Persistent kidney dysfunction after acute kidney injury predicts short-term outpatient mortality.

BACKGROUND: Acute kidney injury (AKI) during hospitalisation is frequent and associated with adverse outcomes. AIMS: To evaluate the association between renal function recovery after AKI and short-term post-discharge mortality. METHODS: This is a retrospective study of all AKI episodes codified in the electronic records of a single centre in 2013 and 2014. Epidemiological data and comorbidities at baseline and laboratory values at admission and discharge were collected. Persistent kidney dysfunction after AKI was defined as a last serum creatinine equal or above 1.2-fold over baseline level. Patients were followed for 30 days after discharge. RESULTS: Out of 1720 evaluated patients, 1541 (89%) were analysed. Of them, 869 (56%) recovered renal function. Independent predictors of renal function recovery after AKI were lower baseline estimated glomerular filtration rate (eGFR) (P < 0.001), higher admission eGFR (P < 0.001) and haemoglobin (P = 0.016), milder AKI (P = 0.037), absence of a history of heart failure (P < 0.001) and lower admission blood pressure (P < 0.001). After discharge, 46 (3%) patients died in the first 30 days. Persistent kidney dysfunction was associated (P = 0.01) with and independently predicted (odds ratio 2.6; 95% confidence interval 1.2-5.4; P = 0.01) short-term post-discharge mortality. CONCLUSIONS: Persistent kidney dysfunction after an AKI episode is an independent predictor of 30-day post-discharge mortality. This information might help select AKI patients who require closer follow up and monitoring after discharge.

Tasa de ultrafiltración horaria ajustada a peso corporal y mortalidad en hemodiálisis / Ultrafiltration rate adjusted to body weight and mortality in hemodialysis patients

Antecedentes y objetivo: La mortalidad de los pacientes en hemodiálisis es alta. Una tasa de ultrafiltración horaria ajustada por peso (UFR/W) elevada se ha asociado con episodios de hipotensión arterial y con mayor riesgo de muerte y/o eventos cardiovasculares. Material y métodos: Hemos evaluado la asociación entre UFR/W y mortalidad en 215 pacientes en hemodiálisis prevalentes seguidos durante 28 ± 6,12 meses. Se estimaron características clínicas basales y UFR/W media a lo largo del seguimiento. Resultados: La UFR/W media fue 9,0 ± 2,4 y los terciles 7,1 y 10,1 mL/kg/h. Se categorizó a la población en función del tiempo que habían estado con UFR/W igual o superior a los puntos de corte descritos en la literatura como relacionados con mayor mortalidad (10,0 mL/kg/h y 13,0 mL/kg/h). Los pacientes con mayor UFR/W fueron más jóvenes, con mayor ganancia de peso interdiálisis y porcentaje de reducción de peso, pero con menor peso seco, inicial y final. Durante el seguimiento, fallecieron 46 (21,4%) personas de las cuales la mayoría eran > 70 años, diabéticas o con enfermedad cardiovascular. No hubo diferencias en la mortalidad entre los grupos de UFR/W ni en la UFR/W entre los fallecidos y no fallecidos. En comparación con estudios previos donde describieron la asociación entre UFR/W y mortalidad, en nuestra población había más prevalencia de medicación protectora cardiovascular y no se observaron UFR/W tan altas. Conclusión: En nuestro medio, la UFR/W más elevada se observó en pacientes más jóvenes y de menor peso y no se asoció con mayor mortalidad. (AU)

Background and aims: Mortality among hemodialysis patients remains high. An elevated ultrafiltration rate adjusted by weight (UFR/W) has been associated with hypotension and higher risk of death and/or cardiovascular events. Methods: We evaluated the association between UFR/W and mortality in 215 hemodialysis patients. The mean follow-up was 28 ± 6.12 months. We collected patientś baseline characteristics and mean UFR/W throughout the follow-up. Results: Mean UFR/W was 9.0 ± 2,4 and tertiles 7.1 y 10.1 mL/kg/h. We divided our population according to the percentage of sessions with UFR/W above the limits described in the literature associated with increased mortality (10.0 mL/kg/h and 13.0 mL/kg/h). Patients with higher UFR/W were younger, with higher interdialytic weight gain and weight reduction percentage but lower dry, pre and post dialysis weight. Throughout the follow-up, 46 (21.4%) patients died, the majority over 70 years old, diabetic or with cardiovascular disease. There were neither differences regarding mortality between groups nor differences in UFR/W among patients who died and those who did not. Contrary to previous studies, we did not find an association between UFR/W and mortality, maybe due to a higher prevalence in the use of cardiovascular protection drugs and lower UFR/W. Conclusions: The highest UFR/W were observed in younger patients with lower weight and were not associated with an increased mortality. (AU)

Slo-Mo anti-neutrophil cytoplasmic antibody-associated renal vasculitis.

Nephrologists are familiar with severe cases of anti-neutrophil cytoplasmic antibodies-associated vasculitis (AAV) presenting as rapidly progressive glomerulonephritis. However, less is known about AAV with slowly progressive renal involvement. While its existence is acknowledged in textbooks, much remains unknown regarding its relative frequency versus more aggressive cases as well as about the optimal therapeutic approach and response to therapy. Moreover, this uncommon presentation may be underdiagnosed, given the scarce familiarity of physicians. In this issue of Clinical Kidney Journal, Trivioli et al. report the largest series to date and first systematic assessment of patients with AAV and slowly progressive renal involvement, defined as a reduction in estimated glomerular filtration rate (eGFR) of 25-50% in the 6 months prior to diagnosis after excluding secondary causes. Key findings are that slowly progressive AAV may be less common than previously thought, although it still represents the second most common presentation of renal AAV, it usually has a microscopic polyangiitis, anti-myeloperoxidase, mainly renal phenotype in elderly individuals, diagnosis may be late (over one-third of patients had end-stage kidney disease at diagnosis), clearly identifying an unmet need for physician awareness about this presentation, but those not needing renal replacement therapy at diagnosis still responded to immunosuppression.

Ultrafiltration rate adjusted to body weight and mortality in hemodialysis patients.

BACKGROUND AND AIMS: Mortality among hemodialysis patients remains high. An elevated ultrafiltration rate adjusted by weight (UFR/W) has been associated with hypotension and higher risk of death and/or cardiovascular events. METHODS: We evaluated the association between UFR/W and mortality in 215 hemodialysis patients. The mean follow-up was 28 ±â€¯6.12 months. We collected patients' baseline characteristics and mean UFR/W throughout the follow-up. RESULTS: Mean UFR/W was 9.0 ±â€¯2,4 and tertiles 7.1 y 10.1 mL/kg/h. We divided our population according to the percentage of sessions with UFR/W above the limits described in the literature associated with increased mortality (10.0 ml/kg/h and 13.0 mL/kg/h). Patients with higher UFR/W were younger, with higher interdialytic weight gain and weight reduction percentage but lower dry, pre and post dialysis weight. Throughout the follow-up, 46 (21.4%) patients died, the majority over 70 years old, diabetic or with cardiovascular disease. There were neither differences regarding mortality between groups nor differences in UFR/W among patients who died and those who did not. Contrary to previous studies, we did not find an association between UFR/W and mortality, maybe due to a higher prevalence in the use of cardiovascular protection drugs and lower UFR/W. CONCLUSIONS: The highest UFR/W were observed in younger patients with lower weight and were not associated with an increased mortality.

Efecto regulador de paricalcitol sobre parámetros inflamatorios, fibróticos y anticalcificantes en el paciente con enfermedad renal crónica. Más allá de la regulación de la enfermedad óseo-mineral / Paricalcitol regulatory effect on inflammatory, fibrotic and anticalcificating parameters in renal patiente. Far beyond mineral bone disease regulation

ANTECEDENTES: La principal causa de morbimortalidad en el paciente con enfermedad renal crónica (ERC) es la cardiovascular. La inflamación y las alteraciones en el metabolismo óseo-mineral en estos pacientes conllevan aumento del riesgo cardiovascular. OBJETIVOS: Valorar el papel de paricalcitol sobre distintos parámetros séricos relacionados con inflamación, fibrosis y enfermedad óseo-mineral en la ERC. MATERIAL Y MÉTODOS: Estudio prospectivo, no controlado en 46 pacientes con ERC estadios III-V sin diálisis, con niveles elevados de paratohormona, según su estadio de ERC, por lo que se introdujo tratamiento con el análogo de vitamina D paricalcitol. Durante 4 meses de tratamiento valoramos los parámetros clásicos y novedosos del metabolismo óseo-mineral en suero (calcio, fósforo, paratohormona, factor de crecimiento fibroblástico-23 [FGF-23], Klotho y calcidiol) y parámetros relacionados con el proceso de inflamación-fibrosis y anticalcificantes (interleucina-6 y 10, factor de necrosis tumoral alfa [TNF-a], factor de crecimiento transformante beta [TGF-b], proteína ósea morfogénica-7 [BMP-7], y fetuína-A). RESULTADOS: Tras el uso de paricalcitol los niveles de Klotho aumentaron (p = 0,001) y los de FGF-23 se mantuvieron estables al igual que los de calcio y fósforo; calcidiol aumentó de forma significativa (p = 0,010) y paratohormona descendió (p = 0,002). Los parámetros de inflamación, fibrosis y calcificación mostraron una regulación benigna con descenso significativo de interleucina-6 (p = 0,001), TNF-alfa (p = 0,005) y TGF-β (p = 0,001) y aumento de BMP-7 (p = 0,001), fetuína-A (p = 0,001) e interleucina-10 (p = 0,001). El filtrado glomerular y la proteinuria se mantuvieron estables. CONCLUSIONES: El tratamiento con paricalcitol en el paciente renal sin diálisis parece ser beneficioso en la regulación de los parámetros inflamatorios y anticalcificantes, preservando la función renal y el eje óseo-mineral. Los marcadores elegidos en nuestro estudio podrían indicarnos un efecto positivo de paricalcitol a nivel vascular

BACKWARD: Cardiovascular events are the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). Inflammation and mineral-bone disorder are pathological conditions that have been associated with an increased cardiovascular risk. OBJECTIVE: Show paricalcitol regulation overinflammatory, fibrotic and mineral disorder parameters in CKD. MATERIAL AND METHODS: Prospective Study in 46 CKD stages III-V patients without dialysis patients whith elevated parathormone in which we introduced paricalcitol. We evaluated classic and newest mineral and bone metabolism serum parameters (calcium, phosphorus, parathormone, fibroblast growth factor-23 [FGF-23], Klotho, calcidiol), inflammatory-fibrosis and anticalcifying parameters (interleukin-6 and 10, tumor necrosis factor-a [TNF- alfa], transforming growth factor-b [TGF-β],bone morphogenic protein-7 [BMP-7] and fetuin-A) for four months. RESULTS: At the end of study soluble Klotho increased (p = .001), FGF-23 remained stable, calcium and phosphorus levels were not increased, calcidiol increased (p = .010) and PTH decreased (p = .002). Inflammation-fibrosis and calcification parameters showed positive regulation after paricalcitol treatment: interleukin-6 decreased significantly (p = .001) and also TNF-alfa did (p = .005), on the contrary, interleukin-10 and fetuin-A increased (p = .001 for both). Anti-fibrosis marker BMP-7 increased (p = .001) and TGF-b decreased (p = .001). We did not find significant changes in renal function. CONCLUSIONS: Paricalcitol treatment might be profitable in regulating inflammatory and anticalcificant parameters, unmodified calcium or phosphorus seric levels and preserving kidney function in renal patients with no dialysis. Our selected parameters could indicate paricalcitol effects in mineral and endothelial disorder related to renal disease

Paricalcitol regulatory effect on inflammatory, fibrotic and anticalcificating parameters in renal patiente. Far beyond mineral bone disease regulation. / Efecto regulador de paricalcitol sobre parámetros inflamatorios, fibróticos y anticalcificantes en el paciente con enfermedad renal crónica. Más allá de la regulación de la enfermedad óseo-mineral.

BACKWARD: Cardiovascular events are the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). Inflammation and mineral-bone disorder are pathological conditions that have been associated with an increased cardiovascular risk. OBJECTIVE: Show paricalcitol regulation overinflammatory, fibrotic and mineral disorder parameters in CKD. MATERIAL AND METHODS: Prospective Study in 46 CKD stages III-V patients without dialysis patients whith elevated parathormone in which we introduced paricalcitol. We evaluated classic and newest mineral and bone metabolism serum parameters (calcium, phosphorus, parathormone, fibroblast growth factor-23 [FGF-23], Klotho, calcidiol), inflammatory-fibrosis and anticalcifying parameters (interleukin-6 and 10, tumor necrosis factor-a [TNF- α], transforming growth factor-b [TGF-ß],bone morphogenic protein-7 [BMP-7] and fetuin-A) for four months. RESULTS: At the end of study soluble Klotho increased (p=.001), FGF-23 remained stable, calcium and phosphorus levels were not increased, calcidiol increased (p=.010) and PTH decreased (p=.002). Inflammation-fibrosis and calcification parameters showed positive regulation after paricalcitol treatment: interleukin-6 decreased significantly (p=.001) and also TNF-α did (p=.005), on the contrary, interleukin-10 and fetuin-A increased (p=.001 for both). Anti-fibrosis marker BMP-7 increased (p=.001) and TGF-b decreased (p=.001). We did not find significant changes in renal function. CONCLUSIONS: Paricalcitol treatment might be profitable in regulating inflammatory and anticalcificant parameters, unmodified calcium or phosphorus seric levels and preserving kidney function in renal patients with no dialysis. Our selected parameters could indicate paricalcitol effects in mineral and endothelial disorder related to renal disease.

Mecanismos inflamatorios y fibróticos en la enfermedad renal. Protagonistas y terapéutica / Inflammatory and fibrotic process in kidney disease. Protagonists and therapy

La enfermedad renal es un problema de salud pública por su incidencia, prevalencia y morbimortalidad. La inflamación y fibrosis son el motor de toda alteración del daño renal, independientemente de su origen. El proceso inflamatorio y fibrótico se caracteriza por infiltración de células inflamatorias, liberación de citoquinas, activación de fibroblastos, de señales químicas y vías de señalización. Este proceso conlleva la generación de células efectoras productoras de matriz extracelular o de complejos de ataque que desemboca en el daño orgánico. Ninguna terapia ha demostrado eficacia total frente al daño inflamatorio o fibrótico. Muchos fármacos, en desarrollo experimental, ejercen su inmunomodulación a través de la regulación de la actividad de muchos tipos de células inmunes y presentan un perfil antiinflamatorio y fibrótico. El objetivo es ser conocedores de la importancia de los procesos que son capaces de provocar el proceso inflamatorio y fibrótico dado que podría tratarse de marcadores diagnósticos y dianas terapéuticas

Chronic kidney disease is a serious public health problem, due to its high incidence and prevalence, as well as its significant morbidity and mortality. Inflammation and fibrosis are the final step in renal failure. The inflammatory and fibrotic process is highlighted by infiltration by inflammatory cells, cytokine release, fibroblast accumulation, and activation of numerous chemical signals. Those processes involve the generating of immunomodulatory cells that produce an extracellular matrix and attack complex, leading to organ damage. There is no an effective therapy against fibrotic and inflammatory damage. There are different drugs that have shown to be beneficial over inflammation and fibrosis in experimental and in vitro studies. The aim is to be aware of the processes that are able to trigger fibrosis and inflammation, given that they could be used as diagnostic markers and therapeutic targets