Replacement of amino acid and protein losses with 1.1% amino acid peritoneal dialysis solution.

OBJECTIVE: Losses of nutrients into dialysate may contribute to malnutrition. Peritoneal dialysis (PD) patients are reported to lose 3-4 g/day of amino acids (AAs) and 4-15 g/day of proteins. The extent to which one exchange with a 1.1% AA dialysis solution (Nutrineal, Baxter, Deerfield, IL, U.S.A.) offsets these losses was investigated in a 3-day inpatient study in 20 PD patients. DESIGN: Simple, open-label, cross-over study on consecutive days in a clinical research unit. On day 1 all patients were given a peritoneal equilibration test (PET). On day 2 they received 1.5% dextrose Dianeal (Baxter) as the first exchange of the day and their usual regimen thereafter. On day 3, the first exchange of the day was the 1.1% AA solution in place of 1.5% Dianeal and the usual PD regimen thereafter. On days 2 and 3 all dialysate effluent was collected and analyzed for AAs and proteins. Patients were maintained on a constant diet. RESULTS: Losses of AAs and total proteins on day 2 were 3.4 +/- 0.9 g and 5.8 +/- 2.4 g, respectively, totaling 9.2 +/- 2.7 g. The net uptake of AAs on day 3 was 17.6 +/- 2.6 g (80 +/- 12% of the 22 g infused). Mean gains of AAs on day 3 exceeded losses of proteins and AAs on day 2, p < 0.001. Losses of total proteins, but not losses of AAs, and the net absorption of AAs from the dialysis solution were correlated directly with peritoneal membrane transport characteristics, obtained from the PET. CONCLUSION: Daily losses of AAs and proteins into dialysate are more than offset by gains of AAs absorbed from one exchange with 1.1% AA-based dialysis solution. Net gains of AAs exceeded losses of proteins and AAs in all patients studied. The difference was relatively constant across a wide range of membrane transport types. Net AA gains were approximately two times the total AA and protein losses.

Hemoperitoneum complicating chronic peritoneal dialysis: single-center experience and literature review.

Hemoperitoneum is a well-recognized, if uncommon, complication of chronic peritoneal dialysis. In this review of 424 patients maintained on peritoneal dialysis at a single center during an 11-year period, 26 patients (6.1%) developed one or more episodes of hemoperitoneum. Three patients had hemoperitoneum on two separate occasions with different etiologies. One additional patient was seen on a hospital consultative service. Three types of bleeding episodes were observed. Twenty-one of 30 (70%) were benign, consisting of pink-tinged dialysate with little clinical consequence (group 1). Three (10%) consisted of minor hemoperitoneum associated with significant intra-abdominal pathology (group 2), and six (20%) required active intervention (group 3). The most frequent cause of hemoperitoneum was bleeding related to menstruation or ovulation; hemoperitoneum was more common in women than in men. Two patients had hemoperitoneum occurring after more than 6 years on dialysis. In both, the etiology was sclerosing peritonitis, an association not previously noted. The less common etiologies of hemoperitoneum encountered in our patients were similar to those in reports from other centers and are compiled here.

Hypercalcemia in patients with advanced chronic renal failure not yet requiring dialysis.

Six patients with progressive chronic renal failure not yet requiring dialysis and not consuming supplemental calcium or vitamin D developed hypercalcemia. Three had proven and 1 suspected tertiary hyperparathyroidism, 1 parathyroid carcinoma and 1 aplastic bone. None of the 3 patients who underwent bone biopsy had heavy bone aluminum staining. The patients with proven parathyroid-mediated hypercalcemia had marked elevation of C-terminal parathyroid hormone and alkaline phosphatase values and, when performed, radiographs consistent with osteitis fibrosa. When these findings are absent or the diagnosis is otherwise uncertain, a bone biopsy may provide a definitive diagnosis and guide management.

Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations.

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.

Renal osteodystrophy in patients on hemodialysis for more than 10 years.

We performed bone biopsies on 13 patients who had been on dialysis from 11.1 to 17.6 years (mean 14.5 +/- 2.1 years) to evaluate renal osteodystrophy in long-term dialysis patients. Seven patients had osteitis fibrosa and 6 had a mineralization defect. Stainable bone aluminum was present in 9 of the patients. Serum phosphorus and parathyroid hormone levels were higher and bone aluminum lower in patients with osteitis fibrosa compared to those with a mineralization defect. Those seriously disabled with decreased mobility due to bone pain (7 of 13) had more bone aluminum than those patients with minimal or no disability (1.55 +/- 1.0 mm/mm2 vs. 0.11 +/- 0.18, respectively, p less than 0.01). A history of fractures during the years on dialysis was also associated with elevated stainable bone aluminum (p = 0.04). We conclude that in long-term dialysis patients aluminum-related osteodystrophy results in greater morbidity than osteitis fibrosa. We recommend that aluminum-containing phosphate binders be used sparingly in patients who are to remain indefinitely on dialysis.

Peritoneal eosinophils during intermittent peritoneal dialysis.

Peritoneal eosinophil counts were investigated in 61 intermittent dialysis patients over the course of 1 year. The peritoneal eosinophil percentage fell from 18 +/- 2% (mean +/- SEM) in the first 2 months of dialysis to 3 +/- 0.4% after 6 months of dialysis. Absolute eosinophils per cubic millimeter fell from 586 +/- 126 to 61 +/- 18 (p less than 0.01 for both percentage and absolute values). There was a wide range in the mean eosinophil percentages per patient in the first 6 months of dialysis (0-84%) that narrowed to 0-9% after 6 months. The majority of the high initial eosinophil counts resolved after 2 months. Peripheral eosinophilia was seen in 8 of the 10 patients with the highest mean peritoneal eosinophil percentages during the first 2 months of dialysis. Patients who developed peritonitis had a significantly lower percentage of eosinophils in the first 1.5 months of dialysis than patients who did not develop peritonitis. At the time of diagnosis of peritonitis, the peritoneal eosinophil count was near zero. 4 cases of peritoneal eosinophilia which developed after antibiotic therapy are described.