Nocturia and Blood Pressure Elevation in Adolescents.

Nocturia has been increasingly recognized as a manifestation of various non-urological conditions including hypertension. In adults, blood pressure (BP) elevation has been identified as a robust correlate of nocturia, but such a relationship has not been studied in pediatric populations where nocturia is often attributed to hormonal, sleep, physiological or psychological disorders. Accordingly, this study aimed to determine the relationship between nocturia and BP elevation in adolescents. We prospectively studied 100 patients, aged 10-18 years, recruited from pediatric clinics at our institution. Nocturia (defined as ≥ 1 voids on voiding diary analysis) was present in 45% of the study sample (range: 1-4 voids/night). 37% of subjects self-reported awakening to urinate, and 34% of subjects had BP elevation according to age-dependent thresholds from current Pediatrics guidelines. On multivariate analyses, BP elevation was strongly associated with nocturia determined by both voiding diary (OR 26.2, 95% CI: 6.5, 106.0) and self-report. Conversely, nocturia was associated with increased odds of elevated BP by diary (26.3, 95% CI: 6.5, 106.4) and self-report (OR 8.1, 95% CI: 3.2, 20.5). In conclusion, nocturia appears to be common and is strongly associated with BP elevation in adolescents. These findings suggest that eliciting a history of nocturia holds promise as a simple method of identifying adolescents at risk for hypertension.

Impact of immediate post-transplant parenteral iron therapy on the prevalence of anemia and short-term allograft function in a cohort of pediatric and adolescent renal transplant recipients.

Anemia is common but under-diagnosed and often inadequately treated in KTX recipients. ID is the major cause of early-onset anemia. We introduced routine use of parenteral (IV) iron in patients (2-18 years) who had KTX between January 2011 and December 2015. We explored the clinical benefits of this practice by comparing the iron-treated subjects [TX] with historical controls who had KTX between 2005 and 2010. The prevalence of anemia at 6 months (early-onset) for the cohort (both the study group and controls) was 55% and for anemia at 12 months (late-onset) was 60%. Although cause-effect relationship may not be proven in a retrospective study design, there was a significant greater frequency of ID and anemia at 3 (P < .02) and 6 months (P < .04), and a reduced allograft function (eGFR < 60 mL/min/1.73 m2 ) at 12 (P = .03) and 24 months (P = .04) of KTX in the control arm. Furthermore, a greater proportion of the control arm required either ESA (P = .03) or blood transfusion (P = .04) as a rescue treatment for moderate-to-severe anemia. In conclusion, routine parenteral iron treatment was associated with a lower prevalence of early- and late-onset anemia, and a lower requirement for either ESA rescue or blood transfusion.

Infective dermatitis associated with HTLV-1 infection in a girl from Trinidad: Case report and review of literature.

Infective dermatitis (ID) associated with Human T-cell leukemia virus type-1 (HTLV-1) is a rare form of severe superinfected eczema seen mostly in the Caribbean islands and Latin America. Although rapid response to antibiotic treatment is observed, patients should be monitored for development of complications associated with this retroviral infection, including T-cell leukemia/lymphoma (ATLL) and HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). Infective dermatitis is rarely seen in the United States and therefore may be under-recognized by physicians unfamiliar with this condition. Herein, we present an additional case report of an ID associated with HTLV-1 in an 11-year-old girl from Trinidad.

Cost analysis on the use of rituximab and calcineurin inhibitors in children and adolescents with steroid-dependent nephrotic syndrome.

BACKGROUND: Rituximab (RTX) is increasingly being used in place of calcineurin inhibitors (CNI) in pediatric patients with steroid-dependent nephrotic syndrome (SDNS). However, despite its favorable safety profile, its unit cost is prohibitive. We therefore compared the healthcare costs associated with the use of both agents in a retrospective cohort. METHODS: This study was a retrospective analysis of data retrieved from the medical charts and electronic databases of pediatric patients (age range 2-18 years) with SDNS who were treated with either CNI or RTX from January 2008 to December 2012 at Children's Hospital of New Orleans, Louisiana. The minimum follow-up period was 12 months. RESULTS: Of the 18 patients whose medical data were analyzed, ten received RTX and eight were treated with CNI. The annualized healthcare cost for the rituximab group was $197,031 versus $189,857 (all values in US dollars) for the CNI group (p > 0.05). At the 12-month follow-up, more patients in the RTX group were in remission (40 vs. 25%). Duration of freedom from steroid use was longer in the RTX group, while body mass index was higher in the CNI arm (p > 0.05). No significant adverse events occurred in either group. CONCLUSION: The expenditure for the RTX and CNI groups was comparable, but there were fewer clinical encounters in the former group, potentially reducing the burden of healthcare on the patient's family.

Spectrum of anemia after kidney transplantation: pathophysiology and therapeutic implications.

The prevalence of anemia in the first month after transplant is 70%-80%. The rate declines to 30%-40% at 3 months and 20% by 12 months. Its occurrence is influenced by the quality of the transplanted organ, bone marrow regenerative capacity, amount of surgical blood loss, and increased iron recycling. There is also a blunted response by oxidative inflammation to the effectiveness of supranormal levels of erythropoietin (EPO) release during ischemic-reperfusion allograft injury. The prevalence rate of late-onset post-transplant anemia (PTA) is 30%-50%. This category of patients falls into two ill-defined groups: (i) those with impaired renal capacity for EPO synthesis and (ii) those with bone marrow resistance. Given the difference in pathophysiology, the current KDIGO guideline that adopts uniform therapeutic approach for the two groups may be inappropriate. Comorbidity due to iron deficiency is common. Anemia is predictive of cardiovascular morbidity and shorter graft survival. Perhaps due to concern for the safe use of EPO stimulating agent (ESA) to correct anemia, there is often inadequate treatment of late-onset PTA. However, universal application of ESA may be harmful. Therefore, clinical trials are needed to define parameters for selecting patients (e.g., EPO assay) that will benefit the most from therapy for anemia.

Success with plasmapheresis treatment for recurrent focal segmental glomerulosclerosis in pediatric renal transplant recipients.

FSGS recurs in approximately 30% of transplanted kidneys and may lead to graft loss. We retrospectively examined the efficacy of early and intensive PP without additional IS in pediatric kidney transplant patients with recurrent FSGS at our center. Seven of 24 patients (29%) had nephrotic proteinuria and histologic evidence of FSGS recurrence within 1-5 days post-transplantation. PP was initiated early after transplantation and initially performed daily until sustained decline in proteinuria. PP frequency was then individually tapered according to proteinuria. Recurrent FSGS in all seven patients responded to a four- to 32-wk course of PP. Two of seven patients had a second recurrence of FSGS, and both recurrences remitted after an additional 3-6 wk of PP. Median observation period was 4.5 yr (0.8-16.3 yr). Complete remission of recurrent FSGS has been sustained in all seven patients, and all patients have stable graft function with recent plasma creatinine <1.5 mg/dL in six of seven patients. Most recent urine protein/creatinine is 0.13-0.61 mg/mg in six of seven patients. One patient has heavy proteinuria secondary to chronic allograft nephropathy 16 yr post-transplant. Intensive and prolonged PP, when initiated early in the post-operative period, is effective in treating recurrent FSGS and preventing graft loss without the use of additional immunosuppressants.

Urinary schistosomiasis.

Schistosomiasis is the second most common socio-economically devastating parasitic disease after malaria, affecting about 240 million residents of developing countries. In Africa, it predominantly manifests as urogenital disease, and the main infective agent is Schistosoma hematobium. Endemicity is propagated by poor socio-economic status and environmental degradation due to rapid urbanization. Recreational swimming is a potent medium for the spread of disease in children and adolescents. Most affected individuals are asymptomatic. The male and female worms are equipped with an extraordinary capacity for immune evasion and are able to co-habit for several decades within the pelvic venous plexus. Eggs deposited in the bladder wall resist elimination by type 1 T lymphocytes. Instead, they are sustained by pro-fibrogenic encapsulation (as modulated by type 2 helper cells). Progressive bladder disease results in obstructive uropathy and predisposes to (mostly) squamous cell carcinoma. Schistosomal glomerulopathy manifests as a clinical spectrum of asymptomatic proteinuria, nephrosis and/or nephritic syndrome. Findings on renal biopsy may be influenced by co-morbidity with Salmonella bacteria, amyloidosis and hepatitis C infection. Potentially fatal Katayama fever and spinal radiculopathy may ensue in tourists visiting an endemic zone. Early detection by urine microscopy is hampered by low urinary excretion rates of the parasite eggs. Although useful in travelers with newly acquired disease, the results of the serological antibody assay may be false positive in residents of an endemic zone. Cystoscopy, however, may be invaluable. Due to its safety, effectiveness and once-daily dosing, praziquantel is the drug of choice. An integrated approach that includes mass chemotherapy, environmental health programs and public health education is the most cost-effective preventive strategy.

Diagnostic Challenges of Urinary Schistosomiasis Among Adolescent Immigrants in New York City: A Report of Three Cases.

Urinary schistosomiasis is endemic in the tropical world. It is uncommon in geographical areas with advanced public health resources. Modern immigration from endemic communities to the United States supports the need to improve our diagnostic awareness. We describe 3 Brooklyn adolescent immigrants from Africa with urinary schistosomiasis, all of whom had an initial misdiagnosis that led to delay in therapeutic intervention.

Resistance to erythropoietin-stimulating agents: etiology, evaluation, and therapeutic considerations.

Routine clinical and laboratory assessments facilitate diagnosis of erythropoietin (EPO) resistant anemia by allowing early identification of patients with non-adherence. Any new event that impairs response to EPO (e.g., catheter sepsis) must be promptly controlled. Because of the confounding interaction of its risk factors, initial evaluation should include nutrition, dialysis adequacy, hemorrhage, bone mineral metabolism, and inflammation. Prevention of EPO resistance is more cost effective and should include adequate dialysis and nutritional supplements. Blood loss during hemodialysis (HD) procedures should be minimized. If there is laboratory proof of iron deficit intravenous repletion is most effective. Oxidative stress may be attenuated by vitamins E and C, while optimal control of hyperparathyroidism will enhance EPO stimulation. Contaminated dialysates should be suspected if there is EPO-stimulating agents (ESA) resistance at the same time among most members of a dialysis program. Heavy metal toxicity should be suspected in high-risk patients. The impact of co-morbidities such as hemoglobinopathy, glucose 6 phosphate dehydrogenase (G6PD) deficiency and connective tissue diseases must be excluded in an appropriate setting. In conclusion, given the multiple risk factors of EPO resistance promotion of the overall health status will most likely yield an enduring benefit. Finally, there are experimental trials of gene-based (therapy) to stimulate endogenous EPO synthesis with the goal of avoiding the off-target effect of excessive dosing.

Review of the Pathophysiologic and Clinical Aspects of Hypokalemia in Children and Young Adults: an Update.

This article examines the regulatory function of the skeletal muscle, renal, and adrenergic systems in potassium homeostasis. The pathophysiologic bases of hypokalemia, systematic approach for an early diagnosis, and therapeutic strategy to avert life-threatening complications are highlighted. By promoting skeletal muscle uptake, intense physical exercise (post), severe trauma, and several toxins produce profound hypokalemia. Hypovolemia due to renal and extra-renal fluid losses and ineffective circulation activate secondary aldosteronism causing urinary potassium wasting. In addition to hypokalemic alkalosis, primary aldosteronism causes low-renin hypertension. Non-aldosterone mineralocorticoid activation leading to low-renin and low-aldosterone hypertension occurs in Liddle's syndrome and apparent mineralocorticoid excess. Although there is enzymatic inhibition of cortisol synthesis in congenital adrenal hyperplasia, precursors of aldosterone produce low-renin hypokalemic hypertension. In addition to the glucocorticoid effect, hypercortisolism activates mineralocorticoid receptors in Cushing's syndrome. Genetic mutations involving furosemide-sensitive Na+-K+-2Cl- co-transporters and thiazide-sensitive Na+-Cl- transporters result in (non-hypertensive) salt-wasting nephropathy. Proximal and distal renal tubular acidosis is associated with hypokalemia. Eating disorders causing hypokalemia include bulimia, laxative abuse, and diuretic misuse. Low urinary potassium (<15 mmol/day) and/or low urinary chloride (<20 mol/L) suggest a gastrointestinal pathology. Co-morbidity of hypokalemia with chronic pulmonary and cardiovascular diseases may increase the fatality rate.

Structural Inequities and Barriers to Accessing Kidney Healthcare Services in the United States: A Focus on Uninsured and Undocumented Children and Young Adults.

The population of children living in poverty and lacking healthcare insurance has increased in the United States of America in the last decade. Several factors have been responsible for this trend including illegal immigration, socioeconomic deprivation, young age, racial segregation, environmental degradation, and discriminatory housing policies. These systemic barriers have contributed to the exclusion of families from essential healthcare services. They are also contributory to the development of chronic illnesses (such as dialysis-dependent kidney disease) that are debilitating and frequently require considerable therapeutic resources. This unfortunate scenario creates a never-ending vicious cycle of poverty and diseases in a segment of society. For pediatric nephrologists, the challenges of caring for uninsured children with chronic kidney disease are all too familiar. Federally funded healthcare programs do not cover this patient population, leaving them the option of seeking care in emergency healthcare settings. Presentation with a critical illness often necessitates urgent placement of vascular catheters and the choice of acute hemodialysis. Adverse social environment influences the need for protracted chronic hemodialysis and a delay in kidney transplantation. Consequently, there is greater comorbidity, recurrent hospitalization, and a higher mortality rate. New policies should address the deficit in health insurance coverage while promoting social programs that will remove structural barriers to health care resources for undocumented children and young adults.

Pattern of resistance to erythropoietin-stimulating agents in chronic kidney disease.

Routine administration of erythropoietin (EPO)-stimulating agents (ESAs) for the control of anemia has improved the quality of life of subjects with chronic kidney disease (CKD). However, a wide variation in individual response to ESA is often observed. The reasons for EPO resistance include demographic variables such as age and gender distribution, morbidity pattern, and modality of dialysis. Despite suggestions by observational data, there is no biological characteristic that puts children at a disadvantage for adequate response to ESA. On the contrary, children possess a superior capacity for red cell production, including extramedullary erythropoiesis. The reasons for larger requirement of ESA in children (than in adults) are greater inflammatory burden, disproportionate blood loss, and greater EPO dosing by pediatric physicians. To minimize the harmful (including fatal) consequences of EPO resistance, surveillance programs must replenish nutrient (for example, iron and folate) stores, minimize oxidative hemolysis, control hyperparathyroidism, avoid catheter infection, and optimize uremic clearance. This clinical approach is justified by the inadequacy of laboratory diagnosis of pertinent etiological factors. Indeed, the best proof for functional nutrient deficiency is often a therapeutic trial. Finally, there are upcoming therapeutic agents that exploit the capacity for an endogenous EPO synthesis in CKD subjects, and may therefore minimize the off-target effect of excess dosages.

Erratum: Differential diagnosis of perinatal Bartter, Bartter and Gitelman syndromes.

[This corrects the article DOI: 10.1093/ckj/sfaa172.][This corrects the article DOI: 10.1093/ckj/sfaa172.].

Differential diagnosis of perinatal Bartter, Bartter and Gitelman syndromes.

The common finding of hypokalemic alkalosis in several unrelated disorders may confound the early diagnosis of salt-losing tubulopathy (SLT). Antenatal Bartter syndrome (BS) must be considered in idiopathic early-onset polyhydramnios. Fetal megabladder in BS may allow its distinction from third-trimester polyhydramnios that occurs in congenital chloride diarrhea (CCD). Fetal megacolon occurs in CCD while fecal chloride >90 mEq/L in infants is diagnostic. Failure-to-thrive, polydipsia and polyuria in early childhood are the hallmarks of classic BS. Unlike BS, there is low urinary chloride in hypokalemic alkalosis of intractable emesis and cystic fibrosis. Rarely, renal salt wasting may result from cystinosis, Dent disease, disorders of paracellular claudin-10b and Kir4.1 potassium-channel deficiency. Acquired BS may result from calcimimetic up-regulation of a calcium-sensing receptor or autoantibody inactivation of sodium chloride co-transporters in Sjögren syndrome. A relatively common event of heterozygous gene mutations for Gitelman syndrome increases the likelihood of its random occurrence in certain diseases of adult onset. Finally, diuretic abuse is the most common differential diagnosis of SLT. Unlike the persistent elevation in BS, urinary chloride concentration losses waxes and wanes on day-to-day assessment in patients with diuretic misuse.

Validation of a composite scoring scheme in the diagnosis of folate deficiency in a pediatric and adolescent dialysis cohort.

BACKGROUND: Laboratory indices are often poorly diagnostic of folate deficiency (FD). Compared with iron depletion in hemodialysis (HD) populations, the impact of FD is less appreciated. The composite scoring of hematologic indices of FD may facilitate a prompt and accurate diagnosis, and enhance operational research on folic acid therapy. OBJECTIVE: Our objectives were to (1) validate composite scores of folate diagnostic indices, and (2) determine the reliability index of the diagnostic tool. METHODS: A cohort of 30 subjects, with a mean age of 16 (SD +/- 3.2 years), on HD and erythropoietin (EPO) for a minimum of 3 months was studied. After a baseline hematologic assessment, routine folates were administered for 6 months. Composite FD scores (FDS) of baseline mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), random distribution width (RDW), and hemoglobin were determined. Validation and reliability statistics were then analyzed, using the quantitative change in red blood cell folate/plasma homocysteine, or EPO requirement after 6 months of folate use, as diagnostic criteria. RESULTS: The mean FDS for FD and non-FD subsets were 3.0 +/- 1.3 and 1.4 +/- 0.9, respectively (analysis of variance; P = .0001). The correlation coefficient, r(2), between FD total and FDS was 0.61 (P = .001), and the coefficient between 2 (weekly) values of RDW, MCV, MCH, and MCHC was >0.84 (P = .0001). Scoring tools derived from the first (P = .002) and second (P = .01) halves of the laboratory indices remained discriminatory for the FD and non-FD groups. Baseline serum folate is poorly specific for FD, whereas FD score >or=3 had sensitivity, specificity, and positive and negative predictive values close to 90%. CONCLUSIONS: Composite scoring of erythrocyte indices was predictive of the FD diagnosis, as defined by the quantitative response of red blood cell folate, homocysteine, and EPO dose to folate therapeutic intervention. The diagnostic items yielded a high reliability coefficient. The FDS scheme is a potential tool for the diagnosis and surveillance of FD, particularly in at-risk populations (e.g., dialysis subjects).

Endemic Esherichia coil O157:H7 infections and hemolytic-uremic syndrome in Oklahoma, 2002-2005.

Hemorrhagic enterocolitis caused by Escherichia coli O157:H7 and its complication of hemolytic-uremic syndrome (HUS) are well known from large outbreaks caused by contaminated meats and vegetables. However most cases may be endemic, not related to an outbreak. We identified cases of HUS in Oklahoma, 2002-2005, from the Inpatient Hospital Discharge Database of the Oklahoma State Department of Health (OSDH) and also the cases of HUS and E. coli O157:H7 reported to the OSDH. 110 cases of HUS were identified from the hospital discharge database; only 14 (12.7%) were reported to the OSDH; 122 cases of E. coli O157:H7 infections were reported to the OSDH. Of the 110 cases of HUS, only six (5.5%) patients in two separate clusters may have had a common source of infection. Although interpretation is limited by the few reports to OSDH, our data suggest that E. coli O157:H7 infections and HUS, presumably related to contaminated food, are endemic throughout Oklahoma.

The role of obesity and its bioclinical correlates in the progression of chronic kidney disease.

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.

Metabolic consequences of modern immunosuppressive agents in solid organ transplantation.

Among other factors, sophistication of immunosuppressive (IS) regimen accounts for the remarkable success attained in the short- and medium-term solid organ transplant (SOT) survival. The use of steroids, mycophenolate mofetil and calcineurin inhibitors (CNI) have led to annual renal graft survival rates exceeding 90% in the last six decades. On the other hand, attrition rates of the allograft beyond the first year have remained unchanged. In addition, there is a persistent high cardiovascular (CV) mortality rate among transplant recipients with functioning grafts. These shortcomings are in part due to the metabolic effects of steroids, CNI and sirolimus (SRL), all of which are implicated in hypertension, new onset diabetes after transplant (NODAT), and dyslipidemia. In a bid to reduce the required amount of harmful maintenance agents, T-cell-depleting antibodies are increasingly used for induction therapy. The downsides to their use are greater incidence of opportunistic viral infections and malignancy. On the other hand, inadequate immunosuppression causes recurrent rejection episodes and therefore early-onset chronic allograft dysfunction. In addition to the adverse metabolic effects of the steroid rescue needed in these settings, the generated proinflammatory milieu may promote accelerated atherosclerotic disorders, thus setting up a vicious cycle. The recent availability of newer agent, belatacept holds a promise in reducing the incidence of metabolic disorders and hopefully its long-term CV consequences. Although therapeutic drug monitoring as applied to CNI may be helpful, pharmacodynamic tools are needed to promote a customized selection of IS agents that offer the most benefit to an individual without jeopardizing the allograft survival.

Review of vancomycin-induced renal toxicity: an update.

In recent times the use of larger doses of vancomycin aimed at curbing the increasing incidence of resistant strains of Staphylococcus aureus has led to a wider report of acute kidney injury (AKI). Apart from biological plausibility, causality is implied by the predictive association of AKI with larger doses, longer duration, and graded plasma concentrations of vancomycin. AKI is more likely to occur with the concurrent use of nephrotoxic agents, and in critically ill patients who are susceptible to poor renal perfusion. Although most vancomycin-induced AKI cases are mild and therefore reversible, their occurrence may be associated with greater incidence of end-stage kidney disease and higher mortality rate. The strategy for its prevention includes adequate renal perfusion and therapeutic drug monitoring in high-risk individuals. In the near future, there is feasibility of renoprotective use of antioxidative substances in the delivery of vancomycin.

Pilot validation of objective malnutrition-inflammation scores in pediatric and adolescent cohort on chronic maintenance dialysis.

BACKGROUND: In recognition of the challenges inherent with the use of single-item indices for the diagnosis of malnutrition-inflammation morbidity in pediatric dialysis patients, to enhance accuracy, we validated a composite scoring system in a pilot study. The objective malnutrition-inflammation score seeks to validate the use of a composite scoring system as a tool for assessing malnutrition-inflammation burden in a pediatric dialysis population. METHODS: We enrolled 20 patients on hemodialysis (n = 14) and peritoneal dialysis (n = 6) over a period of 12 months. We derived composite scores from selected indices of renal pathology, nutrition, dialysis adequacy, protein catabolism, and dialysis modality. We assessed reliability by a test-retest method and measured validity by defining the relationship of the indices with serum C-reactive protein in a multiple regression analysis. We calculated sensitivity, specificity, accuracy, and precision for the malnutrition-inflammation score. RESULTS: The mean age was 12.8 years (standard deviation = 6.1), and male-female ratio was 12:8. Patients (n = 8) with elevated serum C-reactive protein (>0.3 mg/dL) had higher composite score for malnutrition-inflammation morbidity. Similarly, the pediatric cohort on hemodialysis had higher score than those on peritoneal dialysis. Upon reliability testing, a low value of typical error (0.07) and high correlation coefficient (r = 0.95) supported validity of the instrument. Moreover, multiple regression analysis showed a strong predictive relationship (R(2) = 0.9, p = 0.03) between the indices and serum C-reactive protein. Sensitivity of malnutrition-inflammation score was 62.5%, specificity was 83%, accuracy was 75%, and precision was 71%. CONCLUSION: Using criterion-validation method, we established the potential use of multi-diagnostic approach to quantify malnutrition-inflammation morbidity in a pediatric dialysis cohort. Given the small sample size, large-scale population-specific studies are needed to ratify these findings and to demonstrate its clinical effectiveness.