Phosphorus control in peritoneal dialysis patients.

Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean+/-s.d. age of 55+/-16 years and mean duration of PD of 33+/-25 months. Serum calcium (Ca(2+)), ionized Ca(2+), phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D(3), 1,25-dihydroxy vitamin D(3), total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3+/-0.65, weekly creatinine clearance 78.5+/-76.6 l, and daily urine output 550+/-603 ml day(-1). Fifty-five percent of patients had a urine volume of <400 ml day(-1). Mean serum phosphorus level was 4.9+/-1.3 mg per 100 ml, serum Ca(2+) 9.4+/-1.07 mg per 100 ml, iPTH 267+/-356 pg ml(-1), ionized Ca(2+) 1.08+/-0.32 mg per 100 ml, calcium phosphorus (Ca x P) product 39+/-19 mg(2)dl(-2), 25(OH)D(3) 8.3+/-9.3 ng ml(-1), 1,25(OH)(2)D(3) 9.7+/-6.7 pg ml(-1), total alkaline phosphatase 170+/-178 U l(-1), and bone alkaline phosphatase 71+/-108 U l(-1). While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca(2+) level was > or =9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca x P product was >55 mg(2)dl(-2) in 136 patients (26%) and lower than 55 mg(2)dl(-2) in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1+/-1.4 and 4.5+/-1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca x P in 73%, serum Ca(2+) in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosphorus control in the majority of patients.

Effect of the hemodialysis session on bcl-2 expression in peripheral blood mononuclear cells in vivo.

bcl-2 is a proto-oncogene with a regulatory role in many conditions due to its marked inhibitory action on apoptosis. Reports regarding the effect of hemodialysis (HD) on apoptosis of mononuclear cells and in association with bcl-2 expression in particular, are controversial. The aim of the present study was to examine in vivo the influence of an HD session on bcl-2 expression of lymphocytes and monocytes. We measured quantitative bcl-2 expression with flow cytometry, in terms of antibodies bound per cell, in blood samples taken from 44 HD patients before and after an HD session. 27 patients (group I) were dialyzed with synthetic-type membranes and 17 (group II) with cellulose-type membranes. bcl-2 expression increased statistically significantly in lymphocytes (1,616 +/- 718 to 1,894 +/- 715 molecules/cell, p < 0.01) at the end of HD. Monocyte expression of bcl-2 was lower than in lymphocytes and almost did not change after the HD session (654 +/- 446 to 698 +/- 375 molecules/cell, p = NS). Comparison between the two groups did not reveal a significant difference in either the baseline bcl-2 expression or in the value of the increase after HD. We conclude that HD seems to decrease lymphocyte apoptosis independent of the biocompatibility of the dialyzer membrane.

Severe vitamin D deficiency in chronic renal failure patients on peritoneal dialysis.

UNLABELLED: The aim of this study was to evaluate the prevalence of vitamin D deficiency in chronic renal failure (CRF) patients on peritoneal dialysis (PD) and to correlate the findings with various demographic and renal osteodystrophy markers. METHOD: This cross-sectional, multicenter study was carried out in 273 PD patients with a mean age of 61.7 +/- 10.9 years and mean duration of PD 3.3 +/- 2.2 years. It included 123 female and 150 male patients from 20 centers in Greece and Turkey, countries that are on the same latitude, namely, 36-42 degrees north. We measured 25(OH)D3 and 1.25(OH)2D3 levels and some other clinical and laboratory indices of bone mineral metabolism. RESULTS: Of these 273 patients 92% (251 patients) had vitamin D deficiency i.e. serum 25(OH)D3 levels less than 15 ng/ml, 119 (43.6%) had severe vitamin D deficiency i.e., serum 25(OH)D3 levels, less than 5 ng/ml, 132 (48.4%) had moderate vitamin D deficiency i.e., serum 25(OH)D3 levels, 5-15 ng/ml, 12 (4.4%) vitamin D insufficiency i.e., serum 25(OH)D3 levels 15 - 30 ng/ml and only 10 (3.6%) had adequate vitamin D stores. We found no correlation between 25(OH)D3 levels and PTH, serum albumin, bone alkaline phosphatase, P, and Ca x P. In multiple regression analyses, the independent predictors of 25(OH)D3 were age, presence of diabetes (DM-CRF), levels of serum calcium and serum 1.25(OH)2D3. CONCLUSION: We found a high prevalence (92%) of vitamin D deficiency in these 273 PD patients, nearly one half of whom had severe vitamin D deficiency. Vitamin D deficiency is more common in DM-CRF patients than in non-DM-CRF patients. Our findings suggest that these patients should be considered for vitamin D supplementation.

Life-threatening hemorrhage from abdominal aorta following a percutaneous renal biopsy.

We report on a case of life-threatening abdominal aorta hemorrhage following percutaneous renal biopsy. A 42-year-old woman with chronic kidney disease stage 2 and microscopic hematuria underwent a percutaneous renal biopsy to evaluate renal insufficiency. One hour following the biopsy procedure, she complained of an abdominal pain and developed signs ofoligemic shock. In despite of 4 blood units transfusion, the patient continued to be in shock. She was transmitted urgently to the operating room without any other examinations (such as abdominal computer tomography) and underwent an emergency laparotomy. A transverse tear in the abdominal aorta was identified as the bleeding site, and after occlusion, the hemorrhage was stopped. The patient gradually recovered and she was discharged in good clinical condition after a few days.

Effectiveness of aluminum hydroxide timing administration in relation to meals in controlling hyperphosphatemia in dialysis patients.

Phosphate binder compounds contribute to the control of hyperphosphatemia in hemodialysis (HD) patients. However, the most effective schedule of administration of phosphate binders in relation to meals is not well documented. We examined the effectiveness of aluminum hydroxide intake as the sole phosphate binder in relation to meals. Eighty-five patients on regular HD (45 male, 40 female), age 21-72 years, with a duration of 6-216 months HD participated in the study. In all patients, phosphate binders were discontinued for a one month period. Thereafter, and according to the protocol, all patients were advised to take aluminum hydroxide [Al(OH)3 ] 30 min before, during and 30 min after meals for 3 periods of one month each, in a random order. One month washout period preceded the periods of Al(OH)3 ingestion. When Al(OH)3 was administered 30 min prior to the meals, serum phosphate decreased by 7.0% (0.59 mg/dL), while when administrated with or 30 min after meals, it decreased statistically significantly by 28.5% (2.08 mg/dL), and 16% (1.29 mg/dL) respectively. Our results suggest that the efficacy of Al(OH)3 to bind phosphate salts and thus to prevent the hyperphosphatemia in HD patients is higher when this drug is taken with meals.

Accuracy and clinical utility of dialysis dose measurement using online ionic dialysance.

BACKGROUND: Statistical associations between urea removal and survival have been described in a number of publications. Urea removal during treatment may be quantified by the delivered dose of dialysis. Methods in clinical use to measure delivered dose are retrospective and reliant on accurate blood sampling. The new generation of single patient proportionating systems incorporate the facility to automatically measure ionic dialysance throughout dialysis. METHODS: In a prospective study on 9 anuric patients with a stable dialysis prescription, we have compared the agreement of the dose of dialysis determined from ionic dialysance (Dt/V) with that derived from equilibriated Kt/V (eKt/V) and Kt/V measured by direct dialysis quantification (Kt/V(DDQ)) using 2 types of hemodialysis membrane (hemophan and low-flux polysulfone). The variability of the delivered dose over a 1-month period was also determined. RESULTS: Ionic dialysance was independent of membrane type. It was comparable to that established for plasma urea water clearance for hemophan but lower for polysulfone (p < 0.001). The mean (+/- SD) delivered dose of dialysis (Dt/V) was similar for both membranes (1.18 +/- 0.15 (hemophan) and 1.18 +/- 0.11 (low-flux polysulfone)). Bland Altman comparisons showed the limits of agreement between Dt/V and Kt/V(DDQ) were +/- 0.17 and for Dt/V compared with eKt/V +/- 0.15. A 1-month measurement of Dt/V demonstrated considerable treatment to treatment variability indicating that delivered dose cannot be considered stable. CONCLUSION: The availability of online measurement of ionic dialysance provides a step towards monitoring dialysis more closely at the time of delivery, and its clinical application will ensure that a more constant dialysis dose is delivered.

Renal abnormalities in patients with sickle cell-beta thalassemia.

We examined renal abnormalities in Greek patients with sickle-cell beta thalassemia (S-beta thal). A total of 17 patients aged 16-59 years suffering from S-beta thal and 17 age- and sex-matched healthy controls were studied. In all individuals we carried out a detailed study of renal function including electrolytes in serum and urine, concentrating or diluting ability, urine acidification ability, glomerular filtration rate (GFR), and hormones [such as plasma renin activity (PRA), serum aldosterone, and erythropoietin (EPO)]. Though the GFR did not differ significantly in patients and controls, half the patients had either supranormal or subnormal values. Serum potassium and uric acid were significantly higher in patients than controls. Serum phosphorus was similar in both groups, though patients with S-beta thal had significantly lower phosphate excretion indices. All patients were unable to maximally concentrate the urine, and seven also had limited ability to maximally dilute it. Five patients had incomplete distal renal tubular acidosis. Four had mild proteinuria, and six had microalbuminuria. Serum EPO and aldosterone were higher in S-beta thal patients than controls, but there was no difference in PRA between the two groups. There was a strong correlation between hemoglobin concentration and EPO levels, which was strongest in patients with GFR < 50 ml/min. We conclude that patients with S-beta thal, like sickle-cell anemia patients, present multiple abnormalities of renal function.

Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis.

We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18-61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 +/- 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios delta anion gap/delta bicarbonate (delta AG/delta HCO3) and sodium/chloride (Na/Cl)). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status.