RESUMEN
The prevalence of chronic kidney disease (CKD) continues to rise globally, paralleled by an increase in associated morbidity and mortality, as well as significant implications for patient quality of life and national economies. Chronic kidney disease often progresses unrecognized by patients and physicians, despite diagnosis relying on two simple laboratory measures: estimated glomerular filtration rate (eGFR) and urine analysis. GFR measurement has been grounded in renal physiology, specifically the concept of clearance, with creatinine identified as a suitable endogenous marker for estimating creatinine clearance (CrCl). On this foundation, various equations have been developed to calculate CrCl or estimated GFR (eGFR) using four variables that incorporate creatinine and certain demographic information, such as sex and age. However, creatinine measurement requires standardization to minimize assay variability across laboratories. Moreover, the accuracy of these equations remains contentious in certain patient subgroups. For these reasons, additional mathematical models have been devised to enhance CrCl estimation, for example, when urine collection is impractical, in elderly or debilitated patients, and in individuals with trauma, diabetes, or obesity. Presently, eGFR in adults can be immediately measured and reported using creatinine-based equations traceable through isotope dilution mass spectrometry. In conclusion, leveraging insights from renal physiology, eGFR can be employed clinically for early diagnosis and treatment of CKD, as well as a public health tool to estimate its prevalence.
Asunto(s)
Creatinina , Tasa de Filtración Glomerular , Insuficiencia Renal Crónica , Humanos , Creatinina/orina , Creatinina/sangre , Insuficiencia Renal Crónica/diagnóstico , Insuficiencia Renal Crónica/fisiopatología , Reproducibilidad de los Resultados , Biomarcadores/orina , AdultoRESUMEN
47-year-old woman suffering from minimal lesion glomerulonephritis previously undergone high-dose steroid therapy and subjected to exacerbations of nephrotic syndrome after therapy discontinuation. It was decided to initiate off-label treatment with Rituximab at a dosage of 375 mg/m2 administred at zero-time, one-month and three months with good therapeutic response and resolution of the clinical laboratory picture. The therapy was well tolerated and had no side effects. This scheme could be an alternative to the conventional therapeutic scheme with steroids or other classes of immunosuppressive drugs, especially in order to avoid problems related to prolonged exposure to steroid therapy.
Asunto(s)
Nefrosis Lipoidea , Síndrome Nefrótico , Femenino , Humanos , Rituximab/efectos adversos , Síndrome Nefrótico/complicaciones , Síndrome Nefrótico/tratamiento farmacológico , Nefrosis Lipoidea/complicaciones , Nefrosis Lipoidea/tratamiento farmacológico , Anticuerpos Monoclonales de Origen Murino/uso terapéutico , Inmunosupresores/efectos adversos , Esteroides , Recurrencia , Resultado del TratamientoRESUMEN
Hepatitis E virus (HEV) is a significant public health problem that affects almost 20 million individuals annually and cause acute liver injury in 3,5 million. Hepatitis E virus can cause acute, fulminant and chronic hepatitis and has been associated with a range of extrahepatic manifestation. The spectrum of these manifestation is still emerging. Acute pancreatitis and neurological, renal, hematologic, and muscoloskeletal manifestations have been described. Renal injury include membranoproliferative glomerulonephritis with or without cryoglobulinemia, membranous glomerulonephritis and tubular necrosis. The etiopathogenesis of extrahepatic manifestation is only supposed. It could be caused by a direct tossic effect of HEV or by an autoimmune process. We report a case of a 46 years old man who presented with acute hepatitis E. He was diagnosed to have acute severe renal failure and severe pancreatitis due to hepatitis E. Few cases have been reported in the literature concerning patients suffering from hepatitis E and severe extraepatic manifestations with a benign course and complete recovery.
Asunto(s)
Lesión Renal Aguda/etiología , Hepatitis E/complicaciones , Pancreatitis Aguda Necrotizante/etiología , Lesión Renal Aguda/terapia , Comorbilidad , Tratamiento Conservador , Hepatitis E/diagnóstico , Humanos , Masculino , Persona de Mediana Edad , Isquemia Miocárdica/complicaciones , Isquemia Miocárdica/cirugía , Complicaciones Posoperatorias , Diálisis RenalRESUMEN
Glucocorticoid-induced osteoporosis (GIO) is a major cause of secondary osteoporosis that starts early after the beginning of therapy even for low drug doses. Glucocorticoids are used for the treatment of immunologic nephropathies and in the setting of kidney transplant. In clinical practice, a number of algorithms are available; they allow us to estimate the long-term risk of major osteoporotic fracture; but none of them is specific for GIO. To date, the therapeutic approach comprises both general measures aimed at correcting calcium and vitamin D intake, and drugs (bisphosphonates, teriparatide, hormone replacement therapy, denosumab) that ameliorate bone mineral density and patient outcomes.