Enes Murat Atasoyu

The Role of Prolidase Activity in the Diagnosis of Uremic Bone Disease

The derangements in bone metabolism in patients with chronic renal failure (CRF) are summarized as uremic bone disease (UBD). In this study, we planned to determine the serum prolidase to compare it with the other biochemical markers. This study was performed on 44 patients (19 females, 25 males, mean age = 56.8 ± 15.6 years) with end-stage renal disease (ESRD). The patients were divided into three groups according to serum bone alkaline phosphatase (bAP) levels. The patients whose bAP was ≥77 U/L were accepted as having high-turnover UBD (n = 18), the patients whose bAP was ≤50 U/L were accepted as having low-turnover UBD (n = 14), and the patients whose bAP levels were between these two values were accepted as having bone disease with normal turnover (n = 12). The serum prolidase levels did not increase in patients with ESRD. There were no significant differences between the serum prolidase levels of patients according to types of the UBD (p > 0.05). Kidney is the most prolidase-rich tissue of the human body. The serum prolidase activity is low in all patients with ESRD, irrespective of the type of UBD. Therefore, we concluded that prolidase had no value in the diagnosis of UBD.

Effects of Different Doses of Hyperbaric Oxygen on Cisplatin-Induced Nephrotoxicity

Cisplatin, an effective antineoplastic agent, frequently induces acute renal failure in animals and humans. Hyperbaric oxygen (HBO) has been shown to prevent cisplatin-induced nephrotoxicity in rats. This study investigated the effect of two different HBO regimes on renal functions, oxidative stress, and histopathological changes in rat kidneys after cisplatin treatment. Wistar rats were divided into five groups: control, HBO, cisplatin, cisplatin plus once daily HBO, and cisplatin plus twice daily HBO. Cisplatin was given as a single intraperitoneal dose of 6 mg/kg, and HBO was applied for 60 min at 2.5 atm for six days. HBO alone did not alter any biochemical parameters or histopathological findings compared with the control group. Cisplatin increased serum urea and creatinine levels and caused severe histopathological injury. In addition, cisplatin increased lipid peroxidation and impaired superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in kidney tissue. Once daily HBO after cisplatin treatment slightly reduced serum urea and creatinine levels and attenuated histopathological injury. HBO also reduced lipid peroxidation and increased SOD and GSH-Px activities significantly. Although twice daily HBO was determined to be more effective than once daily HBO on oxidative stress parameters, it increased serum creatinine levels and histopathological injury compared with the cisplatin group. It was concluded that HBO alone does not induce nephrotoxicity and oxidative stress in rat kidneys; once daily HBO may prevent cisplatin-induced nephrotoxicity, an effect that is partially mediated by the modification of oxidant/antioxidant systems in the kidneys; and twice daily HBO potentiates cisplatin nephrotoxicity by a ROS-independent mechanism.

Hyperbaric Oxygen Therapy Attenuates Renal Ischemia/Reperfusion Injury in Rats

Objective: Renal ischemia/reperfusion (I/R) injury occurs in both native and transplanted kidneys. Hyperbaric oxygen (HBO) has been shown to prevent I/R injury in different tissues. The aim of this study was to evaluate the effect of HBO on renal I/R injury in rats. Materials and Methods: Sprague-Dawley rats were randomly assigned to one of three groups. The Control group (n = 6) received right nephrectomy. The I/R (n = 6) and I/R+HBO groups (n = 6) received 30 min left renal ischemia followed by 24 h of reperfusion after right nephrectomy. The I/R+HBO group (n = 6) received additional HBO therapy for 60 min at 2.5 absolute atmospheres starting at the initial 15th minute of reperfusion. Results: In the I/R group, blood urea nitrogen (BUN) and creatinine levels increased significantly compared with the Control and I/R+HBO groups (p < 0.05). BUN and creatinine levels were similar in the Control and I/R+HBO groups. Kidney samples from I/R group rats revealed severe tubular damage and neutrophil infiltration at histopathological examination. The animals treated with HBO showed markedly improved lesions and less neutrophil infiltration compared with the I/R group (p < 0.05). Conclusions: HBO exhibited marked protection against I/R injury in this study as measured using BUN and creatinine levels and renal histopathology. However, further studies are needed to clarify the renoprotective effect of HBO on I/R injury.

Leptospirosis in Istanbul, Turkey: a wide spectrum in clinical course and complications.

Patients with high fever and multiorgan involvement were investigated for the determination of frequency, clinical course and complications of leptospirosis in Istanbul. Leptospirosis was determined in 22 cases among the 35 hospitalized patients that were prediagnosed as leptospirosis according to ‘Probable Leptospirosis Diagnosis and Follow-up’ form. Among the leptospirosis cases 19 were male and 16 were military staff. Mean age was 35.6 y. Dark field examination (DFE), latex agglutination test (LAG), ELISA IgM, leptospirosis culture (LC) and microscopic agglutination test (MAT) were performed to confirm the diagnoses. The most frequent initial symptoms and findings were fever, fatigue, headache, nausea-vomiting and increased muscle sensitivity. Jaundice was noted only in 2 cases. A 74-y-old female patient died after the recurrence of the disease with severe rhabdomyolysis and pulmonary failure. Sagittal sinus thrombosis, perimyocarditis and chronic renal failure were major complications in another 3 patients. ELISA IgM, LC, DFE, LAG and MAT tests were positive in 68, 72, 82, 100 and 100% of the patients, respectively. As a conclusion, diagnosis of leptospirosis is usually overlooked. Clinical awareness, use of probable leptospirosis diagnosis forms and the application of different laboratory methods in the diagnosis of suspected cases may offer the chance to diagnose the leptospirosis accurately.

Relationship between P-Wave Dispersion and Effective Hemodialysis in Chronic Hemodialysis Patients

Objective: To investigate whether or not P-wave dispersion (PWD) can be used as a good indicator of effective hemodialysis. Subjects andMethods: The study included 35 patients (20 males, 15 females, mean age 61 ± 10 years) who regularly received hemodialysis treatment for chronic renal failure. Following hemodialysis, the patients whose hemodynamic parameters were preserved and who reached dry body weight were included. Twelve-lead resting electrocardiogram (ECG) at a speed of 25–50 mm/s, the value of total body fluid (TBF) and bioelectric impedance using bipedal bioelectric impedance equipment were obtained before and immediately after hemodialysis. Blood samples were also taken for the assessment of blood electrolytes, urea and creatinine. PWD was defined as the difference between the maximum and minimum P-wave duration calculated on a standard 12-lead ECG before and after dialysis. Results: The following parameters were obtained before and after hemodialysis: blood pressure 132 ± 21 vs. 130 ± 10 mm Hg (p > 0.05), TBF 33.9 ± 6 vs. 32 ± 5.6 liters (p = 0.001), impedance 499 ± 110 vs. 596 ± 136 Ω (p = 0.001), P-max 103.1 ± 8.9 vs. 106.3 ± 12.7 ms (p > 0.05), P-min 70.2 ± 11 vs. 72.5 ± 7.9 ms (p > 0.05), PWD 32.2 ± 11.9 vs. 33.8 ± 13.4 ms (p > 0.05). Although statistically significant decreases were observed in urea and creatinine levels after hemodialysis, no such changes were observed in blood electrolytes. Conclusion: The P-max and PWD did not change significantly after hemodialysis, hence these two parameters can be used as an indicator of effective hemodialysis.

Effect of Hyperbaric Oxygen on Cyclosporine-Induced Nephrotoxicity and Oxidative Stress in Rats

Reactive oxygen species have been suggested to be involved in cyclosporine nephrotoxicity. Hyperbaric oxygen is known to induce the generation of reactive oxygen species in tissues. The aim of this study was to investigate whether the use of hyperbaric oxygen concurrently with cyclosporine potentiates cyclosporine nephrotoxicity by inducing oxidative stress in kidneys. The study consisted of four groups of rats: a control group, a cyclosporine group (15 mg/kg/day intraperitoneally for 14 days), a hyperbaric oxygen group (60 min. every day for five days at 2.5 atmosphere absolute), and a cyclosporine + hyperbaric oxygen group (cyclosporine 15 mg/kg/day intraperitoneally for 14 days + hyperbaric oxygen for 60 min at 2.5 atmosphere absolute every day for five days on the last five days of cyclosporine treatment). Oxidative stress was determined by measuring renal thiobarbituric acid-reactive substances content, renal superoxide dismutase, and glutathione peroxidase activities. Cyclosporine increased serum urea and creatinine levels, indicating the development of nephrotoxicity, and induced significant oxidative stress in rat kidneys. Hyperbaric oxygen alone did not alter any of the biochemical and oxidative stress parameters compared to the control group. When used concurrently with cyclosporine, hyperbaric oxygen significantly reduced cyclosporine-induced oxidative stress, but it neither attenuated nor aggravated cyclosporine-induced nephrotoxicity. These results suggest that reactive oxygen species are involved in cyclosporine nephrotoxicity, but are not the direct cause of the toxicity. Although concurrent use of cyclosporine and hyperbaric oxygen did not exacerbate cyclosporine nephrotoxicity in this model, we recommend that the renal functions of patients be monitored periodically when these treatments are used concurrently.

A rare complication of idiopathic membranous nephropathy: crescentic transformation.

Introduction. In this study, the cause of rapidly deteriorating renal functions in a follow-up period of a 65-year-old female patient, who applied with nephrotic syndrome findings and diagnosed as membranous nephropathy, is presented. Case report. A 65-year-old patient with findings of nephrotic syndrome had normal kidney size and serum complement level, and was negative for autoantibodies and viral serology. In histopathologic examination, 20 glomeruli were consistent with membranous glomerulonephritis. The patient, evaluated for idiopathic membranous nephropathy, was followed-up monthly with supportive treatment. In the second month of follow-up, a re-evaluation of the patient due to nausea and urine discoloration revealed 144 mg/dL urea, 6.3 mg/dL creatinine, and 2.5 g/dL albumin. Urine sediment revealed dysmorphic erythrocytes and granular silenders. Renal re-biopsy was done. Of 11 glomeruli, three global sclerosis and eight crescentic glomeruli with fibrosis and scarce cellular component were seen. The case was accepted as crescentic glomerulonephritis, a rare complication of idiopathic MN. Before the treatment, antiGBM, pANCA, cANCA, and ANA were negative. Pulse metil prednisolone and pulse cyclophosphamide treatment protocol was administered. Hemodialysis was needed nine times. At the end of first month of the treatment, hemodialysis was no longer needed. Conclusion. Due to a risk of spontaneous remission up to 30% of membranous nephropathy, there is no consensus on specific treatment applicable to all cases. However, crescentic GN should be investigated immediately when sudden and rapid deterioration of renal functions appeared.

Analyses of Subjects with Hypokalemic Metabolic Alkolosis, Gitelman's and Bartter's Syndrome

The two most common forms of inherited normotensive hypokalemic metabolic alkalosis are Bartters and Gitelmans syndromes. Bartters is mostly seen in children, while Gittelmans is mostly seen in adolescents and adults. We analyze three subjects of adult-onset Gitelmans and Bartters syndrome. The patients applied to our hospital due to severe hypokalemia with little clinical expression (paresthesia, cramp, polyuria, polydipsia, and/or weakness). All had normal blood pressure, hypokalemia, hyperreninemic hyperaldosteronism, and a decrease in the fractional chloride reabsorption. Key elements in differential diagnosis of chronic hypokalemia are blood pressure assessment, acid base equilibrium, serum calcium concentration, and 24-hour urine potassium and calcium excretion.

Anicteric leptospirosis and renal involvement.

We read the clinical study report entitled ‘‘Acute renal failure: a common manifestation of leptospirosis’’ by Cetin et al. with great interest. We work in another teaching and research hospital serving the same city as the medical center in which the cases described in the article were observed. We prospectively investigated leptospirosis in patients applying to the GATA Haydarpasa Training and Research Hospital with fever and multiorgan involvement between February 2004 and October 2004 (over a 9-month period), and leptospirosis was determined in 39 cases within that time frame. Dark field examination, macroagglutination, culture, ELISA IgM, and microagglutination tests aimed toward leptospirosis were performed, and leptospirosis was diagnosed when at least two tests resulted positive. While only three cases were icteric course leptospirosis (Weil’s disease), 36 (92%) were determined to be anicteric course leptospirosis. This finding was in agreement with the information in the literature to the effect that 90% of leptospirosis cases are anicteric. Urinary abnormalities (leukocyturia and/or hematuria and/or proteinuria) were determined in 26 of the 39 cases diagnosed as leptospirosis (66%), similar to Cetin et al.’s findings. Acute renal failure (ARF), an indicator of poor prognosis, was determined in eight cases. Hyperbilirubinemia was present in only two (25%) of the cases in which ARF occurred. This finding suggests that the classic idea that severe leptospirosis equals icteric leptospirosis may not always be accurate. A severe clinical course was observed in 10 of our leptospirosis cases. ARF was present in eight of these. All responded to supportive therapy and crystallized penicillin (12–24 MIU/day) or doxycycline (200 mg/day b.i.d.). Hemodialysis therapy was administered to only one patient (a 20-year-old male), monitored for 9 months, who was diagnosed with end-stage renal disease due to lack of improvement in kidney functions and was included in a regular hemodialysis program for 4 h, three days a week. Apart from Cetin et al.’s reports and the case we report here, leptospirosis has not been described as a complication leading to ESRD in the literature. It was regarded as particularly interesting that our case had no previous kidney pathology. Two cases presenting with anicteric leptospirosis died. One of these died due to ‘‘pulmonary involvement Address correspondence to Dr. Vedat Turhan, GATA Haydarpasa Egitim Hastanesi İnfeksiyon Hastaliklari ve Klinik, Mikrobiyoloji Servisi, Kadikoy-Istanbul 34668, Turkey; Fax: +90-216-348-7880; E-mail: vedatturhan@yahoo.com

Dissection of the Thoracic Aorta in a Patient with Autosomal Dominant Polycystic Kidney Disease

Internal Medicine,Gulhane Military Medical Academy, Haydarpasa Training Hospital, Istanbul, Turkey.Autosomal dominant polycystic kidney disease(ADPKD) is a systemic illness with a number of extra-renal manifestations. A 61-year-old male patient withknown ADPKD was admitted to the emergency roomof our hospital in May 2003 with severe chest painradiating to his neck and back, and a sense ofbreathlessness. There was no history of trauma.On admission, he was hypotensive (90/50 mmHg)and his heart rate was 110 beats/min. He had a mid-systolic murmur, which was most marked at the leftsternal edge. His peripheral pulses were weak. Bilater-al basal crepitations were found on pulmonaryexamination. Abdominal examination was normalexcept for large palpable polycystic kidneys. He hadno focal neurologic signs. Laboratory examinationshowed no significant abnormalities except for raisedserum urea (121 mg/dL) and creatinine (4.1 mg/dL).An electrocardiogram showed depression of ST seg-ments in the anterior leads. Emergency computerizedtomography scanning of the thorax and abdomen de-monstrated dissection and intramural thrombus withinthe descending thoracic aorta and bilateral polycystickidneys (Panels A and B).He was transferred immediately for aortic surgery.During the operation, a type II thoracic aortic dissectionwas observed. His recovery was complicated by theexpansion of the dissection and he died on the thirdpostoperative day.Numerous cardiovascular abnormalities have beenreported in ADPKD patients, including heart valvelesion, cerebral aneurysm, splenic artery aneurysm,aortic root dilatation, abdominal aortic aneurysm,thoracic aortic dissection, and cervical artery dissection[1–3]. The prevalence of intracranial aneurysm andrupture are five-fold higher in ADPKD patients than inthe general population [4]. However, the prevalence ofextracerebral aneurysms is not clear. One autopsy seriesdescribed aortic dissection as being seven times morecommon in patients with ADPKD than in the generalpopulation [2]. Spontaneous artery dissection wasreported as a major complication in five unrelatedADPKD patients. All underwent spontaneous dissect-ion and none had phenotype of elastic tissue disorderor thoracic aortic dissection. Torra et al, in their case-control study, found a similar distribution of aorticdiameters in 139 ADPKD patients and their 149unaffected relatives [5]. The case reported by Paynteret al appears to be very similar to our case [3]. Arterialdissection may belong to the spectrum of extrarenalmanifestations of ADPKD. The association of ADPKD