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A Bakkaloglu

Publications and source records attributed to A Bakkaloglu.

At least 19 recordsLinked to original sources

Recessive missense mutations in LAMB2 expand the clinical spectrum of LAMB2-associated disorders.

Congenital nephrotic syndrome is clinically and genetically heterogeneous. The majority of cases can be attributed to mutations in the genes NPHS1, NPHS2, and WT1. By homozygosity mapping in a consanguineous family with isolated congenital nephrotic syndrome, we identified a potential candidate region on chromosome 3p. The LAMB2 gene, which was recently reported as mutated in Pierson syndrome (microcoria-congenital nephrosis syndrome; OMIM #609049), was located in the linkage interval. Sequencing of all coding exons of LAMB2 revealed a novel homozygous missense mutation (R246Q) in both affected children. A different mutation at this codon (R246W), which is highly conserved through evolution, has recently been reported as causing Pierson syndrome. Subsequent LAMB2 mutational screening in six additional families with congenital nephrotic syndrome revealed compound heterozygosity for two novel missense mutations in one family with additional nonspecific ocular anomalies. These findings demonstrate that the spectrum of LAMB2-associated disorders is broader than previously anticipated and includes congenital nephrotic syndrome without eye anomalies or with minor ocular changes different from those observed in Pierson syndrome. This phenotypic variability likely reflects specific genotypes. We conclude that mutational analysis in LAMB2 should be considered in congenital nephrotic syndrome, if no mutations are found in NPHS1, NPHS2, or WT1.

Child, Preschool↗

How does the presence of urologic problems change the outcome of kidney transplantation in the pediatric age group.

PURPOSE: We retrospectively reviewed the impact of functional and anatomic urologic disorders on kidney transplantation outcomes in terms of the surgical and long-term results of pediatric renal transplantation. MATERIALS AND METHODS: Of the 55 kidney transplantations in the pediatric age group, end-stage renal disease (ESRD) was secondary to genitourinary disorders in 23 patients (42%). The urologic abnormalities were vesicoureteral reflux in 13 patients (59%), neurogenic bladder in 4 patients (18%), posterior urethral valves in 3 patients (14%), renal stone disease in 4 patients (18%), bilateral ureterovesical junction obstruction in 3 patients (14%), and unilateral renal agenesis with concomitant contralateral ureteropelvic junction obstruction in 1 patient (4%). RESULTS: Of the 23 patients with urologic problems, 19 (83%) had functioning grafts with a mean follow-up of 49 months (range, 7-120 months). In the other 32 patients, 26 (81%) had functioning grafts with a mean follow-up of 43 months (range, 1-144 months). The graft survival, mean serum creatinine, and urinary tract infection rates of the patients did not differ between the two groups. CONCLUSIONS: The presence of functional urologic disorders as the cause of ESRD did not seem to change the outcome of renal transplantation in terms of graft survival when compared with patients without any urologic disorders. Urinary tract infections seem to be a little more common and yet clinically not significant in those patients. Reflux does not always need to be corrected before transplantation, unless it is causing symptoms or infection.

Child↗

Semen variables and hormone profiles after kidney transplantation during adolescence.

Our aim was to investigate the semen variables and hormone profiles among transplant patients who received kidneys during adolescence. Seven postpubertal transplant patients who underwent successful renal transplantation during adolescence (13-19 years; 3 were preemptive) were enrolled in our clinical follow-up. Serum levels of prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone were checked together with the semen analysis. The ages of the patients ranged from 18 to 25 years (median, 22 years). The median age was 15 years (range, 12-18 years) at initial presentation. The median time between initial diagnosis and transplantation was 12 months (range, 2-60 months). The median follow-up after transplantation was 51 months (range, 23-134 months). Three of the seven patients had unilateral low testicular volume. The renal function tests were within normal limits, as well as serum levels of prolactin, FSH, LH, and testosterone. Sperm counts ranged from 0.2 to 55 million/mL (median, 1.7 million/mL). Only 1 patient (14.2%) had normal sperm parameters. Oligoteratozoospermia (low sperm count and defects in morphology) was observed in 1/7 (14.2%), asthenoteratozoospermia (low levels of motility and defects in morphology) in 1/7 (14.2%), and all parameters were abnormal in 4/7 (57.1%) cases. Our data suggest that in contrast to adult patients, semen variables are severely affected and spermatogenesis does not improve after renal transplantation when the patient was subjected to uremia before or during adolescence, the crucial period for spermatogenesis.

Adolescent↗

Renal transplantation in children with augmentation enterocystoplasty.

INTRODUCTION: We report our experience with renal transplantation in patients with severe bladder dysfunction who underwent prior augmentation cystoplasty. PATIENTS AND METHODS: Among 58 pediatric patients, three underwent bladder augmentation prior to renal transplantation. The patients' ages at transplantation were 10, 13, and 17. The etiologies of bladder dysfunction were posterior urethral valves in two patients and contracted bladder in one patient. Vesicoureteral reflux was concomitantly present in three patients. Pretransplant ileocystoplasty was created in two patients and gastrocystoplasty in one patient. All patients received kidneys from cadaveric donors and were treated with calcineurin-based immunosuppressive therapy. RESULTS: The patients had normal renal function without hydronephrosis of the transplanted kidney at 13, 22, 49 months follow-up. No patients had morbidity due to technical complications. All the patients were continent. Two of three patients required clean intermittent catheterization from a Mitrofanoff conduit, while one patient spontaneously voids without significant residual urine. Urinary tract infections observed in two patients were successfully treated without any permanent deterioration in graft kidney function. CONCLUSIONS: Our data suggest that augmentation cystoplasty is a safe and effective option to treat patients with end-stage renal disease undergoing kidney transplantation. Experience of the transplantation team with a qualified pediatric urologist is essential due to the potentially high risk of surgical complications during the long term management of these patients.

Adolescent↗

E148Q is a disease-causing MEFV mutation: a phenotypic evaluation in patients with familial Mediterranean fever.

BACKGROUND: Familial Mediterranean fever (FMF) is one of the periodic fever syndromes. It is common among Turks, Jews, Arabs, and Armenians. Several mutations in the MEFV gene, including E148Q, have been identified as causing this disease. It has been suggested that the E148Q mutation is the mildest mutation and some reports have questioned its disease association. OBJECTIVE: To evaluate the phenotypic features of the patients with E148Q mutation. SUBJECTS: 26 patients homozygous for E148Q, 10 compound heterozygous for E148Q, and eight complex cases were assessed. RESULTS: Although four of the 26 patients with E148Q/E148Q were asymptomatic at the time of evaluation, abdominal pain was seen in 77% of the patients, fever in 66%, arthralgia in 50%, arthritis in 15.4%, and vomiting in 23.8%. Compound heterozygotes and complex cases had a higher frequency of abdominal pain, fever, arthralgia, arthritis, myalgia, and chest pain than subjects who were homozygous for E148Q, but none of these symptoms reached statistical significance. None of our patients had amyloidosis but two with E148Q/E148Q had a family history of amyloidosis and one had rapidly progressive glomerulonephritis secondary to vasculitis, which progressed to chronic renal failure. CONCLUSIONS: Patients homozygous for E148Q have a heterogeneous clinical presentation. Most are symptomatic and colchicine treatment is required in these patients.

Abdominal Pain↗

Bone mineral density in children with familial Mediterranean fever.

The aim of this study was to evaluate bone mineral content (BMC), serum and urinary bone turnover parameters in patients with familial Mediterranean fever (FMF), an autosomal recessive disease characterized by recurrent episodes of inflammation of serous membranes. Demographic characteristics and MEFV mutations were defined in 48 children diagnosed with FMF (23 F, 25 M; median age 7.0 years (3.0-10.0)). We evaluated the blood counts, acute-phase proteins and serum and urinary bone turnover parameters during attack-free periods. The BMC and BA (bone area) of vertebrae L1-L4 were measured by DEXA. Thirty-eight age-, sex- and ethnicity-matched healthy children constituted the control group. Mean L1-L4 BMC in Group I (patients with two mutations) and II (patients with no or single mutations) were 15.49+/-5.99 g and 15.68+/-4.89 g, respectively, both significantly lower than the mean L1-L4 BMC of control patients, which was 19.59+/-6.7 g (p<0.05). Mean L1-L4 BMD in Group I, Group II and the control group were 0.466+/-0.066 g/cm(2), 0.487+/-0.085 g/cm(2 )and 0.513+/-0.079 g/cm(2), respectively. Mean z-scores in Group I, Group II and the control group were -1.87+/-0.74, -1.55+/-0.92 and -1.39+/-0.84, respectively. Mean L1-L4 BMD and z-score of Group I were lower than in the control group (p<0.05). ESR and SAA (serum amyloid A) levels were higher in Group I patients: 28.3+/-14.5 mm/h and 350+/-62 mg/l in Group I; and 20.5+/-11.7 mm/h and 190+/-68 mg/l in Group II, respectively. In conclusion, FMF patients had lower BMC, BMD and z-scores than a control group. We suggest that decreased BMD, BMC and z-score in FMF patients may be secondary to subclinical inflammation.

Bone Density↗

Allelic variants in genes associated with hereditary periodic fever syndromes as susceptibility factors for reactive systemic AA amyloidosis.

We investigated the hypothesis that low-penetrance mutations in genes (TNFRSF1A, MEFV and NALP3/CIAS1) associated with hereditary periodic fever syndromes (HPFs) might be risk factors for AA amyloidosis among patients with chronic inflammatory disorders, including rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), Crohn's disease, undiagnosed recurrent fevers and HPFs themselves. Four of 67 patients with RA plus amyloidosis had MEFV variants compared with none of 34 RA patients without amyloid (P value=0.03). The E148Q variant of MEFV was present in two of the three patients with TNF receptor-associated periodic syndrome (TRAPS) complicated by amyloid in two separate multiplex TRAPS families containing 5 and 16 affected members respectively, and the single patient with Muckle-Wells syndrome who had amyloidosis was homozygous for this variant. The R92Q variant of TNFRSF1A was present in two of 61 JIA patients with amyloidosis, and none of 31 nonamyloidotic JIA patients. No HPF gene mutations were found in 130 healthy control subjects. Although allelic variants in HPFs genes are not major susceptibility factors for AA amyloidosis in chronic inflammatory disease, low-penetrance variants of MEFV and TNFRSF1A may have clinically significant proinflammatory effects.

Amino Acid Substitution↗

Decreased prevalence of atopy in paediatric patients with familial Mediterranean fever.

BACKGROUND: A number of inflammatory diseases, including familial Mediterranean fever (FMF), have been shown to be driven by a strongly dominated Th1 response, whereas the pathogenesis of atopic diseases is associated with a Th2 response. OBJECTIVE: Because dominance of interferon gamma has the potential of inhibiting Th2 type responses-that is, development of allergic disorders, to investigate whether FMF, or mutations of the MEFV gene, have an effect on allergic diseases and atopy that are associated with an increased Th2 activity. METHOD: Sixty children with FMF were questioned about allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis, as were first degree relatives, using the ISAAC Study phase II questionnaire. The ISAAC Study phase II was performed in a similar ethnic group recruited from central Anatolia among 3041 children. The same skin prick test panel used for the ISAAC Study was used to investigate the presence of atopy in patients with FMF and included common allergens. RESULTS: The prevalences of doctor diagnosed asthma, allergic rhinitis, and eczema were 3.3, 1.7, and 3.3%, respectively, in children with FMF, whereas the corresponding prevalences in the ISAAC study were 6.9, 8.2, and 2.2%, respectively. Only the prevalence of allergic rhinitis was significantly different between the two groups (p<0.001). The prevalence of atopy in these patients with FMF (4/60 (7%)) was significantly lower than in the children of the population based study (20.6%) (p<0.001). CONCLUSION: Family Mediterranean fever seems to be protective against development of atopic sensitisation and allergic rhinitis.

Asthma↗

The role of apoptosis in childhood Henoch-Schonlein purpura.

The pathogenesis of vasculitis is complex and is yet to be fully elucidated, although it is known that inflammatory cells play a major role. Dysregulation of apoptosis and defective clearance of inflammatory cells could lead to the persistence of inflammation and excessive tissue injury. In this study we aimed to investigate Fas (CD95) and apoptosis on peripheral blood (PB) neutrophil and lymphocytes in Henoch-Schonlein purpura, both in the acute phase and after resolution to determine the role of apoptosis in this self-limited vasculitis. Leukocytoclastic vasculitis presenting with Henoch-Schonlein purpura (HSP) was diagnosed according to ACR 1990 criteria and confirmed by skin biopsy. Thirty-seven patients (22 boys, 15 girls) aged 2.5-17 years (9 +/- 3.3) were enrolled in the study. Expression of CD95 and apoptosis were investigated by the annexin/PI method on peripheral blood neutrophils and lymphocytes in both the acute and the resolution phases of the disease. The mean neutrophil and lymphocyte CD95 expression was 65.4 +/- 37.6% and 33.3 +/- 7.3%, respectively, in the acute stage and 62.8 +/- 44.2% and 41 +/- 20%, respectively, in the resolution ( P > 0.05). The percentage of apoptotic peripheral blood neutrophils and lymphocytes as determined by annexin positivity was 13.3 +/- 11.31% and 8.6 +/- 9.5%, respectively, during the acute phase and 4.6 +/- 3.4% and 3.1 +/- 3.1%, respectively, in the resolution (P = 0.002, P = 0.008). These results suggest that increased apoptotic process in the immune effector cells in the acute phase of the disease may play an important role in the early control of inflammatory response and repair in leukocytoclastic vasculitis, thereby contributing to the self-limited nature of the disease.

Adolescent↗

Triple immunosuppression with or without basiliximab in pediatric renal transplantation: acute rejection rates at one year.

Acute rejection (AR) is a major determinant of chronic allograft dysfunction and graft survival. This study evaluated the effect of basiliximab on AR in pediatric renal transplantation on triple immunosuppression. Forty-three transplantations (25 males and 18 females; mean age 14.9 +/- 3.6 years) were performed between 1996 and 2002. Thirteen of the grafts came from cadaveric donors and 30 from living-related donors. All patients were placed on immunosuppression with prednisolone + (azathioprine or mycophenolate mofetil) + (cyclosporine [CYA] or tacrolimus). Basiliximab was also administered in 20 cases. The respective rates of biopsy-proven AR in the basiliximab group (BG) and the standard-regimen group (N-BG) were 0% vs 17.4% (P >.05) at 1 month posttransplantation; 0% vs 26.1% (P <.05) at 3 months; 0% vs 26.1% (P <.05) at 6 months, and 7.1% vs 26.1% (P >.05) at 12 months. In the N-BG group the 1- and 3-year graft survival rates were 91.3% (21/23) and 83.3% (15/18), respectively. The mean glomerular filtration rate (GFR) in the first year after the transplantation was 75 +/- 33 mL/min/1.73 m(2) in the N-BG and 98 +/- 21 mL/min/1.73 m(2) in the BG patients (P <.05). Basiliximab significantly reduced the rates of acute rejection at 3 and 6 months after pediatric renal transplantation. The GFR in the first year was significantly higher among the patients treated with basiliximab, which was well tolerated by all patients and caused no significant adverse effects. The effect of basiliximab on long-term graft survival and chronic allograft dysfunction deserves further investigation.

Adolescent↗

A phenocopy of CAII deficiency: a novel genetic explanation for inherited infantile osteopetrosis with distal renal tubular acidosis.

The rare bone thickening disease osteopetrosis occurs in various forms, one of which is accompanied by renal tubular acidosis (RTA), and is known as Guibaud-Vainsel syndrome or marble brain disease. Clinical manifestations of this autosomal recessive syndrome comprise increased bone density, growth failure, intracerebral calcification, facial dysmorphism, mental retardation, and conductive hearing impairment. The most common cause is carbonic anhydrase II (CAII) deficiency. Several different loss of function mutations in CA2, the gene encoding CAII, have been described. To date, there have been no exceptions to the finding of CAII deficiency in patients with coexistent osteopetrosis and RTA. Most often, the RTA is of mixed proximal and distal type, but kindreds are reported in which either distal or proximal RTA predominates. We report the molecular genetic investigation of two consanguineous kindreds where osteopetrosis and distal RTA (dRTA) were both manifest. One kindred harbours a novel homozygous frameshift alteration in CA2. In the other, CAII levels were normal despite a similar clinical picture, and we excluded defects in CA2. In this kindred, two separate recessive disorders are penetrant, each affecting a different, tissue specific subunit of the vacuolar proton pump (H(+)-ATPase), providing a highly unusual, novel genetic explanation for the coexistence of osteopetrosis and dRTA. The osteopetrosis is the result of a homozygous deletion in TCIRG1, which encodes an osteoclast specific isoform of subunit a of the H(+)-ATPase, while the dRTA is associated with a homozygous mutation in ATP6V1B1, encoding the kidney specific B1 subunit of H(+)-ATPase. This kindred is exceptional firstly because the coinheritance of two rare recessive disorders has created a phenocopy of CAII deficiency, and secondly because these disorders affect two different subunits of the H(+)-ATPase that have opposite effects on bone density, but which have only recently been determined to possess tissue specific isoforms.

Acidosis, Renal Tubular↗

Tumour necrosis factor alpha G-->A -238 and G-->A -308 polymorphisms in juvenile idiopathic arthritis.

OBJECTIVES: To study G-->A -238 and G-->A -308 polymorphisms in the promoter region of the tumour necrosis factor (TNF) alpha gene in patients with juvenile idiopathic arthritis (JIA). We analysed whether there were any associations between these polymorphisms and the type of JIA and/or the clinical course of the disease in two populations. METHODS: The first group consisted of 51 Turkish JIA patients and the second consisted of 159 JIA patients from the Czech Republic. Healthy individuals (93 and 100) from each country served as controls. Subgroups of JIA were defined according to the Durban criteria. The course of the disease was defined on the basis of the physician's global evaluation of disease activity, the swollen and tender joint count and the erythrocyte sedimentation rate. RESULTS: In both JIA cohorts, the distribution of genotypes was not significantly different among the types of JIA. The G-->A -238 polymorphism did not have an effect on the patients' outcome in either group. The G-->A -308 polymorphism was significantly associated with a poor outcome in the Turkish group (P=0.005) but there was no association in the Czech patients. Some features of JIA in Turkish patients differed from those in Czech patients. CONCLUSIONS: Genetic differences may accompany the phenotypic differences found in the Turkish group. Although larger numbers of patients are clearly needed to verify this, we suggest that the G-->A -308 polymorphism may be operative in defining disease outcome in selected groups.

Adolescent↗

Novel ATP6V1B1 and ATP6V0A4 mutations in autosomal recessive distal renal tubular acidosis with new evidence for hearing loss.

Autosomal recessive distal renal tubular acidosis (rdRTA) is characterised by severe hyperchloraemic metabolic acidosis in childhood, hypokalaemia, decreased urinary calcium solubility, and impaired bone physiology and growth. Two types of rdRTA have been differentiated by the presence or absence of sensorineural hearing loss, but appear otherwise clinically similar. Recently, we identified mutations in genes encoding two different subunits of the renal alpha-intercalated cell's apical H(+)-ATPase that cause rdRTA. Defects in the B1 subunit gene ATP6V1B1, and the a4 subunit gene ATP6V0A4, cause rdRTA with deafness and with preserved hearing, respectively. We have investigated 26 new rdRTA kindreds, of which 23 are consanguineous. Linkage analysis of seven novel SNPs and five polymorphic markers in, and tightly linked to, ATP6V1B1 and ATP6V0A4 suggested that four families do not link to either locus, providing strong evidence for additional genetic heterogeneity. In ATP6V1B1, one novel and five previously reported mutations were found in 10 kindreds. In 12 ATP6V0A4 kindreds, seven of 10 mutations were novel. A further nine novel ATP6V0A4 mutations were found in "sporadic" cases. The previously reported association between ATP6V1B1 defects and severe hearing loss in childhood was maintained. However, several patients with ATP6V0A4 mutations have developed hearing loss, usually in young adulthood. We show here that ATP6V0A4 is expressed within the human inner ear. These findings provide further evidence for genetic heterogeneity in rdRTA, extend the spectrum of disease causing mutations in ATP6V1B1 and ATP6V0A4, and show ATP6V0A4 expression within the cochlea for the first time.

Acidosis, Renal Tubular↗

Higher frequency of allele 2 of the interleukin-1 receptor antagonist gene in patients with juvenile idiopathic arthritis.

OBJECTIVE: An increased incidence of allele 2 of the interleukin-1 receptor antagonist gene (IL1RN*2) in several inflammatory diseases has recently been reported. The aim of this study was to examine a variable number tandem repeat (VNTR) polymorphism of the IL1RN gene in patients with juvenile idiopathic arthritis (JIA). METHODS: Findings in 185 Czech patients with JIA were compared with those in 168 Czech controls, 50 JIA patients and 52 controls of Turkish origin, and 79 controls from central England. VNTR polymorphism analysis of IL1RN was performed by polymerase chain reaction using 2 flanking primers to amplify an 86-bp tandem repeat region in intron 2. RESULTS: The frequency and carriage rate of IL1RN*2 were significantly increased in Czech JIA patients compared with the Czech controls (frequency 27.6% versus 15.8%; carriage rate 44.3% versus 26.2%). Increased frequency and carriage rate of IL1RN*2 were found in 23.3% and 40.0% of Turkish JIA patients and in 17.3% and 34.6% of ethnically matched controls. The high representation of IL1RN*2 in 52.3% of the 22 patients with extended oligoarthritis, 31.3% of the 56 patients with enthesitis-related arthritis, and 42.9% of the 14 patients with other arthritis was particularly responsible for the increased frequency of IL1RN*2 in the Czech JIA patients. We found no association of IL1RN*2 with disease activity or severity parameters. CONCLUSION: Inheritance of IL1RN*2 may contribute to genetic susceptibility in several forms of autoimmune diseases, including JIA. The IL1RN*2 allele may be useful as a prognostic indicator of the evolution of an extended oligoarticular course of JIA.

Alleles↗

Pulmonary haemorrhage in a 6-year-old boy with Henoch-Schönlein purpura.

Henoch-Schönlein purpura (HSP) is the most common vasculitis in children. It is a multisystemic disease but pulmonary haemorrhage is extremely rare. We present the case of a 6-year-old boy with Henoch-Schönlein purpura, pulmonary haemorrhage and severe renal involvement. The patient responded to a combination of intravenous methylprednisolone and cyclophosphamide. A review of the literature revealed that young age may be a good prognostic sign and that immunosuppressive drugs and supportive management are essential in the treatment. Renal biopsy is helpful in the differential diagnosis of HSP-mimicking pulmonary vasculitic syndromes. Combining cyclophosphamide with glucocorticoids may improve the outcome in severe HSP cases with pulmonary haemorrhage.

Child↗