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Leal Moreira, Carla

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  • Does Cystatin C have a role as metabolic surrogate in peritoneal dialysis beyond its association with residual renal function?
    Publication . Leal Moreira, Carla; Cunha, Liliana; Correia, Sofia; Silva, Filipa; Castro, Ana; Tavares, Joana Manuel; Carvalho, Maria João; Oliveira, José Carlos; Santos, Maria Olivia; Cabrita, Antonio; Rodrigues, Anabela
    Introduction: It has been suggested that cystatin C levels are modified by obesity and inflammation. Furthermore, cystatin C has been associated with cardiovascular events and mortality outcomes. Aim: To study the association of cystatin C with the metabolic profile and cardiovascular disease of peritoneal dialysis patients. Methods: Data collected included clinical, laboratorial, and multifrequency bioimpedance assessment of 52 stable peritoneal dialysis patients. Minimal residual renal function was defined as > 2mL/min/1.73m2. Results: Serum cystatin C was not significantly associated with peritoneal or urinary cystatin C excretion. Negative correlation of cystatin C with normalized protein catabolic rate (rho -0.33, p = 0.02) and a trend towards positive correlation with relative body fat (rho 0.27, p = 0.05) were not independent from residual renal function. Cystatin C was not significantly associated with cardiovascular disease (p = 0.28), nor with glycated hemoglobin (p = 0.19) or c-reactive protein (p = 0.56). In the multivariate model, both age and diabetes were the strongest predictors of cardiovascular disease (odds ratio 1.09, p = 0.029 and odds ratio 29.95, p = 0.016, respectively), while relative body fat was negatively associated with cardiovascular disease (p = 0.038); neither cystatin C (p = 0.096) nor minimal residual renal function (p = 0.756) reached a significant association with cardiovascular disease. Conclusions: In this group of peritoneal dialysis patients, cystatin C did not correlate with the metabolic or inflammatory status, nor cardiovascular disease, after adjustment for residual renal function.
  • Nephrotic Syndrome as a Cause of Transient Clinical Hypothyroidism
    Publication . Benido Silva, Vânia; Pereira, Maria Teresa; Leal Moreira, Carla; Santos Monteiro, Sílvia; Inácio, Isabel; Cardoso, Helena
    Nephrotic syndrome may trigger the onset of hypothyroidism, promoting massive urinary protein losses including thyroxine (T4) and triiodothyronine (T3) along with their binding proteins. At an early stage, a clinical and biochemical euthyroid state is expected. However, in patients with prolonged and severe proteinuria, especially with concomitant low thyroid reserve, urinary losses of free and protein-bound thyroid hormones are sufficiently pronounced to induce a subclinical or overt hypothyroidism. Despite its high prevalence in clinical practice, the literature lacks case reports of newly diagnosed clinical hypothyroidism due to NS in adults, making this condition under-recognized. We report a case of a 23-year-old man with previous normal thyroid function who developed overt hypothyroidism due to a severe nephrotic syndrome, requiring supplementation with levothyroxine (LT). After the patient had undergone bilateral nephrectomy, treatment with LT was discontinued and thyroid function normalized.