Miguel Moyses Neto

Acyclovir and valacyclovir have been widely used for the treatment of herpes virus infections, including herpes zoster, with generally favorable outcomes. However, in patients with chronic kidney disease, particularly those undergoing peritoneal dialysis or hemodialysis treatment, neurotoxicity can be a significant complication as renal excretion is the primary elimination pathway. Here, we report three cases of automated peritoneal dialysis patients treated for herpes zoster who developed neurotoxicity following acyclovir or valacyclovir administration. Symptoms appeared 2 to 4 days after treatment initiation. They included mental confusion, psychomotor agitation, dizziness, dysgeusia, anosmia, blurred vision, gait instability, hallucinations, dysarthria, paresis, involuntary lower-limb movements, ataxia, and anorexia. Neurological symptoms gradually resolved after drug discontinuation, alongside complete regression of zoster lesions. Despite decades of clinical experience and numerous reports, acyclovir and valacyclovir-induced neurotoxicity continue to occur in patients with severe renal impairment. This report underscores the importance of dose adjustment and close monitoring, emphasizing that neurotoxicity, although rare, can occur even at apparently safe doses in patients undergoing peritoneal dialysis.

Objective: This study aims to evaluate the correlation between parathyroid hormone measured by a second-generation assay (PTHG2) and by a third-generation assay (PTHG3), and their association with mineral and bone disorder (MBD) biochemical parameters and radiographic vascular calcification score in kidney transplant recipients (KTRs). Materials and methods: We evaluated 87 KTRs and measured PTHG2, PTHG3, biochemical profile, urinary fractional excretion of calcium (FE Ca) and phosphate, 25(OH)D3, and Kauppila score for vascular calcification. Statistical analysis: Non-parametric tests and logistic [...] Abstract Objective: This study aims to evaluate the correlation between parathyroid hormone measured by a second-generation assay (PTHG2) and by a third-generation assay (PTHG3), and their association with mineral and bone disorder (MBD) biochemical parameters and radiographic vascular calcification score in kidney transplant recipients (KTRs). Materials and methods: We evaluated 87 KTRs and measured PTHG2, PTHG3, biochemical profile, urinary fractional excretion of calcium (FE Ca) and phosphate, 25(OH)D3, and Kauppila score for vascular calcification. Statistical analysis: Non-parametric tests and logistic

O comprometimento do estado nutricional é muito frequente nos pacientes com doença renal crônica (DRC), especialmente os pacientes em diálise e candidatos a transplante renal. É conhecido que a desnutrição em transplantados renais está associada a uma alta taxa de morbimortalidade no período pós-operatório¹ 1. Molnar MZ, Keszei A, Czira ME, Rudas A, Ujszaszi A, Haromszeki B, et al. Evaluation of the malnutrition-inflammation score in kidney transplant recipients. Am J Kidney Dis. 2010;56(1):102–11. doi: http://dx.doi.org/10.1053/j.ajkd.2010.02.350. PubMed PMID: 20471737. https://doi.org/10.1053/j.ajkd.2010.02.3... . A avaliação criteriosa do estado nutricional é fundamental para o planejamento de condutas que atendam efetivamente às demandas dessa realidade. Diretrizes do KDIGO recomendam avaliação de riscos perioperatórios para candidatos a transplante renal, como estado de sensibilização, transfusões de sangue e derivados, gestações, doença cardiovascular, doenças pulmonares, infecções e neoplasias malignas² 2. Chadban SJ, Ahn C, Axelrod DA, Foster BJ, Kasiske BL, Kher V, et al. KDIGO clinical practice guideline on the evaluation and management of candidates for kidney transplantation. Transplantation. 2020;104(4S1, Suppl 1):S11–103. doi: http://dx.doi.org/10.1097/TP.0000000000003136 https://doi.org/10.1097/TP.0000000000003... , mas não há destaque para a avaliação nutricional. Em uma meta-análise com mais de 50 pacientes com DRC foi verificado através da avaliação global subjetiva ou um escore de desnutrição-inflamação que a prevalência de desnutrição energético-proteica foi de 28%–54% nos pacientes em diálise³ 3. Carrero JJ, Thomas F, Nagy K, Arogundade F, Avesani CM, Chan M, et al. Global prevalence of protein-energy wasting in kidney disease: a meta-analysis of contemporary observational studies from the international society of renal nutrition and metabolism. J Ren Nutr. 2018;28(6):380–92. doi: http://dx.doi.org/10.1053/j.jrn.2018.08.006.PubMed PMID: 30348259. https://doi.org/10.1053/j.jrn.2018.08.00... . Todavia, há escassez de padrões de referência e de definição de pontos de corte associados aos riscos clínicos e nutricionais; portanto o acompanhamento periódico é a melhor forma de detectar as anormalidades do estado nutricional, seus desfechos e impactos⁴ 4. Ikizler TA, Burrowes JD, Byham-Gray LD, Campbell KL, Carrero JJ, Chan W, et al. KDOQI clinical practice guideline for nutrition in CKD: 2020 update. Am J Kidney Dis. 2020;76 (3, Suppl 1):S1–107. doi: http://dx.doi.org/10.1053/j.ajkd.2020.05.006. PubMed PMID: 32829751. https://doi.org/10.1053/j.ajkd.2020.05.0... .

Compromised nutritional status is very common in patients with chronic kidney disease (CKD), especially patients on dialysis and candidates for kidney transplantation. Malnutrition in kidney transplant recipients is associated with a high rate of morbidity and mortality in the postoperative period¹ 1. Molnar MZ, Keszei A, Czira ME, Rudas A, Ujszaszi A, Haromszeki B, et al. Evaluation of the malnutrition-inflammation score in kidney transplant recipients. Am J Kidney Dis. 2010;56(1):102–11. doi: http://dx.doi.org/10.1053/j.ajkd.2010.02.350. PubMed PMID: 20471737. https://doi.org/10.1053/j.ajkd.2010.02.3... . The careful assessment of nutritional status is essential for planning behaviors that effectively meet the demands of this reality. KDIGO guidelines recommend assessment of perioperative risks for kidney transplant candidates, such as sensitization status, blood transfusions and derivatives, pregnancies, cardiovascular disease, lung diseases, infections and malignant neoplasms² 2. Chadban SJ, Ahn C, Axelrod DA, Foster BJ, Kasiske BL, Kher V, et al. KDIGO clinical practice guideline on the evaluation and management of candidates for kidney transplantation. Transplantation. 2020;104(4S1, Suppl 1):S11–103. doi: http://dx.doi.org/10.1097/TP.0000000000003136 https://doi.org/10.1097/TP.0000000000003... , but there is no emphasis on nutritional assessment. In a meta-analysis with more than 50 patients with CKD, through subjective global assessment or a malnutrition-inflammation score, the researchers reported that the prevalence of protein-energy malnutrition was 28%–54% in dialysis patients³ 3. Carrero JJ, Thomas F, Nagy K, Arogundade F, Avesani CM, Chan M, et al. Global prevalence of protein-energy wasting in kidney disease: a meta-analysis of contemporary observational studies from the international society of renal nutrition and metabolism. J Ren Nutr. 2018;28(6):380–92. doi: http://dx.doi.org/10.1053/j.jrn.2018.08.006.PubMed PMID: 30348259. https://doi.org/10.1053/j.jrn.2018.08.00... . However, there is a lack of reference standards and definition of cut-off points associated with clinical and nutritional risks; therefore, periodic monitoring is the best way to detect abnormalities in nutritional status, their outcomes and impacts⁴ 4. Ikizler TA, Burrowes JD, Byham-Gray LD, Campbell KL, Carrero JJ, Chan W, et al. KDOQI clinical practice guideline for nutrition in CKD: 2020 update. Am J Kidney Dis. 2020;76 (3, Suppl 1):S1–107. doi: http://dx.doi.org/10.1053/j.ajkd.2020.05.006. PubMed PMID: 32829751. https://doi.org/10.1053/j.ajkd.2020.05.0... .

Membranous nephropathy is a glomerulopathy, which main affected target is the podocyte, and has consequences on the glomerular basement membrane. It is more common in adults, especially over 50 years of age. The clinical presentation is nephrotic syndrome, but many cases can evolve with asymptomatic non-nephrotic proteinuria. The mechanism consists of the deposition of immune complexes in the subepithelial space of the glomerular capillary loop with subsequent activation of the complement system. Great advances in the identification of potential target antigens have occurred in the last twenty years, and the main one is the protein “M-type phospholipase-A2 receptor” (PLA2R) with the circulating anti-PLA2R antibody, which makes it possible to evaluate the activity and prognosis of this nephropathy. This route of injury corresponds to approximately 70% to 80% of cases of membranous nephropathy characterized as primary. In the last 10 years, several other potential target antigens have been identified. This review proposes to present clinical, etiopathogenic and therapeutic aspects of membranous nephropathy in a didactic manner, including cases that occur during kidney transplantation.

RESUMO A nefropatia membranosa é uma glomerulopatia, cujo principal alvo acometido é o podócito, e acarreta consequências na membrana basal glomerular. Tem maior frequência em adultos, principalmente acima dos 50 anos. A apresentação clínica é a síndrome nefrótica, mas muitos casos podem evoluir com proteinúria não nefrótica assintomática. O mecanismo consiste na deposição de complexos imunes no espaço subepitelial da alça capilar glomerular com subsequente ativação do sistema do complemento. Grandes avanços na identificação de potenciais antígenos alvo têm ocorrido nos últimos vinte anos, e o principal é a proteína “M-type phospholipase-A2 receptor” (PLA2R) com o anticorpo anti-PLA2R circulante, o que possibilita avaliar a atividade e o prognóstico dessa nefropatia. Essa via de lesão corresponde aproximadamente a 70% a 80% dos casos da nefropatia membranosa caracterizada como primária. Nos últimos 10 anos vários outros antígenos alvo potenciais têm sido identificados. Esta revisão se propõe a apresentar de modo didático aspectos clínicos, etiopatogênicos e terapêuticos da nefropatia membranosa, incluídos os casos com ocorrência no transplante renal.

Background: Acute kidney injury is a frequent cause of hospital readmission in kidney transplant recipients (KTR), usually associated with infections and graft rejection. Herein, we report a case of an unusual cause of acute kidney injury in a KTR (massive histiocytes renal interstitial infiltration). Case presentation: A 40-year-old woman was submitted to a second kidney transplant. One year after surgery, she presented asthenia, myalgia, and fever, haemoglobin 6.1 g/dL; neutrophils: 1.3 × 109/µL; platelets: 143 × 109/µL; blood creatinine 11.8 mg/dL, requiring dialysis. A kidney biopsy revealed diffuse histiocytic infiltration, which was assumed due to dysregulated immunological activation triggered by infections. The patient had multiple infections, including cytomegalovirus infection (CMV), aspergillosis, bacteraemia, and urinary tract infections, which could trigger the immune response. Haemophagocytic lymphohistiocytosis (HLH) was ruled out. The present case highlights the occurrence of isolated massive renal interstitial infiltration of histiocytes that does not meet the criteria for HLH or other related pathologies. Conclusions: Renal histiocyte activation and infiltration may have been initiated by an immunological mechanism similar to what occurs in HLH and infectious processes. The present case highlights the occurrence of isolated massive renal interstitial infiltration of histiocytes that does not meet the criteria for HLH or other related pathologies.

Hypercalcemia is common in patients after kidney transplantation (KTx) and is associated with persistent hyperparathyroidism in the majority of cases. This retrospective, single-center study evaluated the prevalence of hypercalcemia after KTx. KTx recipients were evaluated for 7 years after receiving kidneys from living or deceased donors. A total of 301 patients were evaluated; 67 patients had hypercalcemia at some point during the follow-up period. The median follow-up time for all 67 patients was 62 months (44; 80). Overall, 45 cases of hypercalcemia were classified as related to persistent post-transplant hyperparathyroidism (group A), 16 were classified as “transient post-transplant hypercalcemia” (group B), and 3 had causes secondary to other diseases (1 related to tuberculosis, 1 related to histoplasmosis, and 1 related to lymphoma). The other 3 patients had hypercalcemia of unknown etiology, which is still under investigation. In group A, the onset of hypercalcemia after KTx was not significantly different from that of the other groups, but the median duration of hypercalcemia in group A was 25 months (12.5; 53), longer than in group B, where the median duration of hypercalcemia was only 12 months (10; 15) (P<0.002). The median parathyroid hormone blood levels around 12 months after KTx were 210 pg/mL (141; 352) in group A and 72.5 pg/mL (54; 95) in group B (P<0.0001). Hypercalcemia post-KTx is not infrequent and its prevalence in this center was 22.2%. Persistent hyperparathyroidism was the most frequent cause, but other important etiologies must not be forgotten, especially granulomatous diseases and malignancies.