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Home hemodialysis is the most cost-effective form of dialysis and is associated with the lowest mortality. Home hemodialysis patients are usually highly motivated, independent, and actively employed. Because of the minimal supervision they require and the fact that they are not in a controlled environment, it is easy to overlook the measurement of their dialysis adequacy. We studied 6 home hemodialysis patients and demonstrated that blood urea measured 30 min before the end of dialysis (Ct-30) is equivalent to that measured 30 min after the end of dialysis (Ct+30). The Kt/V results using Ct-30, Kt/V(Ct-30), were almost equivalent to Kt/V(Ct+30) (p = 0.5). The Kt/V Kt/V(Ct) using blood urea measured at the end of dialysis (Ct) significantly overestimated Kt/V(Ct-30) and Kt/V(Ct+30) (p = 0.007) The calculated percent reduction of urea (PRU) was about 5% less when using Ct-30 compared with Ct (p = 0.001). Taking blood samples 30 min before the end of dialysis for urea kinetics is more convenient for the home dialysis patients, since no other technical aspects of dialysis need their attention. The samples can be delivered to the laboratory the following day, because the blood may be stored in heparinized tubes at 4°C without deterioration of urea and creatinine concentrations. The Kt/V(Ct-30) was almost equal to Kt/V(Ct+30), so there is no longer any concern for the errors introduced by urea rebound. The blood pump must be reduced to 80 mL/min for about 10 sec to eliminate the errors due to fistula and cardiopulmonary recirculation. A simple programmable calculator will facilitate the calculation of accurate results using the Daugirdas second-generation formula.

In the late 1970s, continuous ambulatory peritoneal dialysis was first introduced as a mode of treatment for patients with end-stage renal disease. Since that time many patients, themselves or with the help of family members, have routinely performed the therapy at home. There are now 2935 home peritoneal dialysis patients in Canada (36% of the total dialysis population}. Today, however, the average patient on dialysis is likely to be older and have other complicating illnesses; moreover, patients may live alone, or have family members who are working. Over the past three years, through the use of innovative assistive devices and strong educational links with community nursing agencies, we have been able to manage peritoneal dialysis patients with complex needs in the home. We performed a retrospective analysis of 18 patients, with severe comorbid conditions, who were managed in the home with the help of community nurses. We will show that this is an economic, efficient, and effective method of caring for home dialysis patients with severe disabilities. Home care agencies need our support so that they can continue to help us manage the complex peritoneal dialysis patient in the 1990s.

Aplastic osteodystrophy without aluminum: The role of “suppressed” parathyroid function. We evaluated 259 dialysis patients using serum parathyroid hormone (PTH, IRMA; normal range 1 to 5.5 pM or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various forms of renal osteodystrophy and their risk factors. Although half of the biopsied patients had low turnover osteodystrophy, evidence of aluminum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ingestion of calcium carbonate, diabetes mellitus and advanced age. The PTH levels in patients with the aplastic lesion were significantly lower than in patients with normal or high bone turnover lesions [7.7 ± 6.1 vs. 36.9 ± 3.2 pM (77 ± 61 vs. 369 ± 32 pg/ml), P < 0.0001]. Aside from hypercalcemia, these patients were relatively asymptomatic. In a second study, 10 patients on peritoneal dialysis with the aplastic lesion had their dialysate calcium lowered from 1.62 to 1.0 mM. This resulted in a significant increase in PTH levels, from [3.7 ± 0.8 to 10.6 ± 1.9 pM (37 ± 8 to 106 ± 19 pg/ml), P < 0.001] which persisted over the nine-month observation period. In conclusion, the aplastic lesion is the most common form of renal osteodystrophy, with aluminum intoxication implicated in only 1/3 of the cases. In the remainder, factors identified include therapy with peritoneal dialysis using supraphysiological dialysate calcium, oral CaCO3 intake and diabetes mellitus. These factors may modulate their effect by lowering serum PTH to levels which are inadequate in maintaining normal bone turnover. The long-term sequelae of this non-aluminum related lesion remain to be defined.

To assess the risk factors associated with renal osteodystrophy, we examined the database of 256 patients who were prospectively studied in three Toronto dialysis centers between October of 1987 and 1989. The potential risk factors examined included age, sex, type and duration of dialysis, type and dose of phosphate binders, vitamin D treatment, and history of diabetes mellitus, renal allograft failure, parathyroidectomy, and bilateral nephrectomy. All patients had undergone a bone biopsy and were categorized into one of four disease groupings: (1) osteitis fibrosa and mixed bone disease, (2) aluminum bone disease, (3) mild bone disorder, and (4) aplastic bone disorder. The mean (+/- SD) age of the patients at bone biopsy was 57 +/- 15 years, and 62% were men. Forty-five percent of patients were treated by hemodialysis and 55% by peritoneal dialysis. The mean duration of dialysis was 4 +/- 4 years. Twenty-five percent were also diabetic. The most common disorder was the aplastic (or "adynamic") bone disorder, found in 34% of patients. Aluminum bone disease was found in 27%, osteitis fibrosa or mixed bone disease in 27%, and mild bone disorder in 12% of patients. Cumulative intake of aluminum gels was associated with aluminum bone disease, whereas peritoneal dialysis with supraphysiologic calcium concentrations, ingestion of calcium carbonate, and diabetes mellitus were associated with both mild bone disorder and aplastic bone disorder. These three latter risk factors may be important in predisposing patients to a low bone turnover state through modulation of parathyroid hormone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal osteodystrophy in diabetic patients. To assess the effects of diabetes mellitus on renal osteodystrophy, we examined the database of 256 patients (45% on hemodialysis and 55% on peritoneal dialysis) who were prospectively studied in three Toronto dialysis centers between October of 1987 and 1989. All patients had serial documentation of their clinical, laboratory and risk parameters of bone disease, and completed a series of investigations that included the deferoxamine test, measurement of intact 1–84 PTH levels, and an iliac crest bone biopsy. Twenty-five percent of these patients were diabetic. When compared to non-diabetic patients, they were on dialysis for a shorter duration (2.4 ±0.3 vs. 4.7±0.3 years; P < 0.0002), used calcium carbonate as the only phosphate binder more frequently (40 vs. 25%; P < 0.007), and had lower parathyroid hormone levels (12 ± 1.4 vs. 24 ± 2.3 pmol/liter; P < 0.002). High-turnover bone disorders (that is, osteitis fibrosa and mixed disorder) were distinctly uncommon (8 vs. 33%; P < 0.01 by Fisher's exact test), while the mild (19 vs. 9%; P = NS) and the aplastic disorders (with mean stainable bone surface aluminum of 6.5 ± 0.7%) (46 vs. 31%; P = NS) tended to be more common in diabetic patients. The prevalence of aluminum bone disease was the same in both groups (27%). Diabetic patients ingested a smaller cumulative dose of aluminum gels (3.7 ± 0.6 vs. 9.3 ± 1.1 kg; P < 0.005), yet had a higher rate of aluminum accumulation on bone surfaces than non-diabetic patients (1.5 ± 0.19 vs. 0.96 ± 0.10% per month on dialysis; P < 0.015). Although the cumulative exposure to aluminum gels remained the major risk factor for aluminum bone disease (P < 0.0001), a positive interaction was noted for diabetic mellitus to increase this risk (P < 0.05). Thus, diabetes mellitus appears to predispose dialysis patients to low bone-turnover states. In addition, it appears to increase aluminum accumulation on bone surfaces and predisposes to aluminum bone disease. The clinical significance of the aplastic disorder remains to be defined.

The spectrum of bone disease in end-stage renal failure—An evolving disorder. We have assessed the bone histology in 259 chronic dialysis patients, all of whom were in the same dialysis program. All patients had bone biopsies with quantitative histomorphometry, intact parathyroid hormone (PTH) measurements, basal and deferoxamine stimulated serum aluminum levels. Results demonstrate the increased incidence of the recently described aplastic bone lesion, particularly in patients treated with peritoneal dialysis (PD). Aluminum-related bone disease is much less common than previously described, perhaps in relation to the declining use of aluminum as a phosphate binder. A different pattern of bone lesions is seen in PD as compared with hemodialysis (HD), with low turnover disorders comprising 66% of the lesions seen in PD and high turnover lesions accounting for 62% of the bone histologic findings in HD. The difference in these patterns may relate to alterations in PTH levels, as mean PTH levels in HD patients were 2-1/2 times the levels found in PD patients (P < 0.0005), while older age, higher prevalence of diabetes and a shorter duration of dialysis may also have contributed to the findings in the PD patients. We suggest that PD, perhaps by maintaining calcium at higher levels, may more effectively suppress the parathyroid gland.

Non-invasive prediction of aluminum bone disease in hemo- and peritoneal dialysis patients. Between October 1987 and October of 1989, we conducted a prospective study to evaluate non-invasive test strategies for predicting aluminum bone disease (ABD) in a group of largely unselected dialysis patients based on their deferoxamine (DFO) test alone, or the combined results of their DFO test and intact 1-84 parathyroid hormone (PTH) levels. These test parameters were evaluated against the pathological diagnosis of ABD based on bone biopsy (“gold standard”). A total of 445 patients in three dialysis centers in Toronto were serially followed for their clinical, laboratory and risk parameters for renal osteodystrophy during the study, and 259 (142 PD and 117 HD) patients underwent a series of investigations which included the DFO test, measurement of intact 1-84 PTH levels, and an iliac crest bone biopsy. Serum aluminum ([A]) level ≥ 3700nM (or 100 µg/liter) had a positive predictive value (PPV) of 75% for ABD in our PD and 88% in our HD patients, but its sensitivity was low (10 and 37%). Delta [Al] (that is, incremental rise of serum [Al] from baseline post-DFO) was useful in predicting ABD in our PD but not HD patients. Test combination based on delta [Al] ≥ 5550nM (or 150 µg/liter) and PTH level < 20 pM (or 200 pg/ml) yielded the best PPV ≥ 95% for ABD in both PD and HD patients. This test cut-off would remain highly predictive of ABD even if the prevalence of ABD decreases to as low as 5% for the PD patients and 10% for the HD patients. However, for patients who have discontinued their aluminum gels for ≥6 months these test strategies would not be useful due to a very high frequency of false-negative cases (or low sensitivity). Thus, the main utility of these non-invasive strategies will be in those patients who continue to require treatment of aluminum gels for their phosphate control.Non-invasive prediction of aluminum bone disease in hemo- and peritoneal dialysis patients. Between October 1987 and October of 1989, we conducted a prospective study to evaluate non-invasive test strategies for predicting aluminum bone disease (ABD) in a group of largely unselected dialysis patients based on their deferoxamine (DFO) test alone, or the combined results of their DFO test and intact 1-84 parathyroid hormone (PTH) levels. These test parameters were evaluated against the pathological diagnosis of ABD based on bone biopsy (“gold standard”). A total of 445 patients in three dialysis centers in Toronto were serially followed for their clinical, laboratory and risk parameters for renal osteodystrophy during the study, and 259 (142 PD and 117 HD) patients underwent a series of investigations which included the DFO test, measurement of intact 1-84 PTH levels, and an iliac crest bone biopsy. Serum aluminum ([A]) level ≥ 3700nM (or 100 µg/liter) had a positive predictive value (PPV) of 75% for ABD in our PD and 88% in our HD patients, but its sensitivity was low (10 and 37%). Delta [Al] (that is, incremental rise of serum [Al] from baseline post-DFO) was useful in predicting ABD in our PD but not HD patients. Test combination based on delta [Al] ≥ 5550nM (or 150 µg/liter) and PTH level < 20 pM (or 200 pg/ml) yielded the best PPV ≥ 95% for ABD in both PD and HD patients. This test cut-off would remain highly predictive of ABD even if the prevalence of ABD decreases to as low as 5% for the PD patients and 10% for the HD patients. However, for patients who have discontinued their aluminum gels for ≥6 months these test strategies would not be useful due to a very high frequency of false-negative cases (or low sensitivity). Thus, the main utility of these non-invasive strategies will be in those patients who continue to require treatment of aluminum gels for their phosphate control.