The incidence and course of acute renal failure following cardiopulmonary bypass (CPB) was retrospectively analyzed. The incidence of oliguric acute renal failure was 1.5% and the mortality rate was 27%, a figure substantially lower than previously reported. Both peritoneal dialysis and hemodialysis were initiated early, with a mean of 3.6 days between the onset of acute renal failure and initiation of dialysis. Survivors had a mean duration of acute renal failure of 24 days. Deaths were caused by cardiac failure (one) and sepsis (two). Mortality rate from acute renal failure complicating CPB resembles that from acute renal failure related to other causes and may be lowered by early aggressive dialysis.

Chawla, R.; Gailiunas, P. Jr.; Lazarus, J. M.; Gottlieb, M. N.; Lowrie, E. G.; Collins, J. J.; Merrill, J. P. Author Information

A convertible and versatile dialysis system consisting of a PMMA hollow fiber unit and UFR controller is shown to be useful for evaluating the effect of solute and fluid removal rates on adequacy of dialysis. Post-dilution mode where high UFR is applied to the patient with matching or comparable dilution rate is concluded to be most effective modification for enhancing the clearance for "middle molecules", without sacrificing the removal rates for the small solutes.

Reliable estimation of blood flow to hemodialyzers is essential to the accurate prescription of therapy. Customarily an air bubble is timed as it traverses a racetrack of known volume and blood flow is calculated from the formula Qb (ml/min) = (volume/BT) (60 sec/min). The linearity of this relationship has recently been questioned. Air bubble velocities were statistically fit to measured blood flows over 6 hematocrit values. From the resulting relationship, Qb (ml/min) = 62 (vol/L) (L/BT)0.96, one can generate a table relating velocity to flow for clinical use.

While hemodialysis therapy in its present form is capable of sustaining life, dialysis patients are not metabolically normal and we are unable to say what technical factors contribute adequate therapy. Recent efforts to resolve these problems have led to the assumption that substances in the molecular weight range of 800 to 3000 daltons may be pathogenic in uremia and these may not be effectively removed by dialysis. Accordingly, four groups of patients (ten each) underwent changes in their routine which were theoretically designed to alter independently the concentration of small (urea) and "middle" molecules in the blood. In two groups, the concentration of urea was theoretically increased or decreased while the concentration of so-called middle molecules was maintained unchanged. In the remaining two groups, middle molecule concentration was theoretically increased or decreased while small molecule concentration was unchanged. Patients were evaluated prior to and after completing altered dialysis therapy. The results suggest three related conclusions. First, the uremic syndrome may be viewed as a constellation of abnormalities which can be subgrouped by association so that azotemia may be correlated with neuropathic disease and hypertension with weight gain or body size, for example. Second, those physiologic variables which changed after altered dialysis tended to deteriorate with increasing concentration of small molecules in the blood and remained independent of theoretical changes in middle molecules. Finally, when patients are relatively under-dialyzed, they may spontaneously modulate the reduced removal of metabolites such as urea by decreasing the dietary intake of nutrients.

A hemodialysis-ultrafiltration system has been developed and evaluated. It may be used either as a conventional hemodialyzer or as a nondialytic ultrafilter. When used as a dialyzer an ultrafiltration controller is required to fix ultrafiltration rate at the desired level. Rates of low molecular solute removal are compatible with those observed in commercially available artificial kidney systems, higher clearances are obtained for middle molecules, and the rate of ultrafiltration can be controlled within narrowly prescribed limits.

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.

The minimum parameters, which I have stressed in the first section, should be measured at least once a week, as should the chest films, the films of the vessels and so on, plus the chemistries, probably when determined by the investigator. If we are going to compare program to program, these intervals should, of course, be synchronized. The more sophisticated parameters, which I have mentioned, should be measured perhaps only when specific areas are to be investigated because the number of things which we think need to be measured is, indeed, enormous for any one laboratory. Now, if such studies are to be carried out by a number of investigators, the standard form mentioned should be instituted and yearly meetings of such groups should be held to compare notes, and particularly the adequacy of the data obtained and the method of obtaining it. Initially perhaps, after the program is underway, if enough groups are actively involved, the first meeting probably should be held six months after the beginning of the evaluation. I realize what we have put forth here is ambitious. I think it is probably wise to put in as many things as possible which might be important, and then with a little rethinking time, obviously some of these things can be eliminated. To my knowledge, we have covered almost everything that needs to be covered, and what we need to do now, perhaps, is to thin this out a little bit with discussion and consultation.

30 patients undergoing regular, three times weekly hemodialysis were treated with large doses of intramuscular testosterone with evaluation of hematopoiesis before and after treatment. A control group of 30 patients not using the drug was evaluated in similar fashion. The presence or absence of native kidneys was the most important factor determining hematocrit level and transfusion requirements in these patients, whether treated with testosterone or not. The mean hematocrit was lower and the transfusion requirements were higher in bilaterally nephrectomized patients. A significant increase in hematocrit occurred in testosterone treated nephric patients, but untreated nephric patients also had a significant rise. Important adverse side effects occurred with testosterone. Anephric patients did not increase hematocrit levels with or without testosterone.

Twenty-six patients with chronic renal failure treated by long-term hemodialysis were studied. Radiologic parathyroid bone disease was observed in 15 patients, and in these, serum parathyroid hormone (PTH) levels were significantly higher (p<0.01) than in those with no bone disease. In 14 patients, dialysate magnesium concentration was raised from the routine of 1.5–2.5 meq/liter (high) for a period of 2 mo, and in 12 patients it was reduced to 0.5 meq/liter (low). A double crossover was then performed for a further 2 mo. The increase in dialysate magnesium resulted in a decrease in serum PTH, calcium, and phosphate concentration, while a decreased dialysate magnesium caused a marked rise in serum PTH without a concomitant increase in serum calcium and phosphate. Following the cross-over, the reciprocal relation between serum PTH and dialysate magnesium was again evident. The changes in serum PTH levels with different dialysate magnesium concentrations suggest that magnesium and calcium influence parathyroid gland secretion in a similar manner, high levels suppressing PTH secretion and low levels stimulating it. The decrease in serum calcium and phosphate with low circulating PTH in high magnesium dialysis is probably due to decreased bone resorption, while the relative lack of change in serum calcium and phosphate concentrations with high PTH levels in low-magnesium dialysis is consistent with end organ refractoriness. Twenty-six patients with chronic renal failure treated by long-term hemodialysis were studied. Radiologic parathyroid bone disease was observed in 15 patients, and in these, serum parathyroid hormone (PTH) levels were significantly higher (p<0.01) than in those with no bone disease. In 14 patients, dialysate magnesium concentration was raised from the routine of 1.5–2.5 meq/liter (high) for a period of 2 mo, and in 12 patients it was reduced to 0.5 meq/liter (low). A double crossover was then performed for a further 2 mo. The increase in dialysate magnesium resulted in a decrease in serum PTH, calcium, and phosphate concentration, while a decreased dialysate magnesium caused a marked rise in serum PTH without a concomitant increase in serum calcium and phosphate. Following the cross-over, the reciprocal relation between serum PTH and dialysate magnesium was again evident. The changes in serum PTH levels with different dialysate magnesium concentrations suggest that magnesium and calcium influence parathyroid gland secretion in a similar manner, high levels suppressing PTH secretion and low levels stimulating it. The decrease in serum calcium and phosphate with low circulating PTH in high magnesium dialysis is probably due to decreased bone resorption, while the relative lack of change in serum calcium and phosphate concentrations with high PTH levels in low-magnesium dialysis is consistent with end organ refractoriness.

Hypertension is a frequent and early component in the uremic syndrome. Extracellular volume expansion causes hypertension in approximately 75% of patients with chronic renal failure and therefore is responsive to hemodialysis. The other major cause of hypertension in uremic patients is hyperreninemia. The degree of hypertension in this small group of patients is more extreme, is not responsive to volume manipulations by dialysis, and often will require bilateral nephrectomy. The route of excretion and drug-dosage alteration in hypertension treatment before initiation of dialysis are important. Indications for hemodialysis and bilateral nephrectomy for complicated hypertension and in preparation for renal transplantation vary in different programs. The increased incidence of cardiovascular death in chronic hemodialysis patients should modify these indications to obtain earlier and better control of hypertension.

No AccessJournal of Urology1 Dec 1974Transplantation without Bilateral Nephrectomy John H. Ball, J. Michael Lazarus, Edmund G. Lowrie, Nicholas L. Tilney, Alan H. Bennett, and John P. Merrill John H. BallJohn H. Ball More articles by this author , J. Michael LazarusJ. Michael Lazarus More articles by this author , Edmund G. LowrieEdmund G. Lowrie More articles by this author , Nicholas L. TilneyNicholas L. Tilney More articles by this author , Alan H. BennettAlan H. Bennett More articles by this author , and John P. MerrillJohn P. Merrill More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)59833-XAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1974 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited ByKabler R and Cerny J (2018) Pre-Transplant Urologic Investigation and Treatment of End Stage Renal DiseaseJournal of Urology, VOL. 129, NO. 3, (475-478), Online publication date: 1-Mar-1983.Lawson R (2018) Editorial CommentJournal of Urology, VOL. 129, NO. 3, (478-478), Online publication date: 1-Mar-1983.Barry J, Larson B, Fischer S, Norman D and Bennett W (2018) Beneficial Effect of Pre-Transplant Splenectomy for Leukopenia in Primary Cadaver Kidney TransplantsJournal of Urology, VOL. 129, NO. 3, (478-480), Online publication date: 1-Mar-1983.Freed S (2018) The Present Status of Bilateral Nephrectomy in Transplant RecipientsJournal of Urology, VOL. 115, NO. 1, (8-11), Online publication date: 1-Jan-1976. Volume 112Issue 6December 1974Page: 706-709 Advertisement Copyright & Permissions© 1974 by The American Urological Association Education and Research, Inc.MetricsAuthor Information John H. Ball More articles by this author J. Michael Lazarus More articles by this author Edmund G. Lowrie More articles by this author Nicholas L. Tilney More articles by this author Alan H. Bennett More articles by this author John P. Merrill More articles by this author Expand All Advertisement Loading ...

A method for assessing cellular immunity to alloantigens has been applied to clinical transplantation. Direct lymphocyte-mediated cytotoxicity (L.M.C.) was more sensitive in detecting presensitisation in potential renal allograft recipients than was the standard test for cytotoxic antibody. Twenty-five patients on hæmodialysis were studied. All twelve patients who had cytotoxic antibody against a donor also had direct L.M.C. against that donor. However, eleven patients had positive direct L.M.C. assays with donors against whom negative antibody cross-matches were obtained. Early results in a prospective study of renal transplantation suggest some predictive value for direct L.M.C. as an assay of presensitisation.

Baroreceptor activity and postural blood volume changes were evaluated in four normotensive and nine hypertensive uremic patients before and after bilateral nephrectomy. Baroreceptor activity, reflected by the slope of linear regression of R-R interval with drug-induced systolic blood pressure elevation, was significantly lower in hypertensive than in normotensive patients. Six of nine patients had normal blood pressure following bilateral nephrectomy; however, the mean slopes of all nine patients, irrespective of postnephrectomy blood pressure, approached that of normotensive uremic patients. The slopes of both normotensive and hypertensive patients, before and after bilateral nephrectomy, were significantly less than normal controls. Similar results were found in lowering blood pressure with amyl nitrite.Depressed baroreceptor activity is suggested to be secondary to neuropathy of the autonomic nervous system, chronic hypertension, heart disease, and anemia. It is speculated that this reduced baroreceptor sensitivity may accentuate the postural symptoms primarly induced by volume reduction on hemodialysis. There is no evidence in this study that depressed baroreceptor activity, as opposed to a reset baroreceptor, is a cause of hypertension in patients with chronic renal failure.