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INTRODUCTION: Expanded hemodialysis (HDx), being based on medium cut-off (MCO) membranes, improves the removal of medium molecule uremic toxins. HDx efficacy has been proven with blood flow rates (Qb) of 350-400 ml/min, while low Qb have only been assessed in single sessions. We evaluated the effectiveness of HDx in patients with tunneled central venous catheters (CVCs) and low Qb over six months, comparing it with high-flux hemodialysis (HF-HD). METHODS: The study included 10 patients with a mean age of 79±12 years and mean Qb of 237 ± 12 ml/min. Reduction ratios (RRs) and predialysis serum levels were measured for ß2-microglobulin (B2M), free κ and λ light chains (FLC), prolactin (PRL), interleukin-6 (IL-6), albumin, and urea after HF-HD and at one, three, and six months of HDx. Erythropoiesis-stimulating agent (ESA) resistance index (ERI) was also evaluated. RESULTS: B2M, κ-FLC, λ-FLC, and PRL RRs were significantly higher with HDx. IL-6, albumin, and urea RRs did not show a statistical difference between the two treatments. Predialysis B2M concentrations were significantly lower after three and six months of HDx, matching up to increased B2M clearance (spKt/V). A decrease in albumin concentrations was observed, with median levels significantly reduced at months seven and eight (35.3 and 35.5 g/L, respectively) but recovering afterwards. ERI was significantly lower during HDx, reaching a 30% reduction at month six. CONCLUSIONS: HDx was feasible, safe, and superior to HF-HD in patients with low Qb rates of tunneled dialysis catheters. The present data expand options for HDx prescription, with particular regard for patients who cannot achieve high convective volumes due to inadequate vascular access.
RESUMO
This case report can be considered a rare occurrence of scleroderma renal crisis (SRC) presenting with a severe clinical course and multiple organ failure. A patient diagnosed with systemic sclerosis four years earlier was admitted to the hospital because of severe malignant systolic-diastolic arterial hypertension and acute kidney injury (AKI). Exacerbating disease suggested thrombotic microangiopathy (TMA) and the PLASMIC (Platelet count; combined hemoLysis variable; absence of Active cancer; absence of Stem-cell or solid-organ transplant; MCV; INR; Creatinine) score was used in the differential diagnosis. Despite the timely initiation of therapy with ACE inhibitors (ACE-I), the progressive renal failure required hemodialysis treatment, but renal function never recovered. Disease duration, skin involvement, and previous specific pharmacological therapy represented multiple risk factors that determined a clinical course complicated by pericardial tamponade with acute heart failure, acute pancreatitis, and ischemic stroke, with fatal evolution. These complications presented a challenging clinical sequence of events requiring an interdisciplinary course of action. Timely ascertainment of the SRC is important given the possible severe organ involvement as well as mortality. A diagnosis of scleroderma renal crisis should be considered in cases of acute kidney injury associated with known risk factors. Early treatment and collaboration between rheumatology and renal physicians can improve patient outcomes.