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Biomedical subjects

S G Massry

Publications and source records attributed to S G Massry.

At least 19 recordsLinked to original sources
PubMed1996

Abnormalities in hepatic lipase in chronic renal failure: role of excess parathyroid hormone.

Post-heparin hepatic lipase activity is reduced in chronic renal failure (CRF). This could be due to reduced synthesis, decreased activity, and/or impaired secretion of the enzyme. Further, the factor(s) responsible for such derangements are not elucidated. We examined hepatic lipase metabolism in normal, 6-wk-old CRF rats, CRF-PTX (parathyroidectomized) rats, and CRF and normal rats treated with verapamil (CRF-V, normal-V) using liver homogenate, hepatic cell culture for 8 h, and in vitro liver perfusion. The Vmax of hepatic lipase in liver homogenate was significantly (P < 0.01) reduced and the Km was significantly (P < 0.01) increased in CRF rats, but the values were normal in CRF-PTX, CRF-V, and normal-V rats. Culture of hepatic cells for 8 h was associated with an increase in hepatic lipase activity but the increment in CRF rats was significantly (P < 0.01) lower than that of normal, CRF-PTX, CRF-V, and normal-V rats. Both parathyroid hormone (PTH)-(1-84) and 1-34 inhibited the production of hepatic lipase in cultured cells from normal, CRF-PTX, CRF-V, and normal-V rats. The expression of the mRNA of the hepatic lipase was significantly reduced in CRF animals with the ratio between it and that of house keeping gene G3DPH being 15 +/-3% compared to 40 +/- 1.3% in normal, 44+/-2.9% CRF-PTX, 44 +/- 5.4% in CRF-V, and 39 +/- 3.9% in normal-V rats. Infusion of heparin to the in vitro hepatic perfusion system increased the activity of hepatic lipase in the effluent in all groups of rat except in CRF animals. Infusion of PTH-(1-34) in dose of 10(-6) M into the liver perfusion system inhibited the increase in post-heparin hepatic lipase activity. The data show that in CRF (a) the mRNA of hepatic lipase is downregulated, and hepatic lipase production, activity and release are impaired, (b) that this is due to the state of secondary hyperparathyroidism of CRF since both acute and chronic excess of PTH were associated with these abnormalities, (c) and that prevention of excess PTH by PTX of CRF rats or blocking the effect of PTH by treatment with verapamil corrected the derangement in hepatic lipase metabolism.

Animals↗
PubMed1996

Elevation of cytosolic calcium of rat cardiac myocytes in phosphate depletion.

Phosphate depletion is associated with a rise in cytosolic calcium ([Ca2+]i) of cells and such a derangement is responsible in major part for organ dysfunction in phosphate depletion (PD). Cardiac function is impaired in PD, and it is possible that PD is also associated with rise in [Ca2+]i of cardiac myocytes. The present study examined the effect of PD on [Ca2+]i of cardiac myocytes and explored the mechanisms that may lead to the rise in their [Ca2+]i. The [Ca2+]i of cardiac myocytes began to rise and ATP content began to fall at the third week of PD. After six weeks of PD, the values of [Ca2+]i were significantly higher (P < 0.01) and those of ATP content were significantly lower (P < 0.01) than in control (PW) rats. The Vmax of Ca2(+)-ATPase and Na+,K(+)-ATPase as well as the Na(+)-Ca2+ exchange were significantly lower (P < 0.01) in PD than in PW animals. The data of the present study are consistent with the notion that the rise in [Ca2+]i of cardiac myocytes of PD rats is due to a decrease in calcium efflux out of them.

Adenosine Triphosphate↗
PubMed1996

Acne: a potential side effect of cyclosporine A therapy.

A renal transplant recipient who developed severe acne 6 months after transplantation is described. Maintenance immunosuppression consisted of cyclosporine A (CsA), azathioprine and prednisone. Tapering the prednisone dose to as low as 5 mg/day, in addition to topical tetracycline, Retin-A cream, and systemic antimicrobial therapy failed to control the progression of the skin lesions. Despite therapy with isotretinoin (Accutane), the lesions continued to progress with nodulocystic transformation (acne conglobata) and isotretinoin was discontinued after 4 months. However, the condition continued to worsen with the development of a systemic illness with daily fever, diaphoresis, and depression. High fever (103 degrees F) with shaking chills prompted hospitalization. Withdrawal of CsA resulted in rapid and continuous improvement of the skin lesions. After 12 months of follow-up, the lesions significantly resolved except for residual areas of scarring. No episodes of acute allograft rejection occurred. In conclusion, we suggest that CsA therapy may be associated with the development of acne. Nodulocystic transformation (acne conglobata) may occur despite the use of isotretinoin. Finally, withdrawal of CsA may lead to resolution of the skin disease and should, therefore, be considered as a therapeutic option for severe and treatment-resistant cases.

Acne Vulgaris↗
PubMed1996

Effects of parathyroid hormone on renal tubular proteinases.

Parathyroid hormone (PTH) has been implicated to exert detrimental effects on remnant nephrons in chronic renal failure. The present investigation addressed the influence of PTH on the proteolytic capacity of isolated proximal tubules both from normal (SHAM) and partially nephrectomized rats (5/6-NX). Proteolytic activities were measured either against azocasein (pH 5.4) or with specific fluorogenic peptidyl substrates for individual cysteine proteinases. Azocaseinolytic activity was enhanced 6 weeks after 5/6-NX in tubules (SHAM 19.0 +/- 1.0 vs. 5/6-NX 24.4 +/- 1.5 U/mg protein), while thereafter activities declined progressively with time (5/6-NX 16 weeks: 12.9 +/- 1.2 U/mg protein). This loss in proteolytic activity could almost completely be prevented by parathyroidectomy (PTX) (5/6-NX + PTX 16 weeks: 18.6 +/- 1.1 U/mg protein). By contrast, severe hyperparathyroidism (induced by a low calcium/high phosphorus diet fed for 6 weeks) in 5/6-NX animals resulted in a significant decline in proteolytic activities in remnant tubules (5/6-NX 24.4 +/- 1.5 vs. 5/6-NX+diet 16.4 +/- 1.9 U/mg protein). When specific activities of tubular cathepsins were measured in healthy rats who had received exogenous PTH, each individual cysteine proteinase (cathepsin L: -42%; cathepsin B: -27%; cathepsin H: -51%) was suppressed. This effect of PTH could readily be abolished by the simultaneous administration of verapamil. These results suggest that chronic PTH excess exerts a suppressive effect on tubular proteinase activities both in normal and partially nephrectomized rats. This PTH effect seems to be mediated by an increase of cytosolic calcium.

Animals↗
PubMed1995

Polymorphonuclear leukocytes in non-insulin-dependent diabetes mellitus: abnormalities in metabolism and function.

OBJECTIVE: To determine basal levels of cytosolic calcium ([Ca2+]i) and phagocytic activity in polymorphonuclear leukocytes (PMNLs) from patients with non-insulin-dependent diabetes (NIDDM). DESIGN: Prospective cohort study. SETTING: A university-county hospital. MEASUREMENTS: Cytosolic calcium levels, adenosine triphosphate (ATP) content, and phagocytosis of PMNLs from patients with NIDDM and from controls. INTERVENTION: In patients with NIDDM, we evaluated the effect of treatment with an oral hypoglycemic agent (glyburide) on [Ca2+]i levels, ATP content, and the phagocytosis of PMNLs. PATIENTS: 22 controls and 34 patients with NIDDM were examined. Fifteen patients were studied before and after 3 months of treatment with glyburide. RESULTS: Polymorphonuclear leukocytes from patients with NIDDM showed significantly elevated basal levels of [Ca2+]i (68 +/- 9.6 compared with 43 +/- 4.9 nmol/L; P < 0.01); reduced ATP content (1.30 +/- 0.58 compared with 2.35 +/- 0.45 nmol/10(6) PMNLs; P < 0.01); and impaired phagocytosis (117 +/- 21.0 compared with 145 +/- 17.4 micrograms oil/10(7) PMNLs per minute; P < 0.01) compared with controls. There was a direct and significant correlation (P < 0.01, r = 0.80) between [Ca2+]i levels in PMNLs and serum glucose levels and an inverse correlation between phagocytic ability and [Ca2+]i levels (P < 0.01; r = 0.62) as well as between phagocytic activity and fasting serum glucose levels (P < 0.01, r = 0.54) in patients with NIDDM. Glyburide therapy resulted in significant reduction in fasting serum glucose levels; in PMNLs, this treatment resulted in a significant reduction in [Ca2+]i levels, a significant increase in ATP content, and a significant improvement of phagocytosis. CONCLUSIONS: Patients with NIDDM have elevated [Ca2+]i levels in PMNLs. This abnormality is probably induced by hyperglycemia and is primarily responsible for the imparied phagocytosis seen in these patients.

Adenosine Triphosphate↗
PubMed1995

Blood pressure control, proteinuria, and the progression of renal disease. The Modification of Diet in Renal Disease Study.

OBJECTIVE: To examine the relations among proteinuria, prescribed and achieved blood pressure, and decline in glomerular filtration rate in the Modification of Diet in Renal Disease Study. DESIGN: 2 randomized trials in patients with chronic renal diseases of diverse cause. SETTING: 15 outpatient nephrology practices at university hospitals. PATIENTS: 840 patients, of whom 585 were in study A (glomerular filtration rate, 25 to 55 mliters/min.1.73 m2) and 255 were in study B (glomerular filtration rate, 13 to 24 mliters/min.1.73 m2). Diabetic patients who required insulin were excluded. INTERVENTIONS: Patients were randomly assigned to a usual blood pressure goal (target mean arterial pressure, < or = 107 mm Hg for patients < or = 60 years of age and < or = 113 mm Hg for patients > or = 61 years of age) or a low blood pressure goal (target mean arterial pressure, < or = 92 mm Hg for patients < or = 60 years of age and < or = 98 mm Hg for patients > or = 61 years of age). MAIN OUTCOME MEASURES: Rate of decline in glomerular filtration rate and change in proteinuria during follow-up. RESULTS: The low blood pressure goal had a greater beneficial effect in persons with higher baseline proteinuria in both study A (P = 0.02) and study B (P = 0.01). Glomerular filtration rate declined faster in patients with higher achieved blood pressure during follow-up in both study A (r = -0.20; P < 0.001) and study B (r = -0.34; P < 0.001), and these correlations were stronger in persons with higher baseline proteinuria (P < 0.001 in study A; P < 0.01 in study B). In study A, the association between decline in glomerular filtration rate and achieved follow-up blood pressure was nonlinear (P = 0.011) and was stronger at higher mean arterial pressure. In both studies, the low blood pressure goal significantly reduced proteinuria during the first 4 months after randomization. This, in turn, correlated with a slower subsequent decline in glomerular filtration rate. CONCLUSIONS: Our study supports the concept that proteinuria is an independent risk factor for the progression of renal disease. For patients with proteinuria of more than 1 g/d, we suggest a target blood pressure of less than 92 mm Hg (125/75 mm Hg). For patients with proteinuria of 0.25 to 1.0 g/d, a target mean arterial pressure of less than 98 mm Hg (about 130/80 mm Hg) may be advisable. The extent to which lowering blood pressure reduces proteinuria may be a measure of the effectiveness of this therapy in slowing the progression of renal disease.

Adolescent↗
PubMed1995

Nephrology.

Captopril given in dosages of 25 mg reduced the doubling of serum creatinine levels by 48% in patients with insulin-dependent diabetes mellitus. Intensive insulin therapy in patients with IDDM delays the onset and slows the progression of diabetic nephropathy, retinopathy, and neuropathy.

Humans↗
PubMed1995

Effect of treatment of hemodialysis patients with nifedipine on metabolism and function of polymorphonuclear leukocytes.

Both animals and patients with chronic renal failure have impaired phagocytosis, which is most likely due to elevated basal levels of cytosolic calcium ([Ca2+]i) and reduced adenosine triphosphate (ATP) content of their polymorphonuclear leukocytes (PMNLs). In animals with chronic renal failure, these derangements are prevented or reversed by their treatment with a calcium channel blocker. This observation may have important clinical implications if these drugs exert a similar effect in humans with chronic renal failure. We examined the basal levels [Ca2+]i, ATP content, and phagocytosis in PMNLs from 11 normal subjects, 18 hemodialysis patients (seven of whom had diabetes mellitus), and 18 hemodialysis patients treated with nifedipine (eight of whom had diabetes mellitus). The basal levels of the [Ca2+]i content of the PMNLs in hemodialysis patients without nifedipine therapy were significantly (P < 0.01) elevated (nondiabetic patients, 77 +/- 3.2 nmol/L; diabetic patients, 75 +/- 1.9 nmol/L) compared with normal values (42 +/- 0.9 nmol/L). Treatment with nifedipine was associated with the return of [Ca2+]i toward normal values in both the nondiabetic (51 +/- 4.5 nmol/L) and diabetic (54 +/- 2.5 nmol/L) hemodialysis patients. The ATP content of PMNLs from hemodialysis patient was significantly (P < 0.01) reduced compared with normal, and nifedipine therapy restored the ATP content to normal values. Phagocytosis was significantly (P < 0.01) impaired in hemodialysis patients (nondiabetic patients, 78 +/- 4.0 micrograms oil/10(7) PMNLs/min; diabetic patients, 77 +/- 4.8 micrograms oil/10(7) PMNLs/min). Nifedipine therapy returned the impaired phagocytosis toward normal (nondiabetic patients, 133 +/- 2.5 micrograms oil/10(7) PMNLs/min; diabetic patients, 129 +/- 6.4 micrograms oil/10(7) PMNLs/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Down-regulation of PTH-PTHrP receptor of heart in CRF: role of [Ca2+]i.

The mRNA of PTH-PTHrP receptor in the kidney and liver of CRF rats is down-regulated. It is not known whether this is a generalized phenomenon and the signals that mediate such down-regulation are not evident. Excess PTH in CRF induces a rise in basal levels of cytosolic calcium ([Ca2+]i), and the high [Ca2+]i is implicated in the genesis of cell dysfunction in CRF. Therefore, it is reasonable to propose that the PTH-induced rise in [Ca2+]i provides a negative feedback control system for the down-regulation of the mRNA of the PTH-PTHrP in order to protect the cells from the harmful effects of progressive rise in blood levels of PTH in CRF. The heart contains the mRNA for this receptor and it is a target organ for PTH action. We examined whether the message of the PTH-PTHrP receptor is down-regulated in the heart of CRF animals and evaluated the role of [Ca2+]i in this process. The expression of the mRNA of the PTH-PTHrP was significantly reduced in the heart of CRF rats as compared to normal animals. Also, the CRF rats had elevated blood levels of PTH and high [Ca2+]i of cardiac myocytes. The parathyroidectomy of CRF rats prevented the rise in blood PTH levels and normalized [Ca2+]i of cardiac myocytes and returned the mRNA of their PTH-PTHrP receptor towards normal levels. The treatment of CRF rats with verapamil normalized [Ca2+]i of cardiac myocytes and returned the mRNA of their PTH-PTHrP receptor towards normal levels, despite marked elevation of blood levels of PTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1995

Excess PTH in CRF induces pulmonary calcification, pulmonary hypertension and right ventricular hypertrophy.

Calcification of the lungs occurs in chronic renal failure (CRF) and may adversely affect both pulmonary and right ventricular function. The present study examined the role of excess parathyroid hormone (PTH) in the genesis of pulmonary calcifications in dogs with experimental CRF and evaluated calcium content of lungs, diffusing lung capacity (DCO), mean pulmonary artery pressure (MPAP), right ventricular pressure (RVP), and right ventricular hypertrophy (RVH) in six normal, six with CRF, and six thyroparathyroidectomized (CRF-PTX) dogs. CRF-PTX animals were maintained normocalcemic and euthyroid. The degree and duration of CRF were not different between the two groups with CRF. The mean value of the serum PTH in CRF dogs was 166 +/- 42 microliters Eq/ml, but was undetectable in CRF-PTX animals. Thallium scan provided evidence consistent with RVH in CRF dogs but not in CRF-PTX animals. Calcium content of lungs was markedly elevated in CRF dogs (7656 +/- 1657 mg/kg dry wt) but modestly increased in CRF-PTX (1057 +/- 117 mg/kg dry wt) as compared to normal (673 +/- 34 mg/kg dry wt). RVP and MPAP were significantly (P < 0.01) higher and DCO significantly lower in CRF dogs than in normal or CRF-PTX animals. These parameters were not different in the latter two group of dogs. In three additional dogs with CRF of one year duration which were followed for an additional year after parathyroidectomy, these abnormalities were corrected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Elevated cytosolic calcium of adipocytes in chronic renal failure.

Chronic renal failure (CRF) is associated with increased calcium content of, and impaired lipase release from lipid cells. This has been attributed to a rise in the cytosolic calcium ([Ca2+]i) of these cells. However, data on [Ca2+]i of lipid cells in CRF and on the mechanisms responsible for such an abnormality are lacking. To study this issue we examined the [Ca2+]i and ATP content of lipid cells and Vmax of Na(+)-K(+)-ATPase and Ca2+ ATPase of membrane preparation and Na(+)-Ca2+ exchange of membrane vesicles of adipocytes from normal rats, 6 week CRF, CRF normocalcemic parathyroidectomized (CRF-PTX) and CRF, and normal rats treated with verpamil (CRF-V, normal-V). [Ca2+]i in adipocytes of CRF rats was higher (199 +/- 8.5 nM) and ATP lower (2.9 +/- 0.31 nmol/10(6) cells) than in normal (120 +/- 4.3 nM; 5.7 +/- 0.27 nmol/10(6) cells), CRF-PTX (128 +/- 4.7 nM; 5.8 +/- 0.39 nmol/10(6) cells), normal-V (121 +/- 3.2 nM; 5.3 +/- 0.36 nmol/10(6) cells), CRF-V (123 +/- 7.4 nM; 5.5 +/- 0.30 mmol/10(6) cells). Vmax Ca2+ ATPase and the activity of Na(+)-K(+)-ATPase and of Na(+)-Ca2+ exchanger were reduced in CRF rats as compared to the other four groups of rats. The values in normal, CRF-PTX, CRF-V and normal-V rats were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Verapamil reverses abnormal [Ca2+]i and carbohydrate metabolism of PMNL of dialysis patients.

The basal levels of cytosolic calcium ([Ca2+]i) of polymorphonuclear leukocytes (PMNL) are elevated in hemodialysis (HD) patients, and this abnormality has been implicated in the dysfunction of the PMNL of these patients. The elevated [Ca2+]i appears to be due to PTH-induced entry of calcium into PMNL, an action that may be prevented by calcium channel blockers. We examined [Ca2+]i and carbohydrate metabolism of PMNL of normal subjects and of HD patients before, after eight to nine weeks of verapamil therapy (120 mg/day), and after eight to ten weeks of discontinuation of verapamil treatment. In HD patients, the basal levels of [Ca2+]i of PMNL are elevated and their glucose uptake, the activity of total and active forms of glycogen synthetase, and glycogen content are reduced compared to values in normal subjects (P < 0.01). These derangements were normalized after verapamil therapy and re-emerged after discontinuation of treatment with verapamil despite no change in blood levels of PTH. The results indicate that the elevation in [Ca2+]i of PMNL and the consequent derangements in carbohydrate metabolism of these cells are treatable with a calcium channel blocker. The data assign a valuable role for calcium channel blockers for the amelioration of some aspects of cell dysfunction of uremia.

Aged↗
PubMed1995

Impaired agonist-induced calcium signaling in hepatocytes from chronic renal failure rats.

Some hormones exert their action by inducing a rise in cytosolic calcium [Ca2+]i (calcium signal), and therefore, a blunting in hormone-induced calcium signal would engender resistance to the action of the hormone. Chronic renal failure (CRF) is associated with resistance to the action of a variety of hormones, a rise in [Ca2+]i and decrease in the amount of mRNA of one hormone receptor, the PTH-PTHrP receptor. We examined the calcium-signal induced by PTH, angiotensin II, vasopressin and glucagon in hepatocytes from CRF animals, evaluated the effect of the basal level [Ca2+]i on the calcium signal and explored the effect of [Ca2+]i on the mRNA of the receptors of these agonists. Hepatocytes from CRF rats have elevated basal levels of [Ca2+]i and display significantly reduced calcium signals induced by all these hormones, while the calcium signals were normal in PTX-CRF animals and those treated with verapamil both of which have normal levels of [Ca2+]i despite CRF. The calcium signals induced by dibutyryl cyclic AMP and G protein activator (GTP gamma S) were normal in hepatocytes from CRF animals despite the high levels of [Ca2+]i. Northern blotting experiments revealed that the levels of the mRNA of the receptors of PTH-PTHrP, angiotensin II and vasopressin were significantly reduced in hepatocytes from CRF animals but PTX-CRF rats and those treated with verapamil had either significantly greater or even normal amounts of the mRNA of these receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Function and metabolism of brain synaptosomes in chronic renal failure.

Patients with advanced renal failure have derangements in the function of their nervous system. The available clinical and experimental data indicate that the state of the secondary hyperparathyroidism of renal failure plays a major role in the genesis of the nervous system dysfunction. The excess parathyroid hormone (PTH) mediates its deleterious effect by causing an elevation in cytosolic calcium of brain cells. This report reviews the evidence leading to the conclusion that PTH is a major uremic toxin.

Acetylcholine↗
PubMed1995

Chronic renal failure increases cytosolic Ca2+ of hepatocytes.

Chronic renal failure (CRF) is associated with increased Ca2+ content of liver and reduced hepatic lipase activity. This has been attributed to a rise in cytosolic Ca2+ ([Ca2+]i) of the hepatocytes, but data on this issue are lacking. We examined the [Ca2+]i and ATP content of hepatocytes as well as the activity of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase), Ca(2+)-ATPase, and Na+/Ca2+ exchanger of hepatic membrane vesicles from normal rats, animals with 6 wk of CRF, CRF normocalcemic parathyroidectomized (CRF-PTX) rats, and CRF and normal animals treated with verapamil (CRF-V, normal-V). [Ca2+]i in hepatocytes of CRF rats was higher (281 +/- 7.4 nM) and ATP lower (6.4 +/- 1.8 nmol/mg protein) than in normal (209 +/- 5.3 nM; 12.5 +/- 0.89 nmol/mg protein), CRF-PTX (212 +/- 1.0 nM; 13.7 +/- 0.79 nmol/mg protein), normal-V (215 +/- 2.3 nM; 14.2 +/- 0.77 nmol/mg protein), and CRF-V rats (209 +/- 7.4 nM; 14.8 +/- 0.72 nmol/10(6) cells). The Na(+)-K(+)-ATPase, the maximal velocity of Ca(2+)-ATPase, and the activity of the Na+/Ca2+ exchanger were reduced, whereas the Michaelis constant of Ca(2+)-ATPase was increase in CRF rats compared with the other four groups of rats. The values in the latter groups were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Pathways involved in PTH-induced rise in cytosolic Ca2+ concentration of rat renal proximal tubule.

Parathyroid hormone (PTH) raises cytosolic Ca2+ concentration ([Ca2+]i) in isolated or cultured renal proximal tubule cells. The pathways through which this action is mediated are not fully delineated. This study explored these pathways utilizing fura 2. [Ca2+]i of freshly prepared renal proximal tubular cells increased from 150 +/- 3.6 to 281 +/- 9.0 nM after the exposure to 10(-7) M angiotensin II, which served as a positive control. Both PTH-(1-84) and PTH-(1-34) produced a dose-dependent rise in [Ca2+]i. The effects of both moieties were similar up to 10(-7) M, but with higher doses the rise in [Ca2+]i with PTH-(1-84) was greater (P < 0.01) than with PTH-(1-34). This effect of the hormone occurred in the presence or absence of calcium in the media, but the rise in [Ca2+]i was significantly greater in the presence of calcium. The PTH-induced rise in [Ca2+]i was markedly inhibited by PTH antagonist [Nle8,18,Tyr34]bPTH-(7-34)-NH2 (bPTH is bovine PTH), verapamil, or nifedipine. 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, increased [Ca2+]i of cells, but its effect was less than PTH. Staurosporine abolished the TPA effect and partially inhibited that of PTH. A G protein activator raised [Ca2+]i, whereas a G protein inhibitor and pertussis toxin partially blocked the effect of PTH. Sodium or chloride channel blockers or sodium-free media did not modify the effect of PTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Renal transplantation in systemic lupus erythematosus: a single-center experience with sixty-four cases.

The outcome of renal transplantation in 64 patients with end-stage renal disease (ESRD) secondary to lupus nephritis is the subject of this report. The patients were transplanted over a 150-month (12.5-year) period (between July 5, 1979, and January 30, 1992). The study population is predominantly made up of young females (mean age, 34.7 +/- 9 years, n = 54, 81.3%). Fifty-one transplants (79.7%) are cadaveric, and 13 (20.3%) are from living-related donors. Fifty-eight patients (90.6%) had primary (first) allografts, and 6 (9.4%) received a second allograft. Posttransplantation immunosuppression consisted of azathioprine and prednisone (AZA group, n = 22, 34.3%) or AZA, prednisone and cyclosporine (CsA group, n = 42, 65.6%). For all 64 patients combined, the 1-year graft and patient survival rates are 68.8 and 86.5%, respectively, whereas 5-year graft and patient survival rates are 60.9 and 85.9%, respectively. Patients whose immunosuppressive regimen was CsA-based had a 1-year graft survival of 71.5 versus 63.6% in the AZA group. However, this 7.9% difference did not reach statistical significance (p = 0.95). The 5-year graft survival of the CsA-based group was 69.1 versus 45.5% for the AZA group, p < 0.05. One-year patient survival was 77.3% for the AZA group and 92.9% for the CsA group, p < 0.05). The data show that patients with ESRD secondary to lupus nephritis can undergo renal transplantation with satisfactory outcome. Immunosuppression based upon CsA improves first-year patient and allograft survival by 15.6 and 7.9%. respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗