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עמוד בית
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April 2011
S. Kivity, I. Danilesko, I. Ben-Zvi, B. Gilburd, O.L. Kukuy, R. Rahamimov and A. Livneh

Background: Amyloidosis of familial Mediterranean fever (FMF) may lead to end-stage renal failure, culminating in kidney transplantation. Since amyloidosis is prompted by high serum amyloid A (SAA) levels, increased SAA is expected to persist after transplantation. However, no data are available to confirm such an assumption.

 Objectives: To determine SAA levels in kidney-transplanted FMF-amyloidosis patients and evaluate risk factors for the expected high SAA levels in this patient group.

Methods: SAA, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) values were obtained from 16 kidney-transplanted FMF-amyloidosis patients, 18 FMF patients without amyloidosis and 20 kidney-transplanted patients with non-inflammatory underlying disease. Demographic, clinical and genetic risk factors evaluation was based on data extracted from files, interviews and examination of the patients.

Results: SAA level in FMF patients who underwent kidney transplantation due to amyloidosis was elevated with a mean of 21.1 ± 11.8 mg/L (normal ≤ 10 mg/L). It was comparable to that of transplanted patients with non-inflammatory disorders, but tended to be higher than in FMF patients without amyloidosis (7.38 ± 6.36, P = 0.08). Possible risk factors for the elevated SAA levels in kidney transplant patients that were excluded were ethnic origin, MEFV mutations, gender, age and disease duration.

Conclusions: Kidney-transplanted patients with FMF-amyloidosis and with other non-FMF causes displayed mildly elevated SAA levels, possibly resulting from exposure to foreign tissue rather than from various FMF-related factors. 

 

August 2010
J. Malyszko, H. Bachorzewska-Gajewska, J. Malyszko, N. Levin-Iaina, A. Iaina and S. Dobrzycki

Background: Kidney disease and cardiovascular disease seem to be lethally synergistic and both are approaching the epidemic level. A reduced glomerular filtration rate is associated with increased mortality risk in patients with heart failure. Many patients with congestive heart failure are anemic. Anemia is very often associated with chronic kidney disease.

Objectives: To assess – in relation to New York Heart Association class – the prevalence of anemia and chronic kidney disease in patients with normal serum creatinine in a cohort of 526 consecutive patients with coronary artery disease undergoing percutaneous coronary interventions.

Methods: GFR[1] was estimated using the simplified MDRD formula, the Cockcroft-Gault formula, the Jeliffe and the novel CKD-EPI formula.

Results: According to the WHO definition the prevalence of anemia in our study was 21%. We observed a progressive decline in GFR and hemoglobin concentration together with a rise in NYHA[2] class. Significant correlations were observed between eGFR[3] and systolic blood pressure, diastolic blood pressure, age, NYHA class, complications of PCI[4], including bleeding, and major adverse cardiac events.

Conclusions: The prevalence of anemia and chronic kidney disease is high in patients undergoing PCI despite normal serum creatinine, particularly in higher NYHA class. Lower eGFR and hemoglobin are associated with more complications, including bleeding after PCI and higher prevalence of major adverse cardiac events. In patients with risk factors for cardiovascular disease, GFR should be estimated since renal dysfunction and subsequent anemia are important risk factors for cardiovascular morbidity and mortality.






[1] GFR = glomerular filtration rate



[2] NYHA = New York Heart Association



[3] eGFR = estimated GFR



[4] PCI = percutaneous coronary intervention


March 2010
M. Sofer, G. Lidawi, G. Keren-Paz, R. Yehiely, A. Beri and H. Matzkin

Background: Tubeless percutaneous nephrolithotomy is defined as PCNL[1] without postoperative nephrostomy tubes. It is reported to reduce postoperative pain, hospital stay and recovery time. To date the procedure has been reserved for selected patients.

Objectives: To assess our initial experience in extending the implementation of tubeless PCNL without preoperative patient selection.

Methods: All consecutive PCNLs performed during 2004–2008 were evaluated. Tubeless PCNL was performed when residual stones, bleeding and extravasation were excluded intraoperatively. Staghorn stones, stone burden, supracostal and multiple accesses, anatomic anomalies, solitary kidneys and operative time were not considered contraindications. We analyzed the clinical data and the choice of tubeless PCNL over time.

Results: Of 281 PCNLs performed during the study period, 200 (71%) were tubeless. The patients' average age was 53 years (range 28–82 years), the stone burden was 924 mm2 (400–3150 mm2), operative time was 99 minutes (45–210 min), complication rate was 14% and immediate stone-free rate 91%. There were 81 conversions to standard PCNL (29%) due to expected second-look (n=47, 58%), impression of bleeding (n=21, 26%), suspected hydrothorax (n=7, 9%) and extravasation (n=6, 7%). The transfusion rate was 1%. The median hospital stay was 1 day (1–15 days) and recovery time 7 days (5–20 days). The rate of implementing the tubeless procedure increased steadily along time from 46% to 83% (P = 0.0001). 

Conclusions: Tubeless PCNL can be safely and effectively performed based on intraoperative decisions, without preoperative contraindications. They are easily accommodated by experienced endourologists and provide real advantages.

 






[1] PCNL = percutaneous nephrolithotomy

 



May 2009
L. Shema, L. Ore, R. Geron and B. Kristal

Background: Acute kidney injury remains a common significant clinical problem. Yet there are scant data in Israel on the incidence of hospital-acquired AKI[1] and on diagnosis validity.

Objectives: To describe the epidemiology of AKI among hospitalized patients in the Western Galilee Hospital, Nahariya, compare discharge summaries to laboratory diagnosis, and investigate the impact of AKI on mortality and length of stay.

Methods: Computerized medical and laboratory data of 34,802 hospitalized subjects were collected. AKI was diagnosed according to three different definitions. We calculated the sensitivity and specificity of AKI based on ICD-9 diagnosis compared to patient's laboratory data as the gold standard.

Results: The overall AKI annual incidence rate was 1–5.1%, depending on the AKI definition used. The incidence of AKI based on ICD-9 diagnosis was significantly lower compared to the laboratory-based diagnosis. Average in-hospital length of stay was 2.4 times longer among patients with AKI compared to subjects without this condition. Furthermore, the in-hospital death rate among AKI patients was 14 times higher than among non-AKI hospitalized subjects, with a positive association between AKI severity and risk of death.

Conclusions: Using AKI laboratory diagnosis as the gold standard revealed ICD-9 diagnosis to be 9.1% sensitive and 99.4% specific. Hospital-acquired AKI is a major contributor to prolonged length of stay and high mortality rates; therefore, interventions to reduce in-hospital disease incidence are required.






[1] AKI = acute kidney injury


April 2008
B. Kristal, R. Shurtz-Swirski, O. Tanhilevski, G. Shapiro, G. Shkolnik, J. Chezar, T. Snitkovsky, M. Cohen-Mazor and S. Sela

Background: Polymorphonuclear leukocyte priming and low grade inflammation are related to severity of kidney disease. Erythropoietin-receptor is present on PMNLs[1].

Objectives: To evaluate the effect of 20 weeks of EPO[2]-alpha treatment on PMNL characteristics in relation to the rate of kidney function deterioration in patients with chronic kidney disease.

Methods: Forty anemic chronic kidney disease patients, stage 4-5, were assigned to EPO and non-EPO treatment for 20 weeks. A group of 20 healthy controls was also studied. PMNL priming and PMNL-derived low grade inflammation were estimated, in vivo and ex vivo, before and after EPO treatment: The rate of superoxide release, white blood cells and PMNL counts, serum alkaline phosphatase and PMNL viability were measured. EPO-receptor on PMNLs was assayed by flow cytometry. The effect of 20 weeks of EPO treatment on kidney function was related to the estimated glomerular filtration rate.

Results: EPO treatment attenuated superoxide release ex vivo and in vivo and promoted PMNL survival ex vivo. Decreased low grade inflammation was reflected by reduced WBC[3] and PMNL counts and ALP[4] activity following treatment. EPO retarded the deterioration in GFR[5]. The percent of PMNLs expressing EPO-R[6] was higher before EPO treatment and correlated positively with the rate of superoxide release. After 20 weeks of EPO treatment the percent of PMNLs expressing EPO-R was down-regulated.

Conclusions: These non-erythropoietic properties of EPO are mediated by EPO-R on PMNLs, not related to the anemia correction. A new renal protection effect of EPO via attenuation of PMNL priming that decreases systemic low grade inflammation and oxidative stress is suggested.






[1] PMNL = polymorphonuclear leukocytes

[2] EPO = erythropoietin

[3] WBC = white blood cells

[4] ALP = alkaline phosphatase

[5] GFR = glomerular filtration rate

[6] EPO = EPO-receptor


November 2007
A.H. Abbasi, R. Ramadan, A. Hoffman and Z. Abassi
October 2007
A. Lipey, A. Kogan, T. Ben-Gal, E. Mor, A. Stamler, B. Medalion, B.A. Vidne, E. Porat and G. Sahar
May 2007
M. Witz and Z. Korzets

Renal vein occlusion in adults is usually a result of vein thrombosis, which is frequently associated with the nephrotic syndrome. The anatomy of renal vascularization is of primary importance for understanding its pathophysiological responses and the clinical and diagnostic presentation of patients with this condition. The reaction of the kidney to its vein occlusion is determined by the balance between the acuteness of the disease, extent of the development of collateral circulation, involvement of one or both kidneys and the origin of the underlying disease. Renal vein occlusion is generally a complication of some other condition, but may also occur as a primary event. The main goals of therapy should be to conserve renal parenchyma in order to maintain renal function and prevent thromboembolic phenomena.

September 2005
October 2004
M. Korem, Z. Ackerman, Y. Sciaki-Tamir, G. Gino, S. Salameh-Giryes, S. Perlberg and S.N. Heyman
September 2003
A.B. Chkhotua, T. Klein, E. Shabtai, A. Yussim, N. Bar-Nathan, E. Shaharabani, S. Lustig and E. Mor

Background: Recent advances in immunosuppressive therapy have led to a substantial improvement in the outcome of kidney transplantation. Living unrelated donors may become a source of additional organs for patients on the kidney waiting list.

Objectives: To study the impact of combination of calcineurin inhibitors and mycophenolate-mofetile, together with steroids, on outcomes of living related and unrelated transplants. 

Methods: Between September 1997 and January 2000, 129 patients underwent living related (n=80) or unrelated (n=49) kidney transplant. The mean follow-up was 28.2 months. Immunosuppressive protocols consisted of MMF[1] with cyclosporine (41%) or tacrolimus (59%), plus steroids. Patient and graft survival data, rejection rate, and graft functional parameters were compared between the groups.

Results: LUD[2] recipients were older (47.8 vs. 33.6 years) with higher number of re-transplants (24.5% vs. 11.2% in LRD[3] recipients, P < 0.05). Human leukocyte antigen matching was higher in LRD recipients (P < 0.001). Acute rejection developed in 28.6% of LUD and 27.5% of LRD transplants (P = NS). Creatinine levels at 1, 2 and 3 years post-transplant were 1.6, 1.7 and 1.7 mg/dl for LRD patients and 1.5, 1.5 and 1.3 mg/dl for LUD recipients (P = NS). There was no difference in patient survival rates between the groups. One, 2 and 3 year graft survival rates were similar in LRD (91.3%, 90% and 87.5%) and LUD (89.8%, 87.8% and 87.8%) recipients.

Conclusions: Despite HLA[4] disparity, rejection and survival rates of living unrelated transplants under current immunosuppressive protocols are comparable to those of living related transplants.






[1] MMF = mycophenolate-mofetile



[2] LUD = living unrelated donor



[3] LRD = living related donor



[4] HLA = human leukocyte antigen


December 2002
Jayson Rapoport BSc MB MRCP, Alexander Kagan MD and Michael M. Friedlaender BM FRCP
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