Development of Potent Cellular and Humoral Immune Responses in Long-Term Hemodialysis Patients After 1273-mRNA SARS-CoV-2 Vaccination.

Long-term hemodialysis (HD) patients are considered vulnerable and at high-risk of developing severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection due to their immunocompromised condition. Since COVID-19 associated mortality rates are higher in HD patients, vaccination is critical to protect them. The response towards vaccination against COVID-19 in HD patients is still uncertain and, in particular the cellular immune response is not fully understood. We monitored the humoral and cellular immune responses by analysis of the serological responses and Spike-specific cellular immunity in COVID-19-recovered and naïve HD patients in a longitudinal study shortly after vaccination to determine the protective effects of 1273-mRNA vaccination against SARS-CoV-2 in these high-risk patients. In naïve HD patients, the cellular immune response measured by IL-2 and IFN-É£ secretion needed a second vaccine dose to significantly increase, with a similar pattern for the humoral response. In contrast, COVID-19 recovered HD patients developed a potent and rapid cellular and humoral immune response after the first vaccine dose. Interestingly, when comparing COVID-19 recovered healthy volunteers (HV), previously vaccinated with BNT162b2 vaccine to HD patients vaccinated with 1273-mRNA, these exhibited a more robust immune response that is maintained longitudinally. Our results indicate that HD patients develop strong cellular and humoral immune responses to 1273-mRNA vaccination and argue in favor of personalized immune monitoring studies in HD patients, especially if COVID-19 pre-exposed, to adapt COVID-19 vaccination protocols for this immunocompromised population.

Acute kidney failure in patients admitted due to COVID-19.

BACKGROUND AND AIM: In December 2019, a coronavirus 2019 (COVID-19) outbreak, caused by SARS-CoV-2, took place in Wuhan and was declared a global pandemic in March 2020 by the World Health Organization (WHO). It is a prominently respiratory infection, with potential cardiological, hematological, gastrointestinal and renal complications. Acute kidney injury (AKI) is found in 0.5%-25% of hospitalized COVID-19 patients and constitutes a negative prognostic factor. Renal damage mechanisms are not completely clear. We report the clinical evolution of hospitalized COVID-19 patients who presented with AKI requiring attention from the Nephrology team in a tertiary hospital in Madrid, Spain. METHODS: This is an observational prospective study including all COVID-19 cases that required hospitalization and Nephrology management from March 6th to May 12th. We collected clinical and analytical data of baseline characteristics, COVID-19 and AKI evolutions. RESULTS: We analyzed 41 patients with a mean age of 66.8 years (SD 2.1), 90.2% males, and with a history of chronic kidney disease (CKD) in 36.6%. 56.1% of patients presented with sever pneumonia or acute respiratory distress syndrome (ARDS), and 31.7% required intensive care. AKI etiology was prerenal in 61%, acute tubular necrosis in the context of sepsis in 24.4%, glomerular in 7.3% and tubular toxicity in 7.3% of the cases. We reported proteinuria in 88.9% and hematuria in 79.4% of patients. 48.8% of patients required renal replacement therapy (RRT). Median length of stay was 12 days (interquartilic range 9-23) and 22% of the population died. Patients who developed AKI during hospital stay presented with higher C-reactive protein, Lactate dehydrogenase-LDH and d-dimer values, more severe pulmonary damage, more frequent intensive care unit-ICU admission, treatment with lopinavir/ritonavir and biological drugs and RRT requirement. CONCLUSIONS: Hypovolemia and dehydration are a frequent cause of AKI among COVID-19 patients. Those who develop AKI during hospitalization display worse prognostic factors in terms of pulmonary damage, renal damage, and analytical findings. We believe that monitorization of renal markers as well as individualized fluid management can play a key role in AKI prevention.

[Acute kidney failure in patients admitted due to COVID-19]. / Fracaso renal agudo en pacientes hospitalizados por COVID-19.

BACKGROUND AND AIM: In December 2019, a coronavirus 2019 (COVID-19) outbreak, caused by SARS-CoV-2, took place in Wuhan, China, and was declared a global pandemic in March 2020 by the World Health Organization. It is a prominently respiratory infection, with potential cardiological, hematological, gastrointestinal and renal complications. Acute kidney injury (AKI) is found in 0.5-25% of hospitalized COVID-19 patients and constitutes a negative prognostic factor. Renal damage mechanisms are not completely clear. We report the clinical evolution of hospitalized COVID-19 patients who presented with AKI requiring attention from the Nephrology team in a tertiary hospital in Madrid, Spain. METHODS: This is an observational prospective study including all COVID-19 cases that required hospitalization and Nephrology management from March 6th to May 12th 2020. We collected clinical and analytical data of baseline characteristics, COVID-19 and AKI evolutions. RESULTS: We analyzed 41 patients with a mean age of 66.8 years (SD 2.1), 90.2% males, and with a history of chronic kidney disease in 36.6%. A percentage of 56.1 presented with severe pneumonia or acute respiratory distress syndrome, and 31.7% required intensive care. AKI etiology was prerenal in 61%, acute tubular necrosis in the context of sepsis in 24.4%, glomerular in 7.3% and tubular toxicity in 7.3% of the cases. We reported proteinuria in 88.9% and hematuria in 79.4% of patients. A percentage of 48.8 required renal replacement therapy. Median length of stay was 12 days (IQR 9-23) and 22% of the population died. Patients who developed AKI during hospital stay presented with higher C-reactive protein, LDH and D-dimer values, more severe pulmonary damage, more frequent ICU admission, treatment with lopinavir/ritonavir and biological drugs and renal replacement therapy requirement. CONCLUSIONS: Hypovolemia and dehydration are a frequent cause of AKI among COVID-19 patients. Those who develop AKI during hospitalization display worse prognostic factors in terms of pulmonary damage, renal damage, and analytical findings. We believe that monitorization of renal markers, as well as individualized fluid management, can play a key role in AKI prevention.

Fracaso renal agudo en pacientes hospitalizados por COVID-19 / Acute kidney failure in patients admitted due to COVID-19

ANTECEDENTES Y OBJETIVO: En diciembre de 2019 surgió en Wuhan, China, la COVID-19, causada por el virus SARS-CoV-2 y declarada pandemia global por la Organización Mundial de la Salud en marzo de 2020. Es una infección respiratoria con complicaciones a nivel cardiaco, hematológico, digestivo, neurológico y renal. El fracaso renal agudo (FRA) en pacientes hospitalizados por COVID-19 se presenta en el 0,5-25% y es un factor de mal pronóstico. Los mecanismos de afectación renal no están completamente aclarados. Presentamos la evolución clínica de pacientes ingresados por COVID-19 con FRA que requirieron atención por Nefrología en un hospital terciario de la Comunidad de Madrid, España. MÉTODOS: Este es un estudio observacional prospectivo de todos los casos que ingresaron por COVID-19 entre el 6 de marzo y el 12 de mayo de 2020 y requirieron atención por Nefrología. Se recogieron datos clínicos y analíticos de características basales, y la evolución de la COVID-19 y del FRA. RESULTADOS: Se analizaron 41 pacientes con una edad media de 66,8 años (DE 2,1), el 90,2% varones, y con enfermedad renal crónica previa en el 36,6%. El 56,1% presentaron neumonía grave o síndrome de distrés respiratorio agudo y el 31,7% requirió ingreso en UCI. El FRA fue de etiología prerrenal en el 61%, necrosis tubular aguda en contexto de sepsis en el 24,4%, glomerular en el 7,3% y por toxicidad tubular en el 7,3%. Se registró proteinuria en el 88,9% y hematuria en el 79,4%. El 48,8% de los pacientes requirió terapia de sustitución renal. La mediana de estancia fue de 12 días (RIC 9-23), y el 22% fallecieron. Los pacientes que desarrollaron FRA durante el ingreso presentaron valores más altos de proteína C reactiva, LDH y dímero-D, una afectación pulmonar más grave, más necesidad de ingreso en UCI, más tratamiento con lopinavir/ritonavir y fármacos biológicos, y mayor necesidad de terapia de sustitución renal. CONCLUSIONES: La hipovolemia y la deshidratación son una causa frecuente de FRA en pacientes con COVID-19. Aquellos que desarrollan FRA intrahospitalario presentan un perfil de peor pronóstico respiratorio, analítico y renal. Creemos que la monitorización de marcadores renales, así como el manejo individualizado de la volemia, pueden ser determinantes para prevenir el FRA

BACKGROUND AND AIM: In December 2019, a coronavirus 2019 (COVID-19) outbreak, caused by SARS-CoV-2, took place in Wuhan, China, and was declared a global pandemic in March 2020 by the World Health Organization. It is a prominently respiratory infection, with potential cardiological, hematological, gastrointestinal and renal complications. Acute kidney injury (AKI) is found in 0.5-25% of hospitalized COVID-19 patients and constitutes a negative prognostic factor. Renal damage mechanisms are not completely clear. We report the clinical evolution of hospitalized COVID-19 patients who presented with AKI requiring attention from the Nephrology team in a tertiary hospital in Madrid, Spain. METHODS: This is an observational prospective study including all COVID-19 cases that required hospitalization and Nephrology management from March 6th to May 12th 2020. We collected clinical and analytical data of baseline characteristics, COVID-19 and AKI evolutions. RESULTS: We analyzed 41 patients with a mean age of 66.8 years (SD 2.1), 90.2% males, and with a history of chronic kidney disease in 36.6%. A percentage of 56.1 presented with severe pneumonia or acute respiratory distress syndrome, and 31.7% required intensive care. AKI etiology was prerenal in 61%, acute tubular necrosis in the context of sepsis in 24.4%, glomerular in 7.3% and tubular toxicity in 7.3% of the cases. We reported proteinuria in 88.9% and hematuria in 79.4% of patients. A percentage of 48.8 required renal replacement therapy. Median length of stay was 12 days (IQR 9-23) and 22% of the population died. Patients who developed AKI during hospital stay presented with higher C-reactive protein, LDH and D-dimer values, more severe pulmonary damage, more frequent ICU admission, treatment with lopinavir/ritonavir and biological drugs and renal replacement therapy requirement. CONCLUSIONS: Hypovolemia and dehydration are a frequent cause of AKI among COVID-19 patients. Those who develop AKI during hospitalization display worse prognostic factors in terms of pulmonary damage, renal damage, and analytical findings. We believe that monitorization of renal markers, as well as individualized fluid management, can play a key role in AKI prevention