Infection of the residual pleural space fifty-nine years after artificial pneumothorax for pulmonary tuberculosis

A 79-year old man with serious comorbidities developed empyema of the residual pleural space that was the sequelae of collapse therapy with artificial pneumothorax performed 59 years ago for pulmonary tuberculosis. Drainage of the infected pleural space through open-window thoracostomy resulted in reversal of systemic toxicity and full recovery

RAAS Blockade as First-Line Antihypertensive Therapy among People with CKD

Hypertension among people with chronic kidney disease is highly prevalent and remains often poorly controlled. To adequately control blood pressure (BP), a combination antihypertensive drug therapy is often required. The choice of the appropriate antihypertensive regimen should be individualized according to the patient clinical characteristics, the severity of chronic kidney disease (CKD), the levels at which BP should be targeted and the presence or absence of proteinuria. In proteinuric CKD, solid evidence from large-scaled randomized trials suggest that agents blocking the renin-angiotensin-aldosterone system (RAAS) should be the antihypertensive therapy of first choice, given their superiority over the other antihypertensive drug classes in reducing proteinuria and delaying nephropathy progression to end-stage-renal-disease (ESRD). In contrast, inhibition of the RAAS is shown to have no additional benefits towards renoprotection in people with non-proteinuric CKD. Combined RAAS blockade as an alternative approach to gain additive reduction in proteinuria and greater retardation of renal function decline is shown to be associated with increased risk of hypotension, serious hyperkalemia and acute kidney injury. In this chapter, we discuss the role of RAAS blockade as first-line antihypertensive therapy among people with proteinuric and non-proteinuric nephropathy, providing an overview of the evidence derived from large-scaled renal outcome trials

The road not so travelled : Should measurement of vitamin D epimers during pregnancy affect our clinical decisions?

Observational studies suggest an adverse effect of maternal hypovitaminosis D during pregnancy. However, intervention studies failed to show convincing benefit from vitamin D supplementation during pregnancy. With analytical advances, vitamin D can now be measured in ten forms—including as epimers—which were thought to be biologically inactive, but can critically impair immunoassays. The aim of this commentary is to highlight the potential clinical and analytical significance of vitamin D epimers in the interpretation of vitamin D roles in pregnancy. Epimers may contribute a considerable proportion of total vitamin D—especially in the neonate—which renders the majority of common assays questionable. Furthermore, epimers have been suggested to have activity in laboratory studies, and evidence suggests that the fetus contributes significantly to epimer production. Maternal epimer levels contribute significantly to predict neonate circulating 25-hydroxyvitamin D concentrations. In conclusion, the existence of various vitamin D forms (such as epimers) has been established, and their clinical significance remains obscure. These results underscore the need for accurate measurements to appraise vitamin D status, in order to understand the current gap between observational and supplementation studies on the field

Changes in kidney function in a population with essential hypertension in real life settings

Introduction. Hypertension has been identified as one of the commonest modifiable determinants for chronic kidney disease progression. A variety of antihypertensive drugs are available and their effect on kidney function has been investigated by a large number of randomized controlled trials. Observational studies, although scarcely been used, outpatient can reflect everyday practice, where drug exposures vary over time, and may provide an alternative for detecting longitudinal changes in kidney function. Materials and Methods. We applied mixed model repeated measures analysis to investigate the effect of antihypertensive drug categories and their combinations on kidney function change over time in a cohort of 779 patients with essential hypertension, using the data from a Greek hypertension outpatient clinic. Antihypertensive drugs were grouped in 5 categories. Their effect was evaluated and their combinations with and without renin-angiotensin-system inhibitors (RASI) to each other. In addition, the combination of RASI with calcium channel blockers (CCBs) was studied. Results. Diuretics, RASI, CCBs, and beta-blockers had a significant renoprotective and blood pressure lowering effect. Combinations with RASI had a smaller beneficial effect on kidney function compared to CCBs (0.75 mL/min/1.73 m2 per year of drug use versus 0.97 mL/min/1.73 m2). There was no additional effect when combining RASI with CCBs. However, the lowering effect on systolic blood pressure was greater (-0.83 mm Hg per year of drug use, P < .001). Conclusions. RASI were found to have a smaller, although significant, renoprotective effect. There was no additional effect on kidney function when combining RASI with CCBs

Characterizing neonatal vitamin D deficiency in the modern era : a maternal-neonatal birth cohort from Southern Europe

International audienc

THE EFECTS OF ENDOGENOUS INSULIN ON ELECTROLYTE BALANCE IN ESSENTIAL HYPERTENTION

THE AIM OF THE STUDY WAS TO DETERMINE WHETHER ESSENTIAL HYPERTENSIVE PATIENTS(HT) MANIFEST A DIFFERENT PATTERN OF BLOOD PRESSURE (BP) AND ELECTROLYTE RESPONSE TO ENDOYENOUS INSULIN AFTER OGTT.20 HT PATIENTS WITH MILD TO MODERATE HYPERTENSION (153.4+-2.9/ 98.4+-2.0MMHG, MISEM) AGED 48.2+-2.2 YS ,BMI 27.1+-0.7KG/M^2 AND 16 MATCHED NORMOTENSIVE (NT) (120.0+-2.2/81.2+-1.3MMHG ) UNDERWENT OGTT , AFTER 3 WKS OF MEDICATION AND STANDARD DIET (10MEQ NA, 40MEQ K ,800MG CA AND 150 GR CURBOHYDRATE PER DAYS )BASELINE (OMIN) AND AT 30,60,90 AND 120MIN THE PLASMA INSULIN , GLYCOSE , ELECTROLYTES (NA,K,CA,P) AND THE URINARY ELECTROLYTES WERE MEASURED. SUPINE BP WAS DECREASED SIGNIFICANTLY FROM BASELINE IN BOTH GROUPS .PLASMA GLYCOSE AND INSOULIN AVC WERE GREATER IN HT TH AN NT (17761+-446 VS 16506+-562 MG.MIN /DL AND 8583+-1187 VS 5140+-514MU.MIN/ML , PL0.05 RESPECTIVELY ).URINARY SODIUM EXCRETION WAS DECREASED (43.6+-7.5 FROM 67.8+-10.2) IN HT (P=0.003) AND 25.4+-2.8 FROM 41.0+-3.7MMOL/2H IN NT (P =0.0002).HT SHOWED A HIG HER THEN NT CULCIURESIS (P<0.0001)40.7+-6.2 VS 29.5+-2.9 MG /2H .IT IS CONCLUDED THAT INSULIN LED TO SODIUM RETENTION IN BOTH HT AND NT BUT TO AUGMENTED CALCIURESIS ONLY IN HT.ΓΙΑ ΝΑ ΜΕΛΕΤΗΣΟΥΜΕ ΤΗΝ ΕΠΙΔΡΑΣΗ ΤΗΣ ΕΝΔΟΓΕΝΟΥΣ ΙΝΣΟΥΛΙΝΗΣ ΣΤΗΝ ΑΡΤΗΡΙΑΚΗ ΠΙΕΣΗ ΚΑΙ ΤΟ ΙΣΟΖΥΓΙΟ ΤΩΝ ΗΛΕΚΤΡΟΛΥΤΩΝ ΤΟΥ ΕΝΔΟΚΥΤΤΑΡΙΟΥ ΚΑΙ ΕΞΩΚΥΤΤΑΡΙΟΥ ΧΩΡΟΥ ΠΡΑΓΜΑΤΟΠΟΙΗΣΑΜΕ ΔΟΚΙΜΑΣΙΑ ΑΝΟΧΗΣ ΓΛΥΚΟΖΗΣ ΣΕ 20 ΥΠΕΡΤΑΣΙΚΑ ΑΤΟΜΑ 48,2+-2,0(Μ+-ΣΕΜ) ΕΤΩΝ ΕΝΩ ΜΕ ΒΜΙ 27.0+-0.7ΚΓ/Μ^2 ΜΕ ΗΠΙΑ ΙΔΙΟΠΑΘΗ ΥΠΕΡΤΑΣΗ (153.4+-2,9/98,5+-2,0 ΜΜΗΓ ) ΚΑΙ ΣΕ 16 ΝΟΡΡΟΤΑΣΙΚΑ ΑΤΟΜΑ (120,0+-2,2/81,2+-1,3ΜΜΗΓ) ΑΝΑΛΟΓΗΣ ΗΛΙΚΙΑΣ ΚΑΙ ΦΥΛΛΟΥ ΜΕΤΑ ΑΠΟ ΣΤΑΘΕΡΗ ΚΑΙ ΕΛΕΓΧΟΜΕΝΗ ΔΙΑΙΤΑ .ΜΕΤΡΗΘΗΚΑΝ ΑΝΑΗΜΙΩΡΟ Η ΣΥΣΤΟΛΙΚΗ ΚΑΙ ΔΙΑΣΤΟΛΙΚΗ ΑΡΤ.ΠΙΕΣΗ , Η ΚΑΡΔ. ΣΥΧΝΟΤΗΤΑ Η ΓΛΥΚΟΖΗ ΚΑΙ Η ΙΝΣΟΥΛΙΝΗ ΤΟΥ ΟΡΟΥ ΟΙ ΗΛΕΚΤΡΟΛΥΤΕΣ (Ν2+,Κ+,ΨΑ++ ΚΑΙ ΜΓ++)ΣΤΟΝ ΟΡΟ ΚΑΙ ΣΤΑ ΟΥΡΑ .ΒΡΕΘΗΚΕ ΟΤΙ Η ΕΝΔΟΓΕΝΗΣ ΙΝΣΟΥΛΙΝΗ ΠΡΟΚΑΛΕΣΕ ~ΠΙΑ ΑΓΓΕΙΟΔΙΑΣΤΑΛΤΙΚΗ ΔΡΑΣΗ ΤΟΣΟ ΣΤΟΥΣ ΟΡΜΟΤΑΣΙΚΟΥΣ ΟΣΟ ΚΑΙ ΣΤΟΥΣ ΥΠΕΡΤΑΣΙΚΟΥΣ ΜΕΙΩΝΟΝΤΑΣ ΤΗΝ ΠΙ ΕΣΗ ΚΑΙ ΑΥΞΑΝΟΝΤΑΣ ΤΗ ΣΥΧΝΟΤΗΤΑ .ΕΛΑΤΤΩΣΗ ΤΟΥ ΚΑΛΙΟΥ ΤΟΥ ΟΡΟΥ ΧΩΡΙΣ ΜΕΤΑΒΟΛΕΣ ΤΟΥ ΝΑΤΡΙΟΥ ΚΑΙ ΑΣΒΕΣΤΙΟΥ .ΜΕΙΩΣΗ ΤΟΥ ΕΝΟΚΥΤΤΑΡΙΟΥ ΝΑΤΡΙΟΥ ΚΑΙ ΑΣΒΕΣΤΙΟΥ .ΜΕΙΩΣΗ ΣΗΜΑΝΤΙΚΗ ΤΗΣ ΝΑΤΡΙΟΥΡΗΣΗΣ ΚΑΙ ΚΑΛΙΟΥΡΗΣΗΣ .AΥΞΗΣΗ ΤΗΣ ΑΣΒΕΣΤΟΟΥΡΟΣΗΣ ΜΟΝΟ ΣΤΟΥΣ ΥΠΕΡΤΑΣΙΚΟΥΣ

The Role of MicroRNAs in Arterial Stiffness and Arterial Calcification. An Update and Review of the Literature

Arterial stiffness is an independent risk factor for fatal and non-fatal cardiovascular events, such as systolic hypertension, coronary artery disease, stroke, and heart failure. Moreover it reflects arterial aging which in many cases does not coincide with chronological aging, a fact that is in large attributed to genetic factors. In addition to genetic factors, microRNAs (miRNAs) seem to largely affect arterial aging either by advancing or by regressing arterial stiffness. MiRNAs are small RNA molecules, ~22 nucleotides long that can negatively control their target gene expression posttranscriptionally. Pathways that affect main components of stiffness such as fibrosis and calcification seem to be influenced by up or downregulation of specific miRNAs. Identification of this aberrant production of miRNAs can help identify epigenetic changes that can be therapeutic targets for prevention and treatment of vascular diseases. The present review summarizes the specific role of the so far discovered miRNAs that are involved in pathways of arterial stiffness