SARS-CoV-2 infection in kidney transplant recipients: clinical impact and outcomes - a single center experience / Infecção por SARS-CoV-2 em receptores de transplante renal: impacto clínico e outcomes - uma experiência de centro único

ABSTRACT Introduction: Kidney transplant recipients are a subgroup of patients at higher risk of critical forms of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection and poor outcomes due to immunosuppression treatment. Herein, we present data from a single center cohort of kidney transplant recipients with SARS-CoV-2 infection. Methods: In a prospective study, baseline characteristics, clinical features, antiviral and immunosuppression management were compared between outpatients and hospitalized patients, during a one-year period. Results: Seventy-seven kidney transplant recipients were analyzed, including outpatients and hospitalized patients, with a median age of 57.7 (IQR 49.7-64.9) years. Twenty-eight (36.4%) were managed as outpatients, while 49 (63.6%) patients required hospital admission. Among hospitalized patients, 18.4% were admitted in ICU, 49% had AKI, and 20.4% died. Immunosuppression adjustments were performed in 95.9% of hospitalized patients, with dose of anti-metabolites adjusted in 83.7%, mTOR inhibitors in 14.3%, calcineurin inhibitors in 12.2%, and corticosteroid therapy in 81.6%. Conclusion: Among hospitalized patients, immunosuppression management included reduction or withdrawal of anti-metabolite and increase of corticosteroid dose. AKI occurred in almost half of patients and mortality in hospitalized patients reached 20%, reflecting greater disease severity than the general population.

RESUMO Introdução: Receptores de transplante renal são um subgrupo de doentes com maior risco de apresentar formas críticas de infecção por Síndrome Respiratória Aguda Grave pelo Coronavirus-2 (SARS-CoV-2) e piores outcomes devido ao tratamento imunossupressor. Aqui, apresentamos dados de uma coorte de um único centro de receptores de transplante renal com infecção por SARS-CoV-2. Métodos: Num estudo prospectivo, características basais, características clínicas, adaptação da terapêutica antiviral e de imunossupressão foram comparados entre doentes seguidos em ambulatório e doentes hospitalizados durante um período de um ano. Resultados: Foram analisados setenta e sete receptores de transplante renal, incluindo doentes de ambulatório e hospitalizados, com idade média de 57,7 (IIQ 49,7-64,9) anos. Vinte e oito (36,4%) foram tratados em ambulatório enquanto 49 (63,6%) doentes necessitaram de internação hospitalar. Entre os doentes hospitalizados, 18,4% foram admitidos na UTI, 49% apresentaram LRA, e 20,4% morreram. Foram realizados ajustes de imunossupressão em 95,9% dos pacientes hospitalizados, com dose de antimetabólitos ajustada em 83,7%, inibidores de mTOR em 14,3%, inibidores de calcineurina em 12,2%, e terapia com corticosteroides em 81,6%. Conclusão: Entre os pacientes hospitalizados, a optimização da terapêutica imunossupressora incluiu redução ou retirada de antimetabólito e aumento da dose de corticosteroides. A LRA ocorreu em quase metade dos pacientes e a mortalidade em pacientes hospitalizados atingiu 20%, refletindo uma maior gravidade da doença em relação à população em geral.

SARS-CoV-2 infection in kidney transplant recipients: clinical impact and outcomes - a single center experience.

INTRODUCTION: Kidney transplant recipients are a subgroup of patients at higher risk of critical forms of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection and poor outcomes due to immunosuppression treatment. Herein, we present data from a single center cohort of kidney transplant recipients with SARS-CoV-2 infection. METHODS: In a prospective study, baseline characteristics, clinical features, antiviral and immunosuppression management were compared between outpatients and hospitalized patients, during a one-year period. RESULTS: Seventy-seven kidney transplant recipients were analyzed, including outpatients and hospitalized patients, with a median age of 57.7 (IQR 49.7-64.9) years. Twenty-eight (36.4%) were managed as outpatients, while 49 (63.6%) patients required hospital admission. Among hospitalized patients, 18.4% were admitted in ICU, 49% had AKI, and 20.4% died. Immunosuppression adjustments were performed in 95.9% of hospitalized patients, with dose of anti-metabolites adjusted in 83.7%, mTOR inhibitors in 14.3%, calcineurin inhibitors in 12.2%, and corticosteroid therapy in 81.6%. CONCLUSION: Among hospitalized patients, immunosuppression management included reduction or withdrawal of anti-metabolite and increase of corticosteroid dose. AKI occurred in almost half of patients and mortality in hospitalized patients reached 20%, reflecting greater disease severity than the general population.

Hepatocellular carcinoma after direct-acting antiviral therapy in kidney transplant recipients infected with hepatitis C virus / Carcinoma hepatocelular después del tratamiento con antivirales de acción directa en pacientes trasplantados renales infectados con el virus de la hepatitis C

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Risk of hepatitis B reactivation in hepatitis B surface antigen seronegative and core antibody seropositive kidney transplant recipients.

BACKGROUND: Previous contact with Hepatitis B virus (HBV) is common in patients undergoing hemodialysis. Literature has shown conflicting results on the risk of HBV reactivation in kidney transplant (KT) recipients with serologic evidence of past HBV infection. METHODS: We reviewed 631 consecutive KT recipients and selected 70 patients simultaneously HBsAg negative and anti-HBc positive before KT, regardless of hepatitis B surface antibody (anti-HBs) status. Demographic characteristics, coinfection with other viruses, the presence of a previous KT, induction and maintenance immunosuppression, length of follow up, biopsy-proven acute rejection episodes, incidence of impaired liver function, and causes of graft loss and mortality were collected. Hepatitis B virus reactivation was defined as detection of HBV DNA viral load >2000 IU/mL during follow up. Outcome data included HBV reactivation episodes, graft function, and patient survival. RESULTS: Median follow-up was 151 months; 91.4% of patients were positive to anti-HBs prior to KT. No patient received HBV prophylaxis and 11 patients (15.7%) received rituximab as part of induction therapy. Anti-HBs titers remained stable in all patients throughout the observation period but two patient showed evidence of HBV reactivation after KT. CONCLUSION: Hepatitis B virus reactivation in HBsAg-negative and anti-HBc-positive after KT is rare but possible. We suggest evaluating HBV serologies, HBV DNA viral load, and liver enzymes before KT and routinely monitoring serologic HBV markers after KT. As only two patients experienced HBV reactivation, it is neither possible to define risk factors for HBV reactivation nor to evaluate the impact of different immunosuppressants or the benefit of prophylactic regimens. Further studies regarding HBV reactivation in solid organ transplant recipients are necessary.

The impact of functioning hemodialysis arteriovenous accesses on renal graft perfusion: Results of a pilot study.

INTRODUCTION: After a kidney transplant, it is unknown whether the maintenance of a functioning hemodialysis arteriovenous access could have deleterious effects on renal grafts. We hypothesize that maintaining an arteriovenous access can deviate a significant proportion of the cardiac output from the renal graft. The aim of this study was to investigate whether a temporary closure of the arteriovenous access could lead to an increase in graft perfusion. METHODS: We conducted a study in 17 kidney-transplanted patients with a functioning arteriovenous access. We evaluated, at baseline and 30 s after compression of the arteriovenous access (access flow occlusion), the hemodynamic parameters and the renal resistive index of the graft by Doppler ultrasound. RESULTS: After arteriovenous access occlusion 82.4% (n = 14) of the patients had a decrease in resistive index. All patients had a decrease in heart rate (67 vs 58 bpm, p < 0.001) and 14 (82.4%) had an increase in mean blood pressure (98.3 vs 101.7 mm Hg, p = 0.044). There was a significant decrease in the resistive index (ΔRI) after the access occlusion (0.68 vs 0.64, p = 0.030). We found a negative correlation in Qa (r2 = -0.55, p = 0.022) with the ΔRI, and Qa was an independent predictor of ΔRI in a model adjusted to pre-occlusion resistive index. CONCLUSION: Our results showed that temporary occlusion of an arteriovenous access causes a significant decline in renal graft resistive index and this decline is higher with the occlusion of accesses with higher Qa. These results suggest that the maintenance of arteriovenous accesses, mainly those with higher Qa, can decrease renal graft perfusion.

Gastrointestinal Bleeding and Diffuse Skin Thickening as Kaposi Sarcoma Clinical Presentation.

A 56-year-old African patient received a kidney from a deceased donor with 4 HLA mismatches in April 2013. He received immunosuppression with basiliximab, tacrolimus, mycophenolate mofetil, and prednisone. Immediate diuresis and a good allograft function were soon observed. Six months later, the serum creatinine level increased to 2.6 mg/dL. A renal allograft biopsy revealed interstitial fibrosis and tubular atrophy grade II. Toxicity of calcineurin inhibitor was assumed and, after a switch for everolimus, renal function improved. However, since March 2014, renal function progressively deteriorated. A second allograft biopsy showed no new lesions. Two months later, the patient was admitted due to anuria, haematochezia with anaemia, requiring 5 units of packed red blood cells, and diffuse skin thickening. Colonoscopy showed haemorrhagic patches in the colon and the rectum; histology diagnosis was Kaposi sarcoma (KS). A skin biopsy revealed cutaneous involvement of KS. Rapid clinical deterioration culminated in death in June 2014. This case is unusual as less than 20 cases of KS with gross gastrointestinal bleeding have been reported and only 6 cases had the referred bleeding originating in the lower gastrointestinal tract. So, KS should be considered in differential diagnosis of gastrointestinal bleeding in some kidney transplant patients.

Use of peritoneal dialysis after surgery for congenital heart disease in children.

Acute kidney injury (AKI) is a common complication in children after surgery for congenital heart disease, and peritoneal dialysis (PD) is usually the renal replacement therapy (RRT) of choice, especially in very young children. The aim of the present study was to describe our experience of using PD to treat AKI after cardiac surgery. We retrospectively analyzed children 1 week to 16 years of age undergoing cardiac surgery during 2000-2008 and found the incidence of AKI treated with PD to be 2.3%. In the 23 patients treated with PD (13 male; average age: 29 ± 48.4 months; weight: 9.1 ± 8.1 kg), the indications for PD initiation were oliguria (n = 13), anuria (n = 9), and acidosis (n = 1). The average time between cardiac surgery and AKI was 4.8 ± 16.8 hours, and between AKI and PD initiation, it was 12 ± 16.8 hours. Patients were treated for a mean of 4.8 ± 3.8 days. Two patients developed peritonitis, and mechanical dysfunction of the PD catheter occurred in 1 patient. In-hospital mortality was 43.4%. Patients treated with PD weighed less (p = 0.004) and had longer bypass time (p = 0.004), inotrope use (p = 0.000), and mechanical ventilation (p = 0.000). However, in a regression analysis, only cardiopulmonary bypass time (odds ratio: 1.021; 95% confidence interval: 0.998 to 1.027; p = 0.032) remained predictive of a subsequent need for PD. We conclude that PD is an efficacious RRT for AKI in children undergoing cardiac surgery and that, in this setting, bypass time is the strongest predictor of a subsequent need for RRT.

Peripheral artery disease: a cause of refractory hypertension after renal transplantation.

The authors report the case of a 44-year-old man, with a history of hypertension, smoking, peripheral artery disease and chronic renal failure. After renal transplantation, the patient developed persistent high blood pressure, despite optimal medical therapy. When angiotensin-converting enzyme (ACE) inhibitor therapy was begun, he developed acute anuric renal failure, which was reversed after interruption of the ACE inhibitor. After the initial clinical evaluation, the patient was referred for renal angiography, which revealed critical stenosis of the proximal left common iliac artery, just above the renal graft artery anastomosis. The patient underwent successful angioplasty and stenting of the lesion, with complete normalization of blood pressure.

Acute renal toxic effect of amiodarone in rats.

Amiodarone is an antiarrhythmic drug now more frequently used after a number of years in which the use had been on the decline due to a number of studies which reported side effects such as chronic toxicity, primarily in the lungs, liver and thyroid glands. Additionally, in some patients an increase in serum creatinine was noted, however the effect of amiodarone on renal function had never been closely examined. Thus, the aim of our study was to analyse the effects of amiodarone on renal function in rats. Experiments were carried out in male Wistar rats divided in two experimental groups: 1) a control group, (n=8), 2) a group that received a daily intraperitoneal injection of amiodarone (50 mg/kg body weight) for 6 days (n=5). At the end of the treatment, renal function was measured by clearance creatinine and acute clearance studies. Renal toxicity was evaluated by urinary N-acetyl-glucosamine and alkaline phosphatase. At the end of the experiment, histology studies were done. Rats treated with amiodarone had a higher serum creatinine (182%) and a lower glomerular filtration rate (53%), renal plasma flow (68%) and filtration fraction (62%) than controls. Rats treated with amiodarone also showed an increase in urinary N-acetyl-glucosamine (221%) and alkaline phosphatase (4.151%) excretion which corresponds with tubular alterations showed on electron microscopy. In conclusion our data confirm that amiodarone induces acute renal damage in the rat.