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Reliable identification and treatment of specific hemodialysis access complications may improve access patency and result in significant cost reduction. Angiography is the gold standard for the evaluation of vascular access; however, it has significant limitations. Intravascular ultrasound (IVUS) is a relatively new technique capable of detecting subtle vascular abnormalities. To investigate the safety, feasibility, and accuracy of IVUS imaging to detect hemodialysis access complications, including stenoses, graft deterioration, and thrombus, we performed 31 IVUS imaging studies in 22 hemodialysis patients. Nineteen studies were performed in the dialysis unit, and 12 studies in the angiography suite. The IVUS catheter was inserted into the graft through the access used for hemodialysis. Findings of 21 studies (17 patients) imaged on the same day by both angiography and IVUS were compared. Grafts and vessels were successfully imaged using IVUS in 29 of 31 studies. There were no adverse effects caused by IVUS. Angiography assessed 17 of 54 vessel segments as normal versus 9 of 54 segments by IVUS (P < 0.001). Angiography detected lesions in 25 segments as opposed to 33 segments by IVUS (P < 0.001). A thrombus was detected in 32 of 54 vessel segments by IVUS, but in only 1 of 54 segments by angiography (P < 0.001). In conclusion, IVUS imaging is feasible and safe to assess hemodialysis access in the angiographic suite and dialysis unit. IVUS detected more vascular abnormalities than angiography. IVUS may be a useful independent imaging and screening modality in the assessment of dialysis access complications, which may help increase graft patency and reduce cost., (Copyright 2002 by the National Kidney Foundation, Inc.)

Patients with chronic renal failure (CRF) are at increased risk for myocardial events that are difficult to evaluate due to atypical symptoms and chronically elevated protein markers of cardiac damage. This study evaluated cardiac troponin T (cTnT), a sensitive marker of cardiac injury, in patients with CRF without myocardial infarction symptoms, and assessed potential causes for elevated cTnT. Blood was obtained from 38 patients with CRF immediately before hemodialysis and from 16 of them post-dialysis, from 21 peritoneal dialysis patients, 10 patients with CRF not on dialysis, 11 patients with cardiomyopathy, and 10 adolescent patients with CRF undergoing hemodialysis. Samples were analyzed for myoglobin, creatine kinase, creatine kinase isoenzyme-MB (CK-MB), lactate dehydrogenase, lactate dehydrogenase isoenzyme-1 (LD-1), and cTnT. Cardiac TnT was elevated in: 71% of patient with CRF undergoing hemodialysis with no significant differences between pre- and post-dialysis values, 57% of patients with CRF on peritoneal dialysis, 30% of patients with CRF without dialysis, 18% of patients with cardiomyopathy, and 20% of adolescent patients with CRF undergoing hemodialysis. Myoglobin was elevated in almost all patients with CRF undergoing hemodialysis and without dialysis, whereas CK-MB and LD-1 were rarely elevated. Cross-reacting dialyzable substances and myocardial stretch were not major causes for elevated cTnT. Until future studies clarify the etiology of elevated cTnT in patients with CRF, results should be interpreted cautiously.

Purpose: To determine the value of a hemodialysis graft surveillance program in reducing the incidence of graft thrombosis and prolonging graft patency by means of early detection and percutaneous transluminal angioplasty (PTA) of graft-related stenoses., Materials and Methods: For 4-1/2 years, routine graft examination and measurement of several dialysis parameters were used to identify 106 cases of suspected graft dysfunction in 57 patients (56 men, one woman; aged 27-76 years). Graft-related stenoses detected with angiography were treated with PTA., Results: Abnormal physical examination findings were the most common sole indication of graft dysfunction. Of the 106 cases referred for angiographic evaluation, 97 (92%) had at least one lesion. PTA was successful in 88 of 90 treated cases. The primary patency rates at 1 year were 16% for arteriovenous fistulas (AVFs) and 23% for polytetrafluoroethylene (PTFE) grafts. Early detection of stenoses by means of surveillance and repeated PTA enabled 1-year primary assisted patency rates of 67% for AVFs and 68% for PTFE grafts. The incidence of graft thrombosis fell from 48% in 1988 to 17% in 1994 (P < .001)., Conclusion: The hemodialysis graft surveillance program resulted in a statistically significant reduction in the incidence of graft thrombosis. Although primary patency rates after PTA were low, repeated PTA of detected stenoses allowed good primary assisted patency rates.

Prolonging the life of vascular access sites is one of the most pressing problems facing the nephrology team in the ongoing care of chronic hemodialysis patients. Thus, the ability to salvage a failing vascular access is important in any circumstance, but salvage is particularly critical in medically complicated situations. The following case presents just such a situation, one in which available access sites were limited and in which salvaging the function of a local access site obviated the need for major surgical intervention for more than 4 years. This example shows the efficacy of nonsurgical thrombolysis and the place of vascular radiology in the long-term preservation of access patency and follow-up care.

The functional renal failure accompanying advanced liver disease is characterized by azotemia, a urine of very low sodium concentration and systemic hypotension with decreased renal perfusion and high renal vascular resistance. Patients with this disorder have a markedly reduced ability to excrete free water and develop hyponatremia, ascites and edema. It is postulated that this renal dysfunction is due to hepatic failure to make renin substrate. Renin released from the kidney is thus unable to exert its pressor effect. The resultant hypotension and renal hypoperfusion continue to stimulate excessive synthesis and release of renin. It is postulated that the overdriven renal renin system increases renovascular resistance at the level of the glomerular arterioles. This causes decreased renal blood flow and decreased glomerular filtration rate leading to salt and water retention and azotemia. Since no renin substrate is available for human infusion, this hypothesis could be tested either by infusion of angiotensin II to restore systemic blood pressure and renal perfusion or by beta adrenergic blockade with propranolol to attempt to decrease the intrarenal effects of renin, restore glomerular blood flow and filtration and thus return of renal function.

Hypoxemia during hemodialysis has variously been attributed to worsening ventilation-perfusion (VA/Q) relationships, alveolar hypoventilation combined with a reduced respiratory quotient, increased right-to-left shunting, and diffusion impairment. It is difficult to separate out these various effects, which explains lack of agreement in the literature. To more critically evaluate the causes of hypoxemia during hemodialysis, we used a multiple inert gas elimination technique to determine the distribution of ventilation-perfusion ratios during hemodialysis in 8 patients with chronic renal failure. Measurements were made before, during (at 60, 120, and 210 min), and after hemodialysis. Whereas arterial PO2 fell from 87 to 74 mmHg by 120 min, ventilation-perfusion relationships actually improved. Cardiac output fell from 5.3 to 4.0 L/min over the same time. Alveolar ventilation, respiratory quotient, and alveolar PO2 all fell, and the alveolar arterial PO2 difference remained essentially unchanged. These findings suggest that the hypoxemia observed during hemodialysis is primarily due to a decrease in alveolar ventilation and respiratory quotient associated with removal of metabolic CO2 in the dialyzer. Secondary factors affecting arterial PO2 were the slight improvement in ventilation-perfusion relationships tending to increase it, and the decrease in cardiac output tending to decrease it. There was no evidence for diffusion impairment because the measured VA/Q inequality accounted for the degree of hypoxemia.

We demonstrate that salts of diatrizoate and iothalamate, radiographic contrast agents, depress the active transport of sodium in the urinary bladder of the Columbian toad, Bufo marinus. Isolated toad bladders were incubated in isotonic Ringer's solutions with isosmolar displacement of sodium chloride by contrast media in experimental solutions. Sodium transport as measured both by short-circuit current (SCC) and by isotopic sodium flux was significantly depressed in the presence of sodium diatrizoate. Sodium transport measured by SCC was significantly depressed with sodium iothalamate and meglumine iothalamate. Equimolar methylsulfate Ringer's solution did not depress SCC. Although contrast media in isotonic Ringer's solutions depressed basal SCC, the vasopressin-stimulated increment in SCC was not depressed by contrast media. Separate experiments with hyperosmolar solutions (786 mM, as utilized in angiography) demonstrated equivalent suppression of SCC by contrast media and by other solutions made hyperosmolar with glucose or sodium methylsulfate, implying a general or nonspecific effect of hyperosomolarity. Inhibition of SCC by contrast media was reversible when the agents were removed by serial changes with standard Ringer's solution. Inhibition of sodium transport by contrast media might provide a basis for studies on some of the clinical toxicities of these agents.

A new three barrier, four compartment model for sodium transport in high resistance urinary epithelia is presented. This model provides a unified and simplified mechanistic explanation for sodium transport and its quantitative regulation. Sodium enters the epithelial cell by passive diffusion. Active extrusion occurs across the lateral cell membrane into the lateral intercellular space (LICS). Sodium movement from the LICS into the serosal compartment is not free and unobstructed as in the models for low resistance epithelia, but rather occurs through a regulatory channel of the LICS passing through desmosomes and the basilar slit. The exact configuration of this regulatory channel controls the rate of sodium movement from the LICS into the serosal compartment. Thus, the configuration of the regulatory channel controls the afterload on the sodium pump and thus ultimately controls the rate of transepithelial sodium transport. Antidiuretic hormone could act by increasing the effective width of this regulatory channel by contraction of intracellular microtubules or microfilaments. Present theories for regulation of transepithelial sodium transport in high resistance epithelia invoke a regulatory barrier at the apical cell membrane or at the active sodium pump located in the basolateral cell membrane. The hypothetical model presented here invokes a new alternative: regulation of the active pump rate by the sodium concentration in the LICS serving as an afterload on the pump; sodium escape from the LICS into the serosal compartment thus becomes the regulatory step for transepithelial transport.

It is theoretically inappropriate to characterize an actively transporting epithelim by "resistance" alone which is correctly applied only to passive circuit elements. Rather, such epithelia (if they actively transport sodium) required, as a minimum, characterization by an active circuit element parameter such as voltage (E Na), current (I Na) or power (WNa) in some configuration with resistances. Recent experimental studies of epithelia which actively transport sodium have omitted consideration of the active circuit element and attributed all measured changes observed to "resistance" changes in the epithelium as the transepithelial sodium gradient is altered. It is suggested that the observed changes in voltage/current ratio could be consequences of changes in the electrical behavior of the active circuit element of such epithelia. It may be biologically impossible to suppress all electromotive forces in epithelia to measure the truly passive characteristics of the epithelim without destroying tissue viability. The actual methods used to date for measurement of "resistance" in epithelia consist of perturbing signals which might alter the electrical behavior of an active element such as an "ion pump"; the observed changes in voltage to current ratio observed in such experiments can be better explained by a change in the active ion pump rather than by changes in passive epithelial "resistance".

The rate of urinary acidification by toad urinary bladders was measured in vitro by following the pH changes of the HCO3-/CO2-buffered Ringer's solutions bathing the mucosal and serosal sides of the bladder. Within the tolerated range of transepithelial potential differences (PD) (-100 to +100 mv), the rate of acidification was found to be a linear function of the PD. The rate of acidification could be increased by a favorable PD whether the PD was the spontaneous transepithelial PD due to sodium transport or a PD imposed in the absence of sodium transport, as when choline was substituted for Na or when amiloride blocked sodium transport. Acetazolamide inhibited both active and PD-driven acidification. Acidification rate was the same in 2.4 mM HCO3- and 1% CO2 as in 12 mM HCO3- and 5% CO2; again, acidification was increased equally by a favorable PD. PD-driven acidification was found to be linearly correlated with acidification occurring at short-circuit conditions. These findings suggest that the rate of acidification can be accelerated by the transepithelial PD in the absence of sodium transport and that the PD-driven component of acidification utilizes a transcellular pathway.