Concentrations of thyroxine-binding globulin in sera and peritoneal dialysates in patients on chronic peritoneal ambulatory dialysis

Losses in thyroxine-binding globulin (TBG) in peritoneal dialysate and thyroid function were evaluated in patients undergoing continuous ambulatory peritoneal dialysis (CAPD), in comparison to patients on hemodialysis (HD) without TBG loss in the dialysate. The TBG concentration in the peritoneal dialysate was 0.26 +/- 0.09 microgram/ml (mean +/- SD, n = 24), with a daily loss of 2.47 +/- 0.94 mg. The serum TBG level in CAPD patients was 21.0 +/- 4.71 micrograms/ml (n = 24), which was not significantly different from that in HD patients (20.0 +/- 5.72 micrograms/ml, n = 24) or in healthy Japanese subjects. The serum TBG level correlated positively with the TBG loss and TBG level in the peritoneal dialysate (p less than 0.001). The serum T4 level in CAPD patients (4.93 +/- 1.38 microgram/dl, n = 24) was significantly greater than in HD patients (4.08 +/- 1.30 microgram/dl, n = 24, p less than 0.05).     

Residual renal function in hemodialysis patients may protect against hyperaluminemia

We investigated 106 home hemodialysis patients whose mean [+/- SEM] serum aluminum (Al) concentration was 60.9 +/- 4.1 micrograms/liter. Serum Al concentration was inversely related to daily urine output (r = -0.52, P less than 0.001). Urine volume and measurements of Al exposure were included in a multivariate analysis of serum Al concentration in the 62 patients whose urine output was greater than 10 ml/day. The multiple correlation coefficient (r) was 0.70 (P less than 0.001) and the percentage contributions to r2 (indicating the relative importance of each factor) were: urine output 57%, oral Al intake 36%, total dialysis hours 7%. The additional contribution from cumulative water Al was negligible. In a subgroup of 26 patients with a urine output exceeding 10 ml/day, urinary Al excretion averaged 15.4 micrograms/day, and renal Al clearance and serum Al concentration were inversely related (r = -0.69, P less than 0.001). We conclude that Al-containing phosphate binders were a more important source of Al than was dialysate in these patients and that residual renal function can reduce the severity of hyperaluminemia in hemodialysis patients.     

High deposition rate of aluminum in tissues in diabetic hemodialysis patients

Aluminum (Al) accumulation in bone is a serious problem in patients on hemodialysis. We studied deferoxamine infusion test (DFO test) in 14 diabetic patients on hemodialysis (HDDM) and 23 hemodialysis patients originated from glomerulo nephritis (HDCGN) to determine whether Al accumulation is different between the two groups or not. There was no difference in hemodialysis duration and total oral intake of Al containing drugs between two groups. Serum C-terminal parathyroid hormone (C-PTH) in HDDM was lower than that in HDCGN group (1.82 +/- 1.30 vs. 3.80 +/- 1.82 ng/ml; P less than 0.01). However serum Al (s-Al) levels were comparable (61.9 +/- 53.0 vs, 45.0 +/- 32.3 micrograms/l). A significant correlation was observed between duration of dialysis period and s-Al in HDDM (r = 0.806, p less than 0.01), but in HDCGN, the relation was not significant. The patients in HDDM whose cumulative aluminum intake was less than 2.0 kg showed the higher serum A1 concentrations before DFO and greater increases in s-Al after DFO test, as compared with those in HDCGN with matched aluminum intake (93.8 +/- 67.6 vs. 35.9 +/- 23.6 micrograms/l; p less than 0.001 and 141.2 +/- 81.8 vs. 70.3 +/- 41.1 micrograms/l; p = 0.035). These results indicate that in uremic diabetic patients with lower intake of Al containing drugs, an early accumulation of Al in the whole body occurs possibly because of the enhanced absorption rate of Al at an intestine and/or the low PTH level.     

Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia

The efficacy of calcium carbonate (CaCO3) as a phosphate binder has been limited by its tendency to cause hypercalcemia. Since standard dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing hypercalcemia with large doses of CaCO3 by inducing positive calcium balance during hemodialysis (HD), we compared control of hyperphosphatemia in 41 HD patients during 4 months each of aluminum hydroxide (Al(OH)3) and CaCO3 when the dialysate calcium concentration was lowered, as required, to maintain the predialysis serum calcium concentration within the normal range. Mean predialysis serum phosphorus and calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(OH)3 therapy (2.9 +/- 0.2 g/day). Reducing the dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed hypercalcemia on CaCO3 decreased serum calcium (-1.1 +/- 0.15 mg/dl) and ionized calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum calcium and phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in acidosis or biochemical hyperparathyroidism was observed during CaCO3 therapy but serum aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic hyperphosphatemia as effectively as Al(OH)3 without increasing the predialysis serum calcium x phosphorus product, provided serum calcium is maintained within the normal range by adjusting the dialysate calcium concentration.     

Effect of body iron stores on serum aluminum level in hemodialysis patients.

To evaluate the influence of body iron stores on the serum aluminum (Al) level, we studied the correlation between iron status (the serum ferritin, serum iron and transferrin saturation) and serum Al levels in 68 severely anemic hemodialysis patients. Among them, 36 underwent the desferrioxamine (DFO) mobilization test. These 68 patients were divided into three groups according to their serum ferritin level. The basal Al level in the patient group was 41.4 +/- 37.4 micrograms/l (control, 4.1 +/- 2.4 micrograms/l). The serum Al level after DFO infusion of the patient group was 111.1 +/- 86.8 micrograms/l. A significantly higher basal Al and peak Al level after DFO infusion were found in group 1 patients (serum ferritin less than 300 micrograms/l) when compared to group 2 (serum ferritin 300-1,000 micrograms/l) and group 3 (serum ferritin greater than 1,000 micrograms/l) patients. A significant negative correlation between serum ferritin and basal serum Al (r = -0.544, p = 0.0001), as well as peak serum Al after DFO infusion (r = -0.556, p = 0.0001), was noted. Similarly, a negative relationship between serum Al (both basal and peak) and either serum iron or transferrin saturation was noted. However, there was no correlation between the serum Al level and the dosage of aluminum hydroxide. In conclusion, serum ferritin, serum iron and transferrin saturation were inversely correlated with serum Al in our hemodialysis patients. Iron deficiency may probably increase Al accumulation in these patients.     

The effects of intraperitoneal calcitriol on calcium and parathyroid hormone

Parathyroid suppression by intraperitoneal calcitriol (1,25(OH)2D3) during peritoneal dialysis. The purpose of this study was to determine if parathyroid hormone (PTH) suppression could be achieved by increasing calcium mass transfer (Ca MT) with high dialysate Ca (4 mEq/liter) or via intraperitoneal (i.p.) 1,25(OH)2D3 in patients undergoing continuous ambulatory peritoneal dialysis. Eleven patients were dialyzed for two months with standard Ca dialysate (3.5 mEq/liter) followed by two months with 4.0 mEq/liter Ca, then by three months of i.p. 1,25(OH)2D3. During the latter period, patients were randomized to groups whose dialysate contained either 3.5 mEq/liter or 4.0 mEq/liter Ca. We found that 4.0 mEq/liter Ca dialysate more than doubled Ca MT (37 +/- 17 mg/day to 84 +/- 6 mg/day) leading to a modest fall (P less than 0.05) in PTH levels (84 +/- 5.5% of controls). Ionized calcium levels did not change. With i.p. 1,25(OH)2D3, however, ionized calcium rose significantly (P less than 0.001) leading to a decline in PTH levels to 53.9 +/- 7.9% of control values. Serum 1,25(OH)2D3 levels rose from undetectable to 47.7 +/- 7.2 pg/dl (normal range 20 to 35). These studies indicate that increasing Ca MT using a 4.0 mEq/liter Ca dialysate leads to a small reduction in PTH concentrations. On the other hand, i.p. 1,25(OH)2D3 is well absorbed into the systemic circulation, raises ionized calcium levels, and leads to a marked suppression of PTH. Thus, i.p. 1,25(OH)2D3 may be a simple and effective means to suppress secondary hyperparathyroidism in patients undergoing CAPD.     

Calcium mass transfer in peritoneal dialysis patients using 2.5 mEq/l calcium dialysate.

Standard peritoneal dialysate has a relatively high calcium concentration of 3.5 mEq/l. Peritoneal dialysis patients thus gain calcium from the dialysate which contributes to the risk of hypercalcemia. Dialysate with 2.5 mEq/l calcium is now available. Theoretically, using dialysate with this calcium content, calcium transfer should be negative (from the patient into the dialysate) when the patient is hypercalcemic, and positive when the patient is normocalcemic or hypercalcemic. Thus, 2.5 mEq/l calcium dialysate may allow larger doses of calcium carbonate to be prescribed. We compared calcium mass transfer (CMT) in 17 stable peritoneal dialysis patients using 3.5 and 2.5 mEq/l calcium dialysate. A solution of 2.05 l, 1.5 g/dl dextrose was dwelled for 4 hours. Calcium was measured in the drained dialysate and serum (total and ionized). Mean CMT was 0.7 +/- 0.5 mEq/exchange using 3.5 mEq/l calcium dialysate and -0.9 +/- 0.9 mEq/exchange using 2.5 mEq/l calcium dialysate (p less than 0.0001). At the time of the CMT studies, the mean serum ionized calcium levels were identical for the two groups (2.6 mEq/l). CMT correlated inversely with serum total calcium, serum ionized calcium, and drained dialysate volume. During hypercalcemia calcium transfer was from the dialysate to the patient when 3.5 mEq/l calcium dialysate was used, but from the patient to the dialysate when 2.5 mEq/l calcium dialysate was used. We conclude that 2.5 mEq/l calcium dialysate is effective in removing calcium and will be helpful in preventing hypercalcemia when large doses of oral calcium compounds are prescribed as a phosphate binder.     

The diagnostic critical value in DFO low dose loading test on patient with aluminum accumulation compared to each parameter of ROD

One hundred two hemodialyzed patients were examined to determine the standard level of delta Al value which is the difference of serum Al concentrations between pre and post DFO loading test. We applied low dose of DFO 15 mg/kg in this loading test. Some significant negative correlations were found between delta Al and MCI, sigma GS/D, osteocalcin, free-Hydroxyproline (dialysate) and free-gamma-Carboxyglutamic acid (dialysate). Each correlation rate was -0.58, -0.44, -0.76, -0.57 and -0.51 respectively. In addition tendencies of correlation were found between delta Al and ALP and between delta Al and %QCT (QCT/mean QCT in patient's age x 100). And statistical significant differences were found between (0 less than delta Al less than or equal to 150 micrograms/l) group and (150 micrograms/l less than delta Al) group in each osteobiochemical parameter. These results indicate that 150 micrograms/l is the lower diagnostic standard level of delta Al in 15 mg/kg DFO loading test.     

Whole blood serotonin levels are markedly elevated in patients on dialytic therapy.

The normal range for whole blood serotonin levels in chronic renal failure patients has not been defined. As serotonin may be implicated in platelet abnormalities, hypo- and hypertension and itch in dialysis patients, serotonin whole blood levels were measured in a group of patients with chronic renal failure and/or who were dialysis dependent. The levels were elevated in 12 patients with moderate (mean serum creatinine 335 +/- 54 mumol/l) chronic renal failure (270 +/- 46 micrograms/l) compared to 11 normals (163 +/- 17 micrograms/l, p less than 0.05; quoted normal range less than 300 micrograms/l) but did not correlate with serum creatinine levels. There was a marked elevation in serotonin levels in dialyzed patients, including those on hemodialysis (polysulfone, n = 6, 747 +/- 234 micrograms/l; cuprophane membranes, n = 6, 708 +/- 198 micrograms/l), hemodiafiltration (n = 12, 695 +/- 130 micrograms/l) and especially peritoneal dialysis (n = 6, 1,148 +/- 162 micrograms/l). All results were significant (p less than 0.01) compared to normals and compared to the nondialyzed group (p less than 0.05). The level of serotonin decreased during hemodialysis regardless of the membrane used. There was no positive correlation of serotonin levels with pruritus or hypertension, although there was a negative correlation with systolic blood pressure. The reference range for serotonin whole blood levels needs to be broadened when considering dialyzed patients.     

Gentamicin removal during intermittent peritoneal dialysis

Gentamicin removal during intermittent peritoneal dialysis was studied in 13 uremic patients. The peak serum level after 80 mg of gentamicin intravenous drip was 6.00 +/- 1.3 micrograms/ml with a serum half-life of 13.6 +/- 4.07 h. The gentamicin dialysate level did not correlate with the corresponding serum concentration. The peritoneal gentamicin clearance (10.0 +/- 3.65 ml/min) correlated with the rate of protein loss, but not with the peritoneal clearances of urea and creatinine. When 4% glucose dialysate was used, the clearance of the drug increased considerably along with the ultrafiltration rate. Adding gentamicin (5 micrograms/ml) to the dialysate resulted in a sustained serum drug level. The mechanism of gentamicin transport through the peritoneal membrane is discussed. The study demonstrated significant removal of gentamicin during intermittent peritoneal dialysis.     

Bone aluminum deposition in maintenance dialysis patients treated with aluminium-free dialysate: role of aluminium hydroxide consumption

Postmortem iliac crest biopsies were performed on 16 uremic patients. 3 had been treated conservatively while 13 had been entered into a maintenance dialysis program. The dialysate was treated by reverse osmosis for more than 10 years, and the aluminium concentration was consistently below the detection limit of 0.15 mol/l. 14 patients had been treated with aluminium hydroxide. Bone histomorphometry, aluminium labelling intensity, osteoid surface aluminium labelling extent (Al/OBI) and bone aluminium concentration were measured. 14 patients had significant bone aluminium deposition, including 2 who were not on dialysis of whom 1 had not received aluminium hydroxide. Bone aluminium concentration and labelling intensity were correlated to total aluminium hydroxide consumption (p less than 0.001, p less than 0.05) and present dose (p less than 0.01, p less than 0.01), while Al/OBI was not. The two patients with the highest aluminium concentrations had symptomatic osteomalacia, but 4 patients with significantly raised concentrations and mineralisation front labelling had secondary hyperparathyroidism. It is concluded that bone aluminium deposition occurs despite the use of aluminium-free dialysate and is associated with total and present aluminium hydroxide consumption; heavy aluminium deposition is associated with severe and symptomatic osteomalacia, but can also be observed in the presence of predominant hyperparathyroidism; aluminium deposition can occur in the absence of treatment with dialysis or aluminium hydroxide; bone aluminium concentration and labelling intensity are a better measure of bone deposition than Al/OBI.     

Pharmacokinetics of oral cephradine in continuous ambulatory peritoneal dialysis patients

Parenteral cephalosporins are widely used to treat peritonitis associated with continuous ambulatory peritoneal dialysis (CAPD). Few data exist on oral antibiotics in treating this disease. This study examined the pharmacokinetics of oral cephradine in noninfected patients on CAPD. Assays for cephradine in dialysate and urine were performed by high-performance liquid chromatography. Following a 500-mg dose, the peak dialysate cephradine concentration was 8.7 +/- 1.4 micrograms/ml. The peak urinary concentration was 201 +/- 119 micrograms/ml. The maximum peritoneal clearance was 4.3 +/- 0.3 ml/min/1.73 m2. Dialysate cephradine concentrations were inadequate against Staphylococcus epidermidis and most gram-negative bacteria found in CAPD-associated peritonitis, but may be adequate for most strains of other gram-positive organisms causing this disease.     

Increase of body iron stores estimated by the increase of serum ferritin concentration during a treatment of 200 mg Fe++ daily after gastrointestinal surgery

A 6-week iron therapy of 200 mg Fe++ daily was given to 13 men and 12 women who had previously undergone various kinds of common gastrointestinal surgery and who had empty iron stores estimated from low serum ferritin concentration. The results were compared with those of a control group corresponding to the study group in respect of sex, number of patients, primary disease, previous operation, empty iron stores (serum ferritin), blood hemoglobin, serum iron, sedimentation rate, blood leukocytes, serum transferrin, folate and vitamin B12. The iron therapy restored the lack of body iron, for the serum ferritin concentrations increased from 12 +/- 7 to 30 +/- 11 micrograms/l (p less than 0.001) in the men and from 10 +/- 6 to 30 +/- 12 micrograms/l (p less than 0.001) in the women, whereas the corresponding changes in the control group were from 10 +/- 9 to 11 +/- 8 micrograms/l and from 11 +/- 8 to 13 +/- 11 micrograms/l in the men and women, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

1,25-Dihydroxycholecalciferol and peritoneal macrophage chemotaxis in patients on continuous ambulatory peritoneal dialysis.

Single graded doses of 1,25-dihydroxycholecalciferol of 2 and 4 micrograms were added intraperitoneally into the overnight 1.5% glucose dialysate of 6 patients on continuous ambulatory peritoneal dialysis. The effect on peritoneal macrophage chemotaxis and random migration was studied and compared with the baseline when no 1,25-(OH)2D3 was added. No consistent effect on peritoneal macrophage chemotaxis was observed. Random migration was significantly depressed at 4 micrograms when compared with baseline (5.4 +/- 1.9 vs. 12.2 +/- 3.7 cells/high-power field, p less than 0.05). The potential clinical role of 1,25-(OH)2D3 as an immune modulator requires further study.     

The nutritional/metabolic and hormonal effects of 8 weeks of continuous ambulatory peritoneal dialysis with a 1% amino acid solution

Circulating intermediary metabolites, hormones and plasma amino acids (AA) were measured at intervals over 24 hours in seven non-diabetic patients with chronic renal failure treated by continuous ambulatory peritoneal dialysis (CAPD), before and after an 8-week period during which a 1% amino acid dialysis solution replaced two of the four dextrose exchanges. Mean 24-hour concentrations of plasma total and essential amino acid were higher following the AA dialysate (total pre: 2893 +/- 185; total post: 3357 +/- 244; p less than 0.05; essential pre: 751 +/- 47; essential post: 1064 +/- 57 mumol/l; p less than 0.001). Mean 24-hour concentrations of the branched chain amino acids leucine, isoleucine and valine were higher following the AA dialysate (valine pre: 201 +/- 18; valine post: 321 +/- 19; p less than 0.001; leucine pre: 102 +/- 6; leucine post: 127 +/- 9; p less than 0.01; isoleucine pre: 67 +/- 5; isoleucine post: 85 +/- 7 mumol/l; p less than 0.05). Serum albumin increased with use of the AA dialysate (pre: 36 +/- 1; 2 weeks, 40 +/- 1; 4 weeks, 40 +/- 1; 6 weeks, 41 +/- 1; 8 weeks, 38 +/- 2 g/l). 24-hour profiles and mean 24-hour concentrations of blood glucose, serum insulin, serum triglyceride, plasma non-esterified fatty acids (NEFA), plasma 3-hydroxybutyrate and plasma alanine were unchanged after the AA period. Plasma bicarbonate decreased with use of the amino acid solution (pre: 21 +/- 1; 2 weeks, 18 +/- 1; 4 weeks, 18 +/- 1; 6 weeks, 16 +/- 1; 8 weeks, 16 +/- 1 mmol/l). Use of a 1% amino acid solution over an 8-week period in CAPD patients improves the plasma amino acid profile but results in a metabolic acidosis. The other endocrine and metabolic abnormalities of uremia remain unchanged.     

Aluminium determination in the skin of patients with and without end-stage renal failure

Aluminium (Al) concentration in the skin was determined by inductively coupled plasma optical emission spectrometry to look for a correlation between Al exposure and skin content in patients with end-stage renal failure. Skin Al concentrations were higher in dialyzed patients than in the nondialyzed group (1.02 +/- 0.30 vs. 0.26 +/- 0.10 micrograms/g; p less than 0.001). Moreover, in the dialyzed group, the patients treated for more than 100 months had a higher concentration of Al in the skin than the others (1.20 +/- 0.26 vs. 0.80 +/- 0.18 micrograms/g; p less than 0.05). Al skin content correlated better with the deferoxamine infusion test (DIT) than with Al blood plasma concentration. In conclusion, our data confirm that the DIT is a valuable tool for the evaluation of body Al content.     

Low serum iron concentration in acute cholecystitis. A discriminator of severity of infection

This study demonstrates that serum iron levels are significantly depressed during acute cholecystitis. Mean admission serum iron concentration for 18 patients who had required emergency cholecystectomy within 48 hours of hospitalization was 40.9 micrograms/100 ml +/- 27.08 (7.32 mumol/l) while for 108 patients who had undergone elective cholecystectomy in the same 18-month period the mean concentration was 90.5 micrograms/100 ml +/- 34.27 (16.2 mumol/l); a mean difference of 49.6 micrograms/100 ml (3.92 mumol/l) (t = 5.8395, P less than 0.00001). Mean serum iron level in seven patients with culture positive acute cholecystitis was 26.4 micrograms/100 ml +/- 10.45 (4.73 mumol/l), significantly different (P less than 0.05) than in 11 patients with culture negative cholecystitis, 50.3 micrograms/100 ml +/- 30.41 (9.00 mumol/l). Admission serum iron level averaged 25.6 micrograms/100 ml (4.58 mumol/l) in three patients with gangrenous gallbladders and was 18 micrograms/100 ml (3.22 mumol/l) in one patient with empyema of the gallbladder. Determination of serum iron level may help distinguish patients with significant infections requiring urgent surgery from patients with biliary colic.     

Effect of peritonitis on insulin and glucose absorption during peritoneal dialysis in diabetic rats

The intraperitoneal route is frequently used for the administration of insulin in diabetic continuous ambulatory peritoneal dialysis patients. However, there is conflicting evidence as to whether the dosage of intraperitoneal insulin should be increased or decreased during peritonitis in these patients. Glucose and insulin absorption and glycaemic control were evaluated in 2-hour exchanges using 15 ml of 2.5% dextrose dialysis solution in diabetic rats with (group 1) and without (group 2) peritonitis. Fasting blood glucose values at the beginning of the study exchanges were mean +/- SD 17.9 +/- 3.3 mmol/l in group 1 and 18.2 +/- 3.5 mmol/l in group 2. Even though group 1 had a higher percentage absorption of dialysate glucose (65 +/- 19 vs. 47 +/- 7%; p less than 0.05) and higher percentage absorption of dialysate insulin (49 +/- 12 vs. 44 +/- 14%; p less than 0.1), the hypoglycaemic response to the standard intraperitoneal dose of insulin was similar in each group. Plasma C peptide levels remained very low in both groups, thus excluding significant endogenous release of insulin. These data indicate that peritonitis per se does not change intraperitoneal insulin requirements during standardized peritoneal dialysis exchanges in diabetic rats. Insulin requirements may also be unaltered during peritonitis in diabetic continuous ambulatory peritoneal dialysis patients, provided that dialysate glucose load and oral carbohydrate intake are kept constant.     

A comparison of plasma and muscle carnitine levels in patients on peritoneal or hemodialysis for chronic renal failure

We studied plasma, dialysate, and muscle carnitine levels in patients with stable chronic renal failure on hemodialysis, and intermittent peritoneal, or continuous ambulatory peritoneal dialysis (CAPD). In patients on hemodialysis, plasma carnitine levels fell from 46.2 +/- 4.5 mumol/l (mean +/- SEM) to 18.8 +/- 2.7 mumol/l immediately after the procedure (p less than 0.001). Depletion of muscle carnitine was found after hemodialysis (1,518 +/- 273 nmol/g wet weight of tissue) compared to normal levels of 5,230.5 +/- 142.7 nmol/g tissue (p less than 0.01). However, the plasma and muscle carnitine levels remained in the normal range in patients on intermittent peritoneal dialysis and CAPD. We postulate that the rapid decline in plasma levels of carnitine caused by hemodialysis initiates unilateral transport of the compound from muscle to the plasma, thus depleting the skeletal muscle stores of carnitine.     

Zinc Transport During Hemodialysis

Zinc transfer during hemodialysis and plasma zinc concentrations in hemodialysis patients were examined. Fifteen volunteer outpatients undergoing hemodialysis showed significant increases in plasma zinc from 74.0 +/- 7.8 to 88.1 +/- 9.7 micrograms/dl after a 5-h dialysis. The increase was mainly the result of hemoconcentration as evidenced by a significant increase in the hematocrit and total serum protein during dialysis, but was also due to diffusion. To study the changes resulting from diffusion, zinc was measured in the arterial blood and in the dialysate at the inflow and outflow sites of the dialyzer. There was a significant (p less than 0.01) increase in the plasma zinc of the arterial blood from 74.7 +/- 8.1 to 80.2 +/- 6.5 micrograms/dl, but a nonsignificant decrease in the dialysate zinc from 10.6 +/- 2.5 to 9.5 +/- 5.9 micrograms/dl. Zinc diffused across the dialyzer from the dialysate to the blood in 12 cases and into the dialysate in three others.