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Based on mathematical analysis, a method computing deviations from normal in body weight, water and sodium, and requiring only presenting body weight and hyperglycemic and euglycemic plasma glucose and sodium concentrations in anuria was developed. Data from 18 hyperglycemic episodes (12 anuric patients) treated with insulin alone were analyzed by this method and were compared to clinical estimates. When normal body water and extracellular volume were assumed to be 0.579 and 0.213 of dry weight, respectively, deviations of presenting weight from dry weight (in kg) were as follows (x = clinical estimate, y = new method estimate): x: -2.5 to +17.2 (+4.6 +/- 5.1, SD); y: -4.1 to +16.7 (+4.2 +/- 5.4, NS); y = -0.4 + 1.0008x, r = 0.96 (p less than 0.01). Similar comparisons were obtained for deviation of body sodium from normal and for euglycemic extracellular volume. Estimates by the two methods agreed when normal body water was assumed to vary between 0.525 and 0.625 of dry weight and when normal extracellular volume was assumed to vary between 0.31 and 0.40 of normal body water.

We compared 56 paired measurements of osmolal gaps and serum ethyl alcohol levels in 15 anesthetized dogs. We then repeated these comparisons after correcting the osmolal gaps for the preceding (the administration of ethyl alcohol) difference between measured and calculated osmolalities. No statistical differences were observed between ethyl alcohol levels and either uncorrected or corrected osmolal gaps. However, uncorrected osmolal gaps differed from ethyl alcohol levels by less than 5 mmol/L in 39.3% of the measurements and by more than 10 mmol/L in 19.6% of the measurements. Corresponding percentages for corrected osmolal gaps were 94.6 and 0 respectively. Thus uncorrected osmolal gaps offer a rough screening test, whereas corrected osmolal gaps offer accurate predictions of serum ethyl alcohol levels.

We analyzed routine serum potassium concentration measurements and conditions temporally associated with abnormalities in potassium concentration in outpatients on chronic hemodialysis (136 nondiabetics, 36 diabetics) and continuous ambulatory peritoneal dialysis (16 nondiabetics, 10 diabetics). The following potassium concentration frequencies were found: prehemodialysis, nondiabetics: normal 51.3%, severe hyperkalemia (greater than 6.0 mmol/l) 10%, severe hypokalemia (less than 3.0 mmol/l) 0.3%; diabetics: normal 57.8%, severe hyperkalemia 8.7%, severe hypokalemia 0.5%. Peritoneal dialysis, nondiabetics: normal 73.7%, severe hyperkalemia 0.6%, severe hypokalemia 4.9%; diabetics: normal 72.5%, severe hyperkalemia 0.9%, severe hypokalemia 2.9%. Normokalemia and severe hypokalemia were significantly (chi 2 test) more frequent in peritoneal dialysis than in prehemodialysis, whereas severe hyperkalemia was more frequent in prehemodialysis serum samples. No difference was found between nondiabetics and diabetics for either form of dialysis. 50% of prehemodialysis episodes of hyperkalemia were diet-induced. Hyperkalemic drugs and anuria were not associated with a higher risk of prehemodialysis hyperkalemia, but each one of 3 abnormalities, very high BUN (greater than 40 mmol/l), metabolic acidosis (TCO2 less than 15 mmol/l) and, in diabetics, severe hyperglycemia (serum glucose greater than 30 mmol/l), was associated with a statistically higher risk of hyperkalemia.

To test the osmotic function of body tissues in hypertonic extracellular (ECF) expansion in vivo, we studied 20 anuric dogs either infused (infusion solution was 0.85 M saline for group A, 1.6 M mannitol for group B and isotonic saline for group C), or not infused with any solution (group D). We compared the observed ECF volume increase (radiosulfate, or cold sodium and chloride space changes), final osmolality, and body water (tritiated water space or apparent sodium volume of distribution) to the values predicted from perfect osmometric function. Observed ECF volume expansion was not different from that predicted (groups A-C). Observed final osmolality and body water were significantly greater than predicted final osmolality (groups A-D) and osmotic volume of distribution (groups A and B), respectively. We then computed 'new' solute generated from anuria (groups A-D) and from dilution of ECF solute controlled by hormonal feedback (groups A-C); this solute was comparable for all four groups. Corrected for this solute observed final osmolality and osmotic volume of distribution were not different from the predicted final osmolality (groups A-D) and measured body water (groups A and B), respectively. It is concluded that in hypertonic ECF expansion, perfect osmometric function predicts accurately the degree of ECF expansion and, if appropriate corrections are made for experimental conditions other than hypertonicity, final osmolality and body water.

With the increasing use of continuous ambulatory peritoneal dialysis (CAPD), a number of complications related to the leakage of dialysate from the abdominal cavity have been described (Dubin and Froelich: Clinical Nuclear Medicine 10(3): 173, 174, 1985; Johnson et al.: Archives of Surgery 122(8): 952-954, 1987; Ducassou et al.: Journal of Nuclear Medicine 25(1): 68, 69, 1984; Walker and Fish: Journal of Nuclear Medicine 29(9): 1596-1602, 1988; Eisenberg et al.: Clinical Nuclear Medicine 13(2): 99-101, 1988). The use of intraperitoneal radiolabeled colloid has been previously described to image entities such as hernias, patent processus vaginalis, abdominal wall, and diaphragmatic leakage by other specialities, but has not been described in the general imaging literature. This paper illustrates a simple, noninvasive method of determining the site of dialysate leak and its importance to assist further patient management.

We measured by affinity chromatography glycosylated hemoglobin levels in the blood of 43 diabetic and nondiabetic patients (139 measurements) on long-term dialysis therapy (continuous ambulatory peritoneal dialysis and hemodialysis) to determine the usefulness of this method of estimating glycemic control in diabetic persons on dialysis therapy. In nondiabetic patients, glycosylated hemoglobin levels were within the normal range (4.0% to 6.8% of total blood hemoglobin levels) for both continuous ambulatory peritoneal dialysis and hemodialysis. Glycosylated hemoglobin values correlated significantly with fasting blood glucose levels, serum urea levels, and serum total carbon dioxide content. By stepwise regression, fasting blood glucose values accounted statistically for .54 of the variability (R2) in glycosylated hemoglobin. The contribution of the other variables to this variability was minimal. In 9 diabetic patients (3 on hemodialysis), glycosylated hemoglobin levels correlated significantly with average daily blood glucose levels. Regression of the fasting blood glucose value on glycosylated hemoglobin was similar between continuous ambulatory peritoneal dialysis and hemodialysis. Measuring glycosylated hemoglobin levels by affinity chromatography is a suitable method for assessing glycemia in dialysis patients.

Five patients, one woman and four men, aged 24 to 54 years, developed abnormally high hematocrits between 4 and 22 months after renal transplantation. In four patients, red cell mass was above normal and plasma volume below normal. In one patient, both red cell mass and plasma volume were below normal. The cause of the deranged plasma volume was not evident. Decreased plasma volume may either contribute to or may, in rare instances, be the only cause of apparent erythrocytosis in renal transplant recipients.

This case report documents successful diagnosis and therapy in a case of Mycobacterium chelonae peritonitis associated with continuous ambulatory peritoneal dialysis (CAPD) and reviews problems associated with CAPD peritontis resulting from the rapidly growing mycobacteria, M. chelonae and Mycobacterium fortultum .

The efficacy and safety of peritoneal dialysis in the immediate postoperative period was evaluated by examining the course of 14 patients who were dialyzed 16 times, 4 to 18 days (mean 9 days) following major abdominal surgery. All patients had abdominal drains in place. Seven had abdominal aortic grafts, five had generalized peritonitis, four had active gastrointestinal bleeding, and ten were hypotensive at the time of treatment. The procedure was effective in all patients with improvement in biochemical factors and in the symptoms of the uremic syndrome. Serious complications (wound dehiscence) were observed in association with dialysis in only one patient. Four patients recovered completely; although the remaining ten died, in none was death due directly to uremia or one of its complications.

We analyzed the changes in serum potassium concentration ([K]) and acid-base parameters in 43 episodes of dialysis-associated hyperglycemia (serum glucose level > 33.3 mmol/L), 22 of which were characterized as diabetic ketoacidosis (DKA) and the remaining 21 as nonketotic hyperglycemia (NKH). All episodes were treated with insulin therapy only. Age, gender, initial and final serum values of glucose, sodium, chloride, tonicity and osmolality did not differ between DKA and NKH. At presentation, serum values of [K] (DKA 6.2 ± 1.3 mmol/L; NKH 5.2 ± 1.5 mmol/L) and anion gap [AG] (DKA 27.2 ± 6.4 mEq/L; NKH 15.4 ± 3.5 mEq/L) were higher in DKA, whereas serum total carbon dioxide content [TCO2] (DKA 12.0 ± 4.6 mmol/L; NKH 22.5 ± 3.1 mmol/L), arterial blood pH (DKA 7.15 ± 0.09; NKH 7.43 ± 0.07) and arterial blood PaCO2 (DKA 26.2 ± 12.3 mm Hg; NKH 34.5 ± 6.7 mm Hg) were higher in NKH. At the end of insulin treatment, serum values of [K] (DKA 4.0 ± 0.7 mmol/L, NKH 4.0 ± 0.5 mmol/L), [AG] (DKA 16.3 ± 5.4 mEq/L, NKH 14.9 ± 3.0 mEq/L), [TCO2] (DKA 23.5 ± 5.0 mmol/L, NKH 24.1 ± 4.2 mmol/L), arterial blood pH (DKA 7.42 ± 0.09, NKH 7.51 ± 0.14) and arterial blood PaCO2 (DKA 31.8 ± 6.7 mm Hg, NKH 34.2 ± 8.3 mm Hg) did not differ between the two groups. Linear regression of the decrease in serum [K] value during treatment, (Δ[K]), on the presenting serum [K] concentration,([K]2), was: DKA, Δ[K] = 2.78 – 0.81 × [K]2, r = −0.85, p < 0.001; NKH, Δ[K] = 2.44 – 0.71 × [K]2, r = −0.90, p < 0.001. The slopes of the regressions were not significantly different. Stepwise logistic regression including both DKA and NKH cases identified the presenting serum [K] level and the change in serum [TCO2] value during treatment as the predictors of Δ[K] (R2 = 0.81). Hyperkalemia is a feature of severe hyperglycemia (DKA or NKH) occurring in patients on dialysis. Insulin administration brings about correction of DKA and return of serum [K] concentration to the normal range in the majority of the hyperglycemic episodes without the need for other measures. The initial serum [K] value and the change in serum [TCO2] level during treatment influence the decrease in serum [K] value during treatment of dialysis-associated hyperglycemia with insulin.