PubMed Health⌕ Search

Biomedical subjects

T Ecder

Publications and source records attributed to T Ecder.

At least 19 recordsLinked to original sources
PubMed2006

Early renal injury after myeloablative allogeneic and autologous hematopoietic cell transplantation.

Renal insufficiency is a common complication early after hematopoietic stem cell transplantation (HSCT). Renal function as measured by creatinine clearance (CrCl) was prospectively evaluated in 47 patients undergoing allogeneic (n=22) or autologous (n=25) HSCT during the first 100 days. Renal dysfunction was classified as follows: Grade 0 (<25% decline in CrCl), Grade 1 (>or=25% decline in CrCl but <2 x increase in serum creatinine), Grade 2 (>or=2 x rise in serum creatinine but no need for dialysis) and Grade 3 (>or=2 x rise in serum creatinine and need for dialysis). Thirty-three patients (70%) had Grade 1-3 renal dysfunction. Renal dysfunction was more common after myeloablative allogeneic HSCT (91%) than autologous HSCT (52%) (P=0.004), and was associated with a high risk of mortality (P=0.039). Sepsis in autologous HSCT patients and cyclosporine toxicity in allogeneic HSCT patients were associated with renal dysfunction. We conclude that autologous and allogeneic HSCT differ in the likelihood and causes of renal dysfunction.

Adult↗
PubMed2006

Isolated hepatic tuberculous abscess in a renal transplant recipient.

Tuberculous liver abscess is rare worldwide. We report a 26-year-old renal transplant recipient who presented with fever, fatigue, and weight loss. Ultrasound (US) of the abdomen showed a cystic mass of 7x6 cm in the subcapsular region of right liver lobe. US-guided percutaneous drainage was performed and 100 mL of yellow-colored pus was aspirated. The patient was empirically started on ampicillin sulbactam treatment. Despite this treatment, the symptoms persisted. Subsequent control abdominal US showed the persistence of a cystic mass of 7x6 cm with thin septation in the subcapsular region near the right liver lobe, which were subsequently diagnosed as a focal hepatic tuberculous abscess by positive culture in Löwenstein-Jensen medium. He was concomitantly started on systemic antituberculous therapy. A tuberculous liver abscess must be considered in the differential diagnosis. Percutaneous drainage along with systemic antituberculous chemotherapy must be considered as an alternative to surgery for the management. A greater awareness of this clinical entity is required for successful treatment.

Adult↗
PubMed2001

Endotoxemic renal failure in mice: Role of tumor necrosis factor independent of inducible nitric oxide synthase.

BACKGROUND: Renal failure is a frequent complication of sepsis with a high mortality. Tumor necrosis factor (TNF) has been suggested to be a factor in the acute renal failure in sepsis or endotoxemia. Recent studies also suggest involvement of nitric oxide (NO), generated by inducible NO synthase (iNOS), in the pathogenesis of endotoxin-induced renal failure. The present study tested the hypothesis that the role of TNF in endotoxic renal failure is mediated by iNOS-derived NO. METHODS: Renal function was evaluated in endotoxemic [Escherichia coli lipopolysaccharide (LPS), 5 mg/kg IP] wild-type and iNOS knockout mice. The effect of TNF neutralization on renal function during endotoxemia in mice was assessed by a TNF-soluble receptor (TNFsRp55). RESULTS: An injection of LPS to wild-type mice resulted in a 70% decrease in glomerular filtration rate (GFR) and in a 40% reduction in renal plasma flow (RPF) 16 hours after the injection. The results occurred independent of hypotension, morphological changes, apoptosis, and leukocyte accumulation. In mice pretreated with TNFsRp55, only a 30% decrease in GFR without a significant change in RPF in response to LPS, as compared with vehicle-treated mice, was observed. Also, the serum NO concentration was significantly lower in endotoxemic wild-type mice pretreated with TNFsRp55, as compared with untreated endotoxemic wild-type mice (260 +/- 52 vs. 673 +/- 112 micromol/L, P < 0.01). In LPS-injected iNOS knockout mice and wild-type mice treated with a selective iNOS inhibitor, 1400W, the development of renal failure was similar to that in wild-type mice. As in wild-type mice, TNFsRp55 significantly attenuated the decrease in GFR (a 33% decline, as compared with 75% without TNFsRp55) without a significant change in RPF in iNOS knockout mice given LPS. CONCLUSIONS: These results demonstrate a role of TNF in the early renal dysfunction (16 h) in a septic mouse model independent of iNOS, hypotension, apoptosis, leukocyte accumulation, and morphological alterations, thus suggesting renal hypoperfusion secondary to an imbalance between, as yet to be defined, renal vasoconstrictors and vasodilators.

Acute Kidney Injury↗
PubMed2001

Outcome of living unrelated (commercial) renal transplantation.

BACKGROUND: Due to inadequate cadaveric and living related organ supply, many end-stage renal disease patients go to Third World countries for commercial transplantation, although the high risk of complications is well established and ethical arguments debate this practice. METHODS: The midterm outcome of 115 patients who had been commercially transplanted in various countries and admitted to our center for post-transplant care and follow-up between 1992 and 1999 was retrospectively analyzed. Data considering the transplantation practice and post-transplant course were collected from the patient files. Outcome of these patients was compared with those with a living related transplant performed at our center. RESULTS: The patients (91 male and 24 female; mean age of 42 +/- 12 years) were transplanted in India (N = 106), Iraq (N = 7), and Iran (N = 2). The mean follow-up period was 64.5 +/- 23.9 months. Post-transplant course was complicated by numerous surgical and/or medical complications, and many of the latter were unconventional infections caused by malaria, invasive fungal infections, and pneumonia due to various opportunistic pathogens. Overall, 52 patients still have functioning allografts, while 22 lost their grafts, 20 died, and 21 were lost to follow-up. Graft survival rates at two, five, and seven years were 84, 66, and 53%, respectively, for the study group, while it was 86, 78, and 73% for living related transplantations performed at our center (P = 0.036). Patient survival rates for the same periods were 90, 80, and 74% for the study group and 90, 85, and 80% for the living related transplantations (P = 0.53). CONCLUSIONS: Besides the ongoing ethical debate, commercial transplantation carries a high risk of unconventional complications, and despite that the patient survival rate is comparable, graft survival is worse than conventional living related transplantations at the midterm.

Adult↗
PubMed2001

Impaired IL-18 processing protects caspase-1-deficient mice from ischemic acute renal failure.

We sought to determine whether mice deficient in the proinflammatory caspase-1, which cleaves precursors of IL-1 beta and IL-18, were protected against ischemic acute renal failure (ARF). Caspase-1(-/-) mice developed less ischemic ARF as judged by renal function and renal histology. These animals had significantly reduced blood urea nitrogen and serum creatinine levels and a lower morphological tubular necrosis score than did wild-type mice with ischemic ARF. Since caspase-1 activates IL-18, lack of mature IL-18 might protect these caspase-1(-/-) mice from ARF. In wild-type animals, we found that ARF causes kidney IL-18 levels to more than double and induces the conversion of the IL-18 precursor to the mature form. This conversion is not observed in caspase-1(-/-) ARF mice or sham-operated controls. We then injected wild-type mice with IL-18-neutralizing antiserum before the ischemic insult and found a similar degree of protection from ARF as seen in caspase-1(-/-) mice. In addition, we observed a fivefold increase in myeloperoxidase activity in control mice with ARF, but no such increase in caspase-1(-/-) or IL-18 antiserum-treated mice. Finally, we confirmed histologically that caspase-1(-/-) mice show decreased neutrophil infiltration, indicating that the deleterious role of IL-18 in ischemic ARF may be due to increased neutrophil infiltration.

Acute Kidney Injury↗
PubMed2001

Gibbs memorial lecture. Unifying hypothesis of body fluid volume regulation: implications for cardiac failure and cirrhosis.

Body fluid volume regulation is critically important in maintaining life. In this paper, we review our unifying hypothesis of body fluid volume regulation, which maintains arterial circulatory integrity in health and disease. The integrity of the arterial circulation, as determined by cardiac output and peripheral vascular resistance, is the predominant determinant of renal sodium and water retention. Arterial circulatory integrity can be disturbed either by a decrease in cardiac output, as in low-output cardiac failure, or by a decrease in peripheral vascular resistance, as in high-output states such as high-output cardiac failure and cirrhosis. The resulting arterial underfilling is sensed by baroreceptors that are located in the left ventricle, the aortic arch, the carotid sinus and the renal afferent arterioles. Decreased activation of these receptors during arterial underfilling leads to neurohumoral compensatory responses, which include the stimulation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone system (RAAS) and the non-osmotic release of vasopressin. These compensatory responses maintain arterial circulatory integrity by increasing peripheral and renal arterial vascular resistance together with renal sodium and water retention. However, over the long term, these adaptive responses may have detrimental effects, such as pulmonary congestion, increased myocardial demand, increased cardiac afterload, ascites and hyponatremia. The intensity of the neurohumoral responses correlates with the progression and severity of both cardiac failure and cirrhosis. The understanding of the pathogenesis of sodium and water retention in cardiac failure and cirrhosis has led to therapies that favorably affect the morbidity and mortality of these patients.

Blood Circulation↗
PubMed2000

Effect of antihypertensive therapy on renal function and urinary albumin excretion in hypertensive patients with autosomal dominant polycystic kidney disease.

Hypertensive patients with autosomal dominant polycystic kidney disease (ADPKD) have a faster progression to end-stage renal disease (ESRD) than their normotensive counterparts. The aim of this prospective, randomized study is to compare the effects of the calcium channel blocker amlodipine and the angiotensin-converting enzyme inhibitor enalapril as first-line therapy on blood pressure, renal function, and urinary albumin excretion in hypertensive patients with ADPKD. Twenty-four patients with ADPKD with hypertension with creatinine clearances (Ccrs) greater than 50 mL/min/1.73 m(2) were included in the study. Twelve patients received amlodipine (mean dose, 9 mg/d), and 12 patients received enalapril (mean dose, 17 mg/d). The patients were followed up for 5 years. Baseline mean arterial pressures, which were 109 +/- 3 mm Hg in the amlodipine group and 108 +/- 3 mm Hg in the enalapril group, decreased significantly after 1 year of follow-up (amlodipine, 96 +/- 3 mm Hg; P < 0.005; enalapril, 89 +/- 2 mm Hg; P < 0.0005) and remained stable at year 5 (amlodipine, 97 +/- 3 mm Hg; P < 0.0005 versus baseline; enalapril, 94 +/- 3 mm Hg; P < 0.005 versus baseline). Ccrs, which were 83 +/- 5 mL/min/1.73 m(2) in the amlodipine group and 77 +/- 6 mL/min/1.73 m(2) in the enalapril group, remained stable after 1 year of follow-up and decreased significantly at year 3 in both groups (amlodipine, 67 +/- 5 mL/min/1.73 m(2); P < 0.01 versus year 1 and baseline; enalapril, 58 +/- 4 mL/min/1.73 m(2); P < 0.05 versus year 1 and P < 0.0005 versus baseline) with no significant change thereafter. No change was observed in urinary albumin-creatinine ratio in the amlodipine group (baseline, 68 +/- 21 mg/g; year 1, 52 +/- 21 mg/g; year 5, 148 +/- 74 mg/g), whereas it decreased significantly in the enalapril group at year 1 (baseline, 23 +/- 4 mg/g; year 1, 13 +/- 3 mg/g; P < 0.05) and remained stable until the end of the study at year 5 (14 +/- 6 mg/g). The investigators concluded that blood pressure was similar in both groups but only enalapril had a significant effect to sustain decreased urinary albumin excretion for a 5-year follow-up. Although proteinuria has been considered a surrogate of renal disease progression, further studies will be necessary to confirm this hypothesis in ADPKD, because after 5 years, no differences in renal function were observed between the enalapril and amlodipine groups. In comparison with patients with ADPKD with uncontrolled hypertension, effective control of blood pressure, as undertaken in the present study, should delay the onset of ESRD by approximately 15 years.

Adult↗
PubMed2000

Progress in blood pressure control in autosomal dominant polycystic kidney disease.

Hypertension occurs commonly in autosomal dominant polycystic kidney disease (ADPKD) and is an important factor in the progression of the disease and cardiovascular mortality. The aim of this prospective 15-year study is to report the rate of blood pressure control and the potential effect of a 10-point education program developed by our center for ADPKD patients and their physicians. The patients' blood pressure treatment was managed by their primary care physicians. Three 5-year periods were analyzed in which similar rates of hypertension in patients with ADPKD were present (63% to 68%). In the first period (1985 to 1989), the rate of blood pressure control (<140/90 mm Hg) was 38% for 216 hypertensive patients with ADPKD. From 1990 to 1994, the percentage of blood pressure control increased to 55% in 194 hypertensive patients with ADPKD (P < 0.001 versus 1985 to 1989); and the level of blood pressure control increased to 64% in 181 hypertensive patients with ADPKD during 1995 to 1999 (P < 0.001 versus 1985 to 1989). Although this percentage of blood pressure control in patients with ADPKD remains suboptimal, it compares very favorably with the 27% estimated blood pressure control in patients with essential hypertension from 1991 to 1994 in the United States.

Adult↗
PubMed1999

Reversal of left ventricular hypertrophy with angiotensin converting enzyme inhibition in hypertensive patients with autosomal dominant polycystic kidney disease.

BACKGROUND: Hypertension occurs commonly and early in the natural history of autosomal dominant polycystic kidney disease (ADPKD), affecting both renal and patient outcome. Activation of the renin angiotensin aldosterone system due to cyst expansion and local renal ischaemia plays an important role in the development of ADPKD related hypertension and left ventricular hypertrophy (LVH), a known important risk factor for cardiovascular morbidity and mortality. The aim of this study was to investigate the effects of an angiotensin converting enzyme (ACE) inhibitor, enalapril, on renal function, blood pressure and LVH in hypertensive ADPKD patients. METHODS: Fourteen hypertensive ADPKD patients (11 men, 3 women; mean age: 40 years) were included in the study. All patients had LVH and creatinine clearance (Cer) greater than 50 ml/min/1.73 m2. The patients were followed for 7 years on enalapril therapy. The effects of enalapril on renal function, blood pressure and LVH were investigated. RESULTS: Baseline measurements of mean arterial pressure (MAP), Ccr and left ventricular mass index (LVMI) were 110 +/- 2 mmHg, 84 +/- 6 ml/min/1.73 m2 and 146 +/- 4 g/m2, respectively. After one year of enalapril therapy there was a significant decrease in MAP (94 +/- 3 mmHg, P < 0.005) which remained stable until the end of the study at 7 years (94 +/- 1 mmHg, P < 0.005 vs baseline). There was also a significant decrease in LVMI (131 +/- 6 g/m2, P < 0.05) after year 1 which continued to decrease until the end of the study reaching 98 +/- 6 g/m2 (P < 0.01 vs year 1 and baseline). Although Ccr remained stable after year 1, a significant decrease was observed after 7 years of follow-up (59 +/- 6 ml/min, P < 0.001 vs year 1 and baseline). CONCLUSIONS: ACE inhibition in hypertensive ADPKD patients provided long-term reversal of LVH in association with a mean 3.6 ml/min/year decline of Ccr. These preliminary results have potential important implications for cardiovascular and renal protection in ADPKD.

Adult↗
PubMed1998

Tuberculosis after renal transplantation: experience of one Turkish centre.

BACKGROUND: In this study, renal transplant recipients with tuberculosis of different organs, were retrospectively analysed with respect to prevalence, outcome and drug toxicity. PATIENTS AND METHODS: In 520 patients, 22 (4.2%) tuberculosis of various organs was diagnosed. The time interval between transplantation and diagnosis of tuberculosis was 44.4 +/- 33.5 (range 3-111) months. In 18 (82%) of the patients, tuberculosis was detected after the first year of transplantation. The most common form was pleuro/pulmonary tuberculosis (54%), and other localizations included jejunum, liver, bone, and urogenital tract. RESULTS: Sixteen of the 22 patients responded favourably to the treatment and maintain excellent allograft function, whereas six patients (27.2%) died. Toxic hepatitis was seen in four (18%) patients, and one case was complicated with acute hepatocellular failure due to isoniazide (INH). However, of the 23 patients at risk of tuberculosis who had had INH prophylaxis for 1 year, neither tuberculosis, nor hepatotoxicity was observed. CONCLUSION: Tuberculosis is a common infection of renal transplant recipients in developing countries. The peak incidence is after the first year of transplantation and mortality is considerable. Hepatoxicity is a considerable risk of treatment, possibly as a result of additive toxic effects of immunosuppressive drugs.

Adult↗
PubMed1998

Improvement of uremic autonomic dysfunction after renal transplantation: a heart rate variability study.

Autonomic dysfunction in hemodialysis patients is one of the components of uremic neuropathy. In this prospective study, we investigated the effect of renal transplantation on uremic autonomic dysfunction with long-term time-domain and frequency-domain heart rate variability. Fourteen hemodialysis patients (10 male, 4 female; mean age 33 +/- 11 (range 16-50) years) were examined before and at the early after transplantation period (mean 4.6 +/- 1.5 (range 3-7. 5) months). The mean time spent on hemodialysis was 16.7 +/- 15.6 (range 6-65) months. In time-domain analysis, significant increases in all parameters except pNN50 (SD, SDANN, SDNN, rMSSD) were observed after renal transplantation (p < 0.01). In frequency-domain analysis, low-frequency (LF) (0.04-0.15 Hz) and high-frequency (HF) (0.15-0.40 Hz) spectral power were found to be significantly increased after renal transplantation (4.54 +/- 1.04 vs. 12.58 +/- 8. 69 for LF (p = 0.005), 2.80 +/- 1.0 vs. 6.50 +/- 3.55 for HF (p = 0. 005)), but the LF/HF ratio was not different from a pretransplant period (1.71 +/- 0.349 vs. 1.85 +/- 0.49, p = 0.26). It was concluded that autonomic dysfunction in hemodialysis patients is reversible and renal transplantation reverses the sympathetic and parasympathetic autonomic dysfunction simultaneously and at a relatively early stage.

Adolescent↗
PubMed1998

Fever in dialysis patients with recently rejected renal allografts.

INTRODUCTION: Fever of unknown origin is a complex problem in dialysis patients with recently rejected renal allografts, due to the contribution of the newly withheld immunosuppressive agents to the immunosuppression of uremia, resulting in an atypical presentation of infections, a main cause of fever in these cases. MATERIALS AND METHODS: Two dialysis patients with recently rejected renal allografts who were hospitalized because of fever of unknown origin are reported. Biochemical, bacteriological and imaging studies were performed for specific diagnosis. RESULTS: Extensive laboratory investigations failed to yield any diagnosis and allograft nephrectomy was performed in one patient, with a probable diagnosis of inflammation of the allograft, which resulted in no improvement. Eventually, both patients were found to have adrenal insufficiency responsible for the fever, which improved after steroid replacement. CONCLUSIONS: Adrenal insufficiency should be suspected in all dialysis patients presenting with fever and atypical symptoms, but only after other potential causes are eliminated; since steroid administration may normalize fever regardless of the etiology, it may mask the signs and symptoms and delay the treatment of other (if any) underlying disorder(s).

Adult↗
PubMed1998

Transplantation in renal amyloidosis.

In this report, the results of renal transplantation in patients with renal amyloidosis were retrospectively analysed and compared with the control group. Fifteen (3.04%) of the 493 renal transplant recipients whom were followed up in Istanbul School of Medicine transplant outpatient clinic, between 1983 and 1997, were included in the study. The etiology of amyloidosis was familial Mediterranean fever in all patients. The mean follow-up period was 38.3 +/- 31.8 (range 7-65) months. Twelve of the patients were male and 3 female with the mean age 34.13 +/- 10.87 (range 21-60) years. Seven patients had living related, 4 living-unrelated and 4 cadaveric donors. Five patients were lost because of different complications: Three patients died from cardiac amyloidosis all with well functioning grafts, 2, 3 and 36 months after the operation. Sepsis and cardiovascular failure was the probable cause of death in 1 patient who also had chronic rejection. Another one patient with chronic rejection died from hepatic failure. Acute rejection developed in 2 patients. Renal functions of these patients improved by anti-rejection therapies. Chronic rejection developed in 3 patients. In the control group, acute rejection and chronic rejection were diagnosed in 5 and 1 patients, retrospectively. While 1 patients returned to hemodialysis in control group, the others are alive with satisfactory graft function. There was no death in control group. The 5-yr graft and patient survival rates in amyloidosis and the control groups were 75, 77, 95 and 100%, respectively. It was concluded that although transplantation is not a contraindication for the treatment of end stage renal failure in patients with renal amyloidosis, it carries high risk of cardiac complications in the postoperative period. Detailed preoperative cardiovascular evaluations are mandatory in these patients and this intervention should improve the prognosis by excluding the patients who have already been complicated with this problem.

Adult↗
PubMed1996

Posttransplant malaria.

The frequency and clinical characteristics of plasmodium infection were reported in 420 renal transplant recipients who were followed in the Transplantation Unit and Out-Patient Clinic of the Medical School of Istanbul. Plasmodium infection was diagnosed in eleven (9 male, 2 female) of the 420 patients (2.6%). Ten of the patients were transplanted in India, and one in our institution. The mean duration between the transplantation and the diagnosis of malaria was 21.7 + 44.4 days in patients who were transplanted in India. All of the patients were taking triple immunosuppressive drugs (CsA, AZA, PRED). Plasmodium falciparum was diagnosed in 6 patients, P vivax in 1 patient and P malariae in 1 patient. Also mixed infection with P falciparum and P malariae was diagnosed in 3 patients. After definite diagnosis, the patients were hospitalized. Chloroquine phosphate plus primaquine phosphate was administered for P vivax infection, whereas chloroquine phosphate alone was given for P falciparum and P malariae infection as a first line antimalarial therapy. As a result of therapy, infection improved clinically and the plasmodia disappeared rapidly from the thick blood film in 10 of the patients. Severe hemolysis and acute renal failure developed in one patient, who improved after hemodialysis therapy and exchange transfusions. It was concluded that malaria is quite a frequent infection of transplant recipients who get their allografts from donors living in high-risk areas, and all transplant recipients having this kind of transplantations should be suspected and examined for malaria. This may help to diagnose and treat the complication in the early period, thus resulting in an improved prognosis for this potentially life-threatening complication of the posttransplant period.

Adult↗
PubMed1996

De novo light-chain deposition disease in a cadaver renal allograft.

The deposition of immunoglobulin (Ig) light chains after renal transplantation most commonly occurs as a manifestation of recurrent multiple myeloma or recurrent light chain nephropathy. We report the development of de novo light chain deposition disease (LCDD) in a cadaveric renal transplant recipient 16 years after transplantation with no evidence of prior multiple myeloma or LCDD and no current evidence of myeloma or lymphoproliferative malignancy.

Adult↗