turgan; Sali Caglar
Turgay Arinsoy, Nephrology and Otolaryngology Departments, Hacettepe University Medical School, T-06100 Ankara (Turkey) Sir, Thromboembolic complications constitute an important risk in the postoperative course after renal transplantation. The incidence has been reported to be as high as 24% [1]. We present a case of sudden hearing loss due to a thromboembolic event in a renal transplant recipient on triple immunosup-pressive treatment consisting of cyclosporin A (CsA), azathioprine (Aza) and predniso-lone (Pred). A 22-year-old Caucasian male with end-stage renal disease secondary to membrano-proliferative glomerulonephritis underwent a living-related donor renal transplantation. The patient had been maintained on a hemo-dialysis program for 3 months prior to renal transplantation. Initial laboratory results showed that serum creatinine level and blood urea nitrogen were 397 μmol/l and 18.3 mmol/l, respectively. The remainder of his laboratory results including prothrombin time (FT), partial thromboplastin time (PTT), chest X-ray and electrocardiogram were within normal limits. Before the operation, CsA was given in a single dose of 4 mg/kg orally. Methylpredni-solone 1,000 mg and Aza 150 mg were given intravenously during surgery. On the operation day, Pred 100 mg was given orally and tapered by 10 mg daily until the dose of 20 mg per day. He received CsA (4 mg/kg) b.i.d. and Aza (1.5 mg/kg/day) in a single oral dose. He tolerated the operation well and had good urine output postoperatively. On the 7th postoperative day, the patient complained of right sudden hearing loss. On the same day, his blood CsA level was measured as 200 ng/ml, and serum creatinine level was 106 μmol/l. PT and PTT were within normal limits. Because of right sudden hearing loss, the patient was referred to the Otolaryngology Department. He had not any vestibular symptoms, otolaryngologic examination revealed no abnormality except for tuning fork tests. With the tuning fork at 512 cps, there was no response on the right ear. The patient localized the sound in the left ear on the Weber test. Investigations included a full range of
Nephron | 1995
Colakoğlu M; Tekin Akpolat; Nurol Arık; Utaş C; Arinsoy T; Sindel S; Cem Sungur; Ünal Yasavul; Cetin Turgan; Sali Caglar
Dr. Nurol Arik, Ondokuz Mayis Universitesi, Tip Fakültesi, Hemodiyaliz ve Nefroloji Bölümü, TR-55139 Samsun (Turkey) Dear Sir, Transplantation is the optimal treatment for patients with end-stage renal disease (ESRD). In Turkey, renal transplants (RTs) are mainly obtained from living donors. Unfortunately, due to the insufficient availability of cadaveric grafts and compatible living donors, RTs have to be obtained from abroad. Some units in South-East Asia have run RT commercial programmes for many years [1-4]. Several patients with ESRD have gone to Bombay for RT from unrelated living donors and have returned to Turkey for posttransplantation follow-up. The purpose of this report is to evaluate the results of RT from unrelated living donors in Turkish patients with ESRD and to discuss the ethical and social aspects of organ transplantation. Sixty-three patients (38 males, 25 females, mean age 38.4 years, range 17-63) from 4 Transplantation units were investigated retrospectively. All transplantations were performed in 1992 and 1993. Mean duration of dialytic therapy before transplantation was 26.1 months (range 0-96). Sixty patients have received primary and 3 patients have received secondary grafts. Mean follow-up time after transplantation was 12.1 months (range 1-25 months). Patient data were collected from the hospital file during transplantation in Bombay and regular follow-up in Turkey. All the donors were males with a mean age of 25.4 years (range 23-30). Mean preoperative period for patient preparation was 5-7 days in most of the patients and mean hospitalization time after operation was 10-12 days. Most of the transplanted patients had been admitted to transplantation units in Turkey at 10-15 days after transplantation. The immunosuppres-sive protocol was as follows at the time of admission: cyclosporine 7-10 mg/kg, aza-thioprine 1-2 mg/kg and prednisolone 1 mg/ kg. Dipyridamole, salicylic acid, polyvita-min tablets, iron supplements, 7⁄8 receptor blockers and antacids were other medications in most of the patients and 1 patient was
Nephron | 1999
Nurol Arik; Tarik Basoglu; Cem Sungur; Bahattin Adam; Abdulkerim Bedir; Tolga Kandemir; Candan Coskun; Irem Bernay
Accessible online at: http://BioMedNet.com/karger Dear Sir, Uremic bone disease is a frequent and disabling complication of end-stage renal disease. Over the last decade, several studies have been published on the use of intravenous (IV) calcitriol therapy in the treatment of secondary hyperparathyroidism [1–3]. There remains some uncertainty on the optimum use of IV calcitriol therapy [4]. In this study, we evaluated the effect of long-term IV calcitriol therapy on the parameters that can be used in monitoring uremic bone disease activity such as parathyroid hormone (PTH), alkaline phosphatase (AP) and bone mineral density (BMD) in 8 uremic patients with secondary hyperparathyroidism. Eight uremic patients with secondary hyperparathyroidism on chronic hemodialysis were selected for the study. After the baseline data had been collected, intravenous calcitriol (Calcijex®, Abbott Lab, Chicago, Ill, USA) was administered at the end of each dialysis session. The initial dose was 0.5 Ìg per injection and it was increased in 0.5-Ìg increments to a maximum tolerable dose. The duration of study was 12 months. The levels of intact PTH and AP, and BMD density in different locations were measured before and after 12 months’ therapy with IV calcitriol in all patients. IV calcitriol was temporarily discontinued or its dosage reduced if the serum calcium and phosphorus concentrations exceeded 11.5 and 6.5 mg/dl, respectively, or the calcium-phosphorus product was greater than 70. A dual energy X-ray bone densitometer was used to measure BMD. Regional BMD values were obtained for the lumbar spine [L3 (BMD), L2– L3 (BMD2)], for proximal portions of both femurs [femoral neck (BMD3), femoral trochanter (BMD4), Ward’s triangle (BMD5)]. Right/left average values of femoral measurements were taken for the analysis. In the present study, the numbers of the observed episodes of hyperphosphatemia and hypercalcemia were 37 and 2, respectively. In 5 of these episodes, increased calcium-phosphorus product values were also noted. Because of the frequent episodes of hyperphosphatemia, hypercalcemia, and increased calcium-phosphorus product, IV calcitriol dose could not exceed 2 Ìg/dialysis session on a regular basis in the participating patients. The mean calcitriol dose was 0.92 Ìg/dialysis session throughout the study. The determined changes in biochemical parameters and bone mineral density values during therapy are shown in table 1. As shown in table 1, we could not determine any significant changes in measured parameters after calcitriol therapy in this study. Although several studies have been published on the use of IV calcitriol therapy, the optimal dosage regimen has not yet been clarified [1–3]. But, in general, a dose greater than 2 Ìg/dialysis has been found to be more efficient than one less than 1 Ìg/dialysis [4]. In the present study, the mean calcitriol dose/dialysis session was found to be 0.92 Ìg. Undoubtedly, other factors unrelated with the calcitriol dose might have contributed to the therapy failure in our patients; we think that our failure both to decrease the PTH and AP levels and to improve BMD must be due to our inability to use an effective dose of IV calcitriol. The major limiting factor preventing the use of an effective dose of IV calcitriol in our
Nephron | 1994
Oktay Oymak; Tekin Akpolat; Nurol Arik; Cem Sungur; Colakoğlu M; Ünal Yasavul; Cetin Turgan; Sali Caglar
Dr. Oktay Oymak, Hacettepe University School of Medicine, Department of Nephrology, TR-06100 Ankara (Turkey) Dear Sir, Hepatitis C virus (HCV) is the most common cause of hepatitis in hemodialysis patients and renal transplant recipients. The major transmission routes of HCV infections are blood transfusions and inoculations; furthermore, organ transplantation, vertical and heterosexual transmission have also been documented [1]. In order to evaluate the contribution of end-stage renal disease patients on renal replacement therapy to the spread of HCV infection, we investigated HCV antibody (anti-HCV) and serum alanine amino-transferase levels in the spouses of these patients. Eighty patients on renal replacement therapy (table 1) and their spouses (28 males, 52 females, aged 37.1 years, range 23-62) and 30 controls (16 males, 14 females, aged 41.5 years, range 2665) were included in the study. 65 of the 80 patients on renal replacement therapy were sexually active. Anti-HCV was measured by a 2nd-generation enzyme-linked immunosorbent assay to C100-3 and 33c antigens of HCV(ELISA, Abbott). Four of the 80 spouses of the patients on renal replacement therapy were anti-HCV positive and none of the controls were anti-HCV positive. The characteristics of these 4 partners were as follows: (1) 3 of them were female and 1 of them was male with a median age of 37.8 years (range 31^45); (2) all their partners were in the anti-HCV-positive group (3 renal transplanted and 1 hemodialysis patients); (3) they did not share any risk factor including blood transfusion for HCV infection; (4) 3 of the patients as well as 2 of their spouses had raised serum alanine aminotransferase levels; (5) all of these pairs were sexually active and they were not using condoms during intercourse. Although there are contrary studies [2], many reports have shown higher anti-HCV Table 1. Characteristics of patients on renal replacement therapy (means and range) Hemodialysis patients Transplanted patients
Nephron | 1993
Tekin Akpolat; Nurol Arik; Arinsoy T; Cem Sungur; Mehmet Bakkaloglu; I. Erkan; Ünal Yasavul; Cetin Turgan; Sali Caglar
Dr. Tekin Akpolat, Hacettepe Hastanesi, Nefroloji Bölümü, Hacettepe, TR-06100 Ankara (Turkey) Dear Sir, Chronic liver disease is a frequent and major complication in renal transplant recipients and contributes greatly to morbidity and mortality in these patients [1]. Hepatitis C virus (HCV) is the most common cause of transplant-associated liver disease [1, 2]. Currently, assays are available to detect antibody to recombinant antigens of HCV (anti-HCV). The aim of our study was to evaluate the prevalence of anti-HCV among renal transplant patients and the possible correlations of anti-HCV with chronic liver dysfunction, graft survival, number of blood transfusions, hepatitis B virus serologic markers and duration of hemodialysis therapy before transplantation in this group of patients. One hundred and sixty-one patients (119 men and 42 women; mean age 35.6 years, range 18-65) were included in the study. Seventy of 161 patients were transplanted in our unit and the rest were referred from other centers for long-term follow-up. Anti-HCV was measured by a second-generation enzyme-linked immunosorbent assay to C100-3 and 33c antigens of HCV (ELISA, Abbott). Chronic liver dysfunction was considered to be a persistent elevation of the serum alanin aminotransferase levels for more than 6 months. Statistical analysis was performed by the χ2 test with Yates’ correction or Student’s test. Ninety-two of 161 patients (57.1%) were anti-HCV positive (table 1), and in the anti-HCVpositive group, the number of patients with chronic liver dysfunction was significantly higher and the duration of hemodialysis treatment was significantly longer than in the negative group. There was no significant difference between the two groups regarding the number of blood transfusions, graft survival and hepatitis B virus serologic markers. Preliminary surveys of renal transplant recipients have shown an anti-HCV prevalence ranging from 10 to 41% [2-5]. Anti-HCV was positive in 57.1% of patients in the present
Nephron | 1995
Colakoğlu M; Cem Sungur; Arzu Sungur; Tekin Akpolat; Emin Kansu; Ünal Yasavul; Cetin Turgan; Şali Çağlar
Cem Sungur, MD, PK (PO Box) 272, TR-06693 Kavaklidere, Ankara (Turkey) Dear Sir, AA-type amyloidosis secondary to familial Mediterranean fever (FMF) is a frequent cause of end-stage renal disease in certain countries [1,2]. Although the differential diagnosis of AAand AL-type amyloidosis can be usually made on clinical and laboratory grounds, there are examples of overlapping cases [3]. It is well established that AL amyloidosis is characterized by monoclonal protein production, but overflow proteinuria in the form of monoclonal light-chain protein excretion is also observed under inflammatory conditions [4]. As FMF is a periodic inflammatory disease, we investigated the presence of monoclonal light-chain protein excretion in 16 patients with FMF and renal amyloidosis. The mean age of the patients was 29 ± 2 years. Twelve were men, and 4 were women. They all had a previous medical history compatible with FMF and a histopathological diagnosis of AAtype amyloidosis on renal biopsy. All patients were receiving colchicine. The amount of proteinuria was measured in 24-hour urine samples, and monoclonal light-chain protein was detected with agar gel im-munoelectrophoresis using the same specimen. The results are summarized in table 1. Lambda and kappa light-chain protein excretions detected in 6 patients were associated with a nonselective proteinuria, and in none of them they were of monoclonal origin. Immunoelectrophoresis demonstrated the presence of immunoglobulins in the urine of all these 6 patients. Other patients were characterized by detection of a single band of albumin in the urine. This study showed that monoclonal light-chain protein excretion is not a feature of FMF and AA-type renal amyloidosis. The presence of light-chain proteins in the urine is associated with nonselective proteinuria as in other glomerular diseases. This noninvasive laboratory test may be of value in the differential diagnosis of patients with FMF and renal amyloidosis when specific immunohistopa-thological tests are not available.
Annals of Pharmacotherapy | 1994
Cem Sungur; Bahri Ates; Oral Akbas
I. Grau E, Estivill E, Muiiiz E, Domingo P, de CasteUarnau C, Fontcuberta J, et al. Diatesishernorragica asociada a dosis altas de antibioticos betalactamico: presentacion de tres casos. Med Clin (Bare) 1986; 86:420-4. 2. Grau E, Fontcuberta J, Felez-BruguesJ. Trombopatia por antibi6ticos betalactamicos. Med Clin (Barc) 1986;86:431-3. 3. McClure PK, Casserly JG, Monsier C, Crozier K. Carbenicillin-induced bleeding disorder. Lancet 1970;2:422-3. 4. Bang NU, Kammer RB. Hematologic complications associated with beta-lactam antibiotic. Rev Infect Dis 1983;5:380-93. 5. Johnson GJ, Rao GHR, White JG. Platelet dysfunction induced by parenteral carbenicillin and ticarcillin. Am J PathoI1978;91:85-106.
Nephron | 1992
Nurol Arik; Fatih Demirkan; Belkis Erbas; Arinsoy T; Cem Sungur; Ünal Yasavul; Cetin Turgan; Zehra Koray; Şali Çağlar
Dr. Nurol Arik, Hacettepe Hastanesi, Nefroloji Bölümü, TR-06100 Hacettepe-Ankara (Turkey) Dear Sir, Approximately one third of the patients treated with recombinant human erythropoietin (rhEPO) will experience either an aggravation of preexisting hypertension or will develop de novo hypertension [1]. But the underlying mechanism is unclear and various causes such as the increased blood viscosity and total red cell mass inducing an increase in peripheral resistance [2] and the reversal of compensatory vasodilatation induced by renal anemia [3] have been proposed by several studies before. Besides, some investigators have suggested that rhEPO itself has some effect on renin-angiotensin-aldosterone axis. So, it has been proposed that the alterations in this axis may contribute to the changes in blood pressure during rhEPO treatment [4,5]. In order to clarify the acute effect of rhEPO on plasma renin activity (PRA) and aldosterone secretion, we studied PRA and aldosterone levels after rhEPO injection in 9 predial-ysis uremic patients. We included 9 patients with chronic renal failure, untreated by dialysis previously. The patients had never taken rhEPO, antihyper-tensives, and the drugs affecting the renin-angiotensin axis and aldosterone secretion such as aldosterone antagonists and angiotensinconverting enzyme inhibitors. Patients were maintained at bedrest in supine position for 6 h prior to rhEPO injection and they kept their supine position throughout the test. After the baseline sampling at 8.00 a.m. rhEPO was given intravenously at a dose of 50 U/kg. Blood samples for analysis were taken at 15, 30 and 60 min after injection and blood pressures were recorded simultaneously. 7-ι ε < o. 3
Nephron | 1995
Cem Sungur; Nurol Arik; Tekin Akpolat
Cem Sungur, MD, PK (POBox)272, TR-06693 Kavaklidere, Ankara (Turkey) Dear Sir, We had suggested that hepatitis C virus (HCV) may be a nosocomial pathogen for hemodialysis patients, since we had observed acute hepatitis C in newly admitted cases who denied blood transfusions and other risk factors involved in the transmission of HCV [1]. A later study in our transplant population also disclosed a very high prevalence of HCV antibody positivity in this particular patient group [2]. In order to find the incidence of hepatitis C viremia in hemodialysis patients and to gather concrete evidence about the nosocomial transmission of HCV, we conducted a study in 146 regular hemodialysis patients who were anti-HCV-antibody-positive with a second-generation ELISA test or had chronic ALT elevations. Their sera were initially screened with a recombinant immunoblot assay (RIBA) deTable 1. Results of PCR analysis in 75 samples
Nephron | 1993
Tekin Akpolat; Oktay Özdemir; Nurol Arik; Fatih Demirkan; Cem Sungur; Osman Özcebe; Semra Dündar; Ünal Yasavul; Cetin Turgan; Şerafettin Kirazli; Şali Çaḡlar
The effect of desmopressin (DDAVP) on protein C (PC) and PC inhibitors was investigated in 7 uremic predialysis patients, 7 hemodialysis patients and 7 controls. Significant decrease in PC activity was observed in all groups after DDAVP administration. Desmopressin did not influence PC antigen and two well-known PC inhibitors, plasminogen activator inhibitor-3 and alpha 1-antitrypsin. Thus, it is suggested that DDAVP-induced decrease in PC activity is not related to the changes in PC inhibitors; further studies are needed to clarify the precise mechanisms of the effect of DDAVP on PC in uremia.