Evaluation of the risk factors for BK virus-associated hemorrhagic cystitis in pediatric bone marrow transplantation patients: Does post-transplantation cyclophosphamide increase the frequency?

BACKGROUND: BKV-HC is one of the most significant complications of HSCT. This retrospective study aimed to determine the frequency of BKV-HC in pediatric patients undergoing HSCT, detect the associated risk factors for the development of BKV-HC, and explore the effects of post-transplantation Cy use. METHODS: Three hundred twenty-seven patients (girls: 121, boys: 206) were analyzed according to sex, conditioning regimen, transplantation type, donor relatedness, stem cell source, the presence and grade of aGVHD, CMV co-existence, and Cy use. RESULTS: Multivariate analysis confirmed the prognostic importance of age (OR: 4.865), TBI use, the presence of aGVHD (OR: 2.794), CMV coinfection (OR: 2.261), and Cy use (OR: 27.353). A statistically significant difference was found between the mean BKV-HC follow-up times compared with post-transplantation Cy intake (p < .001). The BKV-HC rate increased as the number of risk factors of the patient increased. CONCLUSION: BKV-HC is an essential complication of HSCT primarily associated with Cy use, the presence of aGVHD, and donor relatedness. The present study shows that the use of Cy in the post-transplantation period further increases BKV-HC risk in pediatric patients, regardless of dose.

A 9.5-year-old boy with recurrent neurological manifestations and severe hypertension, treated initially for polyarteritis nodosa, was subsequently diagnosed with adenosine deaminase type 2 deficiency (DADA2) which responded to anti-TNF-α.

A 9.5-year-old boy was referred with a 2-year history of recurrent fever, myalgia, abdominal pain and various neurological manifestations associated with increased acute phase reactants and IgG level. During the recent episode, severe hypertension and right-sided hemiparesis developed and angiography demonstrated irregularities and stenosis in renal and mesenteric artery branches. Although these manifestations were consistent with polyarteritis nodosa (PAN), the consanguinity of his parents, a cousin with similar clinical features and early disease onset led to suspicion of deficiency of adenosine deaminase type 2 (DADA2) diseases. DADA2 was established by demonstration of decreased ADA2 enzyme activity and a homozygous G47R mutation in the CECR1 gene. The diagnosis of DADA2 is challenging because of the overlapping manifestations with PAN and other periodic fever syndromes. DADA2 should be considered in the differential diagnosis of PAN. Raised IgG levels (usually low in DADA2) should be sought in future cases.Abbreviations: CECR1, cat eye syndrome chromosome region candidate 1; DADA2, deficiency of adenosine deaminase type 2; MEFV, Mediterranean fever; PAN, polyarteritis nodosa.

Diagnostic utility of a targeted next-generation sequencing gene panel in the clinical suspicion of systemic autoinflammatory diseases: a multi-center study.

Systemic autoinflammatory diseases (sAIDs) are a heterogeneous group of disorders, having monogenic inherited forms with overlapping clinical manifestations. More than half of patients do not carry any pathogenic variant in formerly associated disease genes. Here, we report a cross-sectional study on targeted Next-Generation Sequencing (NGS) screening in patients with suspected sAIDs to determine the diagnostic utility of genetic screening. Fifteen autoinflammation/immune-related genes (ADA2-CARD14-IL10RA-LPIN2-MEFV-MVK-NLRC4-NLRP12-NLRP3-NOD2-PLCG2-PSTPIP1-SLC29A3-TMEM173-TNFRSF1A) were used to screen 196 subjects from adult/pediatric clinics, each with an initial clinical suspicion of one or more sAID diagnosis with the exclusion of typical familial Mediterranean fever (FMF) patients. Following the genetic screening, 140 patients (71.4%) were clinically followed-up and re-evaluated. Fifty rare variants in 41 patients (20.9%) were classified as pathogenic or likely pathogenic and 32 of those variants were located on the MEFV gene. We detected pathogenic or likely pathogenic variants compatible with the final diagnoses and inheritance patterns in 14/140 (10%) of patients for the following sAIDs: familial Mediterranean fever (n = 7), deficiency of adenosine deaminase 2 (n = 2), mevalonate kinase deficiency (n = 2), Muckle-Wells syndrome (n = 1), Majeed syndrome (n = 1), and STING-associated vasculopathy with onset in infancy (n = 1). Targeted NGS panels have impact on diagnosing rare monogenic sAIDs for a group of patients. We suggest that MEFV gene screening should be first-tier genetic testing especially in regions with high carrier rates. Clinical utility of multi-gene testing in sAIDs was as low as expected, but extensive genome-wide familial analyses in combination with exome screening would enlighten additional genetic factors causing disease.

Efficacy of anakinra in a patient with systemic amyloidosis presenting as amyloidoma.

Amyloidosis is a heterogeneous group of disorders characterized by extracellular deposition of unique protein fibrils. The least common presentation of an amyloid deposition is as a discrete mass called amyloidoma or amyloid tumor. We report a case of a soft tissue amyloidoma in the abdomen of a 16-year-old girl who was diagnosed as having systemic amyloidosis. A girl aged 16 years was referred to our hospital with a pre-diagnosis of a retroperitoneal mass documented with abdominal ultrasonography and tomography. A laboratory examination revealed nephrotic syndrome. She underwent surgery for a complete resection of the lesion. A histopathologic examination with Congo red and crystal violet dyes verified the diagnosis of amyloidoma. An immunohistochemical study for amyloid A protein was positive. A renal biopsy was also compatible with AA amyloidosis. A detailed search for the etiology of systemic amyloidosis revealed heterozygous mutation in the Mediterranean fever gene. Treatment with colchicine and anakinra were started with the diagnosis of familial Mediterranean fever because the other causes of secondary amyloidosis were ruled out. After 3 months of anakinra treatment, the laboratory findings returned to normal and excessive proteinuria disappeared. In countries where FMF and other autoinflammatory diseases are prevelant, systemic amyloidosis should be kept in mind in the differential diagnosis of children who present with nephrotic syndrome and abdominal mass. Taking previously reported cases and our case together, it appears that anti-interleukin-1 treatment represents a promising new approach in a subset of patients with systemic amyloidosis secondary to autoinflammatory diseases.

Single port laparoscopic and open surgical accesses of chronic peritoneal dialysis in children: A single center experience over 12 years.

INTRODUCTION: The aim of this study was to evaluate patients with end stage renal failure (ESRD) who underwent chronic peritoneal dialysis (CPD). The clinical outcomes of laparoscopic and open placements of catheters were compared. MATERIALS AND METHODS: We reviewed 49 (18 male and 31 female) children with CPD according to age, sex, cause of ESRD, catheter insertion method, kt/V rate, complications, presence of peritonitis, catheter survival rate between January 2002 and February 2014. RESULTS: Thirty-three patients were with open placement and 16 patients were with laparoscopic placement. The rate of the peritonitis is significantly less in patients with laparoscopic access than open access (n = 4 vs n = 25) (P <0.01). Patients with peritonitis were younger than those who had no attack of peritonitis (10.95 ± 0.8 years vs 13.4 ± 0.85 years). According to the development of complications, significant difference has not been found between the open (n = 9) and laparoscopic (n = 3) approaches except the peritonitis. Catheter survival rate for the first year was 95%, and for five years was 87.5%. There was no difference between open and laparoscopic group according to catheter survival rate. The mean kt/V which indicates the effectiveness of peritoneal dialysis was mean 2.26 ± 0.08. No difference was found between laparoscopic and open methods according to kt/V. CONCLUSION: Laparoscopic placement of CPD results in lower peritonitis rate. Catheter survival rate was excellent in both groups. Single port laparoscopic access for CPD catheter insertion is an effective and safe method.

Kidney injury molecule-1 and neutrophil gelatinase associated lipocalin in normoalbuminuric diabetic children.

BACKGROUND: We aimed at evaluating the urinary levels of kidney injury molecule-1 ( KIM-1) and neutrophil gelatinase associated lipocalin (NGAL), and the relationship between these markers and clinical and laboratory variables in normoalbuminuric children with type 1 diabetes (T1D). METHODS: The study group consisted of 60 (F/M: 28/32) children with T1D with a median age of 13 (min: 7.1-max: 17.9) years and a mean HbA1c of 8.6%. The average period of treatment was 6.8±2.2 years. The control group consisted of 60 healthy children [(F/M: 32/28); median age: 13.6 (min: 6.9-max: 17.9) years]. RESULTS: Urinary KIM-1 and NGAL levels were significantly elevated in the diabetic group (KIM-1: 0.50±0.34 ng/mg-cr; NGAL: 33±31 ng/mg-cr) compared with the nondiabetic control subjects (KIM-1: 0.26±0.25 ng/mg-cr, NGAL 13.3±14.5 ng/mg-cr) (p<0.001). No significant associations were observed between NGAL or KIM-1 and the duration of diabetes and HbA1c levels. NGAL was found to be weakly correlated with KIM-1 (p<0.005, r=0.289). CONCLUSIONS: NGAL and KIM are high in normoalbuminuric diabetic children before reduction in glomerular filtration rate. High NGAL and KIM-1 levels may indicate early diabetic kidney injury; however, we did not observe any relationship between these markers and diabetic indices. For clinical usefulness of these markers, long-term studies are required.

Spectrum of steroid-resistant and congenital nephrotic syndrome in children: the PodoNet registry cohort.

BACKGROUND AND OBJECTIVES: Steroid-resistant nephrotic syndrome is a rare kidney disease involving either immune-mediated or genetic alterations of podocyte structure and function. The rare nature, heterogeneity, and slow evolution of the disorder are major obstacles to systematic genotype-phenotype, intervention, and outcome studies, hampering the development of evidence-based diagnostic and therapeutic concepts. To overcome these limitations, the PodoNet Consortium has created an international registry for congenital nephrotic syndrome and childhood-onset steroid-resistant nephrotic syndrome. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Since August of 2009, clinical, biochemical, genetic, and histopathologic information was collected both retrospectively and prospectively from 1655 patients with childhood-onset steroid-resistant nephrotic syndrome, congenital nephrotic syndrome, or persistent subnephrotic proteinuria of likely genetic origin at 67 centers in 21 countries through an online portal. RESULTS: Steroid-resistant nephrotic syndrome manifested in the first 5 years of life in 64% of the patients. Congenital nephrotic syndrome accounted for 6% of all patients. Extrarenal abnormalities were reported in 17% of patients. The most common histopathologic diagnoses were FSGS (56%), minimal change nephropathy (21%), and mesangioproliferative GN (12%). Mutation screening was performed in 1174 patients, and a genetic disease cause was identified in 23.6% of the screened patients. Among 14 genes with reported mutations, abnormalities in NPHS2 (n=138), WT1 (n=48), and NPHS1 (n=41) were most commonly identified. The proportion of patients with a genetic disease cause decreased with increasing manifestation age: from 66% in congenital nephrotic syndrome to 15%-16% in schoolchildren and adolescents. Among various intensified immunosuppressive therapy protocols, calcineurin inhibitors and rituximab yielded consistently high response rates, with 40%-45% of patients achieving complete remission. Confirmation of a genetic diagnosis but not the histopathologic disease type was strongly predictive of intensified immunosuppressive therapy responsiveness. Post-transplant disease recurrence was noted in 25.8% of patients without compared with 4.5% (n=4) of patients with a genetic diagnosis. CONCLUSIONS: The PodoNet cohort may serve as a source of reference for future clinical and genetic research in this rare but significant kidney disease.

Novel NLRP12 mutations associated with intestinal amyloidosis in a patient diagnosed with common variable immunodeficiency.

Heterozygous mutations in the NLRP12 gene have been found in patients with systemic auto-inflammatory diseases. However, the NLRP12-associated periodic fever syndromes show a wide clinical spectrum, including patients without classical diagnostic symptoms. Here, we report on a 20-year-old female patient diagnosed with common variable immunodeficiency (CVID), who developed intestinal amyloidosis and carried novel compound heterozygous mutations in NLRP12, identified by whole exome and transcriptome sequencing. CVID is a primary immunodeficiency characterized by low serum immunoglobulins, recurrent bacterial infections and development of malignancy, but it also presents with a magnitude of autoimmune features. Because of the unspecific heterogeneous clinical features of the disease, a delay in diagnosis is common. Secondary, inflammatory (AA type) amyloidosis has infrequently been observed in CVID patients. Based on our case observation and a critical review of the literature, we suggest that NLRP12 mutations might account for a small fraction of CVID patients with severe auto-inflammatory complications.

Effect of creatine and pioglitazone on Hk-2 cell line cisplatin nephrotoxicity.

Cisplatin is a chemotherapeutic agent, which is used in the treatment of various solid organ cancers, and its main dose limiting side effect of cisplatin is nephrotoxicity. The aim of this study is to investigate the role of pioglitazone and creatine on cisplatin nephrotoxicity in vitro. Real-time cell analyzer system (RTCA) was used for real-time and time-dependent analysis of the cellular response of HK-2 cells following incubation with cisplatin and combination with creatine or pioglitazone hydrochloride. First, half-maximal inhibitory concentrations (IC50) of cisplatin, creatine and pioglitazone were calculated by RTCA system. Afterwards creatine and pioglitazone was administered with serial dilutions under RTCA system. IC50 dose for cisplatin was 7.69 M × 10(-5) at 24th hour and 3.93 M × 10(-6) at 48th hour. IC50 dose for pioglitazone was 1.61 M × 10(-3) at 24th hour and 2.85 M × 10(-4) at 48th hour. Although cells were treated the dose of 40,225 mM creatine, IC50 dose could not been reached. Neither pioglitazone nor creatine had additional protective effect in any dose. Consequently, beneficial effect of creatine and pioglitazone on cisplatin-induced cell death could not be found. Further studies and clinical trials are needed to evaluate the effect of different doses of these drugs in cisplatin-induced nephrotoxicity.

Effect of free creatine therapy on cisplatin-induced renal damage.

Abstract Cisplatin is one of the commonly used anticancer drugs and nephrotoxicity limits its use. The aim of this study is to investigate the possible protective effect of creatine supplementation on cisplatin-induced nephrotoxicity. Sixty male Sprague-Dawley rats were divided into three groups: Group I: Cisplatin (n=20) (7 mg/kg cisplatin intraperitoneal (i.p.) single dose), group II: Cisplatin+creatine monohydrate (n=20) (7 mg/kg cisplatin i.p. single dose and 300 mg/kg creatine p.o. daily for 30 days starting on first day of cisplatin injection), group III: Control group (n=20) (Serum physiologic, 2.5 mL/kg i.p.). Sacrifications were performed at first week and 30th day. Blood urea nitrogen (BUN) and serum creatinine levels, histopathological evaluation, mitochondrial deoxyribonucleic acid (mtDNA) common deletion rates, and body weights of rats were evaluated. A significant decrease in body weight, higher values of kidney function tests, histopathological scores, and mtDNA deletion ratios were observed in group I compared to control group at days 7 and 30 (p<0.05). In group II, there was a slight decrease in body weight at same days (p=0.931 and 0.084, respectively). Kidney function tests, histopathological scores, and mtDNA common deletion ratios were statistically better in group II than group I at 7th and 30th day (p<0.05). Although creatine significantly reversed kidney functions and pathological findings, this improvement was not sufficient to reach normal control group's results at days 7 and 30. In conclusion, the present study demonstrates that creatine administration is a promising adjuvant protective drug for reducing nephrotoxic effect of cisplatin.

Eculizumab therapy in a patient with dense-deposit disease associated with partial lipodystropy.

BACKGROUND: Dense deposit disease (DDD) (also known as membranoproliferative glomerulonephritis type II) in childhood is a rare glomerulonephritis with frequent progression to end-stage renal disease (ESRD) and a high recurrence after kidney transplantation. The pathophysiologic basis of DDD is associated with the uncontrolled systemic activation of the alternative pathway (AP) of the complement cascade. CASE-DIAGNOSIS/TREATMENT: A 14-year-old girl presented with edema and nephrotic range proteinuria. Blood tests showed hypoalbuminemia, nephrotic range proteinuria, normal renal function, and a low C3 level. Renal biopsy confirmed the diagnosis of crescentic DDD. Complement analysis revealed strong AP activation (low C3), positive C3 nephritic factor (C3NeF), and a decreased complement factor H (CFH) levels with CFH polymorphisms. Therapy with eculizumab was considered after the failure of corticosteroid and plasmapheresis to modulate the ongoing massive proteinuria and persistence of low serum C3 levels. There was a marked clinical and biochemical response following the administration of eculizumab. CONCLUSIONS: Our case emphasizes the efficacy of eculizumab in the management of crescentic DDD in a patient with a normal renal function, in a short follow-up period. Considering previously reported cases, it appears that eculizumab represents a promising new approach which may prevent progression to ESRD in a subset of patients with DDD.

The effect of simvastatin and erythropoietin on renal fibrosis in rats with unilateral ureteral obstruction.

Prevention of fibrosis is a very important therapeutic strategy in the treatment of obstructive nephropathy (ON). The aim of this study is to show and compare the actions of Simvastatin (Simv) and Erythropoietin (Epo) in renal expression of nuclear factor kappa B (NFκB), transforming growth factor-ß (TGF-ß), basic fibroblast growth factor (bFGF), platelet-derived growth factor B (PDGF-B), fibronectin and development of interstitial fibrosis in rats with unilateral ureteral obstruction (UUO). A total of 48 Sprague-Dawley rats were allocated to 4 groups of sham, Epo, Simv and control. Unilateral ureteral ligation was performed on all rats except the Sham group. For interstitial fibrosis Masson's trichrome stain and for the expression of TGF-ß, PDGF-B, bFGF, NFκB and fibronectin, immunohistochemical methods were used. In the Epo and Simv groups, expression of TGF-ß and fibronectin and staining with Masson's trichrome were less compared to the control group. In addition, fibronectin expression in the Epo group was less than the Simv group. Unlike the Simv group, NFκB and bFGF expression in the Epo group were less when compared to the control group. Consequently, it was seen that both Epo and Simv prevented fibrosis in ON. Epo was superior in this effect by suppressing the expressions of NFκB and bFGF more effectively than Simv. Based on this finding, Epo might be a better agent than Simv in the prevention of fibrosis in ON.

An uncommon cause of acute kidney injury in young children: cystinuria.

UNLABELLED: Bilateral obstructive nephrolithiasis is a rare cause of acute kidney injury (AKI) in early childhood. As soon as the identification of AKI secondary to ureteral stone is made, it will necessitate an emergency treatment. PATIENTS: We report three infants with AKI caused by bilateral obstructive ureteral cystine stones. They were diagnosed with acute post-renal injury due to obstructive bilateral ureteral stones based on ultrasound scan findings. Immediately, bilateral ureteral stents were inserted for urinary drainage. Once renal function recovered to normal, each patient underwent ureteroscopy and percutaneous nephrolithotomy at the same session. Cystinuria was diagnosed by stone analysis and increased urinary excretion of cystine. Patients were advised to maintain a high fluid intake and were treated with potassium citrate in addition to tiopronin. CONCLUSIONS: With these three cases we would like to emphasize the importance of urolithiasis in the differential diagnosis of acute renal failure in young children, since urolithiasis may only cause nonspecific symptoms in this population. An early diagnosis with prompt treatment and a close follow-up are the key for achieving the best long-term outcome in cystinuria.

Is serum cystatin C a better marker than serum creatinine for monitoring renal function in pediatric intensive care unit?

In critically ill patients, mild to moderate reductions in glomerular filtration rate are not instantly followed by parallel changes in serum creatinine (SCr). The aim of this study was to identify a value of serum cystatin C (cys-C) level as a marker for monitoring renal function in critically ill pediatric patients. Creatinine clearance was used to estimate glomeruler filtration rate (eGFR). The correlation between the inverse of serum cys-C and eGFR (r = -0.70, p < 0.0001) was better than the correlation between the inverse of SCr and eGFR (r = -0.27, p = 0.008). Serum cys-C was found to be superior to SCr to predict renal impairment (area under the curve for cys-C, 0.932 and for SCr, 0.658). It can be concluded that cys-C is superior to SCr for the detection of renal impairment in critically ill children.

Homozygous M694V as a risk factor for amyloidosis in Turkish FMF patients.

Secondary amyloidosis is the most severe complication of familial Mediterranean fever (FMF). Since the M694V mutation was associated with clinical severity, it was expected to be associated with amyloidosis as well. However, a number of contradicting reports have been published, especially pertinent to Turkish patients nearly 10years ago. The aim of this study was to analyze recent data regarding the association between M694V mutation and amyloidosis among FMF patients in Turkey. We conducted a comprehensive review of the literature regarding the role of M694V mutation in the development of amyloidosis secondary to FMF. Twenty-seven papers from 20 centers including 3505 Turkish subjects were reviewed. Four-hundred patients had amyloidosis and homozygous M694V was detected in 189 (47%) of the 400 amyloidotic patients which was significantly higher than that in the FMF patients not developing amyloidosis (p<0.0001). In the presented analysis we were able to reach a patient number of 400 which is much higher than all those published hitherto. Our findings confirmed that homozygous M694V is associated with amyloidosis in the Turkish population as well similar to Armenia, Israel, and Arabian countries. The necessity to treat asymptomatic or mildly symptomatic FMF patients with this genotype, even in countries where amyloidosis is rare, should be considered carefully.

Sarcoid uveitis simulating birdshot chorioretinopathy in a child.

PURPOSE: To report a child with sarcoid choroidopathy that has a similar appearance to birdshot chorioretinopathy. METHODS: Observational case report. Review of the clinical examination, laboratory findings, and histopathologic records of a child with sarcoidosis. RESULTS: A 9-year-old girl was examined in a routine consultation demand in our pediatric clinic. Slit-lamp examination revealed granulomatous anterior uveitis, and funduscopic examination of both eyes revealed numerous, oval, irregular, creamy chorioretinal lesions. These were widespread throughout the fundus, except the macula, and had the characteristic funduscopic appearance of birdshot chorioretinopathy. The patient underwent axillary lymph node biopsy that showed noncaseating granulomas consistent with sarcoidosis. CONCLUSION: Sarcoidosis should be considered in a child with chorioretinal lesions resembling birdshot chorioretinopathy.

Etiology and outcome of acute kidney injury in children.

The aim of this prospective, multicenter study was to define the etiology and clinical features of acute kidney injury (AKI) in a pediatric patient cohort and to determine prognostic factors. Pediatric-modified RIFLE (pRIFLE) criteria were used to classify AKI. The patient cohort comprised 472 pediatric patients (264 males, 208 females), of whom 32.6% were newborns (median age 3 days, range 1-24 days), and 67.4% were children aged >1 month (median 2.99 years, range 1 month-18 years). The most common medical conditions were prematurity (42.2%) and congenital heart disease (CHD, 11.7%) in newborns, and malignancy (12.9%) and CHD (12.3%) in children aged >1 month. Hypoxic/ischemic injury and sepsis were the leading causes of AKI in both age groups. Dialysis was performed in 30.3% of newborns and 33.6% of children aged >1 month. Mortality was higher in the newborns (42.6 vs. 27.9%; p < 0.005). Stepwise multiple regression analysis revealed the major independent risk factors to be mechanical ventilation [relative risk (RR) 17.31, 95% confidence interval (95% CI) 4.88-61.42], hypervolemia (RR 12.90, 95% CI 1.97-84.37), CHD (RR 9.85, 95% CI 2.08-46.60), and metabolic acidosis (RR 7.64, 95% CI 2.90-20.15) in newborns and mechanical ventilation (RR 8.73, 95% CI 3.95-19.29), hypoxia (RR 5.35, 95% CI 2.26-12.67), and intrinsic AKI (RR 4.91, 95% CI 2.04-11.78) in children aged >1 month.

Effect of rosiglitazone on cisplatin-induced nephrotoxicity.

AIM: Nephrotoxicity is a major side effect of cisplatin (Cis), a widely used chemotherapeutic drug. Recent studies have strongly suggested that inflammatory mechanisms may play an important role in the pathogenesis of Cis nephrotoxicity. Rosiglitazone (Ros), a peroxisome proliferator-activated receptor-gamma agonist has been recently demonstrated to regulate inflammation by modulating the production of inflammatory mediators and adhesion molecules. The aim of this study was to evaluate the effect of Ros on the prevention of Cis-induced nephrotoxicity. METHODS: Eighteen male Sprague-Dawley rats weighing 150-200 g were included in the study. The rats were randomly divided into three groups: group 1: Cis-treated group; group 2: Cis-Ros-treated group; group 3: saline-treated group. Blood urea nitrogen (BUN) and serum creatinine concentrations were measured. In addition, extent of histological renal tubular injury in each animal was graded histologically. RESULTS: Mean BUN and serum creatinine concentrations were significantly lower in group 3 than in group 1 (p<0.05) and group 2 (p<0.05). There were no significant differences in terms of BUN and serum creatinine concentrations between groups 1 and 2 (p>0.05). Acute tubular injury with karyomegalic changes in corticomedullary junction was significantly higher in groups 1 and 2 than group 3 (p<0.05). However, there were no significant differences between groups 1 and 2 (p>0.05). CONCLUSION: This study indicates that post-insult administration of Ros does not seem to have a beneficial effect on prevention and severity of nephrotoxicity induced by Cis.

Acute renal failure with acyclovir treatment in a child with leukemia.

Acyclovir is an effective, frequently used antiviral agent. Adverse effects of this drug are well known and are especially seen with high doses and/or dehydration. In this article, we report a 6-year-old boy with leukemia with nonoliguric acute renal failure in normal hydration status after using acyclovir treatment. He had no preexisting renal impairment, and there were no additional symptoms. Dimercaptosuccinic acid radionucleid scyntigraphy and other laboratory findings revealed impairment of proximal tubule function, in addition to distal tubule. We emphasize that renal functions should be monitored carefully during treatment with acyclovir, and asymptomatic nephrotoxicity must be kept in mind.