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Biomedical subjects

V E Torres

Publications and source records attributed to V E Torres.

105 records · Page 6Linked to original sources
PubMed1983

Significance of proteinuria on the outcome of renal function in patients with focal segmental glomerulosclerosis.

Kidney survival analysis was performed for 64 patients with focal segmental sclerosis to ascertain whether the degree of proteinuria and other factors determined at the time of renal biopsy might be associated with progression to end-stage renal failure. On the basis of urinary excretion of protein, which was measured in 63 of the 64 patients, three groups of patients were identified: 15 patients (group A) had asymptomatic proteinuria (less than 3.5 g/24 h), 38 patients (group B) had nephrotic proteinuria (3.5 to 14 g/24 h), and 10 patients (group C) had massive proteinuria (more than 14 g/24 h). Kidney survival curves showed that the median time from biopsy to end-stage renal failure was more than 11, 7, and 3 years for groups A, B, and C, respectively. Thus, patients with massive proteinuria had an accelerated course to renal failure as compared with other nephrotic patients who had a lesser degree of proteinuria (P = 0.014) and patients who had asymptomatic proteinuria (P less than 0.001). Higher initial serum creatinine levels and severe tubulointerstitial damage were associated with a shorter time to end-stage renal failure. Age at onset and at biopsy, systolic and diastolic blood pressure, serum albumin and cholesterol, percentage of sclerotic glomeruli, mesangial proliferation, hyalinosis, vascular sclerosis, and initial response to prednisone were not associated with the time to end-stage renal failure when each of these variables was considered separately.

Biopsy↗
PubMed1982

Acute intrinsic renal failure induced by indomethacin: role of prostaglandin synthetase inhibition.

Nonsteroidal anti-inflammatory agents are often used to treat acute inflammatory arthritis because of their effectiveness and the infrequency of reported serious side effects. This report describes two patients who had acute intrinsic renal failure that was triggered by indomethacin. Both patients were volume contracted and had other circulatory impairments. Azotemia was so severe as to require temporary hemodialysis in one patient. Intrinsic renal function began to recover within 5 days after discontinuation of indomethacin. At the time that recovery began, urinary prostaglandin excretion increased in both patients. A detailed review of pertinent experimental data indicates that renal production of prostaglandin is an important compensatory response that helps to maintain renal function in the face of diminished renal blood flow. Our cases provide clinical support for this hypothesis and illustrate the fact that indomethacin, by interfering with this protective mechanism, can lead to acute intrinsic renal failure. Clinicians must be aware of this possible complication and use the nonsteroidal anti-inflammatory drugs with caution in patients who have compromised prerenal status.

Acute Kidney Injury↗
PubMed1980

The progression of vesicoureteral reflux nephropathy.

The relations among renal function, proteinuria, and glomerular lesions were studied in 54 patients with reflux nephropathy. The clinical course to end-stage renal disease was not appreciably altered by late surgical correction of the reflux, occurrence of urinary tract infection, or hypertension. All patients with progressive renal disease had significant proteinuria. Mesangial glomerular lesions can occur in the absence of proteinuria detectable by routine analysis, whereas lesions similar to those seen in idiopathic focal sclerosing glomerulopathy were present in the renal biopsies from proteinuric patients. Deposition of immunoproteins was limited to glomeruli undergoing sclerosis. Similarly, electron-dense deposits were confined to areas of mesangial alterations. Our results suggest that mesangial alterations occur early in the course of reflux nephropathy and may lead to the development of focal sclerosis. At later stages, counterproductive mechanisms of adaptation to the loss of viable nephrons might result in an acceleration of the clinical course to renal failure.

Adolescent↗
PubMed1980

In search of marker for genetic susceptibility to reflux nephropathy.

The frequency of 40 HLA antigen specificities was determined in 44 patients with end-stage renal disease secondary to reflux nephropathy and compared with those observed in 526 control subjects. Higher than normal frequencies were observed for HLA-B12 in female patients, and HLA-B8 in combination with HLA-A9 or HLA-BW15 in male patients, and HLA-BW15 in patients of both sexes. A comparison of the frequency of HLA antigens in the reflux patients with a history of hypertension versus those without a history of hypertension revealed that HLA-A3 was found with higher frequency and HLA-A1 and HLA-B8 with lower frequency in association with hypertension. These results suggest that the major histocompatibility antigens might be in linkage disequilibrium wih a gene (or genes) determining the susceptibility to renal damage by vesicoureteral reflux and that this linkage, or the clinical expression of this linkage, might be influenced by variations in relation to the sex of the patients.

Child↗
PubMed1978

Cyclic nucleotide phosphodiesterases in glomeruli of rat renal cortex.

The presence and properties of cyclic 3',5'-adenosine monophosphate phosphodiesterase (cAMP-PDIE) and cyclic 3',5'-guanosine monophosphate phosphodiesterase (cGMP-PDIE) were studied in glomeruli isolated from rat renal cortex by sieving and density gradient centrifugation. The specific activity of cGMP-PDIE was higher than the specific activity of cAMP-PDIE in glomeruli; in tubules and renal cortical slices, the specific activity of cAMP-PDIE was higher than that of cGMP-PDIE. In homogenates, X 100,000g supernate of homogenate (cytosol) and X 100,000g pellet (membrane fraction) from glomeruli, the specific activity of cGMP-PDIE was significantly higher than it was in analogous preparations from tubules or renal cortical slices. Cyclic 3',5'-GMP (10(-6)M to 10(-5)M) stimulated glomerular cAMP-PDIE, but it was without effect on cAMP-PDIE from tubules. Structural analogs of cyclic 3',5'-GMP or 5'-GMP did not stimulate glomerular cAMP-PDIE. Cyclic 3',5'-AMP slightly inhibited cGMP-PDIE from both glomeruli and tubules. N6-,2'-0-dibutyryl cyclic 3',5'-AMP inhibited cAMP-PDIE, but not cGMP-PDIE. The addition of calcium increased the activity of cGMP-PDIE, mainly in tubules, but was without effect on cAMP-PDIE. These results suggest the predominance of cyclic 3',5'-GMP catabolism in glomeruli in comparison with other cortical structures, and they demonstrate that both the specific activities and regulatory properties of cyclic nucleotide phosphodiesterase in glomeruli differ markedly from tubules or unfractionated renal cortical tissue.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Modulation of cyclic nucleotides in islated rat glomeruli: role of histamine, carbamylcholine, parathyroid hormone, and angiotensin-II.

Because glomerular functions are modulated by numerous humoral agents, probably acting through cyclic nucleotides, the effects of some polypeptide hormones and biogenic amines on cyclic AMP (cAMP) and cyclic 3',5'-guanosine monophosphate (cGMP) were studied in glomeruli isolated from rat renal cortex. Glomeruli and cortical tubules were prepared by a combination of sieving and density-gradient centrifugation. Under basal conditions, the contents of cAMP and cGMP in glomeruli were significantly higher than in tubules and unfractionated renal cortical tissue.Histamine caused a striking increase in cAMP in glomeruli (+Delta% 675+/-87) and, to a lesser degree, increased cAMP in tubules (+Delta% 103+/-25) or in tissue slices. This stimulation was dose-dependent in the range of 1 muM-1 mM histamine. Metiamide (an H(2)-antagonist), but not pyrilamine (an H(1)-antagonist) blocked the effect of histamine on cAMP, which indicates that histamine causes its effect via interaction with H(2) receptors. Histamine caused less extensive increases in cGMP in both glomeruli and tubules. Carbamylcholine caused a marked increase in cGMP in glomeruli (+Delta 295+/-7) and a much lower increase in tubules (+Delta% 70+/-20); these effects were blocked by atropine. Parathyroid hormone (1 mug/ml) increased cAMP and, to a much lesser degree, also cGMP in glomeruli. In tubules, parathyroid hormone caused much more extensive increases in cAMP than in glomeruli; no changes, or rather a small decline in cGMP, was observed. Angiotensin-II (2 muM) markedly lowered cAMP in glomeruli (-Delta% -45+/-8) and in tubules (-Delta% 33+/-7) but had no effect on cGMP. Bradykinin (20 muM) did not consistently influence either cAMP or cGMP in glomeruli or tubules. Present results demonstrate that cAMP and cGMP metabolism in glomeruli are controlled independently by humoral agents known to alter glomerular functions in vivo. Our findings are consistent with the view that histamine and cholinergic agents generated and (or) released locally in glomeruli or in their vicinity may play important roles as mediators of immunopathological injury of glomeruli, and that these effects are mediated by cAMP and (or) cGMP through interaction with H(2) receptors and muscarinic receptors. Likewise, our results suggest that the effects of angiotensin-II and parathyroid hormone on glomerular dynamics may be mediated by cyclic nucleotides.Thus, we surmise that extrarenal as well as intrarenal humoral agents may play an important role in the pathology and physiology of glomeruli through mediation of either cAMP, cGMP, or both.

Angiotensin II↗
PubMed1975

Indomethacin enhancement of glycerol-induced acute renal failure in rabbits.

Seventy-three rabbits (2 to 3 kg in weight) were studied during a control period and after receiving 50% glycerol (G) or mercuric chloride (M) with or without indomethacin (I) (controls received the diluent used for I). Plasma creatinine, plasma renin activity, blood pressure, sodium and potassium concentrations, hematocrit value, urinary output, body wt and histologic appearance of the kidney were determined. I enhanced the incidence and severity of the acute renal failure produced by G but failed to aggravate that produced by M. Because the dose of I used in this study blocked the synthesis of renal prostaglandins in the rabbit, we suggest that renal prostaglandins protect against the development of G-induced acute renal failure (a circulatory type of renal failure) in this animal model. Furthermore, the failure of I to aggravate M-induced acute renal failure indicates that it is unlikely that I aggravates G-induced acute renal failure by a direct nephrotoxic effect. No evidence was found for other possible side actions of I being responsible for the observed aggravation.

Acute Kidney Injury↗
PubMed1975

Role of prostaglandins in the reversal of one-kidney hypertension in the rabbit.

Hypertensive rabbits with a clip on the renal artery of their solitary remaining kidney show an abrupt decrease in blood pressure after the arterial constriction is released. Although the mechanism underlying this phenomenon remains controversial, some experimental evidence suggests that it could be humorally mediated. The involvement of prostaglandins was investigated by examining the effect of the release of the arterial constriction on blood pressure, renal blood flow, glomerular filtration rate, and urinary output in five conscious single-kidney hypertensive rabbits in which prostaglandin synthesis was blocked with indomethacin (priming intravenous injection of 9 mg/kg followed by a constant infusion of 1 mg/kg hour-1). The results were compared with those obtained in another group of five single-kidney hypertensive rabbits submitted to the same protocol but not treated with indomethacin. The blockade of prostaglandin synthesis with indomethacin prevented the increments in renal blood flow and glomerular filtration rate seen in the control rabbits after unclipping a significantly retarded the appearance of diuresis and the fall in blood pressure. Despite these observations, the results do not indicate a major participation of prostaglandins in the reversal of single-kidney hypertension, because the decrease in blood pressure 9 hours after the removal of the arterial constriction was similar in both groups.

Aminohippuric Acids↗
PubMed1975

Changes in plasma renin substrate, plasma and renal renin, and plasma osmolarity during glycerol-induced acute renal failure in rabbits.

Seven groups of rabbits were studied before or at various intervals after the subcutaneous administration of 50 percent glycerol in isotonic saline (14 ml/kg). A sharp increase in plasma crystalloid osmolarity, due to glycerol reabsorption from the subcutaneous tissue, was detected at 1.5 and 6 hours and was maximal between 12 and 20 hours. Plasma renin activity did not change at 1.5 hours, but it was significantly elevated at 6 hours and maximally increased between 12 and 20 hours. The increase of plasma crystalloid osmolarity might contribute to renin release in this experimental model. Changes in renal renin levels after the administration of glycerol were not significant, although lower renal renin values were consistently found in rabbits with more severe impairment of renal function. Plasma renin substrate increased later than plasma renin activity (20 hours) and remained high after plasma renin activity had returned to normal (48 hours). The increase of plasma renin substrate was interpreted as mainly due to the impairment of renal function, since a positive correlation was found between plasma creatinine and plasma renin substrate.

Acute Kidney Injury↗
PubMedDate not supplied

Inherited renal neoplasms.

The application of positional cloning to the study of families with inherited renal neoplasms has allowed the identification of genes which are also important in the pathogenesis of sporadic tumors and has advanced the understanding of the mechanisms underlying renal carcinogenesis. This review provides a discussion of these mechanisms as well as the diagnosis and management of the inherited renal neoplasms.

Carcinoma, Renal Cell↗