RESUMO
Antiphospholipid syndrome (APS) is a rare autoimmune disease characterized by recurrent arterial and venous thromboembolic events. Renal complications occur in 3â % of patients. Renal artery stenosis is the most common, and APS-related nephropathy is the predominant microvascular complication. APS nephropathy has heterogeneous manifestations ranging from hematuria and non-nephrotic range proteinuria to hypertension and multi-organ failure caused by catastrophic antiphospholipid antibody syndrome. Anticoagulation and thromboprophylaxis are key to management. Immunosuppression has been used with some success but lacks randomized controlled trial validation for their use.
Le syndrome des anticorps antiphospholipides (SAPL) est une maladie auto-immune rare caractérisée par des événements thromboemboliques artériels et veineux récurrents. Les complications rénales surviennent chez 3â % des patients. La sténose de l'artère rénale est la plus courante et la néphropathie liée au SAPL représente la complication microvasculaire principale. La maladie rénale liée au SAPL se traduit par des manifestations hétérogènes allant de l'hématurie et de la protéinurie non néphrotique à l'hypertension jusqu'à la défaillance multi-organique causée par le syndrome catastrophique des anticorps antiphospholipides (SCAPL). L'anticoagulation et la thromboprophylaxie sont clés dans la prise en charge. L'immunosuppression a été utilisée avec un certain succès, mais manque de validation par des essais contrôlés randomisés pour leur utilisation.
Assuntos
Síndrome Antifosfolipídica , Doenças Autoimunes , Obstrução da Artéria Renal , Tromboembolia Venosa , Humanos , Anticoagulantes/uso terapêutico , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/diagnóstico , Síndrome Antifosfolipídica/terapia , Doenças RarasRESUMO
Systemic sclerosis is a rare autoimmune vasculopathy associated with dysregulated innate and adaptive immunity that leads to generalized systemic fibrosis. Renal involvement occurs in a significant proportion of systemic sclerosis patients, and is associated with worse outcome. Scleroderma renal crisis (SRC) is the most studied and feared renal complication described in systemic sclerosis. However, with the emergence of ACE inhibitors and better management, the mortality rate of SRC has significantly decreased. Renal disease in systemic sclerosis offers a wide array of differential diagnoses that may be challenging for the clinician. The spectrum of renal manifestations in systemic sclerosis ranges from an isolated decrease in glomerular filtration rate, increased intrarenal arterial stiffness, and isolated proteinuria due to SRC to more rare manifestations such as association with antiphospholipid antibody nephropathy and ANCA-associated vasculitis. The changes observed in the kidneys in systemic sclerosis are thought to be due to a complex interplay of various factors, including renal vasculopathy, as well as the involvement of the complement system, vasoactive mediators such as endothelin-1, autoimmunity, prothrombotic and profibrotic cytokines, among others. This literature review aims to provide an overview of the main renal manifestations in systemic sclerosis by discussing the most recent epidemiological and pathophysiological data available and the challenges for clinicians in making a diagnosis of renal disease in patients with systemic sclerosis.
Assuntos
Injúria Renal Aguda , Esclerodermia Localizada , Escleroderma Sistêmico , Humanos , Rim , Escleroderma Sistêmico/diagnóstico , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/etiologia , Inibidores da Enzima Conversora de Angiotensina , Esclerodermia Localizada/complicaçõesRESUMO
BACKGROUND: Mycoplasma salivarium is part of our commensal oral flora and readily resides in dental plaque. Although considered indolent, few case reports have documented its pathogenic potential in humans. To this day no case of Mycoplasma salivarium infectious endocarditis has ever been described. CASE PRESENTATION: Our report describes a challenging case of Mycoplasma salivarium endocarditis, with a patient presenting with oligoarticular joint swelling, and later on in the course of his disease developed signs of right-sided heart failure. The diagnosis was initially mistaken for septic gonarthritis and was later established on the basis of echocardiography and eubacterial PCR of joint fluid. CONCLUSION: This report describes a first documented case of Mycoplasma salivarium culture negative endocarditis that was successfully treated with targeted antimicrobial therapy. Specific antimicrobial therapy targeting Mycoplasma spp, lead to clinical improvement, with radiological regression of the lesion and the resolution of the serum inflammation biomarkers.
Assuntos
Endocardite , Infecções por Mycoplasma , Mycoplasma salivarium , Humanos , Valva Mitral/patologia , Infecções por Mycoplasma/microbiologia , Boca/microbiologiaAssuntos
Doenças Renais Císticas , Nefropatias , Doenças Renais Policísticas , Sistema Urinário , HumanosRESUMO
Malignancy-related hypercalcemia is a leading cause of hypercalcemia among hospitalized patients that carries poor prognosis. Parathyroid carcinoma is a rare form of primary hyperparathyroidism that may be associated with PTH dependent hypercalcemia. Severe hypercalcemia is life-threatening and may require management in an intensive care unit by means of medical therapy consisting of volume expansion, loop diuretics, cinacalcet, calcitonin and bisphosphonates. Renal replacement therapy such as intermittent hemodialysis has been successfully used among patients with severe hypercalcemia who become refractory to medical treatment. However, little data are available for cases of severe refractory hypercalcemia that fail to respond to both optimal medical therapy and hemodialysis. Our present case illustrates the successful use of continuous veno-venous hemodiafiltration (CVVHDF) with calcium-free dialysate calcium and markedly increased dialysate flow rate, to restore normal calcemia in a patient with metastatic parathyroid carcinoma with severe refractory hypercalcemia.
Assuntos
Terapia de Substituição Renal Contínua , Hipercalcemia , Neoplasias das Paratireoides , Cálcio , Soluções para Diálise , Humanos , Hipercalcemia/complicações , Hipercalcemia/terapia , Hormônio Paratireóideo , Neoplasias das Paratireoides/complicações , Diálise Renal/efeitos adversosRESUMO
Antiphospholipid antibody syndrome (APLS) is a rare autoimmune disease characterized by recurrent arterial and venous thromboembolic events, pregnancy related complications as well as the persistent detection of antiphospholipid antibodies at a 12 week interval. Renal complications tend to occur in 3% of APLS patients, with renal artery stenosis being the most common kidney related complication. Renal pathology may be subdivided into macro as well as microvascular thrombotic complications with stenosis, thrombosis and infarction representing the principle macrovascular events and APLS nephropathy representing the predominant microvascular complication. APLS related kidney disease may present with an array of heterogenous manifestations ranging from hematuria and non-nephrotic range proteinuria to hypertension or as part of a severe, life threatening and fulminant multiorgan failure disorder known as catastrophic antiphospholipid antibody syndrome (CAPS). Management of APLS related renal complications depends on the site of vascular injury, the thromboembolic risk profile based on the subtype, isotype and titer of the autoantibodies as well as the severity of the injury. Primary prophylaxis in these patients primarily revolves around the use of low dose aspirin, with prophylactic anticoagulation during events that increase thromboembolic like surgery and hospitalization. Anticoagulation is the cornerstone of treatment of APLS related kidney disease with INR targets varying depending on the associated venous or arterial thrombosis. Immunosuppression with the likes of rituximab, mTOR inhibitors, eculizumab and belimumab have been used with some success, but lack randomized control trial validation for their use. Pulsed corticosteroids with Plasmapheresis and intravenous immunoglobulins is the recommended treatment for CAPS.
Assuntos
Síndrome Antifosfolipídica , Nefropatias , Trombose , Anticoagulantes/uso terapêutico , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/diagnóstico , Síndrome Antifosfolipídica/terapia , Feminino , Humanos , Nefropatias/tratamento farmacológico , Masculino , Gravidez , Fatores de Risco , Trombose/tratamento farmacológico , Trombose/terapiaRESUMO
SGLT2 inhibitors (SGLT2i) will change the clinical practice of nephrology with their therapeutic cardiorenal and antidiabetic properties. By inhibiting proximal tubular sodium and glucose reabsorption, these new drugs decrease intraglomerular pressures. Over the last 5 years several breakthrough studies have demonstrated the SGLT2i protective effects on outcomes such as cardiovascular mortality, hospital admission for heart failure, sustained decreases in eGFR in patients with diabetic nephropathy and the development of ESKD. With the new DAPA-CKD study revealing protective effects of SGLT2i in CKD patients without diabetes, therapeutic recommendations will now have to evolve towards including these drugs in the chronic management of all most proteinuric CKD patients.
Les inhibiteurs du cotransporteur du sodium-glucose de type 2 (iSGLT2) révolutionnent la pratique clinique en néphrologie par le biais de leurs effets antidiabétique, cardio et néphroprotecteur. Ces molécules inhibent la réabsorption du glucose et du sodium au niveau du tubule proximal, ce qui résulte en une baisse de la pression intraglomérulaire. Plusieurs grandes études ont démontré l'effet protecteur des iSGLT2 sur la mortalité cardiovasculaire, le taux d'hospitalisation pour une insuffisance cardiaque et le ralentissement de la progression de la néphropathie diabétique. La sortie de DAPA-CKD va certainement modifier les recommandations thérapeutiques pour la prise en charge de l'insuffisance rénale chronique (IRC) non diabétique, en démontrant un effet néphroprotecteur majeur chez les IRC protéinuriques d'origine non diabétique également.
Assuntos
Diabetes Mellitus Tipo 2 , Nefropatias Diabéticas , Inibidores do Transportador 2 de Sódio-Glicose , Nefropatias Diabéticas/tratamento farmacológico , Humanos , Hipoglicemiantes/uso terapêutico , Transportador 2 de Glucose-Sódio , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêuticoRESUMO
Cardiac arrest (CA) is a frequent cause of death and a major public health issue. To date, conventional cardiopulmonary resuscitation (CPR) is the only efficient method of resuscitation available that positively impacts prognosis. Extracorporeal membrane oxygenation (ECMO) is a complex and costly technique that requires technical expertise. It is not considered standard of care in all hospitals and should be applied only in high-volume facilities. ECMO combined with CPR is known as ECPR (extracorporeal cardiopulmonary resuscitation) and permits hemodynamic and respiratory stabilization of patients with CA refractory to conventional CPR. This technique allows the parallel treatment of the underlying etiology of CA while maintaining organ perfusion. However, current evidence does not support the routine use of ECPR in all patients with refractory CA. Therefore, an appropriate selection of patients who may benefit from this procedure is key. Reducing the duration of low blood flow by means of performing high-quality CPR and promoting access to ECPR, may improve the survival rate of the patients presenting with refractory CA. Indeed, patients who benefit from ECPR seem to carry better neurological outcomes. The aim of this present narrative review is to present the most recent literature available on ECPR and to clarify its potential therapeutic role, as well as to provide an in-depth explanation of equipment and its set up, the patient selection process, and the patient management post-ECPR.
RESUMO
Stress hyperglycemia is a transient increase in blood glucose during acute physiological stress in the absence of glucose homeostasis dysfunction. Its's presence has been described in critically ill patients who are subject to many physiological insults. In this regard, hyperglycemia and impaired glucose tolerance are also frequent in patients who are admitted to the intensive care unit for heart failure and cardiogenic shock. The hyperglycemia observed at the beginning of these cardiac disorders appears to be related to a variety of stress mechanisms. The release of major stress and steroid hormones, catecholamine overload, and glucagon all participate in generating a state of insulin resistance with increased hepatic glucose output and glycogen breakdown. In fact, the observed pathophysiological response, which appears to regulate a stress situation, is harmful because it induces mitochondrial impairment, oxidative stress-related injury to cells, endothelial damage, and dysfunction of several cellular channels. Paradigms are now being challenged by growing evidence of a phenomenon called glucotoxicity, providing an explanation for the benefits of lowering glucose levels with insulin therapy in these patients. In the present review, the authors present the data published on cardiac glucotoxicity and discuss the benefits of lowering plasma glucose to improve heart function and to positively affect the course of critical illness.