A randomized, double-blind, crossover design study of sevelamer hydrochloride and sevelamer carbonate in patients on hemodialysis.

AIMS: Sevelamer carbonate is an anion exchange resin with the same polymeric structure as sevelamer hydrochloride in which carbonate replaces chloride as the anion. The study investigated the effects of sevelamer carbonate and sevelamer hydrochloride on serum phosphorus, lipids and bicarbonate levels in hemodialysis patients. MATERIALS AND METHODS: This was a double-blind, randomized, crossover study. 79 hemodialysis patients were randomly assigned to either sevelamer carbonate or sevelamer hydrochloride for 8 weeks followed by a crossover to the other regimen for an additional 8 weeks of treatment. RESULTS: The mean serum phosphorus was 4.6+/-0.9 and 4.7+/-0.9 mg/dl during sevelamer carbonate and sevelamer hydrochloride treatment, respectively. Sevelamer carbonate and sevelamer hydrochloride were equivalent in controlling serum phosphorus, the geometric least square mean ratio was 0.99 (90% CI, 0.95-1.03). Mean total and LDL cholesterol were 144.0+/-33.9 and 59.5+/-24.9 mg/dl, respectively, during sevelamer carbonate treatment and 139.0+/-33.6 and 56.0+/-23.3 mg/dl, respectively, during sevelamer hydrochloride treatment. Serum bicarbonate levels increased by 1.3+/-4.1 mEq/l during sevelamer carbonate treatment. There were fewer gastrointestinal adverse events with sevelamer carbonate. CONCLUSIONS: Sevelamer carbonate and sevelamer hydrochloride were equivalent in controlling serum phosphorus and serum bicarbonate levels increased with sevelamer carbonate. Lipid profiles for both were well-below the levels suggested by KDOQI. Sevelamer carbonate may have advantages over sevelamer hydrochloride in the treatment of hyperphosphatemia in hemodialysis patients.

A controlled trial of the early treatment of secondary hyperparathyroidism with calcitriol in hemodialysis patients.

BACKGROUND: Calcitriol is widely used in conjunction with phosphorus-binders containing calcium to treat secondary hyperparathyroidism in dialysis patients. Its efficacy in patients with severe hyperparathyroidism is diminished, in part, due to glandular hyperplasia associated with decreased calcitriol and calcium receptors. SUBJECTS AND METHODS: We, therefore, developed a prospective, randomized trial comparing i.v. calcitriol plus calcium carbonate (CaCO3) compared to CaCO3 alone (control) in patients with mild to moderate hyperparathyroidism who were within the first year of initiating hemodialysis. Patients underwent calcium (Ca) suppression/stimulation testing at baseline and after six and twelve months of treatment to indirectly assess parathyroid gland hyperplasia. RESULTS: In the calcitriol group, the amino-terminal parathyroid hormone (N-PTH) decreased significantly from a baseline value of 70 +/- 12 pg/ml at month zero to 22 +/- 7 and 19 +/- 6 pg/ml at months 6 and 12, respectively (the conversion factor of amino-terminal PTH to intact PTH is 6, i.e., 10 pg/ml N-PTH equals 60 pg/ml intact PTH). In contrast, the N-PTH levels in the CaCO3 alone group did not change. The change in nadir N-PTH levels at month 12 compared to month zero decreased by 14 +/- 7% in the calcitriol group but increased by 96 +/- 59% in the control group (p < 0.05). In addition, the increment in N-PTH levels during hypocalcemic stimulation decreased by 68 +/- 6% at month 12 compared to month zero but increased by 61 +/- 42% in the control group. Although total calcium and phosphorus levels were not different between the two groups, ionized calcium values were higher in the calcitriol group. The incidence of hypercalcemia was the same in both groups and the episodes were asymptomatic. CONCLUSION: Pulse calcitriol therapy is effective in preventing progression of secondary hyperparathyroidism in hemodialysis patients with mild to moderate disease. Based on Ca suppression/stimulation tests, calcitriol was more successful in preventing gland growth than CaCO3 alone. Further studies are needed to determine if the strategy of early treatment of mild to moderate hyperparathyroidism by pulse calcitriol is safe and effective in hemodialysis in patients.

Factors associated with the prevalence of arteriovenous fistulas in hemodialysis patients in the HEMO study. Hemodialysis (HEMO) Study Group.

BACKGROUND: Arteriovenous (AV) fistulas are the vascular access of choice for hemodialysis patients, but only about 20% of hemodialysis patients in the United States dialyze with fistulas. There is little information known about the factors associated with this low prevalence of fistulas. METHODS: Multiple logistic regression analysis was used to evaluate the independent contribution of factors associated with AV fistula use among patients enrolled in the HEMO Study. The analysis was conducted in 1824 patients with fistulas or grafts at 45 dialysis units (15 clinical centers). RESULTS: Thirty-four percent of the patients had fistulas. The prevalence of fistulas varied markedly from 4 to 77% among the individual dialysis units (P < 0.001). Multiple regression analysis revealed five demographic and clinical factors that were each independently associated with a lower likelihood of having a fistula, even after adjustment for dialysis unit. Specifically, the prevalence of fistulas was lower in females than males [adjusted odds ratio (AOR) 0.37, 95% CI, 0.28 to 0.48], lower in patients with peripheral vascular disease than in those without (AOR 0.55, 95% CI, 0.38 to 0.79), lower in blacks than in non-blacks (AOR 0.64, 95% CI, 0.46 to 0.89), lower in obese patients (AOR per 5 kg/m(2) body mass index, 0.76, 95% CI, 0.65 to 0.87), and lower in older patients (AOR per 10 years, 0.85, 95% CI, 0.78 to 0.94). The differences in the prevalence of fistulas among the dialysis units remained statistically significant (P < 0.001) after adjustment for these demographic and clinical factors. Finally, there were substantial variations in the prevalence of fistulas even among dialysis units in a single metropolitan area. CONCLUSIONS: Future efforts to increase the prevalence of fistulas in hemodialysis patients should be directed at both hemodialysis units and patient subpopulations with a low fistula prevalence.

Insulin-like growth factor 1 enhances renal function in a patient with chronic renal failure on peritoneal dialysis.

Insulin-like growth factor 1 (IGF1) has been shown to improve renal function in healthy subjects, as well as those with chronic renal failure. To our knowledge, IGF1 has not been shown to be efficacious in patients who were already undergoing dialysis. We present the case of a 70-year-old woman with end-stage renal disease (ESRD) and overt uremic symptoms treated with IGF1 after peritoneal dialysis was discontinued because of complications. There was a significant improvement in her inulin clearance during the course of treatment. The patient remained well and did not require dialytic support for 19 weeks. Although further data are necessary, we believe this case shows that IGF1 may be a short-term alternative to dialysis in patients with ESRD.

Association of acidosis and nutritional parameters in hemodialysis patients.

There is extensive literature supporting an important role for acidosis in inducing net protein breakdown, both in experimental animals and humans. However, the clinical importance of the moderate intermittent metabolic acidosis frequently observed in hemodialysis patients has not been determined. We performed a cross-sectional analysis of the baseline laboratory data in the first 1,000 patients recruited to the Hemodialysis Study, looking for correlations between predialysis serum total carbon dioxide levels and parameters related to dietary intake and nutritional status. We found the mean predialysis serum total carbon dioxide level was moderately low (21.6 +/- 3.4 mmol/L; mean +/- SD) despite the use of bicarbonate dialysate and an average single-pool Kt/V of 1.54. Predialysis serum total carbon dioxide level correlated negatively with normalized protein catabolic rate (P < 0.001), suggesting patients with lower serum total carbon dioxide levels have a greater protein intake. The degree of acidosis observed in our patients does not seem to have a deleterious effect on the nutritional status of these patients because correlation of serum total carbon dioxide level with nutritional parameters, such as serum creatinine and serum albumin levels, was either negative or not statistically significant. Further investigation of the effect of modifying serum bicarbonate concentration on nutritional markers is needed to test these hypotheses.

Suppression of parathyroid hormone secretion in hemodialysis patients by a novel vitamin D analogue: 19-nor-1,25-dihydroxyvitamin D2.

In this double-blind, placebo-controlled, randomized, multicenter study, 35 patients with end-stage renal disease undergoing maintenance hemodialysis were treated three times weekly for 4 weeks with either 19-nor-1,25-dihydroxyvitamin D2 (paricalcitol) intravenously at doses ranging from 0.04 to 0.24 microg/kg or placebo. Eligible patients with secondary hyperparathyroidism (HPT; intact parathyroid hormone [iPTH] level > 300 pg/mL) were initially withdrawn from any existing vitamin D therapy over a 4-week washout period and then randomized to treatment for 4 weeks with either paricalcitol or placebo. Overall, there was a clinically and statistically significant reduction in iPTH level for patients receiving paricalcitol compared with placebo (P = 0.006). The study end point for efficacy was at least a 30% reduction from maximum baseline in iPTH level for 75% of the patients receiving paricalcitol per dosing group. The study end point for efficacy was at least a 30% reduction from maximum baseline in iPTH for 75% of patients receiving paricalcitol per dosing group. Sixty-eight percent (15 of 22) of patients receiving paricalcitol attained this efficacy end point regardless of dosage received (0.04, 0.08, 0.16, and 0.24 microg/kg). Eighty-three percent (5 of 6) of the patients in each of the paricalcitol groups receiving 0.16- and 0.24-microg/kg dosages attained the efficacy end point. Only two patients receiving placebo attained the iPTH end point. There were no clinically relevant differences in serum calcium (Ca) or phosphorus (P) levels between the group treated with paricalcitol and that treated with placebo. Although there was a statistically significant difference between the change from baseline to final-visit Ca levels in the paricalcitol group and the placebo group (P < 0.001), the final-visit mean Ca level in the paricalcitol group was within the normal range (9.44 mg/dL). There was no statistically significant difference between groups for the change from baseline in P level (P = 0.625). Only one patient treated with paricalcitol developed hypercalcemia before or coincident with the iPTH end point. Three other patients receiving paricalcitol experienced elevated serum Ca levels subsequent to reaching the iPTH end point, with iPTH reductions of 83% to 98%. There were no significant differences between patients treated with paricalcitol and patients treated with placebo in adverse reactions. These results show that paricalcitol safely and effectively reduces iPTH levels in hemodialysis patients with secondary HPT.

Impaired delivery of hemodialysis prescriptions: an analysis of causes and an approach to evaluation.

Serial kinetic modeling is commonly used in hemodialysis to assess the adequacy of dialysis. A variety of problems lead to declining Kt/V in previously stable patients. These include noncompliance, vascular access recirculation, and dialyzer dysfunction. The purpose of this study was to find the relative frequencies of these problems in a group of patients undergoing routine hemodialysis. Simultaneous urea kinetic modeling and access recirculation were tested during 3 consecutive months. The baseline Kt/V was defined as the average of each patient's Kt/V values obtained during the previous 4 mo. A clinically important fall in Kt/V was defined as a decline of > or =0.2 if the baseline Kt/V was > or =1.2, or a decline of > or =0.1 if the baseline Kt/V was <1.2. Ninety-three of 375 (25%) sessions met the criteria for a significant decline in urea kinetic modeling. The baseline Kt/V in this group was 1.33 +/- 0.20 (mean +/- SEM) and declined to 1.02 +/- 0.18 in the abnormal month (P < 0.05). In 42% of instances with a decline of Kt/V, reduced blood processing due to a lower blood flow or shorter time than prescribed was responsible. Recirculation of >12% was found in 25% of sessions with a decrease in Kt/V. These patients most often had access dysfunction or reversed needles. The remaining one-third of patients with decreases in Kt/V had no problem identified, and subsequent monthly kinetic modeling results returned to baseline. These results suggest that analysis of falling urea kinetic modeling results should include a careful review of the dialysis record for reductions in prescribed time or blood flow rates followed by vascular access testing. If these evaluations are unrevealing, urea kinetic modeling results usually return to baseline in the next month.

Bone disease in long-term dialysis.

We reviewed the clinical features, laboratory findings, and skeletal abnormalities of six patients who have been on dialysis therapy for 12 to 20 years (average, 16.7 years). Hemodialysis has been the major therapeutic modality in five of the six individuals. Ages of the patients ranged from 28 to 67 years (mean, 44.5). Bone biopsy specimens were available for five of the patients. In three of these, the predominant changes in bone were those of osteitis fibrosa. In two patients with severe osteitis fibrosa, there was a decrease in height. Two patients had predominantly osteomalacia, but in one of these, the condition was noted before the initiation of 13 years of chronic ambulatory peritoneal dialysis, supplanted 2 years ago by hemodialysis. Total parathyroidectomies with implants of parathyroid tissue in the forearm were performed in four of the six patients. All four had, and continue to have, markedly elevated levels of parathyroid hormone (PTH). Symptoms and signs of amyloidosis of bone have occurred in all six patients, including carpal tunnel syndrome in two, bone cysts in three, and presumptive tendon involvement of the shoulder in one patient. The pathogenesis of hyperparathyroidism is described briefly, and appropriate treatment is summarized.

Comparison of survival of an expanded polytetrafluoroethylene graft designed for early cannulation to standard wall polytetrafluoroethylene grafts.

BACKGROUND: Placement and maintenance of a well-functioning vascular access are essential for delivery of adequate hemodialysis. Newly placed polytetrafluoroethylene (PTFE) arteriovenous grafts require a period of wound healing and incorporation of fibrous tissue before use, a period typically lasting two to three weeks. An ideal PTFE graft would be one that can be used for vascular access immediately, obviating the need for temporary dialysis catheters. Recently an expanded PTFE (ePTFE) graft with a mesh cannulation segment (Diastat graft) has been proposed for early cannulation. STUDY DESIGN: This is a retrospective single-center study comparing ePTFE graft survival to contemporaneously placed standard wall PTFE (GORE-TEX) grafts. RESULTS: Forty-seven consecutive new or established patients receiving chronic hemodialysis had grafts (25 ePTFE, 22 standard PTFE) placed between November 1994 and July 1995. There were no significant differences between the groups in age, race, gender, incidence of diabetes mellitus, or peripheral vascular disease. By the end of the study, 21 of 25 ePTFE grafts had clotted, compared with 11 of the 22 patients receiving a standard PTFE graft. Median time to first clotting was 53 days for the ePTFE grafts and 164 days for the standard PTFE grafts (p < 0.0001). Nine patients with ePTFE grafts required a temporary catheter after their first clotting episode. CONCLUSIONS: The ePTFE grafts thrombosed at a significantly higher rate than standard wall PTFE grafts. Further experience with the Diastat graft might improve graft survival. However, early experience does not suggest that the avoidance of short-term temporary access outweighs the problem of high clotting rate, and its attendant morbidity.

Pathogenesis of secondary hyperparathyroidism.

Hyperplasia of the parathyroid glands and increased concentrations of immunoreactive parathyroid hormone are among the earlier alterations of mineral metabolism in patients with chronic renal failure. In the past five years several investigators have demonstrated that phosphorus retention plays a key role in the development of secondary hyperparathyroidism and chief cell hyperplasia of the parathyroid glands. Since phosphorus regulates the production of 1,25D3 by altering the enzyme 1-alpha-hydroxylase it is possible that the effect of phosphorus retention is mediated by a decrease in the synthesis of 1,25D3. This has been shown in patients with early renal insufficiency. However, in patients with advanced renal failure the reduced renal mass may limit the production of 1,25D3. It is clear now that phosphorus per se independent of the levels of ionized calcium and 1,25D3 can increase the synthesis and secretion of PTH in vivo and in vitro. The abnormalities in vitamin D metabolism are not only characterized by low levels 1,25D3 but by low number of vitamin D receptors. Thus, the parathyroid glands are resistant to the action of 1,25D3 and high pharmacological concentrations of 1,25D3 in blood are necessary to suppress the levels of parathyroid hormone in advanced renal failure. The development of monoclonal changes in glands obtained from patients with secondary hyperparathyroidism further complicates the treatment of secondary hyperparathyroidism in patients maintained on haemodialysis. Thus, correction of serum phosphorus is imperative for the success of 1,25D3 to control the levels of parathyroid hormone. Currently several laboratories are studying at the molecular level the mechanisms by which dietary phosphorus induces chief cell hyperplasia.

Magnesium carbonate as a phosphorus binder: a prospective, controlled, crossover study.

The use of calcium carbonate (CaCO3) to bind phosphorus (P) in chronic hemodialysis patients has been a popular tactic in the past decade. Nonetheless, problems with hypercalcemia decrease its usefulness, particularly in patients treated with calcitriol. A P binder not containing calcium (Ca) would be of value in these circumstances. In short-term studies, we showed that magnesium carbonate (MgCO3) was well-tolerated and controlled P and Mg levels when given in conjunction with a dialysate Mg of 0.6 mg/dl. We, therefore, performed a prospective, randomized, crossover study to evaluate if the chronic use of MgCO3 would allow a reduction in the dose of CaCO3 and yet achieve acceptable levels of Ca, P, and Mg. We also assessed whether the lower dose of CaCO3 would facilitate the use of larger doses of calcitriol. The two phases were MgCO3 plus half the usual dose of CaCO3 and CaCO3 alone given in the usual dose. It was found that MgCO3 (dose, 465 +/- 52 mg/day elemental Mg) allowed a decrease in the amount of elemental Ca ingested from 2.9 +/- 0.4 to 1.2 +/- 0.2 g/day (P < 0.0001). The Ca, P, Mg levels were the same in the two phases. The maximum dose of i.v. calcitriol without causing hypercalcemia was 1.5 +/- 0.3 micrograms/treatment during the MgCO3 phase and 0.8 +/- micrograms/treatment during the Ca phase (P < 0.02). If these studies are confirmed, the use of MgCO3 and a dialysate Mg of 0.6 mg/dl may be considered in selected patients who develop hypercalcemia during treatment with i.v. calcitriol and CaCO3.

Impaired delivery of dialysis: diagnosis and correction.

Hemodialysis treatments yielding inadequate amounts of dialysis, as defined by urea kinetic modeling, are partially responsible for considerable mortality and morbidity in the United States. In almost 50% of dialysis treatments resulting in a Kt/V of < 1.0, the culprit is impaired delivery of the prescribed amount of dialysis. The factors involved in impaired delivery of dialysis are many and often elusive. If present and widespread, a search for the cause of the problem entails careful examination of the equipment and nursing procedures. If impaired delivery is a sporadic and infrequent event, a patient-specific investigation should be undertaken. In either circumstance, a clear understanding of the principles and practical aspects of hemodialysis greatly assists the nephrologist as a sleuth.

Kinetics of monocyte 1 alpha-hydroxylase in renal failure.

In chronic uremia, the requirement of supraphysiological doses of serum 25-hydroxyvitamin D3 [25(OH)D3] for the normalization of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels has been attributed to impaired substrate availability to renal 1 alpha-hydroxylase. Because serum 1,25(OH)2D3 can also be corrected by 25(OH)D3 supplementation in bilaterally nephrectomized patients, we examined the role of substrate availability on 1,25(OH)2D3 production by peripheral blood monocytes (PBM). In hemodialysis patients (HP), 25(OH)D3 uptake was 50% lower than normal, and the maximal velocity (Vmax) and apparent Michaelis constant (Km) for 25(OH)D3 of 1 alpha-hydroxylase were 2.7- and 4-fold above normal, respectively. When serum 1,25(OH)2D3 of HP was corrected by intravenous 1,25(OH)2D3, 25(OH)D3 uptake, Km, and Vmax returned to normal values. The effect of 25(OH)D3 supplementation was also examined. In normal adults, 25(OH)D3 administration had no effect on serum 1,25(OH)2D3 levels nor on the Km or the Vmax of PBM 1 alpha-hydroxylase but caused a 11-fold increase in serum 24R,25-dihydroxyvitamin D3[24R, 25(OH)2D3]. In HP, 25(OH)D3 therapy raised serum 1,25(OH)2D3 and reduced the Km and Vmax of PBM 1 alpha-hydroxylase, which correlated negatively with serum 1,25(OH)2D3. However, serum 24R,25(OH)2D3 only increased slightly above basal. These results demonstrate that, in HP, 1) impaired uptake of 25(OH)D3 and low affinity for substrate determine the need for high 25(OH)D3 levels to normalize serum 1,25(OH)2D3, despite higher enzymatic activity; 2) 1,25(OH)2D3 deficiency plays a role in enhanced 1,25(OH)2D3 synthesis and impaired access of 25(OH)D3 to PBM 1 alpha hydroxylase; and 3) abnormal 25(OH)D3 delivery also affects 24-hydroxylation.

Modulation of renal osteodystrophy by extrarenal production of calcitriol.

We report a patient with severe chronic renal failure who developed spontaneous bone fractures. He was found to have hypercalcemia, normal calcitriol levels (probably due to extrarenal production by noncaseating granulomas), and functional hypoparathyroidism. The bone biopsy showed low bone turn-over and the presence of noncaseating granulomas. Treatment with corticosteroids decreased the calcium and calcitriol levels and the parathyroid hormone levels rose. No further fractures occurred. A repeat bone biopsy revealed the presence of osteitis fibrosa. Renal osteodystrophy may be modulated by extrarenal production of calcitriol. In this case, excessive suppression of parathyroid hormone by endogenous calcitriol presumably caused an adynamic bone lesion and spontaneous fractures.

Physiologic mechanisms of action of lovastatin in nephrotic syndrome.

The effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on the metabolism of apolipoprotein (apo) B-containing lipoproteins appear to differ according to the predominant lipoprotein profiles present and the condition being treated. In familial hypercholesterolemia, with isolated low density lipoprotein (LDL) elevations, the LDL-apoB elimination rate is increased by up-regulated LDL-receptors. In familial combined hyperlipidemia where very low density lipoprotein (VLDL) and LDL both may be increased and enhanced production of LDL-apoB may be present, HMG-CoA reductase inhibitors seem to diminish increased LDL-apoB production. The drug-induced decreases in LDL-apoB production could be due to decreased production of precursor VLDL-apoB or due to decreased conversion of VLDL-apoB to LDL-apoB after enhanced removal of VLDL by up-regulated LDL-receptors. To distinguish between these possibilities, we assessed the effects of HMG-CoA reductase inhibitors in another condition in which there is both apoB overproduction and accumulation of VLDL and LDL in plasma, the nephrotic syndrome. We used endogenous labeling of apoB with [13C]leucine and a multicompartmental model to calculate the metabolic parameters of apoB-containing lipoproteins. Only subjects with focal segmental glomerular sclerosis (FSGS) were included, as FSGS is a chronic, very slowly progressive form of nephrotic syndrome. A double-blind, randomized, placebo-controlled, crossover design was used. Treatment periods of 6 weeks were separated by a 2-week washout period. Of the four men studied, three had high triglyceride levels and four had high cholesterol levels. Lovastatin (20 mg/day) significantly decreased cholesterol (27.6 +/- 6%), LDL-cholesterol (27.6 +/- 9%) and plasma apoB (17.9 +/- 2.9%) (P < 0.01 for all). During the placebo period, calculation of kinetic parameters revealed VLDL-, intermediate density lipoprotein (IDL)-, and LDL-apoB overproduction and decreased VLDL-apoB fractional catabolic rate. Lovastatin significantly decreased LDL-apoB production rate in all cases (34.1 +/- 14%, P = 0.03). The decreased LDL-apoB was mainly due to a channelling of LDL precursors away from conversion to LDL (conversion of VLDL to LDL decreased from 80.6 +/- 8.3% to 55.9 +/- 17.2%, P = 0.05). Thus, lovastatin decreased LDL-cholesterol in nephrotic subjects mainly by inhibiting LDL-apoB production from VLDL.

Acute effects of different concentrations of dialysate magnesium during high-efficiency dialysis.

It has been suggested that magnesium carbonate (MgCO3) may be an effective and safe alternative to calcium carbonate in binding phosphorus in dialysis patients. In these studies, the concentration of magnesium in the dialysate was either very low or zero. To date, only patients undergoing conventional dialysis have been reported. The primary purpose of the present study was to determine the fluxes of magnesium using dialysate magnesium concentrations of 0 mg/dL, 0.6 mg/dL, and 1.8 mg/dL in eight patients undergoing high-efficiency hemodialysis. The net removal of magnesium was 486 +/- 44 mg, 306 +/- 69 mg, and 56 +/- 50 mg, with the use of dialysate magnesium concentrations of 0 mg/dL, 0.6 mg/dL, and 1.8 mg/dL, respectively (P = 0.001). Plasma magnesium levels significantly decreased from 3.3 +/- 0.2 mg/dL to 1.6 +/- 0.2 mg/dL and from 3.4 +/- 0.3 mg/dL to 2.1 +/- 0.2 mg/dL during the dialysis sessions using 0 mg/dL and 0.6 mg/dL magnesium dialysates, respectively. Plasma magnesium remained unchanged when 1.8 mg/dL dialysate magnesium was used. A significant independent correlation was found between the total magnesium removed and both the dialysate concentration used (P < 0.001) and the predialysis plasma magnesium level (P < 0.001). The measured magnesium removal exceeded the estimated predialysis extracellular fluid (ECF) magnesium pool with the use of magnesium-free dialysate. This was not found with dialysate magnesium concentrations of either 0.6 mg/dL or 1.8 mg/dL. A secondary purpose of the study was to determine the acute clinical tolerance of the low and magnesium-free dialysates.(ABSTRACT TRUNCATED AT 250 WORDS)

The successful treatment of recurrent nephrotic syndrome with the MOPP regimen in a patient with a remote history of Hodgkin's disease.

The association of Hodgkin's disease and minimal-change nephrotic syndrome is well established. We describe a gentleman who developed Hodgkin's disease that was treated successfully. Two years later, he developed minimal-change nephrotic syndrome that responded to steroids. Over the next 9 years, the patient experienced two episodes of nephrotic syndrome due to focal segmental glomerulonephritis that were successfully treated with the mustard/vincristine/prednisone/procarbazine (MOPP) regimen. There was no evidence of recurrence of Hodgkin's lymphoma during any episode of nephrotic syndrome.