In this review we summarized some information regarding the link between kidney and oxidative stress. Accruing evidences indicated the kidney as a fundamental organ in reactive oxygen species (ROS) production. ROS are highly reactive and cause in single cells: protein alteration, DNA damage, cellular senescence and apoptosis; while the effect of ROS in biological tissues leads to a harmful oxidation effect on all their biochemical components: lipids, proteins, carbohydrates, and nucleic acids. Oxidative stress plays a role in the pathophysiology of renal impairment and is a mediator of CKD progression; furthermore, during substitutive therapy with haemodialysis or peritoneal dialysis and in case of transplantation, organism continues to be exposed to oxidation causing the development of major systemic comorbidities in particular cardiovascular diseases.
Psoriasis is an immune-mediated inflammatory disease for a long time considered as a type of pathology characterized by an exclusive skin involvement. Recently it has been shown that patients affected by this disease have a higher risk of developing comorbidities such as cardiovascular diseases, arterial hypertension, diabetes mellitus, and metabolic syndrome. Even the kidneys can be affected by psoriasis through three different mechanisms: immune-mediated renal damage, drug-related renal damage and chronic renal damage. Renal function should be monitored periodically to minimize the risk of renal adverse events.
Glucagon-like peptide-1 receptor agonists are highly effective in improving glycemic control either as monotherapy or in combination with other hypoglycemic drugs and have low incidence of side effects, such as hypoglycemia, nausea and weight gain, thus increasing patients' adherence to therapy. This class of medications is now attracting growing interest from Nephrologist. In fact, accumulating data show that these drugs not only reduce major adverse cardiovascular events in patients with diabetes mellitus type 2 and established cardiovascular disease or high cardiovascular risk profile, but also prevent albuminuria and slow the decline of renal function towards end stage renal disease in patients with diabetic kidney disease. In this review we report the most recent studies demonstrating the beneficial effects of glucagon-like peptide-1 receptor agonists on renal outcomes, and also discuss the direct and indirect mechanisms through which they confer kidney protection. Finally, we discuss the metabolic and anti-inflammatory effects of glucagon-like peptide-1 receptor agonists in diabetic patients with COVID-19 disease.
A coryneform bacterium was isolated from the bronchoalveolar aspirate of a patient with interstitial pulmonary inflammation. Commercial systems identified the isolate as Corynebacterium sp. or Aureobacterium sp./Corynebacterium aquaticum, but 16S rRNA gene analysis unequivocally attributed it to the genus Microbacterium. This represents the first documented case of Microbacterium pulmonary infection. Case reportA 44-year-old man underwent heart transplantation on 8 August 2000 as a consequence of ischaemic cardiomyopathy (previous extended anterior myocardial infarction). Transplantation and the post-operative course were uncomplicated and the patient was discharged on 31 August 2000 and prescribed a cyclosporin A, azathioprine and corticosteroid therapy (cyclosporin blood levels were expected to be 400 ng dl 21 ). Ten days later, the patient showed an acute organ rejection documented by endomyocardial biopsy (Grade 2, Dallas Classification, with diffuse and aggressive infiltrate) and was treated with high doses of intravenous corticosteroid (500 mg methylprednisolone per day for 3 days). Following this therapy, the rejection successfully reversed (Grade 1A at 1 month after treatment).Twelve days after corticosteroid treatment, the patient was readmitted with fever, neck pain, oesophageal discomfort during deglutition and a cough. At that time, the white blood cell count was 0?56 cells ml 21 with 80 % neutrophils, 15 % lymphocytes and a CD4/CD8 ratio of 0?4, thus showing intense immunosuppression. Fever quickly rose to 38?3 u C. Several blood and sputum cultures were negative for aerobic and anaerobic bacteria and for fungal cells. Before and after the transplant, the patient had been monitored for cytomegalovirus by the pp65 antigenaemia test, whose results were constantly negative. At the time of readmission, a further test for cytomegalovirus pp65 antigenaemia was performed and the result again was negative. A chest radiograph showed interstitial inflammation of the inferior left pulmonary lobe. After a few days, pleural effusion developed, as evidenced by physical examination. Computerized axial tomography examination confirmed pulmonary inflammation and pleural effusion, but excluded mediastine involvement. Initially, the patient was treated empirically with meropenem (500 mg three times per day), clarithromycin (500 mg per day), ciprofloxacin (200 mg twice a day) and fluconazole (150 mg per day), all intravenously, and oral trimethoprim/sulfamethoxazole (800 mg per day). This therapy did not lower the fever, nor did it attenuate the other symptoms. After 5 days, a selective bronchoalveolar washing was performed and the aspirate was examined. Direct Gram staining showed the presence of Gram-positive bacilli, whilst observation for Pneumocystis jiroveci (Pneumocystis carinii) after Giemsa and toluidine blue O staining yielded negative results. The aspirate was not checked for the presence of cytomegalovirus, but was cultured for aerobic and anaerobic bacteria, as well as for fungi. Culture on blood agar and ...
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