Chylous ascites is the accumulation of lipid-rich lymph in the peritoneal cavity. The usual cause in adults is lymphatic obstruction or leakage caused by malignancy. Non-malignant causes include postoperative trauma, cirrhosis, tuberculosis, pancreatitis and filariasis. A variety of treatment options have been proposed for the management of chylous ascites; however, their effectiveness in idiopathic or primary form is unknown. Here we report a case of chylous acid rapidly resolved with the treatment of fasting, total parenteral nutrition and somatostatin analogue.

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Various risk scores such as COVID‐GRAM Critical Illness Risk Score (COVID‐GRAM), quick COVID‐19 Severity Index (qCSI), and systemic immune‐inflammation index (SII) have been developed to determine critical illness in hospitalized patients. None of these risk scoring systems was evaluated in HD patients who indeed carry the highest risk of developing critical illnesses. We aimed to evaluate, in hemodialysis (HD) patients with COVID‐19, the performance of these scoring systems for the need of intensive care unit (ICU) and mortality. The qCSI, COVID‐GRAM, and SII scores of the patients at admission to hospital were calculated and grouped according to the scoring results. The primary outcome of the study was mortality and need of ICU. Critical illness was described as a composition of admission to the ICU, invasive ventilation, or death. It was determined that when the qCSI is over 6.5, the need for ICU increased 13.8 times and mortality increased 21.3 times. When the COVID‐GRAM score is >157, the ICU need increased 14.7 times and the mortality increased 33.7 times. We found that the need for ICU increased 4.2 times and mortality increased 3.1 times when the SII score was >1145. These tests, which can be easily calculated, could be used to estimate the risk of developing critical illness among COVID‐19 HD patients. Estimating the risk of critical illness could help to reduce mortality in HD patients.

These data suggest that AVS is strongly and independently interrelated with LVH in chronic haemodialysis patients. The underlying mechanism might be the valve resistance to left ventricular outflow, as shown by increased transaortic flow velocities and maximal pressure gradients in AVS patients.

Atherosclerosis-induced premature vascular diseases are the leading cause of mortality among patients with chronic kidney disease (CKD). The pathogenetic mechanism of atherosclerosis in patients with CKD has not been fully explained. Experimental studies have demonstrated that high dietary sodium intake not only increases circulatory volume and blood pressure, but also facilitates development of atherosclerosis by reducing production-bioavailability of nitric oxide due to oxidative stress and accordingly by enhancing endothelial and arterial stiffness. In this study, we investigated the relationship between sodium consumption and carotid artery intima-media thickness, which is the indicator of atherosclerosis, by determining daily urinary sodium excretion, which is a reliable indicator of sodium consumption, in our patient group. Our patient group included 193 patients with stage 2-4 non-diabetic CKD and without a history of atherosclerotic disease. We determined that 77% of our patients have been consuming more than 2  g of sodium per day, which is the upper limit of sodium consumption recommended for patients with CKD. We determined a positive linear correlation between carotid artery intima-media thickness and patient age (p < 0.001), C-reactive protein (p < 0.001), urinary sodium excretion (p < 0.001), body mass index (p = 0.002), systolic blood pressure (p = 0.002), hemoglobin (p = 0.030), triglycerides (p = 0.043), and diastolic blood pressure (p = 0.049). We also found a negative linear correlation between carotid artery intima-media thickness and glomerular filtration rate (p = 0.008). We found that urinary sodium excretion is the determinant of intima-media thickness even if all factors associated with intima-media thickness are adjusted, and that intima-media thickness increases by 0.031 (0.004-0.059) mm per 2  g increase in daily sodium excretion, independent from overall factors (p = 0.025). Our results reveal a relation between urinary sodium excretion and carotid artery intima-media thickness and suggest that excessive sodium consumption predisposes development of atherosclerosis in patients with CKD.