Israel Medical Association Journal

Background: The ischemic “steal” syndrome complicates angio-access in a growing number of hemodialysed patients. Until now, operative attempts (fistula ligation or banding) to treat this problem have met with only limited success.

Objective: To assess the results of DRIL (distal revascularization-interval ligation) procedure in treating the “steal” syndrome.

Methods: A retrospective review (1996–2002) was conducted of all 11 patients who underwent the DRIL[1] procedure in two tertiary care hemodialysis units.

Results: Two patients were excluded because of inadequate medical documentation. All of the nine patients remaining suffered from overt atherosclerotic disease, six had diabetic nephropathy and four were smokers. The arterio-venous access, which led to the “steal” syndrome, was proximally located in all (antecubital in 8, thigh area in 1). “Steal” symptoms included hand pain, paraesthesia, neurologic deficits and gangrenous ulcers. DRIL was technically successful in all patients. There were no perioperative deaths. Immediate and complete relief of pain was achieved in eight of the nine patients. One patient with gangrene later required a transmetacarpal amputation. No patient required hand amputation. During follow-up (range 1–26 months) hemodialysis was continued uninterruptedly using the problematic AVA[2] in all patients. Thrombosis occurred in the AVA in only two patients after the DRIL procedure at 9 and 24 months postoperatively, respectively. Three patient deaths were unrelated to the DRIL.

Conclusions: In selected patients the DRIL procedure is a safe and effective way to treat the “steal” syndrome. AVA patency is not compromised by this operation. Preoperative angiography, before and after manual compression of the AVA, is crucial for the proper selection of patients who will benefit most from the DRIL procedure.

Background: Acute renal infarction is an oft-missed diagnosis. As a result; its true incidence, although presumed to be low, is actually unknown. Surprisingly, the medical literature on the subject, other than anecdotal case reports, is scarce.

Objectives: To increase physician awareness of the diagnosis and to identify predictive clinical and laboratory features of the entity.

Method: Between 1 November 1997 and 31 October 2000, 11 cases of acute renal infarction in 10 patients were diagnosed in our center by contrast-enhanced computerized tomography. The medical charts of these patients were reviewed regarding risk factor, clinical presentation, possible predictive laboratory examinations, and out-come.

Results: During the 36 month observation period, the incidence of acute renal infarction was 0.007%. The mean age of the patients (5 men and 5 women) was 67.4 + 21.1 (range 30-87 years). In four cases the right and in five the left kidney was involved; in the other. two cases bilateral:involvement was seen. In 7/10 patients, an increased risk for thromboembolic events was found. Six had chronic atrial fibrillation and one had a combined activated protein C resistance and protein S deficiency, Three patients had suffered a previous thromboembolic event. Two cases were receiving anticoagulant therapy with an INR of 1.6 and 1.8, respectively. On admission, flank pain was recorded in 10/11, fever in 5 and nausea/vomiting in 4 cases. Hematuria was detected in urine reagent strips in all cases; Serum lactate dehydrogenase and white blood cell count were elevated in all cases (1,570 + 703 IU/L and 12,988 + 3,841/ l, respectively). In no case was the diagnosis of acute renal infarction  initially entertained. The working diagnoses were .renal colic in 2 pyelonephritis in 3, renal carcinoma, digitails intoxication, and suspected endocarditis in one patient each, and an acute abdomen in 3. Time from admission to definitive CT diagnosis ranged from 24 hours to 6 days; Three patients were treated with intravenous heparin and another with a combination of IV heparin and renal intra-arterial urokinase infusion with, in the latter case, no recovery of function of the affected kidney. With the exception of this one patient (with a contralateral contracted kidney) who required maintenance dialysis, in all other cases serum creatinine levels. remained unchanged or reverted to the baseline mean of 1.1 mg/dl (0.9-1.2).

Conclusions: Acute renal infarction is not as rare as previously assumed. The entity is often misdiagnosed. Unilateral flank pain in a patient with an increased risk for thromboembolism should raise the suspicion of renal infarction. In such a setting, hematuria, leuaocytosis and an elevated LDH level are strongly supportive of the diagnosis.

Background: Multiple factors are involved in the pathogenesis of hypertension in the obese individual.

Objective: To evaluate the role of a decrease in sympathetically mediated thermogenesis and the effect of the correlation between the plasma leptin and daily urinary nitric oxide levels on obesity-related hypertension.

Methods: We evaluated three groups: 25 obese hypertensive patients (age 45.7±1.37 years, body mass index 34.2±1.35 kg/m², systolic/diastolic blood pressure 155±2.9/105±1.3, mean arterial pressure 122±1.50 mmHg); 21 obese normotensive patients (age 39.6±1.72, BMI[1] 31.3±0.76, SBP/DBP[2] 124±2.1/85.4±1.8, MAP[3] 98.2±1.80); and 17 lean normotensive subjects (age 38.1±2.16, BMI 22.1±0.28, SBP/DBP 117±1.7/76.8±1.5, MAP 90.1±1.50). We determined basal resting metabolic rates, plasma insulin (radioimmunoassay), norepinephrine (high performance liquid chromatography) in all subjects. Thereafter, 14 obese hypertensives underwent a weight reduction diet. At weeks 6 (n=14) and 14 (n=10) of the diet the above determinations were repeated. Plasma leptin (enzyme-linked immunosorbent assay) and UNOx[4] (spectrophotometry) were assayed in 17 obese hypertensives and 17 obese normotensives, and in 19 obese hypertensives versus 11 obese normotensives, respectively.

Results: Obese hypertensive patients had significantly higher basal RMR[5] and plasma NE[6] levels. Insulin levels were lower in the lean group, with no difference between the hypertensive and normotensive obese groups. At weeks 6 and 14, BMI was significantly lower, as were insulin and NE levels. RMR decreased to values of normotensive subjects. MAP normalized but remained significantly higher than that of obese normotensives. Leptin blood levels and the leptin/UNOx ratio were significantly higher in the obese hypertensive compared to the obese normotensive patients. Both these parameters were strongly correlated to BMI, MAP⁵, RMR, and plasma NE and insulin .Obese hypertensive patients excreted less urinary NO metabolites. A strong correlation was found between MAP and the leptin/UNOx ratio.  

Conclusions: A reduction of sympathetically mediated thermogenesis, as reflected by RMR, results in normalization of obesity-related hypertension. In contrast, insulin does not seem to play a major role in the pathogenesis of hypertension associated with obesity. Increased leptin levels in conjunction with decreased NO production in the presence of enhanced sympathetic activity may contribute to blood pressure elevation in the obese.

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[1] BMI = body mass index

[2] SBP/DBP = systolic blood pressure/diastolic blood pressure

[3] MAP = mean arterial pressure

[4] UNOx = urinary nitric oxide

[5] RMR – resting metabolic rate

[6] NE = norepinephrine

Background: Cell-mediated immunity is impaired in uremia. Cell-matrix interactions of immune cells such as CD4+T lymphocytes with extracellular matrix are an important requirement for an intact immune response. The adherence of CD4+T cells of healthy subjects (normal T cells) to ECM components is inhibited in the presence of uremic serum. Such decreased adhesive capacity is also found in T cells of dialysis patients. Various chemokines and cytokines affect the attachment of CD4+T cells to ECM.

Objective: To evaluate chemokine (MIP-1β and RANTES) and tumor necrosis factor α-induced adhesion of CD4+T cells to ECM in a uremic milieu.

Methods: We examined adhesion of normal CD4+T cells (resting and activated) to intact ECM in response to soluble or bound chemokines (MIP-1β and RANTES) and to TNF-α following incubation in uremic versus normal serum. Thereafter, we evaluated the adhesion of resting CD4+T cells from dialysis patients in a similar fashion and compared it to that obtained from a healthy control group.

Results: Addition of uremic serum diminished soluble and anchored chemokine-induced attachment of normal resting and activated CD4+T cells to ECM compared to a normal milieu (a peak response of 10–11% vs. 24–29% for soluble chemokines, P<0.001; 12–13% vs. 37–39% for bound chemokines on resting cells, P<0.01; and 18–20% vs. 45–47% for bound chemokines on activated cells, P<0.02). The same pattern of response was noted following stimulation with immobilized TNF-α (7 vs. 12% for resting cells, P<0.05; 17 vs. 51% for activated cells, P<0.01).  Adherence of dialysis patients’ cells to ECM following stimulation with both bound chemokines was reduced compared to control T cells (15–17% vs. 25–32%, P<0.0000). In contrast, adherence following stimulation by TNF-α was of equal magnitude.

Conclusions: Abnormal adhesive capacity of T lymphocytes to ECM in uremia may, in part, be related to a diminished response to MIP-1β, RANTES and TNF-α. However, whereas reduced adhesion to chemokines was present in both normal CD4+T cells in a uremic environment and in dialysis patients’ T cells, TNF-α-induced adhesion was found to be inhibited only in normal cells in a uremic milieu.

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ECM = extracellular matrix

TNF-α = tumor necrosis factor-a