ABSTRACT
BACKGROUND AND AIMS: Age and chronic kidney disease have been described as mortality risk factors for coronavirus disease 2019 (COVID-19). Currently, an important percentage of patients in hemodialysis are elderly. This study aimed to investigate the impact of COVID-19 in this population and to determine risk factors associated with mortality. METHOD: Data was obtained from the Spanish COVID-19 CKD Working Group Registry, that included patients in renal replacement therapy (dialysis and kidney transplantation) infected by COVID-19. From March 18, 2020, to August 27, 2020, 1165 patients on hemodialysis affected by COVID-19 were included in the Registry. A total of 328 patients were under 65 years-old and 837 were 65 years old or older (elderly group). RESULTS: Mortality was 18.6% higher (95% confidence interval (CI): 13.8%-23.4%) in the elderly hemodialysis patients compared to the non-elderly group (see figure). Death from COVID-19 infection was increased 5.5-fold in hemodialysis patients compared to mortality in the general population for a similar period, and there was an age-associated mortality increase in both populations (see figure 1). In multivariate Cox regression analysis, age (hazard ratio (HR) 1.58, 95% CI: 1.31-1.92), dyspnea at presentation (HR 1.61, 95% CI: 1.20-2.16), pneumonia (HR 1.76, 95% CI: 1.12-2.75) and admission to hospital (HR 4.13, 95% CI: 1.92-8.88) were identified as independent mortality risk factors in the elderly hemodialysis population. Treatment with glucocorticoids reduced the risk of death (HR 0.71, 95% CI: 0.51-0.98) in aged patients on hemodialysis. CONCLUSION: Mortality is dramatically increased in elderly hemodialysis patients affected by COVID-19. Age, dyspnea at presentation, pneumonia or hospitalization are factors associated with a worse prognosis, after adjusting dialysis population to other confounding factors. Treatment with glucocorticoids could be a therapeutic option for this specific population. (Table Presented).
ABSTRACT
BACKGROUND AND AIMS: Angiotensin converting enzyme 2 (ACE2) is one of the components of the renin-angiotensin system (RAS) that mainly degrades angiotensin II to angiotensin-(1-7). ACE2 is predominantly expressed in the kidney and the heart, but it has been evidenced in type 2 alveolar lung cells, where it acts as a receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this context, a controversy arose as to whether the use of RAS blockers could increase ACE2 lung expression and the risk infection by COVID-19. This study aimed to investigate the effect of an ACE inhibitor (Ramipril) on ACE2 expression in experimental diabetes. METHOD: 12 weeks old diabetic db/db mice (n=7) were given ramipril (8 mg/Kg/day) during 8 weeks or the respective vehicle. db/m (n=7) vehicle-treated non-diabetic mice were included as controls. ACE2 mRNA expression and enzymatic activity were studied in kidney, heart and lung samples of these animals to identify if the diabetic condition or treatment with ramipril modulated ACE2 expression. RESULTS: In vehicle-treated diabetic db/db animals, ACE2 mRNA expression was significantly increased in the kidney (p<0.001) and ramipril treatment reversed this effect (p=0.026). In the heart, ACE2 expression decreased in db/db when compared to db/m littermates (p=0.035) and ramipril had no effect. We found no differences in ACE2 gene expression in the lung. Besides, ACE2 enzymatic activity was increased in the kidney (29%) and also in the lung (16%) of db/db mice when compared to controls. Ramipril treatment decreased ACE2 activity a 19% in the lung and had no effect in the kidney when compared to untreated db/db (see figure). In the heart, ACE2 activity tended to decrease in db/db mice (29%) when compared to db/m and ramipril increased ACE2 activity (18%) but did not exceed the cardiac ACE2 activity of the db/ m. CONCLUSION: ACE2 is increased in the kidney and the lung, and decreased in the heart of diabetic mice. Ramipril treatment restores ACE2 levels. The results suggest that ACE inhibitors do not increase ACE2 expression and the activity decrease exerted in the lung may be protective against COVID-19 infection.
ABSTRACT
BACKGROUND: COVID-19 infection manifests as pneumonia associated with multiple organ failure, and death. Acute kidney injury is a risk factor for mortality. There is limited scientific literature on COVID-19 infection and allergic tubulointerstitial nephritis, its clinical course and short- and long-term prognosis. METHOD: We performed a retrospective study where medical records of 60 patients with histological diagnosis of allergic tubulointerstitial nephritis from January 2009 to November 2020. In these patients, we studied the incidence of COVID-19 infection, clinical characteristics and prognosis from March to the actual date. RESULTS: Of 60 patients with allergic tubulointerstitial nephritis, 6 (10%) patients were diagnosed with COVID-19. The first case, an 85-year-old woman with a history of metastatic melanoma treated with nivolumab and allergic tubulointerstitial nephritis by immunobiological agents in 2018, diagnosed with mild COVID-19 infection in April 2020 without deterioration of renal function in controls at 3 and 6 months of follow-up. The second case, a 51-year-old woman with a history of large B-cell lymphoma with plasmacytic differentiation and progression to multiple myeloma of lambda light chains and allergic tubulointerstitial nephritis due to chemotherapy since 2019, admitted for acute pyelonephritis and PRES syndrome secondary to first dose of bortezomib complicated with COVID-19 nosocomial pneumonia and acute pancreatitis treated with corticosteroids and broad spectrum antibiotic therapy;she died of abdominal refractory septic shock. The third patient, a 64-year-old man without prior renal impairment, was admitted for severe COVID-19 pneumonia and acute kidney injury secondary to acute tubulointerstitial nephritis of uncertain etiology that required orotracheal intubation and continuous veno-venous hemodiafiltration for a week who received methylprednisolone in bolus for 3 days and continued treatment with corticosteroid therapy with complete recovery of renal function and improvement in proteinuria at 3 months of follow-up. The fourth patient, an 82-yearold woman with acute kidney injury AKIN 3 secondary to acute allergic tubulointerstitial nephritis related to ciprofloxacin complicated with severe COVID-19 nosocomial pneumonia, who died despite ventilatory support and high-dose steroids therapy and tocilizumab. The fifth patient, a 75-year-old with a history of metastatic lung adenocarcinoma treated with immunobiological agents and allergic tubulointerstitial nephritis in 2018, admitted in march 2020 for mild COVID-19 pneumonia treated with steroids and hydroxychloroquine without deterioration of respiratory and kidney function. The sixth patient, an 86-years-old man with acute kidney injury AKIN 3 due to acute allergic tubulointerstitial nephritis secondary to proton-binding inhibitors and nosocomial COVID-19 infección with improvement of kidney function with steroids therapy only. CONCLUSION: Our 6 patients with allergic tubulointerstitial nephritis and COVID-19 infection presented different spectrum of the disease. It seems that nosocomial COVID-19 infection in patients admitted with recent diagnosis of acute allergic tubulointerstitial nephritis presented a worse clinical prognosis compared with long-term diagnosed acute tubulointerstitial nephritis. Further studies with a larger sample size are needed.
ABSTRACT
BACKGROUND AND AIMS: COVID-19 infection is responsible for respiratory infection with variable clinical expression from its asymptomatic form to severe pneumonia associated with acute respiratory distress syndrome and death. Risk factors related to higher mortality are age over 65 years, cardiovascular, pulmonary and kidney disease, hypertension, and diabetes. There is limited scientific literature on COVID-19 infection and previous kidney disease, specifically in patients with glomerular and tubular kidney disease. The aim of this study was to determine general characteristics, analytical parameters and clinical evolution of patients with kidney disease who have undergone kidney biopsy and who presented infection or high suspicion of infection by COVID-19. Identify mortality and associated risk factors. METHOD: we studied patients with high clinical suspicion of infection or confirmed infection by COVID-19 from March 2020 to May 15, 2020 of all patients who underwent percutaneous renal biopsy at the Vall d'Hebron Hospital between January 2013 and December 2019. RESULTS: 39 of the 553 patients have been diagnosed with COVID-19 infection since March 2020. The average age was 63615 years and 48.7% were male. Hypertension was present in 79.5% of patients, chronic kidney disease without renal replacement therapy in 76.9%, and cardiovascular disease in 64.1%. Nasopharyngeal swab was performed in 26 patients;older patients (p=0.01), patients with hypertension (p=0.005), immunosuppression (p=0.01), use of RAS-blocking drugs (p=0.04) and gastrointestinal symptoms (p=0.02) were more likely to be tested for COVID-19. 22 patients required hospitalization and 15.4% died. In the bivariate analysis, mortality was associated with older age (p=0.03), cardiovascular disease (p=0.05), chronic obstructive pulmonary disease (COPD) (p=0.05) and low hemoglobin levels (p=0.006). Adjusted Cox regression showed that low hemoglobin levels (10.12±1.89g/dL) at admission had 1.81 greater risk of mortality [1.04-3.13;p=0.04]. CONCLUSION: Patients with COVID-19 infection and kidney disease confirmed by kidney biopsy presented mortality of 15.4%. Swab test for COVID-19 was more likely to be performed in older, hypertensive, use of RAS-blocking drugs, immunosuppressed patients and those with gastrointestinal symptoms. Low hemoglobin is a risk factor for mortality.