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Biomedical subjects

S Anderson

Publications and source records attributed to S Anderson.

At least 433 records · Page 24Linked to original sources
PubMed1988

Pathogenesis of diabetic glomerulopathy: hemodynamic considerations.

Early stages of diabetes mellitus are characterized by glomerular hyperfiltration in humans and experimental animals. In diabetic rats, single nephron hyperfiltration results from elevations in the glomerular capillary plasma flow rate and hydraulic pressure, which are in turn associated with progressive albuminuria and morphologic injury. Interventions that ameliorate these hemodynamic adaptations afford protection against structural injury. Dietary protein restriction, which lowers glomerular filtration, perfusion, and hydraulic pressure, retards glomerular injury and limits capillary basement membrane thickening in both the glomerular and retinal circulatory beds. Alternatively, selective control of glomerular capillary hypertension using angiotensin I converting enzyme inhibitor therapy limits glomerular injury in this model as well. Each of these interventions is effective even in the absence of improved metabolic control, implying that hemodynamic factors per se are important in this pathogenic process. The pathophysiologic mechanisms of diabetic hyperfiltration remain incompletely elucidated. Recent studies invoke a potential role for atrial natriuretic peptide (ANP). Strict metabolic control abolishes the elevations of glomerular filtration rate and of plasma ANP levels in moderately hyperglycemic diabetic rats. Moreover, infusion of a specific ANP antibody reverses hyperfiltration in diabetic rats. Thus, hyperglycemia-induced chronic volume expansion may trigger ANP release, which in turn contributes to diabetic hyperfiltration. Hemodynamic factors may play an important role in the pathogenesis of extrarenal microangiopathy as well. Elevated peripheral capillary blood flows and/or hydraulic pressure may be found in many peripheral capillaries, in association with thickening of the capillary basement membrane. Dietary protein restriction, which lowers blood flow to many organs, limits retinal as well as glomerular basement membrane thickening in diabetic rats, suggesting that hemodynamically mediated structural injury is a diffuse phenomenon in the diabetic state.

Animals↗
PubMed1988

Enterolithiasis with imperforate anus. Report of two cases with sonographic demonstration and occurrence in a female.

Enterolithiasis has been previously described as a plain film finding of rectovesical or rectourethral fistula in patients with anorectal malformation. Two cases of enterolithiasis with anorectal malformation are described in which the intraluminal nature of the calcifications was identified using ultrasound. The use of ultrasound for this purpose has not been previously reported to our knowledge. This simple, noninvasive technique permits antenatal differentiation between enterolithiasis and meconium peritonitis in some patients and can suggest the prenatal diagnosis of rectourinary communication when enterolithiasis is present. In addition, one of our cases occurred in a female. The entity of enterolithiasis with imperforate anus in a female has not been previously reported.

Anus, Imperforate↗
PubMed1988

Anemia lessens and its prevention with recombinant human erythropoietin worsens glomerular injury and hypertension in rats with reduced renal mass.

Chronic renal disease is frequently characterized by anemia, which may modify systemic and renal hemodynamics. In adult Munich-Wistar rats, the mild anemia (hematocrit, approximately equal to 42 vol/dl) that accompanies five-sixths nephrectomy was either made more severe (approximately equal to 30 vol/dl) by feeding a low iron diet or prevented (approximately equal to 50 vol/dl) by administration of recombinant human erythropoietin (r-HuEpo). In functional studies performed 4 weeks after renal ablation, untreated rats exhibited mild anemia with systemic hypertension and elevation of the single nephron glomerular filtration rate due to glomerular capillary hyperperfusion and hypertension. Preventing anemia with r-HuEpo worsened systemic and glomerular hypertension, effects largely obviated by induction of more marked anemia with the low iron diet. Untreated rats followed for 6 weeks postablation exhibited progressive proteinuria and sclerosis involving 12% of glomeruli, contrasted with 33% in rats given r-HuEpo. Even after 12 weeks, sclerosis involved only 6% of glomeruli in rats with more severe anemia but progressed to 30% in untreated rats. Thus, anemia limits systemic and glomerular hypertension and glomerular injury, whereas its prevention by r-HuEpo severely accelerates hemodynamically mediated glomerular injury in this model. These results suggest that anemia is a hemodynamically favorable adaptation to chronic renal disease and that its overly vigorous correction may have adverse renal hemodynamic and structural consequences.

Anemia↗
PubMed1988

Glucocorticoids amplify glomerular injury in rats with renal ablation.

Male Munich-Wistar rats were subjected to 1 2/3 nephrectomy. One group received no therapy (C). A second group received daily doses of methylprednisolone (MP). A third group received MP plus the angiotensin I converting enzyme inhibitor (CEI) benzazepril. A fourth group received CEI alone. Half of the rats in each group underwent micropuncture study 2 weeks after ablation. Untreated rats exhibited systemic hypertension and elevation of the single nephron glomerular filtration rate (SNGFR), due to glomerular capillary hyperperfusion and hypertension. Administration of MP resulted in comparable systemic hypertension with further elevation of SNGFR due to even higher values for glomerular perfusion and hydraulic pressure (PGC). Concurrent treatment with CEI-controlled systemic and glomerular hypertension despite equivalent renal ablation and comparable doses of MP. After 12 weeks untreated rats demonstrated continued systemic hypertension, progressive proteinuria, and eventual glomerular sclerosis. Addition of MP dramatically accelerated the development of proteinuria and glomerular sclerosis, while CEI afforded striking protection against disease progression. Thus, potent vasodilator glucocorticoids may amplify hemodynamically mediated glomerular injury, whereas control of systemic and glomerular hypertension prevents this undesirable consequence of chronic steroid therapy.

Analysis of Variance↗
PubMed1988

Glomeruli and blood pressure. Less of one, more the other?

A primary role for the kidney in the initiation and maintenance of hypertension has long been recognized, but the pathogenetic interactions among renal hemodynamics, hormonal and hereditary factors, and dietary sodium intake remain enigmatic. Reduction in filtration surface area, whether acquired in the course of intrinsic renal disease or after surgical renal ablation, leads to systemic hypertension as well as to progressive renal insufficiency, sequellae made even more severe by dietary sodium excess. Moreover, hypertension and progressive renal disease eventuate in some individuals born with a solitary kidney, as well as in those with more severe degrees of dysgenesis (ie, oligomeganephronia). Hypertension is also commonly observed in certain inbred rat strains in which filtration surface area is congenitally deficient. Based on these and other lines of evidence reviewed herein, we postulate that a renal abnormality that contributes to essential hypertension in the general population is a reduced number of nephrons. The consequences of this abnormality are limitations in the ability to excrete sodium and thus, salt-sensitive hypertension. Finally, congenital variability in filtration surface area may explain why only some, but not all, patients exposed to potentially injurious renal stimuli eventually manifest chronic nephropathy. This may also account for the susceptibility of subsets of Type I and Type II diabetics to develop overt glomerulopathy.

Diabetic Nephropathies↗
PubMed1988

Therapeutic benefit of converting-enzyme inhibition in progressive renal disease.

Systemic hypertension is both the cause and the consequence of renal disease. Experimental studies suggest that the adverse effects of systemic hypertension on the progression of renal disease may depend upon the intraglomerular hemodynamic consequences. Systemic hypertension accompanied by afferent arteriolar vasoconstriction is associated with normal glomerular capillary pressure and relative protection against morphologic injury. In contrast, systemic hypertension with afferent arteriolar vasodilatation leads to glomerular hypertension and is associated with structural injury. Glomerular hypertension may be present even in the setting of normal systemic pressure, as in experimental diabetes. Therapeutic interventions that attenuate glomerular capillary hypertension slow the development of glomerular injury. Dietary protein restriction, which normalizes glomerular capillary filtration, perfusion, and pressure without lowering blood pressure, retards the development of glomerular sclerosis. Alternatively, selective reduction of glomerular capillary pressure with converting-enzyme inhibitor therapy is also protective against progressive renal injury. In contrast, antihypertensive therapy, which controls systemic hypertension but does not reduce glomerular capillary pressure, fails to protect remnant kidney rats from glomerular injury. These studies suggest that control of glomerular hypertension may be of special benefit to the patient with progressive renal disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Intraglomerular hypertension: implications and drug treatment.

Systemic hypertension is both cause and consequence of progressive renal disease. Recent experimental studies indicate that systemic and glomerular capillary hypertension are not necessarily accompaniments, and that therapeutic interventions may affect systemic and glomerular pressures independently. Therapeutic interventions that control glomerular capillary hypertension protect against progressive renal injury, even in the presence of continued systemic hypertension. Conversely, therapy that controls systemic but not glomerular hypertension does not protect the kidney from continuing damage. Thus, control of intraglomerular hypertension is necessary if antihypertensive therapy is to be effective in preventing progression of renal injury.

Animals↗
PubMed1988

Interrelationships among atrial peptides, renin, and blood volume in pregnant rats.

To determine how changes in intravascular volume are sensed by atrial and renal volume receptors during pregnancy and the puerperium, circulating atrial natriuretic peptide (ANP) levels and plasma renin activity (PRA) were measured in conscious chronically catheterized rats on days 9-10, 15-16, 19-20, and 22 of pregnancy, on the first postpartum day, and in nonpregnant controls. Blood volume measured in a separate group of anesthetized rats increased progressively during pregnancy, and circulating ANP levels tended to decline, although not significantly below the nonpregnant value of 132 +/- 9 pg/ml (mean +/- SE). PRA remained similar to the nonpregnant value of 5.5 +/- 0.6 ng angiotensin I.ml-1.h-1 until day 22 of pregnancy, when it rose to 14.1 +/- 1.8 ng angiotensin I.ml-1.h-1 (P less than 0.001 vs. nonpregnant). In pregnant rats, PRA was suppressed after uninephrectomy and chronic administration of deoxycorticosterone and saline, demonstrating the ability of this hormonal system to respond appropriately to further increments in volume induced during pregnancy. On the first postpartum day plasma ANP rose to 268 +/- 26 pg/ml, and PRA fell to 3.6 +/- 0.4 ng angiotensin I.ml-1.h-1 (P less than 0.005 and P less than 0.05 vs. nonpregnant values, respectively). Thus it appears that the increased blood volume in normal pregnancy is not sensed by renal or atrial volume sensors, presumably because it is accommodated by an enlarged maternal vascular compartment. In the puerperium, however, due to the decreased size of the maternal vascular compartment, atrial and renal volume sensors recognize the intravascular volume as expanded.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome.

Functional and morphologic measurements were performed in Munich-Wistar rats after a single central venous injection of puromycin aminonucleoside (PA) or saline vehicle (sham). During phase I, PA rats exhibited overt nephrotic syndrome and impaired glomerular filtration, primarily due to a reduction in the glomerular capillary ultrafiltration coefficient. The morphologic counterpart of the latter consisted of effacement of glomerular epithelial cell foot processes and decrease in the number of filtration slit diaphragms. Administration of the angiotensin I converting enzyme inhibitor (CEI) enalapril to PA rats did not ameliorate glomerular dysfunction. During phase II, PA rats exhibited spontaneous resolution of proteinuria, impaired function, and morphologic abnormalities. However, PA rats now demonstrated marked glomerular capillary hypertension and continued, albeit lesser, reductions in the ultrafiltration coefficient. Concurrent CEI administration modestly lowered systemic arterial pressure, and normalized the glomerular capillary hydraulic pressure and ultrafiltration coefficient. Additional rats were studied during phase III, 70 wk after injection. In PA rats, prior glomerular hypertension was associated with development of recurrent proteinuria and extensive glomerular sclerosis, whereas concurrent CEI administration limited these parameters to values comparable to those in sham rats. Glomerular hypertension thus may explain the development of glomerular sclerosis and renal failure long after an episode of acute glomerular injury.

Animals↗
PubMed1988

An intermediate filament-associated developmentally regulated protein in corneal fibroblasts.

A developmentally regulated, cytoskeletal-associated protein was identified and partially characterized using a monoclonal antibody developed for this study. Based on the distinctive fibrous pattern of distribution of this antigen in the cytoskeletons of cultured corneal fibroblasts, and a characteristic reorganization of these fibers into perinuclear whorls in response to colchicine treatment, this protein was found to be associated with the intermediate filaments (vimentin filaments). Chronological distribution of this intermediate filament-associated protein (IFAP) and vimentin during fetal development of the cornea in rabbit was analysed immunohistochemically. During an early stage of corneal development (day 13 of gestation), both this IFAP and vimentin were present in the stromal cells in the presumptive corneal region. The IFAP was also present in the surface epithelium. At day 17 and 21, the corneal endothelial layer was developed and contained both the IFAP and vimentin. However, in the corneal stromal cells, the concentration of IFAP (based on the densities of the immunostaining reaction) progressively decreased during the later stages of fetal development (day 24 to day 28), while relative concentrations of vimentin were not reduced significantly. In the corneal stromal cells in the adult rabbit, the IFAP was not detectable while vimentin was still present. For further characterization of this protein, extracts of cultured corneal fibroblasts and fetal corneas were analysed by SDS-PAGE followed by an immunotransblot technique. These analyses indicated that the IFAP was a polypeptide with a Mr of 130k. Therefore, this protein was not vimentin (Mr 55-58k). The presence of this IFAP in the fetal corneas and stromal cells and its absence in the quiescent stromal cells in the adult cornea indicated that this unique IFAP is developmentally regulated in corneal stromal cells, and its association with vimentin filaments may be important during the active state of corneal stromal cells.

Aging↗
PubMed1988

Patients with rheumatoid arthritis at high risk for noncompliance with salicylate treatment regimens.

Recent studies indicate the adherence of many patients with rheumatoid arthritis (RA) to their treatment regimens is poor. Management of this problem depends on identification of noncompliant patients, followed by interventions to increase their level of adherence. In this study, 63 patients with RA receiving salicylate drugs completed a questionnaire during an outpatient visit. The questionnaire contained items believed to be predictive of future compliance, including patient self-predictions regarding future compliance, ratings of behavior in similar situations and barriers to compliance, such as ease of transportation to the clinic. Compliance was estimated via a salicylate assay that was taken during a subsequent outpatient appointment. Multivariate analyses of our data revealed that significant predictions could be made regarding future compliance, with 75% of the noncompliant patients correctly identified. Variables contributing significantly included behavioral self-predictions and a measure of current behavior in similar situations, as assessed by a salicylate assay that was collected during the 1st outpatient visit.

Arthritis, Rheumatoid↗
PubMed1988

Coping strategies in rheumatoid arthritis.

Our purpose was to investigate the importance of the coping process for patients with rheumatoid arthritis (RA). Eighty-four patients with classic or definite RA were examined. The relationship between coping strategies and psychological status, functional status, pain, and disease activity was analyzed. Coping was measured by an adapted version of the Ways of Coping Scale, and measures of psychological status, life stress, functional status, pain, and disease activity were also obtained. Canonical correlation revealed a significant relationship between the coping process and psychological status. Coping also was significantly related to functional status, but not to pain or disease activity. Patients who coped by restructuring life goals were found to have better psychological adjustment and functional status than patients who hoped for unrealistic solutions or engaged in self-blame.

Activities of Daily Living↗
PubMed1988

Diagnostic value of the history and examination in giant cell arteritis: a clinical pathological study of 81 temporal artery biopsies.

To determine the value of the history and examination in predicting a temporal artery biopsy result, 81 temporal artery biopsies between 1974-1980 were studied. Each biopsy was scored blindly and independently by 2 pathologists and correlated with clinical data and the indications for biopsy at the time of the biopsy. Thirteen biopsies had giant cells and were considered positive, 8 had mononuclear inflammatory cells in the wall (7 cases) or healed arteritis (1 case) and were considered probable, and 60 were negative. In patients with an elevated sedimentation rate, the presence of a sign (tenderness or abnormal temporal artery), or a symptom (visual change or headache) predicted 18 of 21 (86%) positive-probable biopsies, but misclassified 32 of 60 negative biopsies. Attempts to derive a clinical decision rule with improved specificity resulted in unacceptably low sensitivity (missing 5 of 21 positive-probable biopsies). A minimum 5-year followup showed that those patients treated with steroids had a 6-fold increase in fractures and a 4-fold increase in cataracts.

Aged↗