Access to treatment in chronic kidney disease, dialysis and transplantation. Is there gender equality?

Sex and gender are often used as synonyms. However, while sex describes only a biological state, gender is a dynamic concept that takes into account psychosocial and cultural aspects of human existence that can change according to place and time. Inequality in medicine has been described in several areas. Among them, gender inequality has been disregarded for many years and is now a matter of concern. Chronic kidney disease (CKD) is a growing epidemic worldwide, affecting approximately 10% of the population. Although both men and women are affected, gender equality, especially in access to different treatments, is a matter of concern. We decided to investigate gender equality in patients with CKD. To this end, we conducted a literature narrative review to determine whether gender inequalities were found in CKD patients in general and in access to different treatment modalities in particular. A non-language restricted search was performed until November 30th 2022 in PubMed, SciELO, Trip Database, Google Scholar, MEDES y MEDLINE. We also investigated the situation in this regard in our country. We found that CKD is more prevalent in women than men, nevertheless this prevalence decreases along the CKD stages to the point that more men reach end stage kidney disease (ESKD) and dialysis. Access to transplant (ATT) is higher in men than in women although posttransplant survival shows no gender differences. Finally, most series have shown that women are more frequently Kidney transplantation (KT) living donors than men. Results in our country are similar to the published literature with the exception of a higher proportion of men as KT living donors. As in other areas, gender inequality in Nephrology has been largely overlooked. In this review we have highlighted gender differences in CKD patients. Gender inequality in Nephrology exists and needs to be looked upon in order to reach a personalized clinical approach.

Trasplante renal en paciente con diagnóstico de esquizofrenia. Reporte de caso / Kidney transplant in a patient with Schizophrenia. Case report

Se presenta el caso de una paciente de sexo femenino de 42 años de edad con diagnóstico de esquizofrenia de larga data e insuficiencia renal crónica estadio V. Tras tratamiento sustitutivo de aproximadamente dos años ingresa en lista de espera para trasplante renal con donante fallecido. Recibe trasplante donante fallecido con buena evolución y favorable adaptación a las intercurrencias acontecidas en el transcurso del proceso. Este caso representa una posibilidad para pacientes con diagnóstico de esquizofrenia puedan recibir un trasplante renal con favorable evolución resaltando diversos aspectos a contemplar a fin de garantizar el éxito de dicha intervención

We report the case of a female patient, aged 42, with long-term schizophrenia and end-stage chronic kidney disease. After approximately two years undergoing replacement therapy, she is put on the waiting list for deceased donor kidney transplant. She receives a transplant from a deceased donor with good progress and favorable adaptation to the intercurrent diseases occurring during the course of the process. This case represents a possibility for patients diagnosed with schizophrenia; they may receive a kidney transplant with good progress, highlighting different aspects to be considered in order to guarantee the success of the procedure

Uso de Cinacalcet en el tratamiento del hiperparatiroidismo persistente post-trasplante renal. Experiencia en un centro de Argentina / Use of Cinacalcet in the treatment of persistent hyperparathyroidism post-renal transplant. A single center experience in Argentina

Introducción: El trasplante renal se asocia con disminución de los niveles séricos de parathormona (PTH). La persistencia de valores elevados de PTH asociado a hipercalcemia es sugestiva de hiperparatiroidismo persistente. El hiperparatiroidismo persistente es un factor de riesgo para calcificaciones vasculares, pérdida de masa ósea y supervivencia del injerto. El cinacalcet actúa sobre los receptores calcio (Ca) sensibles aumentando su activación por el Ca iónico, disminuyendo los niveles de PTH, Ca y fosforo (P) plasmático. El objetivo de este estudio es evaluar la efectividad y seguridad del cinacalcet en pacientes Trasplantados renales con hiperparatiroidismo persistente e hipercalcemia. Material y métodos: Se realizó un estudio retrospectivo y observacional en 14 pacientes trasplantados renales que recibieron cinacalcet durante al menos 3 meses como tratamiento del hiperparatiroidismo. Resultados: La PTHi pre-cinacalcet fue 159 ± 70 pg/ml; al mes fue 151 ± 110 pg/ml; a los 3 meses 150 ± 96 pg/ ml, a los 6 meses de 142 ± 64 y al año 139 ± 75 pg/ml. El descenso de la PTHi no fue significativo. El Ca sérico bajó en forma significativa de 11.3 ± 0.8 a 10.0 ± 0.8 mg/dl al mes del tratamiento (p< 0.001) manteniendo sus valores estables a los 3 (10.2 ± 1.0), 6 (10.3 ± 0.5) y 12 (10 ± 0.4) meses. El P fue 2.7 ± 0.79mg/dl al inicio del tratamiento, manteniendo valores estables en los meses 3, 6 y 12. La dosis media de cinacalcet al inicio fue de 30 mg aumentando en forma no significativa al 3º mes a 32 ± 12 mg/d, al 6º mes 40 ± 22 mg/d y al año 41.6 ± 18 mg/d. Conclusión: En esta pequeña cohorte de estudio de pacientes con hiperparatiroidismo persistente e hipercalcemia, el cinacalcet fue efectivo en bajar los niveles de Ca (p< 0.001), no teniendo el mismo efecto sobre la PTHi.

Background: Renal transplant (RTx) is associated with the decrease in serum parathyroidhormone (PTH) levels. The persistence of high PTH levels associated to hypercalcemia is suggestive of persistent hyperparathyroidism (pHPT). pHPT is a risk factor for vascular calcifications, bone loss, and graft survival. Cinacalcet acts on the calcium sensing receptor increasing their activation by ionic Ca, reducing serum PTH, Ca, and phosphate (P) levels. The objective of this study was to evaluate the efficacy and safety of cinacalcet in RTx patients with pHPT and hypercalcemia. Material and methods: We performed a retrospective, observational study in 14 RTx patients who received cinacalcet for at least 3 months as part of the pHPT treatment. Results: Pre-cinacalcet iPTH levels were 159 ± 70 pg/ml; after one month it was 151 ± 110 pg/ml, 150 ± 96 pg/ml at three months, 142 ± 64 at six months and 139 ± 75 pg/ml after one year. The decrease in the iPTH was not significant. The serum Ca significantly decreased from 11.3 ± 0.8 to 10.0 ± 0.8 mg/dl after one month (p< 0.001) keeping serum levels stable after three (10.2 ± 1.0), six (10.3 ± 0.5), and twelve (10 ± 0.4) months. P was 2.7 ± 0.79 mg/dl at the beginning of treatment, keeping their levels stable after 3, 6, and 12 months. The average dose of cinacalcet at the beginning was 30 mg increasing in a non-significant way on the 3rd month to 32 ± 12 mg/d, on the 6th month to 40 ± 22 mg/d, and on the 12th month to 41.6 ± 18 mg/d. Conclusion: In this small cohort of patients with pHPT and hypercalcemia, cinacalcet was effective in reducing serum Ca levels (p< 0.001), but not iPTH.

Severe neutropenia in a renal transplant patient suggesting an interaction between mycophenolate and fenofibrate.

OBJECTIVE: To describe a patient in whom initiation of micronized fenofibrate precipitated mycophenolate induced neutropenia. CASE SUMMARY: A 57-year-old man was admitted to the hospital because of febrile neutropenia. He had undergone kidney transplantation seventeen years ago. The patient's immunosuppressive maintenance regimen consisted of mycophenolate mofetil (MMF) 500 mg three times a day, and meprednisone 4 mg daily. His medical history included, hypertension treated with losartan 50mg daily, and dyslipidemia treated with ezetimibe 10mg /simvastatin 20mg for four years (until 2 weeks before admission when micronized fenofibrate 200 mg per day was started because of persistently elevated triglycerides levels. On presentation temperature was 37.8°C and initial laboratory tests showed 3130 White Blood Cell Count(WBC)/µL with neutropenia (absolute neutrophil count (ANC) 313/µL) Fenofibrate and mycophenolate mofetil were discontinued, piperacillin tazobactam 4.5gr three times a day and granulocyte stimulation factor 300 µg/day were started. Three days after admission WBC was 7280/µL, neutrophils: 22%, ANC: 1160/mm(3). Mycophenolate mofetil was restarted and granulocyte stimulation factor was discontinued. One month after discharge his WBC was 4480/µL and ANC 1926/µL. DISCUSSION: The initiation of fenofibrate in a patient on stable and therapeutic doses of mycophenolate may have precipitated mycophenolate induced neutropenia, a well described, dose dependent phenomenon. Mycophenolic acid (MPA) displays a complex pharmacokinetic profile susceptible to potential significant interactions with fenofibrate. Since approximately 99% of MPA and fenofibrate bind to albumin, displacement may occur, leading to increased free MPA. Second competition of fenofibric acid for UGT1A9 an enzyme implicated in conjugation of MPA may have decreased its metabolism. The combination of these two effects may increase the risk of dose dependent neutropenia. Using the Interaction Probability Scale (DIPS), the interaction was designated as probable. CONCLUSIONS: Until further evidence is available, when fenofibrate is started in a renal transplant patient on mycophenolate careful monitoring should be considered to avoid potentially fatal complications.