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Kidney International, Vol. /2 (1977), pp. 279—284

Competitive effects of hypokalemia and volume depletion on plasma activity, and catecholamine concentrations in patients

WILLIAM L. HENRICH, FRED H. KATZ, PERRY B. MOLINOFF and ROBERT W. SCHRIER

Departments of Medicine and Pharmacology, University of Colorado Medical Center, and Denver Veterans Administration Hospital, Denver, Colorado

Competitive effects of hypokalemia and volume depletion on toutes les hemodialyses mais Ic potassium plasmatique n'a diminué , aldosterone and catecholamine concentrations (4,8 a 3,4 mEq/litre, P < 0,001) que dans Ic groupe soumis a une in hemodialysis patients. The effects of isokalemic and hypokalemic dialyse hypokaliémique. Les diminutions rnoyennes du poids cor- ultrafiltration dialysis on plasma renin activity (PRA), aldosterone porel (— 1,77 vs. — 1,66 kg) et de Ia pression artérielle moyenne (125 (ALDO) and plasma catecholamine (CA) concentrations were in- a 109 vs. 126 a 108 mm Hg) ont été semblables dans les deux vestigated in eight patients with end-stage renal failure. Plasma groupes. PRA a augmenté au cours de Ia dialyse aussi bien dans Ic concentration was kept constant during each hemodialysis, groupe isokaliémique (4,55 a 8,85 ng/ml/hr, P < 0,02) que dans Ic but plasma potassium decreased (4.8 to 3.4 mEq/liter, P < 0.001) groupe hypokaliémique (2,18 a 3,19 ng/mI/hr, P < 0,01). Ces only in the hypokalemic dialysis group. The falls in mean body modifications do poids corporel, de Ia pression artérielle et de PRA weight (—1.77 vs. —1.66 kg) and mean pressure (125 to 109 ne sont pas significativement différentes darts les deux groupes. Des vs. 126 to 108 mm Hg) were similar in the isokalemic and hypoka- differences importantes, cependant, sont apparues entre les deux lemic dialysis patient groups. PRA increased during dialysis both groupes. Alors que l'ALDO moyenne augmente (105 a 198 pg/mI, in the isokalemic (4.55 to 8.85 ng/ml/hr, P < 0.02) and hypoka- P < 0,05) au cours de Ia dialyse isokaliémique, dIe chute signifi- lemic (2.18 to 3.19 ng/ml/hr, P < 0.01) groups. These changes in cativement au coors de Ia dialyse hypokaliCmique (120 a 36,8 body wt, , and PRA were not significantly different ng/ml, P < 0,005). Avant Ia dialyse les CA sont significativement in the isokalemic and hypokalemic dialyses. There were, however, supérieures aux valeurs normales dans les deux groupes. Avec Ia important differences between the isokalemic and hypokalemic dialyse les CA ne sont pas significativenient modifiées dans Ic groups. While the mean ALDO increased (105 to 198 pg/mI, P < groupe isokaliCmique et chutent dans le groupe hypokaliemique 0.05) during the isokalemic dialyses, ALDO actually fell signifi- (1,27 a 0,93 ng/ml, P < 0,02). Malgré Ia diminution du poids cantly during the hypokalemic dialyses (120 to 36.8 pg/mI, P < corporel et de Ia pression artérielle dans les deux groupes, Ia 0.005). Prior to dialysis, CA's were increased significantly above fréquence cardiaque n'augmente qu'au cours de Ia dialyse isokalié— normal values in both dialysis groups. With dialysis, CA's did not mique. En conclusion, ces résultats obtenus chez des malades change significantly in the isokalemic group and actually fell in the soumis a l'hCmodialyse démontrent l'effet d'une diminution du hypokalemic group (1.27 to .93 ng/ml, P < 0.02). In spite of potassium plasmatique dans le sens de Ia suppression de I'ALDO, decreased body wt and blood pressure in both groups, heart rate effet predominant malgré Ia diminution de Ia pression artérielle et increased only during the isokalemic dialysis. These results demon- du poids corporel et I'augmentation de PRA concomitants. strate a dominant effect of a fall in plasma potassium concentra- L'augmentation des CA, chez ces malades, a peut-Ctre une inter- tion to suppress ALDO, despite a concomitant fall in blood pres- action avec Ic bilan do sodium et contribue a I'hypertension. La sure and body wt and a rise in PRA. The elevated CA diminution des CA et I'absence de tachycardie au cours de Ia concentrations in these patients may possibly interact with sodium dialyse hypokaliCmique soulCve l'hypothèse qu'une chute de Ia balance and contribute to the hypertension in these patients. The concentration de potassium plasmatique puisse determiner ou dé— fall in CA's and absence of tachycardia during hypokalemic masquer une insuffisance du système rerveux autonome chez ces dialysis raises the possibility that a fall in plasma potassium con- malades atteints d'insuffisance rénale chronique, malades dont on centration may cause or unmask aut000mic insufficiency in these sait qu'ils soot exposés a de tels désordres. chronic renal failure patients who are predisposed to this disorder.

Effets compétitifs de l'hypokaliémie et de Ia diminution du volume In nephrectomized patients, dialysis ultrafiltration sur l'activité rénine et lea concentrations plasmatiques d'aldostérone has been found to be associated with a rise in plasma et de catécholamines chez les malades en hémodialyse. Les effets de aldosterone concentration [1]. This observation sug- Ia dialyse par ultrafiltration isokaliémique et hypokaliemique sur l'activité rénine plasmatique (PRA), l'aldostérone (ALDO) et les gests that a rise in plasma renin activity is not a catécholamines (CA) plasmatiques ont été étudiés chez huit mal- necessary accompaniment of the effect of volume de- ades au stade terminal de I'insuffisance rénale. La concentration pletion on plasma aldosterone. During ultrafiltration plasmatique de sodium a été maintenue constante au cours de dialysis, however, a fall in plasma sodium concentra- tion also may occur and account for any rise in Received for publication February 28, 1977; plasma aldosterone concentration [1, 2]. Alterna- and in revised form June I, 1977. tively, any failure of ultrafiltration dialysis to stimu- 1977, by the International Society of Nephrology. late plasma aldosterone levels could be related to a

279 280 Henrichel a! concomitant fall in plasma potassium concentration one set of seven dialyses involving five of the patients, [3—5]. Moreover, circulating catecholamines could af- the dialysate potassium concentration was adjusted fect either the release of renin or aldosterone during so that plasma potassium did not change by more ultrafiltration dialysis. than 0.3 mEq/liter. In another group of dialyses, in In the present studies, ultrafiltration dialysis was which eight patients (including the original five pa- performed on chronic renal failure patients possess- tients) underwent 12 dialyses, plasma potassium con- ing their own kidneys. During all dialyses, plasma centration was allowed to decrease. In both sets of sodium concentration was kept constant. In this set- dialyses, the goal was for the patients to lose weight ting, the effect of isokalemic and hypokalemic ultra- by ultrafiltration, and all patients lost at least 0.5 kg dialysis on plasma renin, aldosterone, and during the dialysis period. catecholamine concentrations was examined. iso- All patients were weighed before and after dialysis; kalemic ultrafiltration dialysis was associated with a food consumed during dialysis was weighed and sub- rise in plasma renin and aldosterone but not plasma tracted from the postdialysis weight. Blood pressures catecholamine concentrations. In contrast, hypokale- and heart rates were measured in the supine position mic ultrafiltration dialysis was associated with a rise in immediately before and after dialysis. No patient had plasma renin activity, but a fall in plasma aldosterone any adverse effects during either dialysis protocol. All and catecholamine levels, Although plasma cate- blood samples were obtained at the beginning and cholamine levels did not increase with ultrafiltration termination of the dialysis from the patient's arterial dialysis in either group, the baseline levels of plasma dialysis line. Plasma for measurement of aldosterone catecholamines in all the patients with chronic renal and peripheral renin activity was collected in iced failure were well above levels found in normal sub- tubes, cold centrifuged, and frozen immediately. The jects. method of analysis of aldosterone and plasma renin From these results, we conclude that hypokalemia activity was by radioimmunoassay [6, 7]. In our labo- may predominate over volume depletion and a ratory, the mean plasma renin activity and aldoste- plasma renin increase as a regulator of plasma al- rone concentrations in normal individuals who were dosterone concentration in chronic renal failure pa- upright for two hours and on a normal sodium intake tients, In these patients, the rise in plasma renin activ- (113 mEq/day) were 4.40.9 ng/ml/hr and 334 30 ity during volume depletion was neither enhanced by pg/mI, respectively. Plasma for measurement of cate- hypokalemia nor accompanied by a rise in plasma cholamines was collected in heparinized tubes and catecholamines. Lastly, although plasma cate- centrifuged at 4°C. Plasma proteins were removed cholamine concentrations were uniformly elevated in following the addition of perchloric acid to a final these patients with end-stage renal failure, these high concentration of 0.lN. Catecholamine concentra- catecholamine levels were not stimulated by iso- tions were determined by a modification of the enzy- kalemic volume depletion, and actually fell during matic technique of Coyle and Henry [8], as described hypokalemic volume depletion. This latter finding by Nelson and Molinoff [9]. The mean ambulatory suggested that hypokalemia might possibly cause or catecholamine concentration in six normal individ- uncover autonomic insufficiency in the uremic pa- uals was 0.36 0.06 ng/ml. Electrolyte concentra- tient. This possibility was supported by the finding tions were determined by flame photometry in the that isokalemic, but not hypokalemic, ultrafiltration routine chemistry laboratory. dialysis significantly increased heart rate in these Statistics were performed using Student's i test and dialysis patients. rank sum test. Data are presented as the mean the standard error of the mean (sEM),anda P value of Methods <0.05 was considered significant. Eight, stable, chronic hemodialysis patients, taking no antihypertensive medicines, were utilized in the Results study. Informed consent was obtained prior to entry Changes in weight during dialysis. Patients in the into the study. All of the patients were male, and the isokalemic dialysis group had a weight decrease from mean age was 48 5 (sEM) yr; the mean length of 70 + 5 to 68 5 kg (P <0.02) during dialysis; the time on dialysis was 45 14 months. All patients hypokalemic group declined from 75 2 to 73 2 kg possessed their own kidneys. All patients were (P < .001) during dialysis. Both the absolute weight dialyzed for six hours on hollow fiber dialyzers (Cobe losses (1.8 vs. 1.7 kg) and the percentage of body wt Hollow Fiber HF 130 [1.3 m2]), using a central deliv- declines (2.3 vs. 2.7%) were thus similar in both ery system (Drake-Willock, model 4009). dialysis groups. Although not significantly different, Two separate dialysis protocols were followed. In the discrepancy between the mean predialysis weights Hypokalemia and volume depletion in dialysis patients 281 ofthe groups is accounted for by higher weights of Before dialysis After dialysis the three additional subjects in the hypokalemic 105______group. Changes in blood pressure during dialysis (Fig. I). Mean blood pressure in the isokalemic dialysis group declined from 125 5 to 109 7 mm Hg (P < 0.001) 100 - during dialysis, and the hypokalemic group had a decrement in mean blood pressure from 126 3 to 108 + 6 mm Hg (P < 0.001). The change in mean blood pressure was, therefore, similar in both isoka- lemic and hypokalemic groups. 95 -

Changes in heart rate during dialysis (Fig. 2). The a, isokalemic dialysis group had a significant increase in

Ca heart rate from 88 5 beats/mm before, to 99 4 a, beats/mm after dialysis (P < 0.02). In the hypo- I90 - kalemic group, however, heart rate was not signifi- cantly altered by ultrafiltration dialysis (873 beats/ mm before, to 90 1 beats/mm after dialysis). The postdialysis heart rate was significantly greater in the 85 - isokalemic group (P < 0.025). Changes in sodium concentration during dialysis. ______S Isokalemic dialysis Plasmasodium concentration was held constant dur- ing dialysis in both groups of dialyses. In the iso O—————O Hypokalemic dialysis 80______kalemic group, the sodium was 136 1 mEq/liter be- fore and 138 1 mEq/liter after dialysis (P = in Fig. 2. Theisokalemic dialysisgroup showing a significant increase in NS); pulse during the course of dialysis. The hypokalemic dialysis group, in contrast, had no significant change in pulse.

Before dialysis After dialysis the hypokalemic group, the serum sodium was 139 I before and 138 I after dialysis (P =NS). Changes in serum potassium during dialysis. The isokalemic dialysis group had a mean serum potas- sium concentration of 40.3 mEq/liter before and 4 130 - 0.2 mEq/liter after dialysis. Thus, no significant change in serum potassium was allowed to occur in this group. In contrast, in the hypokalemic group of E E dialyses, mean serum potassium concentration fell a, 0.2 mEq/liter before, to 3.4 0.1 120 from 4.8 P <0.001 a, mEq/liter after dialysis (P < 0.001). Comparison between groups indicated that the postdialysis potas- I, P<0.001 a, sium concentration was significantly lower (P < 0.02) in the hypokalemic patients. I,C110 a, Changes in plasma renin activity during dialysis. In both groups, a significant increase in plasma renin activity was seen during dialysis. The isokalemic group had an increase in plasma renin activity from 100 4.6 1.8 to 8.9 3.6 ng/ml/hr (P < 0.02), and the hypokalemic group had an increase from 2.20.5 to S Isokalemic dialysis 3.2 0.8 ng/ml/hr (P < 0.01). Although not signifi- O-————-O Hypokalemic dialysis cantly different, the lower predialysis plasma renin in the hypokalemic group may have been influenced by Fig. 1. A comparable and significant fall in blood pressure observed the higher prediaJysis potassium concentration in in both the isokalemic (solid line) and hypokalemic (dashed line) that group; additionally, the three subjects added to dialysis groups. the hypokalemic group had plasma renin activities 282 Henrich et a!

which were lower, and thus lowered the mean value. The inclusion of these three subjects in the analysis Before dialysis After dialysis 2.5______of the results did not, however, alter the statistical sig ______• nificanceof the other variables analyzed in the paper. Isokalemic dialysis Changes in plasma aldosterone concentration during o—————o Hypokalemic dialysis dialysis (Fig. 3). In the isokalemic group of dialyses, 2.0 - plasma aldosterone concentration increased from 105 61 to 198 + 72 pg/mI (P < 0.05). In striking 0 C,

contrast, despite a comparable amount of volume 5, 0C, depletion and a significant increase in plasma renin 0 activity, a decrease in aldosterone concentration oc- — curred, from 12040 to 37 18 pg/mI (P < 0.005), 0 with the hypokalemic dialyses. The predialysis .00 plasma aldosterone values in the groups were com- 5) parable, but the postdialysis values were significantly 1.0- E different (P < 0.05). C, 5- Changes in catecholamines during hemodialysis (Fig. 4). The predialysis plasma catecholamine concentra- tions were significantly higher in both isokalemic and hypokalemic groups when compared to normals (P < 0.01). In the isokalemic dialyses, catecholamine con- 0lrange,mean±2sEM centration was 1.77 0.43 ng/mI before and 1.51 0.21 ng/ml after dialysis (P =NS).In the hypo 0______kalemic patients, the catecholamine concentration decreased from 1.27 0.17 ng/ml before, to 0.93 Fig.4. The catecholamine concentration from a group of normals, depictedby the hatched area at the bottom of the graph. Both dialysisgroups had significantly higher predialysis catecholamine concentrations than normals. lsokalemic dialysis patients had no significant change in catecholamine concentrations, whereas hypo- kalemic dialysis patients had a significant fall in catecholamine concentrations.

0.08 ng/mI after dialysis (P < 0.02). The postdialysis catecholamine concentration was significantly lower in the hypokalemic group than the isokalemic group (P < 0.025). Changes in serum bicarbonate, calcium, magnesium, and cortisol during dialysis. An equivalent increase in serum bicarbonate occurred in both groups during dialysis, from 21.1 0.8 to 24,4 0.5 mEq/liter (P < 0.001) in the isokalemic dialysis group, and from 20.3 0.9 to 24.5 0.7 mEq/liter (P < 0.001) in the hypokalemic dialysis group. Serum calcium did not change in either group. Isokalemic dialysis patients had a calcium concentration of 9.7 + 0.5 mEq/liter before dialysis and a postdialysis calcium concentra- tion of 10.0 0.4 mEq/Iiter, P =NS.The hypo- kalemic patients' calcium concentrations were 9.8 0.3 mEq/liter before and 9.8 0.3 mEq/liter after dialysis, P =NS.Four of the patients had serum cortisol measured during isokalemic and hypo- kalemic dialyses, and no significant change was ob- Fig. 3. The isokalemic dialysis group showing a significant increase in served during either experimental condition. Sim- aldosterone concentration during dialysis. The hypokalemic dialysis group, however, underwent a significant reduction in aldosterone ilarly, the serum magnesium concentrations were not concentration during dialysis. significantly altered during dialysis. Hypokalemia and volume depletion in dialysis patients 283

Discussion phasized that there is evidence that aldosterone is Several potential factors may be involved in the involved in the urinary excretion of both sodium and regulation of plasma aldosterone concentration in potassium over a wide range of renal function, in- patients with advanced chronic renal failure. In- cluding patients with advanced renal failure who do cluded among these are changes in plasma sodium, not require maintenance hemodialysis [11]. potassium, and renin concentrations, or some other Another observation in the present study was the consequence of volume depletion, such as alterations finding of high baseline plasma catecholamine con- in plasma catecholamines. centrations in these patients with advanced renal fail- A fall in plasma sodium concentration has been ure. Preliminary results using the fluorirnetric method suggested to stimulate plasma aldosterone [2]. Dur- of analysis of plasma catecholamines have suggested ing hemodialysis, plasma sodium concentration fre- high concentrations in uremic patients [12, 13]. This quently decreases and, thus, could account, at least in finding was confirmed in the present study using the part, for the increase in plasma aldosterone that has more sensitive radiometric enzymatic technique [8, been observed during fluid removal by ultrafiltration 9]. A preliminary communication, however, also sug- in nephrectomized patients [1, 2]. While such studies gested a correlation between plasma catecholamine in nephrectomized patients seem clearly to in- and renin concentrations [13]. In the present study, criminate a pathway independent of the renin-angio- plasma renin activity rose during both isokalemic and tensin system, the precise pathway has not been de- hypokalemic dialysis, and yet no detectable increase fined. In the present study, there can be little doubt in plasma catecholamine concentrations was ob- that plasma aldosterone concentration may be al- served. The high baseline concentrations of plasma tered in chronic renal failure patients in the absence catecholamines are probably due both to a decreased of changes in plasma sodium concentration. Changes urinary excretion and diminished metabolism which in plasma cortisol, calcium, and magnesium also may be related to a decline in catechol-O-methyl failed to explain the observed effects of ultrafiltration transferase activity [13]. In any case, it is not unrea- hemodialysis on plasma aldosterone concentration. sonable to suggest that the high concentrations of The present results provide further evidence that plasma catecholamines present in patients with ad- changes in plasma aldosterone concentration can vanced renal failure may be a factor in the high clearly be dissociated from changes in plasma renin incidence of hypertension in this population. In this activity. This dissociation between plasma aldoste- regard, it is interesting to note that Kim et al [14] rone and renin was primarily accomplished by alter- have demonstrated that an increase in peripheral vas- ing plasma potassium concentration. During iso- cular resistance, in addition to an increase in extra- kalemic ultrafiltration hemodialysis, rises in both cellular fluid volume, is involved in the hypertension plasma aldosterone and renin were observed. Dur- of patients on maintenance hemodialysis. While the ing ultrafiltration dialysis, however, which lowered role of catecholamines in the hypertension of chronic blood pressure and body weight by a comparable renal failure is intriguing, a comparison of cate- degree, but allowed plasma potassium to fall (4.8 to 3.4 cholamines in normotensive and hypertensive dialysis mEq/liter), plasma renin activity rose but plasma a!- patients, however, will be necessary to confirm this dosterone concentration fell significantly. These find- possibility. ings, therefore, demonstrate that hypokalemia of a The high plasma catecholamine concentrations in degree frequently observed during ultrafiltration patients with advanced renal failure may also relate dialysis may dominate over volume depletion, a fall to dialysis hypotensive syndromes. Orthostatic hypo- in blood pressure, and a rise in plasma renin activity tension is characteristic of patients with pheochro- to suppress plasma aldosterone concentration. The mocytoma and presumably relates to the high level of physiologic importance of such a role of plasma po- supine sympathetic tone which does not increase fur- tassium to influence plasma aldosterone concentra- ther during the venous pooling which occurs on tion in patients with end-stage renal failure remains standing. Similarly, the high concentration of plasma to be defined, but obviously would have to relate to catecholamines in our patients with advanced renal the extrarenal effects of aldosterone. The distribution failure did not increase during ultrafiltration dialysis. of sodium and water between intracellular and extra- This failure of the concentrations of plasma cate- cellular compartments, and thus, the control of blood cholamines to rise may relate to their initial high pressure could be such an extrarenal effect of aldoste- concentration or to the fact that clinical or subclinical rone. Another extrarenal effect may involve modu- autonomic insufficiency is a frequent accompaniment lation of serum electrolytes through effects on the of advanced renal failure [15, 16]. In any case, the gastrointestinal system [10]. Also, it should be em- occurrence of a fall in blood pressure at the onset of 284 Henrichet al

dialysis prior to fluid removal by ultrafiltration could drews, and Nancy Miller. Secretarial assistance was result from the failure of sympathetic tone to increase provided by Ms. Linda M. Benson. in response to the hemodynamic stresses of hemo- Reprint requests to Dr. R. W. Schrier, Medicine/Renal Depart- dialysis, eg., extracorporeal blood in dialysis lines. ment, Box C281, University of Colorado Medical Center, 4200 It is also interesting to note that not only did East Ninth A venue, Denver, Colorado 80262, U.S.A. plasma catecholamines fail to rise in response to re- moval of fluid by ultrafiltration with a consequent fall References in blood pressure, but hypokalemic dialysis was ac- I. MCCAA RE, MCCAA CS, READDG,BOWER JD, GUYTON AC: tually found to be associated with a fall in plasma Increased plasma aldosterone concentration in response to hemodialysis in nephrectomized man. Circ Res 31:473—480, catecholamine concentrations. Hypokalemia has 1972 been found to be associated with dysautonomia in 2. MCCAA RE, BOWERJD,MCCAA CS: Relative influence of patients with primary hyperaldosteronism [17]. It is acute sodium and volume depletion on aldosterone secretion possible that in patients with advanced renal failure, in nephrectomized man. Circ Res 33:555—562, 1973 who already have a propensity for autonomic in- 3. COOKE CR, HORVATH JR, MOORE MA, BLEDSOET,WALKER WG:Modulation of plasma aldosterone concentration by sufficiency [15], a fall in plasma potassium may un- plasma potassium in anephric man in the absence of a change cover or cause impairment in sympathetic responses. in potassium balance. J C/in Invest 52:3028—3032, 1973 In support of this suggestion is the observation in the 4. CANNON PJ, AMES RP, LARAGH JH: Relation between potas- present study that a significant increase in pulse rate sium balance and aldosterone secretion in normal subjects and occurred during ultrafiltration in isokalemic but not in patients with hypertensive or renal tubular disease. J C/in Invest 45:865—879, 1966 hypokalemic hemodialysis. More definitive studies, 5.WEIDMANP,HORTON R, MAXWELLMH,FRANKLINSS,FICH- however, are required to investigate this possibility. MANM: Dynamic studies of aldosterone in anephric man. In conclusion, the present results demonstrate that Ins 4:289—298, 1973 hypokalemia may dominate over volume depletion 6. KATZ FH, SMITH JA: Radioimmunoassay of angiotensin: I. and a rise in plasma renin activity to suppress plasma Comparison of two renin activity methods and use for other measurements of the renin system. C/in Chem 18:528—533, aldosterone concentrations in patients with advanced 1972 renal failure, These patients also were shown to have 7.KATZFH, ROMFH P, SMITH JA: Diurial variation of plasma high plasma catecholamine concentrations which are aldosterone, cortisol, and renin activity in supine man. J C/in not stimulated by either isokalemic or hypokalemic Endocrino/ Metab 40:125—134, 1975 ultrafiltration dialysis and a mean fall in blood pres- 8. COYLE iT, HENRY D: Catecholamines in fetal and newborn rat brain. J Neurochem 21:61—67, 1973 sure of 18 mm Hg. These high catecholamine concen- 9. NELSON DL, MOLINOFF PG: Distribution and properties of trations may have pathogenetic importance both in adrenergic storage vesicles in nerve terminals. J Pharmaco/ the hypertension and dialysis hypotension syndromes Exp TIter 196:346—359, 1976 observed in this population of patients. Lastly, the 10. CHARRONRC,LEME CE, WILSON DR, ING TS, WRONG OM: lack of increase in heart rate and a fall in cate- The effect of adrenal steroids on stool composition, as re- vealed by in vivo dialysis of feces. C/in Sd 37:151—167, 1969 cholamines during hypokalemicultrafiltration II. Sd-tRIER RW, REGAL GM: Influence of aldosterone on so- dialysis suggest that hypokalemia may either cause or dium, water and potassium metabolism in chronic renal dis- uncover autonomic insufficiency in this group of pa- ease. KidneyIn! 1:156—168,1972 tients already prone to this disorder. 12.BRECHTHM, ERNST W, KOCH KM: Plasma norepinephrine concentrations in regular hemodialysis patients (abstr.). Kid- ney In! 8:124,1975 Acknowledgments 13. ATUKNO, WESTERVELT FB, PEACH M: Altered catecholamine metabolism, plasma renin activity and hypertension in renal A portion of this work was presented at the West- failure (abstr). mt Congr Nephro/, Florence, 1975, p. 475 ern Society for Clinical Research, Carmel, California, 14. KIM KE, ONESTI G, SCHWARTZAR,CHINITZ JL, SWARTZ C: February 1977. This study was supported in part by Hemodynamics of hypertension in chronic end-stage renal grants from NIH (HL 15629), NS 10206, and VA disease. Circu/aiion46:456—464,1972 IS. EWING Di, WINNEY R: Autonomic function in patients with Project 4844—01. Dr. Henrich is a recipient of a Na- chronic renal failure on intermittent hemodialysis. tional Kidney Foundation Research Fellowship 15:424—429, 1975 award. Dr. Molinoff is an Established Investigator 16. KERSH ES, KRONFIELD Si, UNGER A, POPPER RW, CANTER 5, of the American Heart Association. The authors COHN K: Autonomic insufficiency in uremia as a cause of acknowledge the assistance of Ms. Anne Bobal, R.N., hemodialysis-induced hypotension. N. Eng/ .1 Med 290:650— Dr. John D. Conger, and the staff of the Denver VA 653,1974 17. BIGLIERI EG, MCILROY MB: Abnormalities of renal function Hospital Dialysis Unit. Technical assistance was pro- and circulatory reflexes in primary aldosteronism. Circulation vided by Ellen F. Roper, Diane E. Loeffel, Jane An- 33:78—86, 1966