Biomedical subjects
Publications and source records attributed to W W Brown.
Stimulated by a mother's desire to find a cure for her child's disease, the National Kidney Foundation has grown from a small local group of interested lay persons and medical professionals Into a major national organization with affiliates around the country and national and International programming in renal research funding, patient and family services, public and professional education, and public policy advocacy.
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The presentation of many renal diseases in older adults is remarkably similar to that in younger patients, although the symptoms and clinical findings are frequently attributed to diseases of aging. Since older patients often respond to treatment as well as younger patients do, they deserve a thorough investigation, including renal biopsy when indicated. It is important to base decisions regarding access to evaluation and treatment, quality of life, and initiation of termination of dialysis on strong moral and ethical grounds.
This study was performed to ascertain the degree to which the care of hospitalized diabetic and hypertensive patients conforms to published guidelines for the detection and management of early renal disease. It was designed as a retrospective chart audit. Six hospitals, four nonurban referral centers, and two urban teaching institutions provided the data. Patients were a random sample of Medicare beneficiaries, with a mean age (SD) of 65.6 (9.1) years, admitted during 1994 with a primary or secondary diagnosis of either diabetes (n = 260) or hypertension (n = 327). A urinalysis was obtained for 163 (62.7%) of the diabetic patients. Among diabetics who had their urine tested, 31.3% had 1+ or greater dipstick proteinuria. A serum creatinine was obtained for 298 (91%) of the hypertensive patients, and 11.8% had a value of 1.5 mg/dL or greater. Abnormal renal function tests were recorded in the discharge summaries of 7.8% of the diabetic and 11.4% of the hypertensive patients. Patients with abnormal renal function were no more likely to be treated with angiotensin-converting enzyme inhibitors (ACEIs). Nonsteroidal antiinflammatory drugs (NSAIDs) were prescribed for 6% of diabetic and 8.8% of hypertensive patients with abnormal renal function at discharge. Despite the high prevalence of renal functional abnormalities detected by routine laboratory tests administered to elderly hospitalized diabetic and hypertensive patients, the medical records of these patients did not document awareness or appropriate management of the potential underlying kidney disease.
Spontaneous bilateral rupture of the extensor mechanisms of the knees, without significant history of trauma, has been reported rarely, generally in association with chronic metabolic disorders, such as chronic renal failure and secondary hyperparathyroidism. We report spontaneous tendon rupture in two patients on chronic hemodialysis for 4 and 11 years, with documented severe secondary hyperparathyroidism. One patient had spontaneous bilateral rupture of his quadriceps and partial avulsion of the left triceps tendons. The other patient had spontaneous rupture of his right quadriceps tendon. Both patients had markedly elevated serum intact parathyroid hormone and moderately elevated serum beta 2-microglobulin levels. Pathologic examination revealed diffuse immunohistochemical staining for beta 2-microglobulin but negative Congo-red staining of the ruptured tendon specimens. These cases and the previous reports in the literature suggest that secondary hyperparathyroidism may play a role in the pathogenesis of this clinical entity.
RATIONALE AND OBJECTIVES: This study was devised to develop a method of measuring the acute effects of radiocontrast media on renal function and assessing the relationship of the dose of radiocontrast media infused with the incidence of radiocontrast-induced renal failure. In addition, the drug adenosine phosphate-magnesium chloride (ATP-MgCl2) was evaluated as a renoprotective agent. METHODS: Eighteen patients with pre-existing renal impairment, (serum creatinine greater than 133 mumol/L) were randomized to receive a continuous infusion of ATP-MgCl2 or placebo before and during a radiocontrast procedure. Subjects were monitored with daily serum creatinine and with radionuclide renal clearance studies at baseline, during, and 24 hours after the radiocontrast procedure. RESULTS: There was an initial deterioration in renal clearance in the entire study group (from 44.2 +/- 4.6 to 32.6 +/- 3.9 mL/min, P = .001) which was independent of the dose of radiocontrast infused. There was a persistent deterioration in renal clearance only in those who received greater than 135 mL of contrast media (from 48.6 +/- 7.8 to 37.1 +/- 3.9 mL/min, P = .05). There also was an increase in serum creatinine that persisted only in those subjects who received greater than 135 mL of contrast media (230 +/- 27 to 283 +/- 44 mumol/L, P = .01). CONCLUSION: Persistent deterioration in renal function after radiocontrast administration appears to be dose-dependent and is not prevented by the use of ATP-MgCl2. Radionuclide techniques are useful in monitoring acute changes in renal function during radiocontrast procedures and may be of value in assessing renal impairment in future intervention studies.
A number of renal disorders are amenable to dietary manipulation. This article reviews nutritional strategies for the management of renal stone disease, chronic renal failure, and nephrotic syndrome. The first portion discusses dietary factors that promote urolithiasis and dietary recommendations utilized in the medical management of stone disease. The second segment discusses the pathophysiology of the progression of renal disease and nutritional interventions to delay progression. Finally, the third portion examines losses of protein, vitamins, and minerals in the nephrotic syndrome and makes recommendations for replacement.
To assess the risk for transmural thermal injury to abdominal viscera during electrosurgical ablation of the endometrium, thermocouples were laparoscopically directed to the surface of the uterus at the time of endometrial ablation. A 2- or 5-mm ball, or a barrel electrode directed through a urologic resectoscope was placed in the cornual area, and current varying from 50 to 150 W of unmodulated ("cutting") or modulated ("coag") current was applied for five seconds without moving the electrode. The resultant temperature rise of the uterine serosa did not exceed 6 degrees C.
The report of a bowel injury's occurring during Nd:YAG laser ablation of the endometrium without associated uterine perforation has raised the question of the safety of the procedure. The fibers used during the initial study on temperatures caused by Nd:YAG laser treatment of uterine tissue were placed directly in contact with the tissue. The results may not be applicable to a noncontact technique. Three patients underwent measurement of surface temperature of the uterus during ablation with the Nd:YAG laser using a noncontact technique. The temperatures were within acceptable ranges in two of the patients but reached potentially dangerous levels in the third. In vitro measurements of temperatures in uterine tissue obtained from fresh hysterectomy specimens were made using fine thermocouples. The temperature rise at 10 mm was greater per joule of delivered energy at 55 W than at 95. The temperature rise varied inversely with the tissue depth when the laser was applied in a continuous fashion with a noncontact technique. When the laser was applied continuously, the temperature rise at a depth of 8 mm was significantly greater than at 10 mm. Precise knowledge of the thickness of the uterine wall may be the limiting factor in determining the safety of the procedure.
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Two patients with renal failure developed N-acetylprocainamide toxicity while receiving procainamide. Treatment consisted of continuous arteriovenous hemofiltration in one and hemodialysis followed by continuous arteriovenous hemodiafiltration in the other. The efficacy of these treatments was compared with the efficacy of three-times-weekly hemodialysis as used in two patients on chronic hemodialysis who had elevated N-acetylprocainamide levels. Continuous methods produced a more rapid reduction in N-acetylprocainamide levels than intermittent hemodialysis.
Numerous anatomic and physiologic alterations occur in the kidney with aging. These changes affect the ability of elderly patient(s) to maintain homeostasis and alter response to medications, stress, illness, or changes in diet, mobility, or environment. Drug-induced illness and drug interactions are major problems in the elderly. Bone disease and fractures are associated with negative calcium balance and decreased production of 1,25-dihydroxycholecalciferol seen with aging. The geriatric patient is not immune to the primary glomerular diseases that occur in younger patients, although the relative incidence of pathologic diagnoses may differ. The high incidence of membranous glomerulonephritis in the elderly, and the well-known association between malignancy and membranous nephropathy strongly favor aggressive evaluation of the nephrotic syndrome in the geriatric age group. Attention must be given to consideration of appropriate end-stage renal disease treatment alternatives for the geriatric population, which now comprises the fastest-growing segment of the end-stage renal disease population.
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Cell pH (pHc) was examined by the [14C]DMO technique in suspensions of proximal tubule fragments from rabbit renal cortex. In buffer with 10 mM HCO3(-), pHc was more alkaline than external pH (pHe) at values of the latter < 7.4. Maximal cell-to-extracellular pH gradients (delta pH) occurred at pHe = 6.8 and below. At pHe > 7.4, pHc was more acid than pHe was. However, pHc was always more alkaline than the electrochemical equilibrium pH. At pHe congruent to 7.0, 60 min of deoxygenation decreased delta pH from 0.22 +/- 0.02 to 0.05 +/- 0.01. Reoxygenation restored delta pH to control values. Incubation with ouabain abolished the delta pH. Both the carbonic anhydrase inhibitor, acetazolamide, and the anion transport inhibitor, 4-acetamido-4'-isothiocyano-2,2'-disulfonic stilbene (SITS), increased delta pH. The studies demonstrate relative intracellular alkalinity in proximal tubule. A fall in pHc occurs with maneuvers that interfere with H+ pumping out of the cells. A rise in pHc occurs with maneuvers that interfere with the disposition of intracellular alkali: slowing of HCO3(-) generation with acetazolamide or blocking of HCO3(-) exit with SITS. The results support a H+-secretory model of proximal tubule acid transport that is dependent on maintenance and dispersal of intracellular alkalinity.
Synthesis of prostaglandin E2 (PGE2) by rabbit bladder was examined. PGE2 synthesis was assessed by thin-layer chromatographic analysis after conversion of [14C]-arachidonic acid to [14C]PGE2 or by a specific radioimmunoassay technique. Intact bladder and microsomes prepared from the bladder transitional epithelium (mucosal) layer and the outer vesicular layer demonstrated synthesis of PGE2. PGE2 synthesis was increased by arachidonic acid and blocked by indomethacin. When the inside medium (bathing the transitional epithelium) contained [14C]arachidonic acid, no detectable radioactivity was observed in the outside medium (bathing the outer layer). Conversely, when the outside medium contained [14C]arachidonic acid, no detectable radioactivity was observed in the inside medium. In addition, [14C]arachidonic acid was incorporated only into tissue directly exposed to bathing media containing the label. These results demonstrate that the rabbit bladder can synthesize PGE2 and that the PGE2- synthesizing systems of the transitional epithelium and outer layer of bladder may be distinct.
Renal inner medullary slices were used to investigate the metabolism and subsequent binding to tissue of [14C]-benzidine metabolite(s) and the effect of benzidine on radioimmunoassayable prostaglandin (PG) E2 synthesis. Benzidine elicited a dose-dependent, reversible inhibition of PGE2 synthesis. By contrast, aspirin inhibition of PGE2 synthesis was not reversible. Binding of [14C]-benzidine metabolite(s) to medullary tissue was observed. This binding was increased by arachidonic acid. Arachidonic acid-mediated binding was prevented by inhibitors of prostaglandin endoperoxide synthetase. Metyrapone and SKF-525A, inhibitors of mixed function oxidase activity, did not inhibit binding of benzidine metabolite(s). Fatty acids which are not substrates for prostaglandin endoperoxide synthetase did not increase binding. These results are consistent with previous studies demonstrating inner medullary microsomal cooxidative metabolism of benzidine by prostaglandin endoperoxide synthetase and document the cooxidative process proceeds in an intact cell preparation, the tissue slice. The renal inner medulla is a potential site for the cooxidative metabolism of drugs and xenobiotics which require activation before eliciting their toxic effects on the urinary tract.
The renal inner medulla may be exposed to high concentrations of organic compounds which are excreted into the urine. This report examines the capacity of the inner medulla to metabolize organic compounds both in vitro and in vivo. The compounds used were 1,3-diphenylisobenzofuran (DPBF), luminol, and benzidine. The inner medulla was shown to possess the capacity to oxidize each of these compounds. Microsomal oxygenation did not require NADPH. Cytochorome P-450 inhibitors carbon monoxide and metyrapone did not reduce DPBF metabolism. Lipoxygenase activity was not detected in inner medullary microsomes. Oxygenation of DPBF was demonstrated in inner medullary slices and was inhibited by indomethacin. The product of DPBF metabolism in renal slices and microsomes was identified as O-dibenzoylbenzene. In vivo experiments demonstrated benzidine metabolism, which was blocked by meclofenamic acid. On the basis of substrate specificity and inhibitor studies, it was concluded that oxygenation of DPBF, luminol, and benzidine was mediated by prostaglandin cyclooxygenase. These results are compatible with cooxygenation being a mechanism of inner medullary drug metabolism.