Reports on acid-base side effects of sevelamer hydrochloride (SH), a new aluminum (Al)- and calcium (Ca)-free phosphate binder are rare and conflicting. In a retrospective analysis, we evaluated SH impact on metabolic acidosis and serum potassium (K) in hemodialysis (HD) patients. Two groups of stable HD patients were studied. Group A included 17 patients, M/F=15/2, 64 (42-80) years old, dialyzed since 130 (34-253) months, under SH for 24 months. Group B serving as controls was made of 7 patients, M/F=4/3, 67 (48-91) years old, dialyzed since 67 (27-174) months, under CaCO3 and/or Al(OH)3 as phosphate binders also for 24 months. Bicarbonate (BIC), K, Ca, phosphorus (P), Ca x P, alkaline phosphatase (ALP), and intact parathyroid hormone (iPTH) were recorded before (MO) and at the end (M24) of 24-month SH or CaCO3-Al(OH)3 treatment in group A and B patients. In group A, BIC fell from 20.02 +/- 1.43 to 17.89 +/- 2.30 mEq/ L, P=.002; and K rose from 5.45 +/- 0.51 to 5.75 +/- 0.49 mEq/L, P=0.02. In group B, BIC (19.8 +/- 3.03 to 19.0 +/- 3.3 mEq/L) and K (5.01 +/- 0.8 to 4.9 +/- 1.1 mEq/L) had nonsignificant changes. In group A, iPTH rose from 132.82 +/- 124.08 to 326.89 +/- 283.91 pg/mL, P=.0008; P fell from 5.92 +/- 1.48 to 4.9 +/- 1.01, P=.02; and Ca x P decreased from 52.04 +/- 9.7 to 45.58 +/- 10.42 mg2/dL2, P=.04. In group B, changes in iPTH from 240.71 +/- 174.7 to 318.57 +/- 260.2 pg/mL, P from 4.9 +/- 0.5 to 4.8 +/- 1.3 mg/dL, and CaxP product from 44.3 +/- 6.6 to 44 +/- 11.2 mg2/dL2 were nonsignificant. The changes observed in Ca and ALP in both groups were nonsignificant. Correlations in group A between metabolic acidosis (BIC) and SH doses, or iPTH and BIC, Ca, or P changes, were also found to be nonsignificant. Long-term use of SH, effectively controlling serum P levels and Ca x P values, is associated with acidosis aggravation and hyperkaliemia. Worsening of secondary hyperparathyroidism, also noted, needs to be confirmed and could be related to Ca/Al salt discontinuation and to metabolic acidosis aggravation itself.

No abstract

Reports on acid-base side effects of sevelamer hydrochloride (SH), a new aluminum (Al)- and calcium (Ca)-free phosphate binder are rare and conflicting. In a retrospective analysis, we evaluated SH impact on metabolic acidosis and serum potassium (K) in hemodialysis (HD) patients. Two groups of stable HD patients were studied. Group A included 17 patients, M/F=15/2, 64 (42-80) years old, dialyzed since 130 (34-253) months, under SH for 24 months. Group B serving as controls was made of 7 patients, M/F=4/3, 67 (48-91) years old, dialyzed since 67 (27-174) months, under CaCO3 and/or Al(OH)3 as phosphate binders also for 24 months. Bicarbonate (BIC), K, Ca, phosphorus (P), Ca x P, alkaline phosphatase (ALP), and intact parathyroid hormone (iPTH) were recorded before (MO) and at the end (M24) of 24-month SH or CaCO3-Al(OH)3 treatment in group A and B patients. In group A, BIC fell from 20.02 +/- 1.43 to 17.89 +/- 2.30 mEq/ L, P=.002; and K rose from 5.45 +/- 0.51 to 5.75 +/- 0.49 mEq/L, P=0.02. In group B, BIC (19.8 +/- 3.03 to 19.0 +/- 3.3 mEq/L) and K (5.01 +/- 0.8 to 4.9 +/- 1.1 mEq/L) had nonsignificant changes. In group A, iPTH rose from 132.82 +/- 124.08 to 326.89 +/- 283.91 pg/mL, P=.0008; P fell from 5.92 +/- 1.48 to 4.9 +/- 1.01, P=.02; and Ca x P decreased from 52.04 +/- 9.7 to 45.58 +/- 10.42 mg2/dL2, P=.04. In group B, changes in iPTH from 240.71 +/- 174.7 to 318.57 +/- 260.2 pg/mL, P from 4.9 +/- 0.5 to 4.8 +/- 1.3 mg/dL, and CaxP product from 44.3 +/- 6.6 to 44 +/- 11.2 mg2/dL2 were nonsignificant. The changes observed in Ca and ALP in both groups were nonsignificant. Correlations in group A between metabolic acidosis (BIC) and SH doses, or iPTH and BIC, Ca, or P changes, were also found to be nonsignificant. Long-term use of SH, effectively controlling serum P levels and Ca x P values, is associated with acidosis aggravation and hyperkaliemia. Worsening of secondary hyperparathyroidism, also noted, needs to be confirmed and could be related to Ca/Al salt discontinuation and to metabolic acidosis aggravation itself.

Insulin-mineral corticoids effects on extrarenal K+ metabolism in dialysis patients. During the inter-dialytic interval in dialyzed patients, hydrogen and potassium ions are regulated by extrarenal mechanisms. We studied the hormonal and acidotic effects on the extrarenal potassium metabolism, in selected, anuric and stable, hemodialysis patients. Fifteen patients, were grouped according to the mean mid-week pre-dialysis K+ over the past 12 months: > 6.0 mEq/L (G1, n=5), = 5.1-6.0 mEq/L (G2, n=5), < or = 5.0 mEq/L (G3, n=5). After a mid-week hemodialysis session and 12 h fasting, they received 1 g/Kg glucose p.os (A). Insulin, aldosterone, renin, pH, HCO3-, glucose, body weight, blood pressure and heart rate were measured before and 60' after the meal. We recorded the same parameters, except insulin, in 15 patients, similarly grouped, before hemodialysis (T0) and on 3 consecutive off dialysis days (T1-T3); G1 received fluorohydrocortisone (FHC) 0.1 mg-0.3 mg/day, according to body weight and G3 spironolactone (SLT) 200 mg per day. G2 were controls (B). (A) A significant rise in glycemia (81 +/- 23 to 157 +/- 52 mg/dL, P<0.001) and insulin (11.8 +/- 6.2 to 46.8 +/- 19.5 microU/mL, P<0.001), with a drop in K+ (5.1 +/- 0.6 to 4.8 +/- 0.7 mEq/L, P=0.001) and aldosterone (453 +/- 373 to 383 +/- 364 pg/mL, P<0.01), were noted at T60 vs. T0, in all groups. Insulin levels correlated negatively (r=-0.54, P<0.04) to serum K+ at T60, in all patients. (B) No major pH, HCO3 and aldosterone changes were observed in the 3 groups. Despite that, K+ dropped in G1 by FHC (6.7 +/- 0.9 to 5.9 +/- 0.6 mEq/L, P<0.05), rose in G3 by SLT (4.4 +/- 0.4 to 5.4 +/- 0.3 mEq/L, P<0.05) and remained unchanged in controls (5.8 +/- 0.2 to 5.8 +/- 0.6 mEq/L), (T0 vs T3 pre-dialysis values). Glucose significantly lowered K+ by promoting adequate insulin secretion. Drugs affecting aldosterone action significantly influenced potassium metabolism. Acid-base balance was not important in K+ handling in steady state anuric dialysis patients.

Encapsulating peritoneal sclerosis is a rare condition of a poorly understood pathogenesis with recognized risk factors, such as medications, surgical interventions, systemic diseases, and malignancies. In endstage renal disease it has been associated with chronic peritoneal dialysis. We hereby report the case of a 59-year-old male hemodialysis patient, who was never treated with peritoneal dialysis and developed an unexplained massive ascites 4 months post laparoscopic cholecystectomy for gallstones. A second laparoscopy and histological evaluation revealed encapsulating peritoneal sclerosis-like findings with parietal peritoneum and spleen involvement. The patient was successfully treated for 12 months with prednisone and tamoxifen. Possible pathogenetic mechanisms of the disease in this case are discussed including peritoneal irritation by chronic cholecystitis, low-grade inflammation of hemodialysis, intraoperative complications and the hypothetical role of oxidized regenerated cellulose used for hemostasis. In conclusion, the suspicion of peritoneal sclerosis should be encountered in cases of unexplained ascites in patients undergoing hemodialysis. The early diagnosis includes laparoscopy and histological evaluation and can result in a good outcome under medical treatment; otherwise, there is a high possibility of bowel obstruction with fatal outcome.