Insurance case managers' perception of quality in back pain programs: a focus study group.

OBJECTIVES: Insurance case managers commonly interact with physiatrists and rehabilitation programs. They influence referrals and patients' decision making. This study was designed to determine which factors affect case managers' perception of back pain program quality. DESIGN: Repeated focus group interview in a neutral facility in an urban Midwestern United States community. Subjects were two groups (n = 12 and 11) of insurance case managers employed by case management firms (large and small), insurers, and self-insured employers. Outcome measures included group and individual responses to a pre-scripted interview and were collected on tape, transcribed, and interpreted by two different persons: the independent expert interviewer and a pain psychologist. RESULTS: There was substantial agreement between the two interpreters. Both groups overwhelmingly chose physiatrists over other specialists. They emphasized timeliness, communication, functionally oriented programs, concrete program goals and time frames, physician knowledge of the legal aspects of disability, and rapid communication of patient noncompliance. CONCLUSIONS: Rehabilitation programs may strive to meet many of these qualities but, in doing so, should be aware that the legal and ethical roles of case managers differ from that of clinicians.

Perturbation of renal amino acid transport by brush border membrane vesicles in the vitamin D-deficient rat.

Vitamin D deficiency is characterized by secondary hyperparathyroidism, phosphaturia, bicarbonaturia, and generalized amino aciduria. While the site at which the phosphaturia ensues has been described to occur at the apical membrane of the renal proximal tubule, no studies are available for amino aciduria. Thus, weanling rats were fed five vitamin D-deficient diets for 4-6 weeks: (i) VLC, 0.02% Ca, 0.3% P; (ii) VLC + 1,25[OH]2D, same + 500 pmole ip for 2 days; (iii) LC, 0.45% Ca, 0.3% P; (iv) HC, 2.5% Ca, 0.3% P; and (v) VLP, 1.2% cA, 0.1% P. The normal diet contained 1.2% Ca, 0.7% P, and 2.5 micrograms% vitamin D. Amino acids, serum 25[OH]D, 1,25[OH]2D, and PTH, using a specific anti-rat PTH antibody, were measured. There were 4.65 +/- 1.1- and 10 +/- 1.39-fold increases in the urinary excretion of taurine and proline, respectively, irrespective of diet. Hypocalcemia, secondary hyperparathyroidism, and increased concentrations of urinary cAMP were demonstrated in all diets, except VLP. Taurinuria and prolinuria manifested at the renal brush border membrane. There was 21-25% and 26-39% attenuation in the peak of the overshoot of Na(+)-dependent uptake of taurine and proline, respectively, that was statistically significant as compared to that of normal diets (P less than 0.01). VLC resulted in a reduction in the Vmax of taurine (VLC, 78.26 +/- 6.88 vs normal, 115.4 +/- 6.26 pmole/mg protein/min, P less than 0.01) and proline (VLC, 402.06 +/- 31.26 vs normal, 589.49 +/- 37.42 pmole/mg protein/15 sec, P less than 0.01) uptake. Acute supplementation with pharmacological doses of 1,25[OH]2D normalized the Vmax of taurine and proline uptake, without affecting their renal excretion. The VLP diet induced and increase in the Km of taurine (VLP, 58.95 +/- 1.88 microM vs normal, 39.75 +/- 2.75 microM P less than 0.01) and proline (VLP, 116.75 +/- 8.87 microM vs normal, 76.82 +/- 7.27 microM P less than 0.01) uptake, without an associated perturbation in the Vmax of uptake. We conclude that the amino aciduria of vitamin D deficiency manifests at the apical membrane of the proximal tubule by an attenuation in the Na(+)-dependent uptake of amino acids. This is associated with a reduction in the initial rate of uptake or number of active transporters in the presence of secondary hyperparathyroidism and hypocalcemia, or a decrease in the affinity of the symport in the presence of P depletion. The data suggest the interplay of multiple factors in the causation of amino aciduria.

Aminoaciduria of vitamin D deficiency is independent of PTH levels and urinary cyclic AMP.

Aminoaciduria and secondary hyperparathyroidism accompany vitamin D deficiency. However, the degree of aminoaciduria and PTH elevation have not been studied relative to different calcium and phosphorus dietary intakes. Weanling rats were fed 5 vitamin D deficient diets for 4-6 weeks: very low Ca (VLC) 0.02% Ca, 0.3% P; VLC + 1,25-dihydroxyvitamin D [1,25(OH)2D3], same + 500 pmol i.p. for 2 days; low Ca (LC) 0.45% Ca, 0.3% P; very low P (VLP) 1.2% Ca, 0.1% P; high Ca (HC) 2.5% Ca, 0.3% P, and control 1.2% Ca, 0.70% P + 2.5 micrograms% vitamin D. Amino acids, serum 25-hydroxyvitamin D [25(OH)D3], 1,25(OH)2D3, and PTH, using a specific antirat PTH antibody, were measured. A significant generalized aminoaciduria (11 amino acids) was found in all vitamin D-deficient groups. Furthermore, it was independent of plasma Ca and PTH, and urinary cAMP excretion irrespective of diet. Serum 25(OH)D and 1,25(OH)2D were significantly reduced in all vitamin D-deficient groups. VLC and VLC + 1,25(OH)2D3 were associated with the highest PTH levels (10- and 13-fold increase, respectively) and urinary cAMP (2.3-fold increase in each) and the lowest serum Ca. LC rats had an 8.8- and a 1.7-fold increase in PTH and urinary cAMP, respectively. Phosphate depletion was found in VLP rats documented by insignificantly elevated PTH, normal urinary cAMP, hypercalciuria, and percent tubular reabsorption of phosphate of greater than 99%. While dietary Ca and P affect plasma and urinary Ca and P plasma PTH and urinary cAMP, it appears that dietary P affects the aminoaciduria observed in this study via mechanisms that remain unclear. The possibility that the mechanism for the tubulopathy is multifactorial should be entertained.

Sensitivity of the physiologically hypertrophied heart to isoproterenol.

Cardiovascular reactions to isoproterenol stimulation (2 and 4 micrograms/min for 12 min each) were evaluated in seven endurance-trained athletes (marathon runners, VO2 max 66.0 +/- 3.7 ml/kg) and seven untrained subjects (VO2 max 54.4 +/- 3.6 ml/kg). At rest and during stimulation, the heart rate, blood pressure as well as one-dimensional (end-diastolic and end-systolic dimensions, shortening fraction) and two-dimensional (end-diastolic and end-systolic volumes, ejection fraction, stroke volume, cardiac output) echocardiographic parameters were determined. The increase in the heart rate of the endurance-trained athletes (28%; 2 micrograms/min) (58%; 4 micrograms/min) was less than in the untrained controls (34%/76%). The blood pressure behaved similarly in both groups. The stroke volume of the endurance-trained subjects rose during stimulation (14%, 4 micrograms/min); the end-diastolic volume remained nearly constant as the end-systolic emptying increased. The stroke volume of the untrained subjects tended to decrease as the end-diastolic and end-systolic volumes were reduced. In absolute terms, the shortening fraction and ejection fraction were identical. Referring to the heart rate, however, they were elevated in the endurance-trained subjects. Hence, under isoproterenol the rise in heart rate was weaker and the increase in ventricular performance seemed to be stronger in the trained subjects compared to the untrained controls. The causes appear to be different regulative effects of the autonomic nervous system on the sinus node and the ventricular myocardium; intrinsic cardiac mechanisms remain to be discussed.

Factors affecting the transport of beta-amino acids in rat renal brush-border membrane vesicles. The role of external chloride.

The effect of a variety of ions and other solutes on the accumulation of the beta-amino acid, taurine, was examined in rat renal brush-border membrane vesicles. Initial taurine uptake (15 and 30 s) is sodium-dependent with a typical overshoot. This Na+ effect was confirmed by exchange diffusion and gramicidin inhibition of taurine uptake. External K+ or Li+ do not increase taurine accumulation more than Na+-free mannitol, except that the combination of external K+ and Na+ in the presence of nigericin enhances uptake. Of all anions tested, including more permeant (SCN- and NO3-) or less permeant (SO4(2-)), chloride supported taurine accumulation to a significantly greater degree. Preloading vesicles with choline chloride reduced taurine uptake, suggesting that external Cl- stimulates uptake. Since this choline effect could be related to volume change, due to the slow diffusion of choline into vesicles, brush-border membrane vesicles were pre-incubated with LiCl, LiNO3 and LiSO4. Internal LiCl, regardless of the final Na+ anion mixture, reduced initial rate (15 and 60 s) and peak (360 s) taurine uptake. Internal LiNO3 or LiSO4 with external NaCl resulted in similar or higher values of uptake at 15, 60 and 360 s, indicating a role for external Cl- in taurine uptake in addition to Na+ effect. Although uptake by vesicles is greatest at pH 8.0 and inhibited at acidic pH values (pH less than 7.0), an externally directed H+ gradient does not influence uptake. Similarly, amiloride, an inhibitor of the Na+/H+ antiporter, had no influence on taurine accumulation over a wide variety of concentrations or at low Na+ concentrations. Taurine uptake is blocked only by other beta-amino acids and in a competitive fashion. D-Glucose and p-aminohippurate at high concentrations (greater than 10(-3) M) reduce taurine uptake, possibly by competing for sodium ions, although gramicidin added in the presence of D-glucose inhibits taurine uptake even further. These studies more clearly define the nature of the renal beta-amino acid transport system in brush-border vesicles and indicate a role for external Cl- in this uptake system.

Developmental aspects of renal beta-amino acid transport. IV. Brush border membrane response to altered intake of sulfur amino acids.

Taurinuria is characteristic of the immature rat. The capacity of the kidney to accumulate the beta-amino acid taurine and D-glucose was examined using isolated brush border membrane vesicles (BBMV) prepared from 28-day-old rats. Taurine accumulation was inversely proportional to osmolarity, indicating uptake rather than binding, and taurine accumulation was Na+-dependent. BBMV from 28-day rats did not accumulate D-glucose to the same degree as in adult BBMV, and the initial rate of uptake was slower. Taurine uptake had a similar Km and Vmax in BBMV from immature rats. Despite similarities in the kinetics of taurine uptake, higher urinary taurine concentrations are found in younger rats, suggesting that other factors, such as an efflux block, account for the taurinuria of young animals. A diet low in methionine and taurine (LTD) given for 7 days resulted in a lower excretion and fractional excretion of taurine than in animals fed a normal sulfur amino acid diet (NTD). A high taurine diet (HTD) causes excessive taurinuria. These patterns of excretion are reflected at the brush border membrane surface with greater uptake after the LTD and reduced uptake after the HTD. A kinetic analysis of adult and 28-day-old animal BBMV reveals that the Vmax of accumulation is altered by diet, whereas the Km remains unchanged. The Vmax is higher in BBMV from LTD animals and lower in BBMV from HTD animals. The kinetics of uptake are similar in adult and 28-day-old rat vesicles on a given diet. Thus, in addition to ontogenic changes in taurine excretion, there is an adaptive response to dietary alteration present at the brush border surface.