RESUMO
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.
Assuntos
Creatinina , Taxa de Filtração Glomerular , Insuficiência Renal Crônica , Humanos , Creatinina/urina , Creatinina/sangue , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/fisiopatologia , Reprodutibilidade dos Testes , Biomarcadores/urina , AdultoRESUMO
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.
Assuntos
Nefrose Lipoide , Síndrome Nefrótica , Feminino , Humanos , Rituximab/efeitos adversos , Síndrome Nefrótica/complicações , Síndrome Nefrótica/tratamento farmacológico , Nefrose Lipoide/complicações , Nefrose Lipoide/tratamento farmacológico , Anticorpos Monoclonais Murinos/uso terapêutico , Imunossupressores/efeitos adversos , Esteroides , Recidiva , Resultado do TratamentoRESUMO
BACKGROUND: Carnitine metabolism in patients on peritoneal dialysis (PD), particularly automated PD (APD), has not been extensively evaluated. Here, we examined levels of a large number of carnitine species in plasma from adult uremic patients treated with continuous ambulatory PD (CAPD) or APD, vetting whether L-carnitine may be used in the solution bag for APD therapy. METHODS: Plasma levels of carnitine and its esters were measured by high-performance liquid chromatography/tandem quadrupole mass spectrometry in 14 patients on CAPD (3 × 1.5 % glucose daily and icodextrin overnight), 16 patients on APD (tidal modality), and 8 age- and gender-matched healthy controls. PD groups did not differ with regard to demographic characteristics, renal function, dialysis features, peritoneal function, or biochemistry. In five APD patients, we also examined the safety and efficacy of L-carnitine (5 g) addition to one night-dwell solution bag over five consecutive days. RESULTS: Several abnormalities were found in plasma carnitine species of PD patients as compared to controls, mainly represented by a reduction of free carnitine and an increase in acetyl-carnitine, dicarboxylic and other carnitines. The main carnitine species (free carnitine, acetyl-carnitine) were significantly lower in plasma from APD than CAPD patients. APD patients tolerated L-carnitine supplementation well, laboratory, physical and dialysis parameters proving stable. CONCLUSIONS: Plasma carnitine metabolism is abnormal in patients on PD, and may be influenced by the PD modality. Given the good tolerability and potential advantages of carnitine used in the PD fluid, L-carnitine-containing solution bags in APD treatment definitely merit further evaluation.