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Biomedical subjects

E S Ricanati

Publications and source records attributed to E S Ricanati.

18 recordsLinked to original sources
PubMed1996

Use of laparoscopy in the management of malfunctioning peritoneal dialysis catheters.

The proper function of peritoneal dialysis (PD) catheters can be compromised by catheter malposition, fibrin clot, or omental wrapping. The purpose of this study was to determine the efficacy of laparoscopy in the treatment of malfunctioning PD catheters. All patients undergoing laparoscopy for catheter dysfunction at MetroHealth Medical Center in Cleveland, Ohio, from 1991 to 1995, were reviewed. Twenty-six laparoscopies were performed in 22 patients, for malfunction occurring an average of 3.9 months following insertion (range 0.5-18 months). Omental and/or small below wrapping as present in all but three cases. Lysis of adhesions was required in 19 of 26 cases, with repositioning only in seven. Eight patients had failed attempts at stiff wire manipulation prior to laparoscopy. Perioperative complications occurred in seven cases, consisting of temporary dialysate leakage (2), enterotomy (1), and early reocclusion (4). Repeat laparoscopy was successful in three of these four reocclusions. The overall success rate (catheter function > 30 days after laparoscopy) was 21/22 (96%). Laparoscopy is highly accurate and effective in the management of peritoneal dialysis catheter dysfunction and results in prolongation of catheter life.

Adult↗
PubMed1986

Dialysis encephalopathy: neuropathologic aspects.

The clinical, epidemiologic, electroencephalographic, and toxicologic features of dialysis encephalopathy (DE) have been clarified, but the neuropathologic and clinicopathologic aspects of the disease have remained obscure. In three cases of DE associated with a dialysate of high aluminum content, spongy change restricted to the upper layers of the cerebral cortex was found. The spongy change was distributed through the cerebral cortex bilaterally and diffusely, but the left hemisphere was involved more severely and extensively than the right hemisphere, and the opercular portions of the frontal and temporal lobes were affected more than the remainder of those lobes. This topographic distribution correlated with the clinical defects in higher cortical functions, including aphasia. The spongy change consisted of vacuoles in the neuropil and inside nerve cell bodies. The vacuoles in the neuropil were located in dendrites, astrocytic processes, and, possibly, other structures. Thus, DE is a disease of neurons and astrocytes of the cerebral cortex. Although spongy change of the upper layers of the cerebral cortex is a nonspecific abnormality, when it occurs in the distribution described and in the absence of other diffuse cerebral diseases, it is characteristic of DE.

Adult↗
PubMed1986

Hepatic veno-occlusive disease associated with renal transplantation and azathioprine therapy.

Four patients with renal transplants developed hepatic veno-occlusive disease after immunosuppressive therapy with azathioprine. Severe progressive portal hypertension developed in all patients, with the clinical presentation varying from a mild viral-like syndrome to rapidly fulminant liver failure and death. The disease was associated with cytomegalovirus infection but not with the dose of azathioprine, the type or duration of transplant, or the type of underlying kidney disease. In view of the high mortality rate associated with veno-occlusive disease (a combined 55% in our four patients and in five reported in the literature) and wide spectrum of clinical presentation in patients with renal transplants, a high index of suspicion is required and aggressive intervention indicated.

Adult↗
PubMed1985

Occlusion of the subclavian vein: a complication of indwelling subclavian venous catheters for hemodialysis.

We are reporting two cases of subclavian vein occlusion following the use of dual lumen subclavian vein catheters as a temporary access to the circulation for hemodialysis. Both patients presented with arm swelling and developed significant collateral circulation established by venography. There was no recanalization of the veins following removal of the subclavian catheters in both cases. This complication has not been previously reported. Its possible pathogenesis is discussed.

Aged↗
PubMed1983

Glucose turnover in chronic uremia: increased recycling with diminished oxidation of glucose.

The effects of chronic renal failure and hemodialysis on the glucose turnover rate, glucose carbon recycling, and glucose oxidation were evaluated in eight chronically uremic subjects. Six normal subjects served as controls. The studies were repeated in seven uremic subjects after they had been established on hemodialysis for 3 to 18 months. Glucose 13C(microliters) was administered by a prime-constant-rate infusion, and the isotopic enrichment of the whole glucose molecule (m + 6), ie, all six carbon atoms of glucose labeled with 13C and that of the C1 atom of glucose in the plasma were measured by mass spectrometry. It was assumed that the C1 atom of the glucose molecule represented the 13C enrichment of the individual glucose carbons. The "true" rate of glucose production was estimated from the dilution of the glucose 13C (microliters) mass (m + 6) in the plasma. In contrast to the whole glucose molecule (m + 6), recycling of tracer carbon resulted in an increased 13C enrichment of the C1 atom of the glucose molecule and an underestimation of glucose turnover ("apparent"). Glucose carbon recycling was estimated from the difference between the "true" and "apparent" rates of glucose turnover. The contribution of glucose to respiratory CO2 was quantified by comparing the 13C enrichment of expired CO2 with that of the plasma glucose carbon. The plasma glucose concentration after an overnight fast was similar in the uremic and control subjects (72.3 +/- 9.5 and 79.0 +/- 9.5 mg/dL, respectively; mean +/- SD).2+ while the "true" rates of glucose production were similar in both groups (normal: 2.02 +/- 0.19 mg/kg X min; uremic: 2.19 +/- 0.53 mg/kg X min).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1983

Silicon as a potential uremic neurotoxin: trace element analysis in patients with renal failure.

We analyzed multiple trace elements in tap water, dialysis fluids, and CSF of patients on dialysis and with chronic renal insufficiency. Before placement of a deionizer in the dialysis unit, we found elevated levels of aluminum, barium, copper, silicon, and zinc in tap water and dialysis fluids. These were corrected by the deionizer. CSF silicon content was increased in patients with chronic renal insufficiency and on dialysis; CSF aluminum, barium, copper, and zinc were normal.

Adult↗
PubMed1983

Glucose metabolism in chronic renal failure: adaptive responses to continuous glucose infusion.

The systemic response to a glucose infusion at 2.7 mg/kg X min was evaluated in 10 undialyzed chronically uremic patients and in 5 controls after they were fasted overnight. Systemic glucose production (Ra) was measured during the steady state using [6,6-2H2]-glucose tracer. In chronic uremic subjects, basal Ra was 1.99 +/- 0.35 ml/kg X min (mean +/- SD) and was not different from that observed in the control subjects (1.86 +/- 0.23). Basal plasma insulin and betahydroxybutyrate concentrations were significantly increased (P less than 0.01) in the uremic group. Glucose infusion resulted in complete suppression of Ra (97%) in the normal subjects. Suppression of Ra in the uremic subjects was virtually complete with the exception of 3 patients who suppressed systemic glucose production by 70%, 79%, and 87%. Glucose utilization (Ru) during glucose infusion rose from the basal state to a plateau level within the 2 hours following the start of infusion and was of the same magnitude in the uremic group as it was in the control group. During the 3rd and the 4th hour of glucose infusion, there was further increase in Ru in the normal subjects, resulting in a decrease in plasma glucose concentration. Only 4 out of 10 uremic subjects showed a similar response. There was no correlation between the metabolic changes noted and the serum creatinine concentration. These data indicate that in chronic uremia, resistance to insulin action in the peripheral tissues is present but is variable, suggesting a spectrum of metabolic disturbances unrelated to the degree of chronic renal failure.

Adolescent↗
PubMed1982

Temporal pattern of secretion of renin in the hemorrhaged dog.

The rate of renin secretion (product of renal plasma flow and the arteriovenous difference for plasma renin concentration) was measured by continuous collection of 2-min samples of arterial and left renal venous blood with continuous electromagnetic monitoring of left renal blood flow in 5 anesthetized male mongrel dogs. Measurements were made for 1 h before and at least 53 min after withdrawal of 16 ml blood/kg BW in 2 min. During the 1-h control period, there were no significant changes in measured variables. The hemorrhage was followed by a sustained reduction in average mean arterial blood pressure to 78.5 +/- 2.24% (SD) of average control values and by a sustained reduction in average renal blood flow to 87.3 +/- 4.47% (SD) of average control values. An increase in rate of secretion of renin began during the hemorrhage in every animal. The increase was transient, reaching a peak at 3-5 min and a nadir at 5-11 min after initiation of hemorrhage. At the peak, the mean value was 1996.9 +/- 977.6% (SE) of mean control, and at the nadir, it was 87.6 +/- 44.7% (SE) of mean control. After the initial treatment increase there was a gradual irregular mean increase in the rate of renin secretion. These data demonstrate that the immediate changes in rate of renin secretion in response to a brief hemorrhage sufficient to cause sustained hypotension are biphasic. This characteristic must be taken into account in modeling regulation of renin secretion and in planning experiments.

Animals↗
PubMed1981

Renal handling of beta-2-microglobulin in renal disorders: with special reference to hepatorenal syndrome.

A study of serum beta 2-microglobulin and urinary beta 2-microglobulin in patients with liver and/or kidney disease was done to determine if such information is of diagnostic help. Serum concentrations and beta 2M/Cr clearance ratios are higher in patients with primary tubular disorders than in those with glomerular diseases, a finding unaltered by hepatic disease. These data suggest either an increased production or decreased tubular degradation of beta 2M, independent of the glomerular filtration rate (GFR), in primary tubular disorders. The marked increase in urinary beta 2-microglobulin that followed insertion of the peritoneal-jugular shunt is evidence that this procedure resulted in improvement of the GFR, in previously underperfused nephrons.

Beta-Globulins↗
PubMed1980

Renal metabolism of beta 2-microglobulin. Experimental animal studies.

beta 2-microglobulin (beta 2M) is a protein of 11,800 daltons which occurs in the plasma of normal individuals at concentrations of approximately 2 microgram/ml. It is presumed to be relatively freely filterable. More than 99% of the filtered beta 2M is taken up by an active reabsorptive mechanism and catabolized by the renal tubule. The data presented here demonstrate that renal extraction is only slightly diminished by complete ureteral obstruction. The renal extraction of beta 2M is greater than can be accounted for by filtration alone. These data indicate that some uptake of beta 2M occurs from the peritubular capillary circulation. The loading of animals with beta 2M is associated with a marked tubular proteinuria suggesting that this protein may play a part in inducing tubular injury.

Animals↗
PubMed1980

Renal artery stenosis with erythrocytosis after renal transplantation.

We present here results of studies on four patients (three men, one woman) who had had cadaver renal transplants and in whom renal artery stenosis and hypertension developed. Erythropoietin-dependent erythrocytosis developed in association with these changes in the three men. All patients had stable renal function and the hypertension was well controlled. Absolute erythrocytosis thought to be secondary to local renal hypoxia due to decreased renal blood flow developed in two of the men. Erythrocytosis developed in the other man but his RBC mass was at the upper limit of normal. In these patients, we suspect that the erythropoietin-dependent erythrocytosis is secondary to intrarenal hypoxia due to renal artery stenosis. Erythrocytosis or elevated erythropoietin levels failed to develop in the woman despite severe renal artery stenosis. Possible reasons for this discrepancy are discussed.

Adult↗
PubMed1977

Characterization of human beta2-microglobulin by isoelectric focusing.

b2-Microglobulin (B2M) isolated from the urine of normal subjects and patients with cadaveric renal transplantation, showed 2 homologues by isoelectric focusing, one with a pI 5.3, the other with a pI 5.7. These proteins show identical molecular weights by dextran gel filtration and sodium dodecyl sulfate acrylamide gel electrophoresis. The immunogenic reactivity demonstrates partial identity using antiserum to human B2M from 2 different sources.

Beta-Globulins↗
PubMed1974

Renal regulation of acid-base equilibrium during chronic administration of mineral acid.

Previous studies in metabolic alkalosis have demonstrated that two factors are the prime determinants of acid excretion and bicarbonate reabsorption; first, the diversion to distal exchange sites of sodium previously reabsorbed in the proximal tubule and loop of Henle; and, second, a stimulus to sodium-cation exchange greater than that produced by a low-salt diet alone. In the present study we have examined the hypothesis that these two factors are also the prime determinants of acid excretion during the administration of mineral acid loads. To test this hypothesis, we have administered to dogs ingesting a low NaCl diet a daily dose of 7 meq/kg of H+ with anions (chloride, sulfate, or nitrate) whose differing degrees of reabsorbability influence the speed and completeness with which each is delivered to the distal nephron with its accompanying Na+. After 2-3 wk of acid administration, and after an initial urinary loss of Na+ and K+, the steady-state value for plasma [HCO3-] was 8.6 meq/liter below control in the HCl group, 3.7 meq/liter below control in the H2SO4 group, and unchanged from control in the HNO3 group; all of these values were significantly different from each other. We would propose the following explanation for our findings: when HCl is administered chronically, marked acidosis occurs because distal delivery of Cl- is restricted by the ease with which the Cl- can be reabsorbed in the proximal portions of the nephron. Only when Cl- retention produces sufficient hyperchloremia to insure delivery of Na+ (previously reabsorbed in proximal tubule and loop of Henle) to the distal nephron in quantities equal to ingested Cl is this primary constraint removed. In the case of sulfuric and nitric acids, there is no constraint on distal delivery, the nonreabsorbability of the administered anion causing prompt, total delivery of Na+ to exchange sites in quantities equal to administered hydrogen. Thus, with H2SO4 and HNO3 the sole constraint on removal of the acid load is the inability of the distal exchange mechanism to conserve the Na+ increment fully by means of H+ exchange. Escape of Na+ and K+ into the urine and the resulting stimulus to Na(+)-H+ exchange remove this constraint and are responsible for establishment of a new steady-state of acid-base equilibrium at plasma [HCO3-] levels significantly higher than those seen with HCl. The feeding of HCl in the presence of a normal salt intake led to a degree of metabolic acidosis not significantly different from that seen in dogs ingesting a low-salt diet. We suggest that the presence of dietary sodium at distal exchange sites did not enhance acid excretion because it is only after a loss of body sodium stores that sodium avidity is increased sufficiently to allow full removal of the acid load. The present findings indicate that the fundamental factors controlling acid excretion and bicarbonate reabsorption in metabolic acidosis are closely similar to those operative in metabolic alkalosis.

Acid-Base Equilibrium↗