A decrease in the incidence of Shiga toxin-related hemolytic uremic syndrome as a cause of kidney transplantation at an argentine referral center.

BACKGROUND: In Argentina, Hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli (STEC HUS), is the main cause of acute kidney injury and the second cause of end-stage renal disease (ESRD) in children. In recent decades, strategies have been implemented to reduce progression to ESRD, but it is not known whether the cumulative incidence of HUS requiring kidney transplantation (KTx) has decreased. We aimed to determine whether the cumulative incidence of STEC HUS in children undergoing KTx decreased and compared outcomes of HUS-related KTx vs. those related to other etiologies. METHODS: All patients who underwent KTx at our institution were evaluated. The cohort was divided into quintiles (Q), and we compared the cumulative incidence of HUS-related KTx vs KTx due to other etiologies. RESULTS: A total of 1000 consecutive KTx were included. The cumulative incidence of HUS-related KTx was 11%. HUS was the second cause of KTx in Q1: 17% (1988-1995); Q2: 13.5% (1996-2003); Q3: 11.5% (2004-2009) and third cause in Q4: 10% (2010-2015) and Q5: 3% (2016-2021). The cumulative incidence of HUS-related KTx decreased in Q4 and Q5 compared to Q1, Q2, and Q3 and the decline was even steeper when comparing Q4 to Q5 (p:0.019). There was no difference in graft survival in patients with HUS vs. congenital anomalies of kidney and urinary tract (CAKUT) but better than in those with focal segmental glomerulosclerosis (FSGS). CONCLUSIONS: In this cohort, the cumulative incidence of HUS-related KTx decreased, which may have been due to the implementation of nephroprotective strategies.

Kidney transplantation in children with CAKUT and non-CAKUT causes of chronic kidney disease: Do they have the same outcomes?

Almost half the children who undergo kidney transplantation (KTx) have congenital abnormalities of the kidney and urinary tract (CAKUT). We compared patient, graft survival, and kidney function at last follow-up between CAKUT and non-CAKUT patients after KTx. We divided the analysis into two eras: 1988-2000 and 2001-2019. Of 923 patients, 52% had CAKUT and 48% non-CAKUT chronic kidney disease (CKD). Of the latter, 341 (77%) had glomerular disease, most frequently typical HUS (32%) and primary FSGS (27%); 102 had non-glomerular disease. CAKUT patients were more often boys, younger at KTx, transplanted more frequently preemptively, but with longer time on chronic dialysis. They had less delayed graft function (DGF) and better eGFR, but higher incidence of urinary tract infection (1 year post-KTx). In both eras, 1-, 5-, and 10-year patient survival was similar in the groups, but graft survival was better in CAKUT recipients vs those with primary glomerular and primary recurrent glomerular disease: Era 1, 92.3%, 80.7%, and 63.6% vs 86.9%, 70.6%, and 49.5% (P = .02), and 76.7%, 56.6%, and 34% (P = .0003); Era 2, 96.2%, 88%, and 73.5% vs 90.3%, 76.1%, and 61% (P = .0075) and 75.4%, 54%, and 25.2% (P < .0001), respectively. Main predictors of graft loss were DGF, late acute rejection (AR), and age at KTx in CAKUT group and disease relapse, DGF, early AR, and number of HLA mismatches in recipients with glomerular disease. Graft survival was better in CAKUT patients. DGF was the main predictor of graft loss in all groups. Disease recurrence and early AR predicted graft failure in patients with glomerular disease.

Series de Pediatría Garrahan. El niño con trastornos renales y de las vías urinarias / Garrahan Pediatrics Series. The child with renal and urinary tract disorders

Las consultas pediátricas por enfermedad renal o de las vías urinarias son frecuentes e incluyen una amplia variedad diagnóstica que desafía al pediatra en su abordaje, la detección de riesgos en el corto y largo plazo, la derivación oportuna al especialista y el seguimiento de las condiciones que generaron cronicidad. En este nuevo volumen de las Series de Pediatría Garrahan se han reunido prestigiosos pediatras y nefrólogos infantiles para actualizar y trasnmitir el manejo integral de algunas de las patologías de mayor prevalencia e impacto, muchas de las cuales causan morbilidad alejada y requieren equipos multidisciplinarios que aseguren una transición en el cuidado del niño, el adolescente y el adulto. Entre sus caracterísitcas se destacan: El estudio detallado de patologías clínicas como las infecciones urinarias, la lesión renal aguda, el síndrome nefrótico, la enfermedad renal progresiva, las terapias de reemplazo renal y la hypertensión arterial. El desarrollo de casos clínicos con las secuencias habituales en el transcurso habitual de las enfermedades que permite destacar las presentaciones clínicas, las alternativas diagnósticas y terapéuticas, así como las posibilidades evolutivas. El cierre de cada capítulo con un recordatorio de puntos clave y lecturas recomendadas y, además, el material complementario disponible en el sitio web. El objetivo es compartir la modalidad de trabajo del hospital, con base en el rol central del pediatra como coordinador de la atención interdisciplinaria en cada una de sus etapas. Una obra actualizada y práctica que aporta información científica y experiencia de los profesionales de una institución de prestigio, de granutilidad para todos aquellos miembros del equipo de salud que atienden y cuidan niños, dondequiera que trabajen al servivio de la salud infantil.

Donor-specific anti-HLA antibodies in pediatric renal transplant recipients with creeping creatinine: Prevalence, histological correlations, and impact on patient and graft survival.

Donor-specific anti-HLA antibodies (DSA) causing CAMR are responsible for a high proportion of long-term graft failures after RTX. We studied the prevalence of DSA in RTX children biopsied for creeping Cr, its relationship with NA, and patient and graft survival according to histopathology. Between 2008 and 2013, 92 children were biopsied at a median of 38 months post-RTX. At biopsy, the prevalence of DSA was 49% and C4d 70%. NA rate was 45%, higher in adolescents (60%). Most frequent diagnoses were CAMR (72%) and interstitial fibrosis with tubular atrophy (IFTA) (28%). Forty-five of 66 patients with CAMR (68%) had detectable DSA. Twenty-one DSA-negative patients with CAMR had histological damage (IFTA + C4d positivity). C4d was detected in 64 of 66 biopsies with CAMR. Recipients with IFTA alone had neither C4d, nor detectable DSA, and were adherent. Graft survival at five yr was 89% in patients with CAMR, 79% in those with CAMR + TCMR Banff I, 33% in those with CAMR + TCMR Banff II, and 96% in those with IFTA. ABMR and complement activation were frequent in children biopsied for creeping Cr. Recipients with DSA were more likely to be non-adherent and have CAMR or CAMR + TCMR and worse graft survival.

Conversion to sirolimus in pediatric renal transplant patients: a single-center experience.

We studied efficacy and safety of conversion from CNI- to SRL-based immunosuppression in 92 kidney TX recipients, mainly due to CAN (69%). Median time of conversion was 31 months (r: 0.3-165); median time of follow-up: 36 months (r: 2-102). In the whole group mean eGFR increased from 53 ± 22 to 67 ± 26mL/min/1.73 m(2) at three months (p = 0.02) and did not change subsequently. Patients with grade I CAN had higher eGFR than those with grade II CAN. Patient and graft survival was 96% and 70% 10 yr after conversion. Patients with grade I CAN had better graft survival than those with grade II CAN: 89% vs. 65% at six yr (p = 0.02) post conversion. There were two episodes of BPAR. Baseline proteinuria >20 mg/kg/day (HR: 10) and baseline eGFR <50 mL/min/1.73 m(2) (HR: 8) were independent predictors of graft loss. Sixty-seven of 92 subjects had ≥1 AEs: diarrhea (n = 52), urinary tract infections (n = 35), and lower respiratory tract infections (n = 12) were the most frequent. Patients with >2 AEs had SRL blood levels >9 ng/mL at month 3 (p = 0.01). In conclusion, patients converted from CNI to SRL had good graft survival and tolerable but frequent AEs. Independent predictors of graft loss were baseline proteinuria and eGFR.