Browsing by Author "Valdivieso, A"
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- ItemEffect of ammonium chloride and dietary phosphorus in the azotaemic rat.: I.: Renal function and biochemical changes(2004) Jara, A; Chacón, C; Ibaceta, M; Valdivieso, A; Felsenfeld, AJBackground. Both dietary phosphorus restriction and the ingestion of ammonium chloride (NH4Cl) given to rats on a high-phosphorus diet have been shown to preserve renal function in the azotaemic rat. Parathyroidectomy also has been reported to preserve renal function and, in addition, to prevent kidney hypertrophy in the remnant kidney model. Our goals were (i) to evaluate in azotaemic rats the effect of dietary phosphorus on renal function in a shorter time frame than previously studied and (ii) to determine whether NH4Cl administration (a) enhances the renoprotective effect of dietary phosphorus restriction and (b) improves renal function in the absence of parathyroid hormone (PTH).
- ItemEffect of ammonium chloride and dietary phosphorus in the azotaemic rat.: Part II -: kidney hypertrophy and calcium deposition(2004) Jara, A; Chacón, C; Ibaceta, M; Valdivieso, A; Felsenfeld, AJBackground. Kidney hypertrophy is stimulated by both partial nephrectomy and NH4Cl administration. Also, parathyroidectomy (PTX) has been reported to prevent kidney hypertrophy induced by a high protein diet. Our goal was to determine in the azotaemic rat: (i) the combined effects of NH4Cl administration and dietary phosphorus on the development of kidney hypertrophy and calcium deposition in the kidney and (11) whether the absence of parathyroid hormone (PTH) affected the development of kidney hypertrophy and calcium deposition.
- ItemEffect of calcitriol treatment and withdrawal on hyperparathyroidism in haemodialysis patients with hypocalcaemia(2001) Jara, A; Chacón, C; Valdivieso, A; Aris, L; Jalil, R; Felsenfeld, AJBackground. Calcitriol is used to treat secondary hyperparathyroidism in dialysis patients. For similarly elevated parathyroid hormone (PTH) levels, the PTH response to calcitriol treatment is believed to he better in hypocalcaemic dialysis patients than in dialysis patients with higher serum calcium values. Furthermore, few studies have evaluated the rapidity of the rebound in serum PTH values after prolonged treatment with calcitriol. Our goal was to evaluate (i) the PTH response to calcitriol treatment in hypocalcaemic haemodialysis patients, (ii) the rapidity of rebound in PTH after calcitriol treatment was stopped, and (iii) whether the effect of calcitriol treatment on PTH levels could be separated from those produced by changes in serum calcium and phosphate values.
- ItemEffect of endothelin receptor antagonist on parathyroid gland growth, PTH values and cell proliferation in azotemic rats(2006) Jara, A; von Höveling, A; Jara, X; Burgos, ME; Valdivieso, A; Mezzano, S; Felsenfeld, AJBackground. A variety of stimuli are involved in the pathogenesis of parathyroid gland hyperplasia in renal failure. Recently, it was shown that blocking the signal from the endothelin-1 (ET-1) receptor (ETAR/ETBR) by a non-selective receptor antagonist, bosentan, reduced parathyroid cell proliferation, parathyroid gland hyperplasia and parathyroid hormone (PTH) levels in normal rats on a calcium deficient diet. Our goal was to determine whether in 5/6 nephrectomized (NPX) rats with developing or established hyperparathyroidism, the endothelin receptor blocker, bosentan, reduced the increase in parathyroid cell proliferation, parathyroid gland hyperplasia and PTH values.
- ItemFailure of high doses of calcitriol and hypercalcaemia to induce apoptosis in hyperplastic parathyroid glands of azotaemic rats(2001) Jara, A; González, S; Felsenfeld, AJ; Chacón, C; Valdivieso, A; Jalil, R; Chuaqui, BBackground. Whether calcitriol administration, which is used to treat secondary hyperparathyroidism in dialysis patients, induces regression of parathyroid-gland hyperplasia remains a subject of interest and debate. If regression of the parathyroid gland were to occur, the presumed mechanism would be apoptosis. However, information on whether high doses of calcitriol can induce apoptosis of parathyroid cells in hyperplastic parathyroid glands is lacking. Consequently, high doses of calcitriol were given to azotaemic rats and the parathyroid glands were evaluated for apoptosis.
- ItemLong-Term outcome of type V lupus membranous glomerulonephritis(SOC MEDICA SANTIAGO, 2005) Pasten, R; Massardo, L; Rosenberg, H; Radrigan, F; Roessler, E; Valdivieso, A; Jacobelli, SBackground: The long-term outcome of the pure form of WHO type V lupus membranous glomerulonephritis is apparently more benign than that of other forms of lupus glomerulonepbritis. However 12% of such patients progress to terminal renal failure. The presence of proteinuria may be an indication of cytotoxic agents. Aim: To study the clinical long-term outcome of WHO type V Inpus membranous glomerulonepbritis. Material and methods: A retrospective analysis of all kidney biopsies of a University Pathology Department, with the diagnosis of WHO type V lupus membranous glomerulonephritis. Review of medical records of patients with the disease and one clinical assessment of all living patients. Results: Between 1973 and 2000, 703 kidney biopsies were done to patients with systemic lupus erytbematosus. Of these, 40 were membranous glomerulonepbritis and in 33 patients (28 women, age range 6-71 years), data on the evolution and survival was obtained. Nineteen bad type Va and the rest type Vb nephritis. Two presented with renal failure and I I with proteinuria over 3.5 g/24h. The median follow-up since the renal biopsy was 63 months (range 1-316). At the end of follow-up, four bad a creatinine clearance of less then 15 ml/h and four a clearance between 15 and 29 ml/h (one of these received a renal allograft). Eleven (33016) patients had died, mostly due to infections. Life expectancy at five years with a creatinine clearance over 15 ml/h was 75%. Bad prognostic factors were an elevated creatinine clearance over 15 ml/h was 75%. Bad prognostic factors were an elevated creatinine and high blood pressure at the moment of the biopsy. Conclusions: The clinical outcome of these patients was bad. Twelve percent reached a stage of terminal renal failure. This is in contrast with the 3% progression to a similar stage of proliferalive glomerulonephritis treated with the 3% cycloposphamide. New tberapies for this condition must be sought.
- ItemOutcome of Chilean patients with lupus nephritis and response to intravenous cyclophosphamide(2003) Velásquez, X; Verdejo, U; Massardo, L; Martínez, ME; Arriagada, S; Rosenberg, H; Valdivieso, A; Jacobelli, SSeveral recent open studies suggest that the response rates of lupus nephritis to intravenous (IV) cyclophosphamide are lower than those observed in clinical trials. One explanation could be ethnic differences; for example, black patients more frequently have treatment-resistant lupus nephritis. Another could be the inclusion of patients who are noncompliant with therapy. From our register of 268 systemic lupus erythematosus (SLE) patients examined between 1973 and 1996, 61 patients were treated for proliferative lupus nephritis (17 had World Health Organization [WHO] type III and 43 had WHO type IV) and were followed through to 2001. Exclusion criteria included a serum creatinine level >3 mg/dL. In this retrospective study, we assessed renal outcome and survival with an endpoint of end-stage renal disease (ESRD) or death (Kaplan-Meier). In the univariate analysis, worse prognostic factors for survival were serum creatinine >1.3 mg/dL (p < 0.001), age <30 years (p < 0.001), class 2 renal function stage (p < 0.03), and renal biopsy activity index >7 (p < 0.02). In the subgroup of 26 patients treated with IV cyclophosphamide, survival at 5 and 10 years was 82% and 73%, respectively. The dosage of IV cyclophosphamide was slightly lower than usual and used for a shorter period (median = 23 months) than what is usually recommended because of the high frequency of complications. Renal outcome of the IV cyclophosphamide-treated patients was poorer than that reported in the National Institutes of Health series (ESRD: 15% versus 3%). This low survival rate could reflect the short course and lower doses of IV cyclophosphamide used or ethnic differences. These data emphasize the need for continuous research for better-tolerated drug schemes for treatment of our lupus nephritis patients.
- ItemReduced natriuresis after oral sodium load in cholestatic rats(2000) Casar, JC; Valdivieso, A; Bravo, JA; Chacón, C; Boric, MPThe purpose of this study was to assess the participation of the atrial natriuretic peptide (ANP)-cGMP system in electrolyte and volume handling of cholestatic rats submitted to an acute oral sodium load. Cholestasis was induced by ligation and section of the common bile duct (n = 51), Control rats were sham operated (n = 56), Three weeks after surgery, 24-hr urinary volume, sodium, potassium, cGMP and creatinine excretion were measured. Three days later, animals received 10 mmol/kg NaCl (1 M) by gavage, and urinary excretion was measured for 6 hr. In parallel groups of rats, plasma volume, electrolytes and ANP concentration, extracellular fluid volume (ECFV), and renal medullary ANP-induced cGMP production were determined in basal conditions or 1 hr after oral sodium overload. As compared with controls, cholestatic rats had a larger ECFV and higher plasma ANP (67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml), but lower hematocrit and blood volume, and were hyponatremic, Cholestatic rats showed higher basal excretion of sodium, potassium, and volume than controls, but equal urinary cGMP, After the NaCl overload, cholestatic rats showed a reduced sodium excretion but equal urinary cGMP, One hr after sodium overload, both groups showed hypernatremia, but whereas in control rats ECFV and ANP increased (50.7 +/- 4.7 pg/ml), in cholestatic rats ECFV was unchanged, and plasma volume and ANP were reduced (37.5 +/- 5.8 pg/ml), ANP-induced cGMP production in renal medulla was similar in cholestatic and control nonloaded rats (14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg), One hr after the load, medullary cGMP production rose significantly in both groups, without difference between them (20.6 +/- 3.1 vs 22.7 +/- 1.7 fmol/min/mg). We conclude that the blunted excretion of an acute oral sodium load in cholestatic rats is associated with lower plasma ANP due to differences in body fluid distribution and cannot be explained by renal refractoriness to ANP.