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M Joannidis

Publications and source records attributed to M Joannidis.

At least 19 recordsLinked to original sources
PubMed2004

Drug-induced renal failure in the ICU.

Drug-induced renal failure is a frequent complication in the setting of ICU. Generally spoken pathomechanisms leading to drug-induced renal failure can be divided into hemodynamic effects, epithelial toxicity or crystalline nephropathy. The risk of drug-induced renal failure is increased by any form of hypovolemia (i.e. true hypovolemia or reduced effective circulating volume), older age, pre-existent renal impairment, and concomitant application of two or more nephrotoxins. This article reviews drugs most frequently responsible for renal failure in the ICU and discusses preventive measures.

Acute Kidney Injury↗
PubMed2003

The effect of marathon cycling on renal function.

The stress of strenuous long-term exercise may alter renal function. Whether this is also true for marathon cycling is unknown so far. The purpose of this study was to evaluate renal function following competitive marathon cycling. We investigated 38-male, well-trained recreational cyclists credibly not taking any kind of doping who participated in the Otztal Radmarathon. Blood and urine specimens were taken the day before, immediately after and one day after competition. Baseline renal functional parameters--normal before competition--increased significantly afterwards and remained elevated during 24 hours of recovery. The rises in serum creatinine, urea and uric acid were 20, 54 and 42 % (p < 0.001 respectively). The corresponding decline in estimated creatinine clearance was 18 %. In all athletes the serum urea/creatinine ratio rose above 40, fractional sodium excretion and fractional uric acid excretion fell below 0.4 % and 15 %, indicating reduced renal perfusion. The observed effects lasted for at least 24 h despite a stable fluid balance during the race and an expanding plasma volume (PV) in the recovery period. Levels of haematocrit remained unchanged immediately post-race but significantly declined from 0.44 to 0.41 on the following day (p < 0.001). The calculated rise in PV was + 10.8 %. Electrolyte homeostasis was preserved throughout the observation period. Post-exercise proteinuria was small and of the mixed glomerular-tubular type. There was neither evidence for exercise-induced haemolysis, nor for significant skeletal muscle damage. The finding obtained from well-hydrated recreational athletes reveals that the extraordinary strains of marathon cycling influence renal function only on a minimal scale. Though minor, the physiological effects were long-lasting. The results obtained suggest that a reduced renal perfusion is the mechanism responsible for the slight impairment of renal function following exhaustive marathon cycling.

Adult↗
PubMed2002

Antifactor Xa activity in intensive care patients receiving thromboembolic prophylaxis with standard doses of enoxaparin.

BACKGROUND: Low-molecular-weight heparins (LMWHs) have become increasingly used to prevent thromboembolic complications in intensive care patients. Unlike in medical and surgical patients, no data on the anticoagulant effectiveness of standard LMWH dosages exist in intensive care patients. Therefore, we prospectively investigated antifactor Xa (aFXa) levels after subcutaneous administration of 40 mg of enoxaparin in 89 intensive care patients over a 24-h period. METHODS: AFXa levels were measured before, 4, 12 and 24 h after subcutaneous administration of enoxaparin. Laboratory parameters including prothrombin time, activated partial thromboplastin time, antithrombin III, fibrinogen as well as platelet count were collected at same intervals. Demographics included age, sex, height, weight, body mass index, admission diagnosis, a thromboembolic risk score and a modified Goris multiple organ dysfunction score. RESULTS: At 4, 12 and 24 h, 56.5%, 39.3% and 12.6% of the study patients were within recommended antithrombotic aFXa levels (0.1-0.3 U ml(-1)). Presence of multiple organ dysfunction as well as high body weight were significantly correlated with low aFXa levels. CONCLUSION: European standard dosages of 40 mg of enoxaparin once daily proved to be ineffective in achieving recommended antithrombotic aFXa levels in intensive care patients. This was most pronounced in patients with high body weight and presence of multiple organ dysfunction.

Adult↗
PubMed2002

Pharmacokinetics of ciprofloxacin in patients with acute renal failure undergoing continuous venovenous haemofiltration: influence of concomitant liver cirrhosis.

To determine an adequate dosage of ciprofloxacin in critically ill medical patients on continuous venovenous haemofiltration, we studied the pharmacokinetics of ciprofloxacin in eight critically ill medical patients with renal failure treated with continuous venovenous haemofiltration using polysulfone membranes. Three of those patients also presented with severe liver dysfunction. For comparison, three patients with approximately normal renal function and two patients with impaired renal function were included. During haemofiltration, plasma concentrations of ciprofloxacin were variable. In all critically ill patients ciprofloxacin elimination was significantly slowed; the mean half-life was similarly prolonged to about 14 h in patients on haemofiltration and those with approximately normal renal function. In critically ill patients with impaired renal function not on haemofiltration, the mean half-life was longest. Ciprofloxacin clearance by haemofiltration was a quarter of the total clearance. Although a unique dose recommendation can hardly be made because of the high variability of pharmacokinetics during haemofiltration, a daily dose of 800 mg (400 mg b.i.d.) in average can be regarded as appropriated for reaching a target plasma concentration of 2 to 3 micrograms/mL (mean concentration). Because the half-life of ciprofloxacin was further prolonged by the presence of liver cirrhosis, the dose should be reduced to 600 mg in patients on haemofiltration with concomitant severe liver dysfunction.

Acute Kidney Injury↗
PubMed2002

Short-term effects of prolonged strenuous endurance exercise on the level of haematocrit in amateur cyclists.

Knowledge is sparse about the extent of potential dehydration due to prolonged strenuous cycling and its haematological acute effects on the haematocrit (Hct) in study populations credibly not taking any kind of doping. With increasing training load levels of Hct and haemoglobin (Hb) decrease in both amateurs and professionals as a long-term consequence due to expanded plasma volume (PV). On a short-term basis, however, counteracting dehydration potentially brought about by endurance exercise may cause a rise in Hct bringing competitive cyclists into conflict with the current condition regulations and Hct cut-off of 50 % set by the International Cycling Union (UCI) in its fight against erythropoietin (rhEPO) doping. On the other hand adequate and sufficient fluid substitution being substantial for a successful endurance performance should prevent any pronounced Hct rises. To study the haematological acute effects of prolonged strenuous cycling we measured Hct, Hb, red blood cell (RBC) count and plasma protein in a reliably 'clean' population of 38 well-trained male amateur cyclists before, immediately after and one day after an extraordinary ultramarathon. The pre-race levels of Hct, Hb and RBC count were placed in the lower range of normal distribution and well below the Hct cut-off limit of the UCI. Immediately post-exercise the mean levels of Hct, Hb, RBC count and protein remained unchanged. One day after race, however, all four parameters significantly dropped by 3 %, 6.7 %, 6.5 %, 9.9 % respectively (p < 0.001), indicating marked post-exercise PV expansion. The calculated percentage increase in PV was 11.9 %. No evidence for coexisting exercise-induced haemolysis was found. Our study shows that in "clean, rhEPO-free" amateur cyclists who involve in strenuous marathon cycling the haematological short-term effects of extraordinary marathon cycling consist in considerable PV expansion making Hct values fall on the following day. The findings - gained from amateurs though - suggest that despite all its disadvantages the UCI Hct cut-off represents an appropriate means to discourage from excessive rhEPO doping at least as long as the available direct methods for detecting this kind of misuse are not yet applied by the international sports federations.

Adult↗
PubMed2002

Elimination of levofloxacin in critically ill patients with renal failure: influence of continuous veno-venous hemofiltration.

OBJECTIVES: Pharmacokinetic data on levofloxacin in critically ill patients are sparse and conflicting. Aim of the study was to assess the clearance of levofloxacin in critically ill patients treated with continuous veno-venous hemofiltration (CVVH). METHODS: Pharmacokinetics of levofloxacin were studied in 11 critically ill patients. Four patients were treated with CVVH because of renal failure, 4 patients had moderately impaired renal function but were not on hemofiltration, and 3 patients had approximately normal renal function. Patients received 0.5 g levofloxacin infused over 0.5 hours. Plasma levels of levofloxacin were determined by HPLC and pharmacokinetic parameters were calculated using a non-compartmental model. RESULTS: Levofloxacin clearance in critically ill patients with approximately normal renal function was similar to that in healthy subjects. In critically ill patients with impaired renal function not on CVVH, mean half-life was prolonged by a factor of about 3 (20-25 hours). The mean residence time and the volume of distribution were also increased. In renal failure treated with CVVH, a wide variability in pharmacokinetics was seen. The half-life was about 30 hours and the mean levofloxacin clearance was raised by a factor of 2. The area under the concentration-time curve was reduced by hemofiltration, while the volume of distribution was increased. There was a positive correlation between blood flow through the hemofilter and levofloxacin clearance. Variable amounts of the drug were recovered from the hemofilter. Most plasma levels, however, were in the therapeutic range and drug accumulation to toxic plasma concentrations was not observed in renal failure patients undergoing CVVH and receiving single daily administration of 0.5 g of levofloxacin i.v. CONCLUSIONS: During CVVH using polysulfone membrane hemofilters, plasma concentrations of levofloxacin are not easily predictable. Levofloxacin clearance may be affected by binding to secondary membranes formed in hemofilters during CVVH and blood flow rates have a significant impact on the pharmacokinetics of levofloxacin.

Adult↗
PubMed2001

Plasma levels of procalcitonin and interleukin-6 in acute myocardial infarction.

Estimation of cardiac morbidity in patients after major surgery is a difficult problem. In addition, infectious complications seriously decrease potential beneficial outcome after cardiovascular surgery. The present study assessed the use of a newer marker of the inflammatory response, procalcitonin, in the field of myocardial infarction, in conjunction with measurements of interleukin-6. Forty-four consecutive cases with acute myocardial infarction were included in the study 4+/-1.3 h after the onset of symptoms. Plasma levels of procalcitonin and interleukin-6 were obtained at admission, and after 3, 6, 12, 18, 24 and 48 h, using commercially available test kits. The range of levels of interleukin-6 and procalcitonin was about normal at admission. Interleukin-6 levels increased significantly following myocardial infarction, whereas procalcitonin were essentially unchanged, i.e. remained close to the normal level threshold of 0.5 ng/ml; only minor variability occurred with a mean peak level of procalcitonin of 1+/-0.4 ng/ml. Data demonstrate that, in contrast to the acute phase reactant interleukin-6, plasma levels procalcitonin are not significantly elevated during uncomplicated acute myocardial infarction. This observation may support the role of procalcitonin measurements in the differential diagnosis of infectious and cardiovascular complications after major surgery.

Acute-Phase Reaction↗
PubMed1999

Thrombolytic therapy in adult meningococcal purpura fulminans with acute renal failure and severe perfusion deficits to the extremities.

OBJECTIVE: To investigate whether systemic administration of recombinant tissue plasminogen activator would improve organ perfusion in an adult patient with fulminant meningococcal disease. DESIGN: Descriptive case report. PATIENT: A 45-year-old female with meningococcal septic shock, purpura fulminans and multiple organ failure who was treated in an eight-bed medical intensive care unit of a University hospital. INTERVENTION: In addition to standard aggressive treatment, on each of three consecutive days the patient received recombinant tissue plasminogen activator infusions at a dose of 20 mg over 4 hrs. RESULTS: Urine output was recorded before, during, and after the recombinant tissue plasminogen activator infusions. In addition, the patient's peripheral perfusion status was documented by clinical assessment. The patient showed a dramatic improvement in urine output, as well as a perceived increase in skin perfusion after recombinant tissue plasminogen activator therapy. The amount of exogenous vasopressor and inotropic support required to maintain the patient's hemodynamic status also rapidly decreased. CONCLUSIONS: In this adult patient, recombinant tissue plasminogen activator therapy resulted in improved organ perfusion similar to that reported for paediatric patients. The findings indicate a need for controlled studies concerning the use of thrombolytics in severe meningococcal disease.

Acute Kidney Injury↗
PubMed1998

Decreased levels of beta-endorphin in circulating mononuclear leukocytes from patients with acute myocardial infarction.

Lymphocytes can be activated to produce and release opioid peptides. We investigated the levels of immunoreactive beta-endorphin in peripheral blood mononuclear cells from 11 patients with acute myocardial infarction. The concentrations of beta-endorphin in mononuclear leukocytes of 30.2 +/- 6.9 pg/10(6) cells on admission were in the normal range of 20-40 pg/10(6) cells and decreased significantly to 6.9 +/- 1.9 pg/10(6) cells after 48 h (p < 0.05). Decreased levels of mononuclear leukocyte-associated beta-endorphin in acute myocardial infarction may be due to the release of endogenous opioid after stimulation by stress and acute-phase reactants and play a role in inflammation and pain.

C-Reactive Protein↗
PubMed1997

Modulation of c-fos and egr-1 expression in the isolated perfused kidney by agents that alter tubular work.

The isolated perfused rat kidney provides a model of selective hypoxia to the medullary thick ascending limb. To investigate the relationship between immediate early gene expression and the extent of hypoxic damage, we determined expression of the immediate early genes (IEG) c-fos and egr-1 in isolated perfused kidneys during standard perfusion and after various measures shown previously to be protective. mRNA levels of c-fos and egr-1 were markedly increased in kidneys after 90 minutes of standard perfusion with Krebs-Henseleit buffer containing albumin. Gene expression was most prominent in the outer medulla followed by papilla and cortex, a pattern reflected by the immunohistochemical demonstration of a prominent accumulation of both egr-1 and c-fos polypetides mainly in the medullary thick ascending limb (mTAL). Protective measures known to minimize morphological damage to the mTAL, including hyperoncotic perfusion, perfusion with glycine, or perfusion with a mixture of amino acids, decreased mRNA levels of c-fos and egr-1 in the outer medulla (by 50% and 35%, respectively) and the papilla (by 60 and 30%, respectively). Renal cortex showed only minor changes. In contrast, prevention of tubular transport by perfusion with 1 mM ouabain increased mRNA levels of c-fos and egr-1 in the outer medulla by 100% and 60%, respectively. Ouabain also dramatically increased mRNA levels of both IEGs in two lines of cultured renal epithelial cells. Changes in the level and distribution of the protein products of these IEGs were not detectable in perfused kidneys by immunohistochemistry. Hypoxic injury of the kidney stimulates IEG expression even in the absence of reperfusion. Protection against hypoxic injury in the mTAL correlates with suppression of IEG mRNA levels when protection is provided by amino acids or hyperoncotic perfusion, but not when provided by inhibition of Na,K-ATPase, which stimulates IEG expression. We conclude that diminished IEG expression is not a necessary concomitant of protection against hypoxic injury.

Amino Acids↗
PubMed1997

Soluble intercellular adhesion molecule-1 (ICAM-1) in serum and urine: correlation with renal expression of ICAM-1 in patients with kidney disease.

A soluble form of intercellular adhesion molecule-1 (sICAM-1) has been described in serum and other body fluids. In order to determine whether sICAM-1 in serum and urine is a useful marker of inflammatory activity in kidney diseases we measured sICAM-1 in serum and urine of fifty patients who underwent renal biopsy, and of twenty healthy individuals. Expression of ICAM-1 on proximal tubular epithelial cells was investigated by immunohistochemistry. Soluble ICAM-1 in serum did not differ between patients and controls (354 +/- 129 ng/ml vs. 305 +/- 52 ng/ml). By multiple regression analysis sICAM-1 correlated with tubular expression of ICAM-1 (p < 0.01), but not with serum creatinine, infiltrating leukocytes, urinary ICAM-1 or proteinuria. In healthy controls mean urinary ICAM-1/cr was 2.5 +/- 3.0 ng/mg creatinine and differed significantly from that of patients (14.5 +/- 14.9 ng/mg) (p < 0.005). Patients with minimal-change disease had the highest uICAM-1 levels. The ratio of urinary ICAM-1 and proteinuria was remarkably constant in all patients with 6.0 +/- 0.9 ng/mg. By multiple regression analysis uICAM-1/cr correlated with proteinuria/cr (p < 0.001) and sICAM-1 (p < 0.005). These data show that sICAM-1 does to some degree reflect ICAM-1 expression in the kidney, whereas uICAM-1 is derived from glomerular filtration and closely parallels proteinuria. Both sICAM-1 and uICAM-1 are not useful to estimate ICAM-1 expression and inflammatory activity in the kidney.

Biomarkers↗