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Biomedical subjects

K Mavromatidis

Publications and source records attributed to K Mavromatidis.

13 recordsLinked to original sources

Deviations of placement/function of permanent central vein catheters for hemodialysis.

Fourteen cases of malposition of a permanent central vein catheter for hemodialysis or poor blood flow associated with thrombosed central veins but correct catheter positioning, in 13 patients suffering from end stage renal disease, presented from September 1991 to December 2003 among 385 permanent central vein catheters for hemodialysis (3.6%). There were 8 episodes of catheter tip malplacement in the azygos vein (1 case), hemiazygos vein (1), left internal thoracic (mammalian) vein (1), contralateral innominate vein (5) and 6 cases with correct anatomical catheter tip placement but with blood inflow from the catheter through the collateral vein system because of thrombosis of a major vein trunk (hemiazygos vein system (2), azygos vein (2), ascending lumbar veins (1), or portal vein system (1)). The malposition was diagnosed using roentgenography, with or without contrast, and computer tomography. In 3 cases the catheter was removed, in 5 cases the position was corrected. In the remaining 6 cases its function was maintained using anticoagulation or/and thrombolytic therapy. In conclusion, the placement of a permanent central vein catheter for hemodialysis must be followed by simple or contrast medium x-ray evaluation of its correct position or function. The malposition must be corrected whereas in the case where there is no alternative solution the function of the catheter may be maintained in the incorrect position using a combination of anticoagulation or/and thrombolytic therapy.

Adolescent↗

The incorrect placement of hemodialysis catheters in veins. The necessity for urgent x-ray evaluation for its position.

We describe a 56-year-old woman with end stage renal failure, who has an unusual complication in relation to catheter placement. She started hemodialysis in 1992 and until October of 1996 had many arteriovenous fistulas in her upper arms and we placed a lot of grafts. Because she had no vascular access for hemodialysis, we decided to place a polyurethane catheter in the left internal jugular vein. The woman had been in good health for 15 months when the blood flow decreased rapidly, so we replaced the catheter with a new one stabilized with silicone in the same place. Because the blood flow again was insufficient for a good dialysis session we decided to check the catheter position angiographically, and were surprised to ascertain that the catheter was placed in the internal thoracic (mammalian) vein. We discuss this patient because she is the first in the international bibliography.

Angiography↗

Anticipation of end stage renal disease in patients with autosomal dominant polycystic kidney disease in successive generations.

Autosomal dominant polycystic kidney disease is a disorder, which is inherited in 50% of offspring, irrelevant the sex and it has a variable clinical expressivity. Initially it was noticed that the clinical expression was interfamilial, but some studies found out that it was different. The aim of this study was to evaluate the age of onset of end-stage renal disease (ESRD) in affected parents in comparison with their offspring in successive generations. We studied 60 families of patients with autosomal dominant polycystic kidney disease (ADPKD). The diagnosis was done by echo criteria and we included only the patients for whom we knew precisely the onset of ESRD (affected parent and offspring), the sex of the parent who suffered from the disease, and offspring. We found out that the ESRD in ADPKD appears at the same age in affected parents and offspring (49,3 +/- 7,9 Vs 51,8 +/- 9,2, p = NS) irrelevant of the sex of the offspring. Patients with paternal inheritance (n = 38) were diagnosed to have ESRD earlier than their affected parents (47,9 +/- 8,3 Vs 52,2 +/- 9,2 p < 0,05), but patients with maternal inheritance had no difference (n = 22) (51,9 +/- 6,8 Vs 51,2 +/- 9,4, p = NS). In all the patients (60 couples) the survival rate was the same between affected parents and offspring (p = NS, Kaplan-Meier test), but significant differences were noticed between offspring with paternal inheritance in comparison with their parents (p < 0,05). In conclusion, we have detected that the onset of ESRD between patients with ADPKD in successive generations: a) Occurs in offspring as in their ancestors, b) anticipation was observed in 55% of couples, c) the sex of offspring does not have any relation with the renal death and d) the ESRD in patients with paternal inheritance occurs earlier in offspring than in their ancestors but not with maternal.

Adult↗

Experimental autoimmune glomerulonephritis (EAG) induced by homologous and heterologous glomerular basement membrane in two substrains of Wistar-Kyoto rat.

BACKGROUND: Goodpasture's, or antiglomerular basement membrane (GBM), disease presents with rapidly progressive glomerulonephritis, and is caused by auto-immunity to the NC1 domain of the alpha 3 chain of type IV collagen. In order to investigate mechanisms involved in the induction and regulation of glomerulonephritis, experimental models of Goodpasture's disease have been developed in the rat which share many characteristics with the human disease. Induction of experimental autoimmune glomerulonephritis (EAG) involves immunization of susceptible strains with either heterologous or homologous GBM in FCA. However, pathological changes have tended to be mild and/or variable, except in certain protocols using Wistar-Kyoto (WKY) rats. METHODS: We studied the susceptibility of inbred WKY rats from two different suppliers to the development of EAG. These substrains of rat had different MHC haplotypes (WKY/CR, RT1-1; WKY/Olac, RT1-k), so we proposed that they might show differences in their immune response to GBM antigens. Both substrains were immunized with sheep GBM, pH 7, or rat GBM buffered to pH 3, pH 5 or pH 7. RESULTS: All immunized rats developed circulating anti-GBM antibodies detectable at 14 days and rising until 28 days, at which time there was linear deposition of IgG on the GBM. WKY/CR rats developed severe focal segmental proliferative and necrotizing glomerulonephritis, with heavy albuminuria, following immunization with rat GBM, pH 7, but only moderate disease following sheep GBM. WKY/Olac rats showed a more variable response, with moderate disease following both rat and sheep GBM. Immunization of either substrain with rat GBM, pH 5, produced a response similar to that with rat GBM, pH 7, but disease was mild following rat GBM, pH 3. CONCLUSION: EAG in the WKY rat varies in severity according to the substrain of animal and preparation of GBM used for immunization. The model with the most severe and consistent changes was that induced in the WKY/CR rat by rat GBM at pH 7. This model of EAG will be of value for investigating mechanisms of autoimmunity and inflammation in glomerulonephritis, and for attempting novel forms of immunotherapy prior to trials in man.

Albuminuria↗

Serum ferritin levels are increased in patients with acute renal failure.

After having observed high serum ferritin concentrations in some patients with acute renal failure (ARF) we decided to evaluate serum ferritin and iron levels in patients with acute and chronic renal failure (CRF). The concentrations of BUN, serum creatinine, Hct, Hb, serum iron and serum ferritin were measured in 47 patients with renal failure who were divided into two groups (A and B). Group A included 24 patients with ARF (19 M, 5 F) and group B 23 patients with CRF (12 M, 11 F). The diagnosis of ARF or CRF was based on patients' history and clinical examination and confirmed by the standard laboratory findings and the subsequent clinical outcome. None of the patients had received iron, blood transfusions or erythropoietin during the last six months and none had malignancy or primary liver diseases. As controls were used 20 normal volunteers (group C) and 10 patients with acute infections (group D). Comparing groups A and B we did not found any difference in BUN, creatinine and serum iron levels. However patients in group A had significantly higher serum ferritin levels (1000 +/- 752 vs 90 +/- 56 ng/dl, p = 0.0001), higher Hct (31.8 +/- 4.4 vs 25.3 +/- 4.1%, p = 0.0001) and higher Hb concentrations (10.5 +/- 1.7 vs 8.1 +/- 1.4 g/dl, p = 0.0001). Ferritin levels in patients with ARF were also higher than the corresponding levels of normal controls (group C) (p = 0.0001), but did not differ significantly from those measured in patients with acute infection (group D). We conclude that in patients with acute renal failure serum ferritin levels are increased and do not reflect serum iron levels.

Acute Kidney Injury↗

Urea concentration gradients during conventional hemodialysis.

To elucidate the intradialytic urea concentration gradients, we examined 26 hemodialysis patients wearing a double-lumen central venous catheter during their first or second fistula-punctured dialysis session. In 17 patients (group A), after 60 and 240 minutes of treatment with a mean blood flow of 196.4 +/- 9.9 mL/min, blood urea nitrogen (BUN) was measured in blood samples taken simultaneously from the central venous catheter, a vein in the arm opposite the access site, and the arterial and venous lines of the dialyzer. In 16 patients (group B), after 60 minutes of treatment with a mean blood flow rate of 197.5 +/- 12.3 mL/min, BUN was measured in blood samples taken from the dialyzer arterial line and then, after decreasing the blood flow to 50 to 60 mL/min for 1 minute, in samples taken from a vein in the arm opposite the access site, the central venous catheter, and the dialyzer arterial line. In group A, the mean BUN values in the dialyzer arterial line at 60 and 240 minutes were found to be 3.7% +/- 3.7% and 3.5% +/- 3.4% higher than the corresponding values in the central veins, respectively (P = NS between 60 and 240 minutes). In group B, after 1 minute of low blood flow, this difference was 1.5% +/- 2.4% (P = 0.06 compared with group A). The peripheral veins in group A patients at 60 and 240 minutes had 9.7% +/- 5.2% and 10.9% +/- 5.3% higher BUN values, respectively, compared with the central veins. This difference in group B patients after 1 minute of low blood flow was 6.8% +/- 4.2%. Urea access recirculation rate in group A, calculated by the classical three-samples method, was found to be 7.6% +/- 5.0% at 60 minutes and 9.9% +/- 5.8% at 240 minutes (P = NS). In group B, BUN values in the dialyzer arterial line after 1 minute of low blood flow increased significantly by 3.4% +/- 4.5% (P < 0.01). Our study shows that during conventional hemodialysis with a blood flow rate of 200 mL/min, urea concentration in the central veins is lower than in the dialyzer arterial line. This gradient after 1 minute of low-flow dialysis had a tendency to decrease. At the same time, however, the urea concentration gradient between the peripheral and central veins remained high, indicating that during conventional hemodialysis, intercompartmental disequilibrium plays a significant role in the arteriovenous gradient.

Arm↗

Influence of continuous haemofiltration-related hypothermia on haemodynamic variables and gas exchange in septic patients.

OBJECTIVE: To investigate the influence of continuous haemofiltration (CHF) on haemodynamics, gas exchange and core temperature in critically ill septic patients with acute renal failure. PATIENTS AND METHODS: In 20 patients (17 male, 3 female) ultrafiltration rate, core temperature, gas exchange and haemodynamic variables were measured at regular intervals during the first 48 h of haemofiltration. Baseline data were compared to those obtained 30 min after initiating CHF and also to those during hypothermia (if observed). MAIN RESULTS: Haemodynamic variables remained remarkably constant throughout the study period. In patients with a relatively low ultrafiltration rate (855 +/- 278 ml/h) temperature did not change, while in patients with a high ultrafiltration rate (1468 +/- 293 ml/h) core temperature significantly decreased from 37.6 +/- 0.9 degrees C to 34.8 +/- 0.8 degrees C (p < 0.001). There was a statistically significant correlation between temperature decrease and ultrafiltration rate (r = -0.68, Y = 1.8-0.003 X, p < 0.01). Hypothermic patients also showed a mean decrease in VO2 from 141 +/- 22 ml/min/m2 to 112 +/- 22 ml/min/m2 (p < 0.01) with a concomitant increase in PaO2 from 103 +/- 37 mmHg to 140 +/- 42 mmHg (p < 0.001) and in PvO2 from 35 +/- 4 mmHg to 41 +/- 5 mmHg (p < 0.001). CONCLUSIONS: 1) Continuous haemofiltration does not cause significant alternations in haemodynamic variables. 2) Hypothermia frequently occurs in patients undergoing continuous haemofiltration with high ultrafiltration rates. These hypothermic patients show a reduction in VO2 leading to an increase in PvO2 and PaO2. This mild hypothermia in these circumstances has no evident deleterious effects.

Acute Kidney Injury↗

Efficacy of dual lumen jugular venous catheter hemodialysis when venous lumen is used as arterial lumen.

In 12 patients who underwent hemodialysis by a dual lumen jugular venous catheter, urea recirculation rate was measured during conventional treatment under normal conditions (R1), as well as when the venous lumen of the catheter was used as arterial lumen and the arterial as venous lumen (R2). Although the mean value of R2 was, as expected, higher than R1 (8.25 +/- 2.7 versus 4.25 +/- 1.00; p = 0.0004), it was still within the acceptable rate. We conclude that during hemodialysis by a dual lumen jugular venous catheter, efficient treatment can be provided when the venous is used as arterial lumen.

Adult↗

Single kidney function: early and late changes in urate transport after nephrectomy.

Renal urate transport was studied by means of pyrazinamide (PZA) and probenecid (PB): (a) before and at 2, 6, 24 weeks (24 patients), (b) 1 to 30 years after uninephrectomy in 27 and 12 patients with Ccr greater than 80 and 30 to 70 ml/min, respectively. Uninephrectomy was followed by important tubular urate transport modifications during at least two weeks, which lead to a marked uricosuria as indicated by significant increase in FEur (mean value +/- SD, 0.228 +/- 0.059 vs. 0.097 +/- 0.014 and 0.099 +/- 0.019 in normals and chronically diseased solitary kidneys). Reduced response to PZA and PB suggests a diminished reabsorptive capacity for urate mainly at the presecretory site which persisted after FENa normalization. Tubular compensations were presumably complete at six weeks, since pattern of urate transport returned to normal with an almost complete reabsorption of filtered urate load (99%) and a percentage of postsecretory reabsorption (80%) very close to those seen in normal subjects with a pair of kidneys. The adjustment in urate excretion in solitary kidneys was achieved by a significant increase of secreted urate as compared with 50% of pre-uninephrectomy values. Thus, increased urate secretion by the remaining intact organ is sufficient to maintain urate balance with a normal serum level.

Adult↗

Insulin-dependent diabetes and renal hypouricemia.

We studied 14 patients (11 women and 3 men) from 18 to 33 years old, suffering from type I diabetes mellitus with normal renal function (creatinine clearance 106.91 +/- 28.73 ml/min) and serum uric acid below 2.5 mg/dl (2.34 +/- 0.11 mg/dl) as well as a high uric acid clearance (23.04 +/- 5.92 ml/min) and fractional urate excretion (21.4 +/- 2.6) versus urate clearance 9.82 ml/min and fractional urate excretion 8.80 +/- 1.3 in 14 normal control subjects. The study of the uricosuric mechanisms was conducted by the combination of probenecid (PB) test which inhibits the reabsorption of secreted urate, and pyrazinamide (PZA) test, which inhibits its tubular secretion. The results of studies indicate that the increase in urate clearance was accounted for by increased PZA-nonsuppressible urate suggesting a decreased reabsorption of filtered urate. Increased PZA-suppressible urate excretion combined with impaired response to a uricosuric drug is consistent with impaired reabsorption of secreted urate. According to our findings, increased urate excretion in diabetic patients may be attributed to the inhibition of both filtered and secreted reabsorption. This reabsorptive tubular abnormality is consistent with the view of an interference of tubular reabsorption of glucose with the tubular capacity for uric acid reabsorption.

Adolescent↗