Impact of different COVID-19 waves on kidney replacement therapy epidemiology and mortality: REMER 2020.

BACKGROUND: Kidney replacement therapy (KRT) confers the highest risk of death from coronavirus disease 2019 (COVID-19). However, most data refer to the early pandemic waves. Whole-year analysis compared with prior secular trends are scarce. METHODS: We present the 2020 REMER Madrid KRT registry, corresponding to the Spanish Region hardest hit by COVID-19. RESULTS: In 2020, KRT incidence decreased 12% versus 2019, while KRT prevalence decreased by 1.75% for the first time since records began and the number of kidney transplants (KTs) decreased by 16%. Mortality on KRT was 10.2% (34% higher than the mean for 2008-2019). The 2019-2020 increase in mortality was larger for KTs (+68%) than for haemodialysis (+24%) or peritoneal dialysis (+38%). The most common cause of death was infection [n = 419 (48% of deaths)], followed by cardiovascular [n = 200 (23%)]. Deaths from infection increased by 167% year over year and accounted for 95% of excess deaths in 2020 over 2019. COVID-19 was the most common cause of death (68% of infection deaths, 33% of total deaths). The bulk of COVID-19 deaths [209/285 (73%)] occurred during the first COVID-19 wave, which roughly accounted for the increased mortality in 2020. Being a KT recipient was an independent risk factor for COVID-19 death. CONCLUSIONS: COVID-19 negatively impacted the incidence and prevalence of KRT, but the increase in KRT deaths was localized to the first wave of the pandemic. The increased annual mortality argues against COVID-19 accelerating the death of patients with short life expectancy and the temporal pattern of COVID-19 mortality suggests that appropriate healthcare may improve outcomes.

Nefritis intersticial tuberculosa, un diagnóstico difícil que precisa de una alta sospecha / Tuberculous interstitial nephritis: A difficult diagnosis that requires a high clinical suspicion

No disponible

Nefropatía por cilindros biliares asociada a disfunción hepática severa causada por esteroides anabolizantes / Bile cast nephropathy associated with severe liver dysfunction caused by anabolic steroids

No disponible

¿Puede ser donante de órganos un paciente con enfermedad de Pompe? / Can a Pompe disease patient be an organ donor?

No disponible

Rechazo agudo del injerto renal no funcionante en pacientes en diálisis después de iniciar tratamiento con interferón y ribavirina / Acute rejection of non-functional renal grafts in dialysis patients after starting treatment with interferon and ribavirin

No disponible

Glomerulopatías C3. Una nueva perspectiva en enfermedades glomerulares / C3 Glomerulopathies. A new perspective on glomerular diseases

El término glomerulonefritis membranoproliferativa denota un patrón general de daño glomerular fácilmente reconocido por microscopía óptica. Con estudios adiciones de microscopía electrónica e inmunofluorescencia, la clasificación en subgrupos es posible. El estudio por microscopía electrónica resuelve las diferencias según la localización de los depósitos electrodensos, mientras que la inmunofluorescencia detecta la composición de los depósitos electrodensos. La glomerulopatía C3 es una entidad descrita de forma reciente, una glomerulonefritis proliferativa (normalmente, pero no siempre), con un patrón de glomerulonefritis membranoproliferativa en la microscopía óptica y con depósitos de C3 aislados en el estudio de inmunofluorescencia, implicando una hiperactividad de la vía alternativa del complemento. La evaluación de un paciente con glomerulopatía C3 debe centrarse en la cascada del complemento, en la desregulación de la vía alternativa del complemento y en la cascada terminal del complemento. Aunque no hay actualmente tratamientos específicos para las glomerulopatías C3, una mejor comprensión de la patogénesis sentaría las bases para el posible uso de drogas anticomplemento como terapia de elección, como el eculizumab. En la presente revisión, se resume la patogenia de las glomerulopatías C3, centrándonos en el papel del complemento, las series de casos recientemente publicados y las opciones terapéuticas hasta el momento actual (AU)

Membranoproliferative glomerulonephritis (MPGN) denotes a general pattern of glomerular injury that is easily recognized by light microscopy. With additional studies, MPGN subgrouping is possible. For example, electron microscopy resolves differences in electron-dense deposition location, while immunofluorescence typically detects the composition of electron-dense deposits. A C3 glomerulopathy (C3G) is a recently described entity, a proliferative glomerulonephritis (usually but not always), with a MPGN pattern on light microscopy, with C3 staining alone on inmunoflouresencie, implicating hyperactivity of the alternative complement pathway. The evaluation of C3G should focus on the complement cascade, as dysregulation of the alternative pathway and terminal complement cascade underlies pathogenesis. Although there are no specific treatments currently available for C3G, a better understanding of their pathogenesis would set the stage for the possible use of anti-complement drugs, as eculizumab. In this review, we summarise the pathogenesis of the C3 glomerulopathies, focusing on the role of complement, the patient cohorts recently reported and options of treatment up to the current moment (AU)

C3 glomerulopathies. A new perspective on glomerular diseases.

Membranoproliferative glomerulonephritis denotes a general pattern of glomerular injury that is easily recognised by light microscopy. With additional studies, MPGN subgrouping is possible. For example, electron microscopy resolves differences in electron-dense deposition location, while immunofluorescence typically detects the composition of electron-dense deposits. A C3 glomerulopathy (C3G) is a recently described entity, a proliferative glomerulonephritis (usually but not always), with a MPGN pattern on light microscopy, with C3 staining alone on immunofluorescence, implicating hyperactivity of the alternative complement pathway. The evaluation of C3G in a patient should focus on the complement cascade, as deregulation of the alternative pathway and terminal complement cascade underlies pathogenesis. Although there are no specific treatments currently available for C3G, a better understanding of their pathogenesis would set the stage for the possible use of anti-complement drugs, as eculizumab. In this review, we summarise the pathogenesis of the C3 glomerulopathies, focusing on the role of complement, the patient cohorts recently reported and options of treatment up to the current moment.

Cholesterol atheroembolism and combined treatment with steroids and iloprost.

Cholesterol atheroembolism (CAE) is a systemic disorder whose incidence has increased in recent decades and that presents high morbidity and mortality. Although several therapeutic alternatives have been reported, there is no consensus about the best treatment for this disease. In this paper we report the case of a patient with CAE with skin, bowel and kidney involvement who presented a good response to combined therapy with steroids and prostaglandin analogues. Although there are no conclusive studies, we recommend this therapeutic alternative in the management of CAE with organic failure.

Acute renal failure due to interstitial nephritis after intravesical instillation of BCG.

Intravesical chemotherapy with bacilli Calmette-Guerin (BCG) has been an established therapy for preventing recurrence of, and for treatment of, superficial transitional cell carcinoma of the bladder, but it is not without side effects. A variety of renal complications have been reported and attributed to mycobacterial infection. Although renal complications are uncommon, several cases of interstitial nephritis (with or without granulomas) and mesangial glomerulonephritis have been reported. We report a 76-year-old male patient who developed acute renal failure due to interstitial nephritis after intravesical instillation of BCG. Corticosteroids may serve the recovery of renal function without concomitant use of anti-tubercular therapy, provided systemic signs and mycobacterial infection are absent. Serum creatinine should be checked in at-risk patients in order to detect this complication early.