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Fourteen patients with uraemic anaemia and having regular haemodialysis were given human recombinant erythropoietin in increasing doses, beginning with 24 U/kg thrice weekly. One patient was dropped from the study because of recurrent thrombosis of vascular access sites. In the other 13 patients, followed up for a mean of 9-1 months (range 8-11), haemoglobin concentrations increased from 62 (SD 8) to 105 (9) g/l. No antierythropoietin antibodies were detected during the study. The correction of anaemia was associated with a tendency to hyperkalaemia and a mild increase of unconjugated bilirubinaemia. In eight previously hypertensive patients antihypertensive treatment had to be reinforced, but in normotensive patients blood pressure did not change. Thrombosis of arteriovenous fistulas occurred in two patients and a cerebral ischaemic lesion in one.Protracted treatment with human recombinant erythropoietin evidently can maintain normal haemoglobin concentrations in uraemic patients over time. Full correction ofanaemia, however, may trigger some vascular problems, particularly in hypertensive patients and those with a tendency to thromboembolism.

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SummaryLow plasma levels of antithrombin III due to excessive urinary loss are thought to be the cause of thrombotic complications in patients with the nephrotic syndrome. To see whether protein C (PC), another antithrombotic protein, is also reduced in plasma by the same mechanism, plasma and urinary protein C were determined in 24 patients with nephrotic syndrome and no thrombotic complication, and compared to plasma and urinary antithrombin III. Twenty patients (83%) had high plasma levels of protein C activity (mean ± SD 157 ± 41 U/dl) and antigen (158 ± 41). Even though measurable amounts of PC antigen were found in the urines of all but two patients the urinary loss of protein C relative to its plasma concentration was about 40 times lower than that of antithrombin III. High protein C might help to counteract hypercoagulability in nephrotic syndrome.

Purpose To analyze the quantitative and qualitative early changes of choroidal neovascularization (CNV) associated with chronic central serous chorioretinopathy (CSC) after treatment using optical coherence tomography-angiography (OCT-A). Methods Charts of consecutive patients with diagnosis of chronic CSC complicated by CNV were retrospectively reviewed. Included patients were divided in photodynamic therapy (PDT) or aflibercept group on the basis of the treatment received (half-fluence PDT or aflibercept 2.0 mg/0.05 ml intravitreal injection). Main outcome measures included the changes between baseline and 1-month follow-up in CNV vessel density (VD) and area on OCT-A images after thresholding and binarization. Results A total of 30 eyes of 26 Caucasian patients were included: 17 eyes of 15 patients in PDT group (mean age 53 ± 11 years) and 13 eyes of 11 patients in aflibercept group (mean age 58 ± 8 years [p = 0.196]). In both PDT and aflibercept groups, best-corrected visual acuity improved at 1 month, and central macular thickness and subretinal fluid significantly decreased. VD did not change after the treatment in both groups (p = 0.502 and p = 0.086) although CNV area decreased significantly (from 0.586 ± 0.449 mm 2 to 0.553 ± 0.453 mm 2 [0.041]) in the PDT group, and nonsignificantly (from 0.767 ± 0.466 mm 2 to 0.733 ± 0.472 mm 2 [p = 0.095]) in the aflibercept group. The same results were confirmed in the subanalysis of the 18 treatment-naïve eyes. Conclusions We demonstrated that, despite all patients showed a favorable clinical response, VD of CNVs complicating chronic CSC did not change after treatment. These findings support the idea that arteriogenesis is the main driving force of CNV in pachychoroid-related macular disorders.

Patients affected by advanced POAG damage have a thinner choroidal thickness compared with normal subjects, using SD-OCT. We also confirmed that age and axial length were the main factors affecting choroidal thickness in these patients.

Into 24 oliguric patients with acute renal failure (ARF) for whom mannitol and high-dose frusemide had failed to promote a diuresis, dopamine (3 μg/kg/min) plus frusemide (10–15 mg/kg/h) were infused for 6–24 h. In 19 of the 24 patients this treatment produced significant increases in diuresis (from 11 ± 7 to 85 ± 51 ml/h; p < 0.001) and natriuresis (from 45 ± 13 to 88 ± 22 mEq/l; p < 0.001), without any significant modification of blood pressure, pulse rate or central venous pressure. 10 of the 24 patients required dialysis: 5 because therapy failed to promote diuresis and the other 5 because of their hypercatabolic state in spite of polyuria. 5 patients died of causes unrelated to ARF. Since all patients who responded were treated within 24 h after the onset of oliguria, it appears to be crucial to administer dopamine and frusemide early, before more severe anatomical and functional damage develops.