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Biomedical subjects

W F Falls

Publications and source records attributed to W F Falls.

At least 19 recordsLinked to original sources
PubMed1983

Chronic hemodialysis of spinal cord injury patients.

Fifteen paraplegics with ESRD have been treated at the Richmond VA Medical Center. The cumulative one year survival was 57%. This is somewhat less than expected for chronic hemodialysis patients from the general population. No patients have received a kidney transplant or been supported with peritoneal dialysis for a long period. The rate of acquisition of patients in this center indicates the rate of treatable ESRD is significantly higher in the spinal cord injury population than in the general population.

Adult↗
PubMed1981

Streptozotocin nephrotoxicity: studies on the defect in renal tubular acidification.

A 64-year-old man developed hyperchloremic acidosis while being treated with streptozotocin for an unresectable hepatoma. Studies done during acid and alkali loading suggested that the defect in urinary acidification resided in the proximal tubule and thus represented a Type II or proximal renal tubular acidosis (RTA).

Acidosis, Renal Tubular↗
PubMed1980

Hyperkalemia: pathophysiology and management.

Huperkalemia, a potentially lethal electrolyte disturbance, is frequently encountered by the practicing physician. Multiple factors, including the level of renal function, acid base status, activity of the renin-angiotension-aldosterone system, and the availability of insulin, normally interact to control the serum potassium concentration. The author approaches hyperkalemia as an aberration of one or more of these controlling factors and discusses appropriate therapeutic modalities.

Addison Disease↗
PubMed1979

Analysis of factors influencing the renin-aldosterone system in a patient with Bartter's syndrome.

The response to indomethacin of a patient with Bartter's syndrome and proximal tubular sodium wasting is described. The patient had evidence of excessive prostaglandin activity (elevated urinary prostaglandin E metabolite [PGE-M] excretion) which returned to normal with indomethacin therapy. Indomethacin administration corrected the defect in proximal tubular sodium resorption, but suppressed plasma renin activity and urinary aldosterone excretion only when sufficient dietary sodium was available to allow for extracellular fluid volume (ECFV) expansion. We conclude that the proximal tubular defect in sodium resorption may have been caused by excessive prostaglandin activity and that the sustained hyperactivity of the renin-aldosterone system was mediated by ECFV depletion.

Aldosterone↗
PubMed1976

Bartter's syndrome. Study of a 52 year old man with evidence for a defect in proximal tubular sodium reabsorption and comments on therapy.

A patient with Bartter's syndrome in whom the disease was recognized at 52 years of age is described. Studies of his renal function suggest that the basic pathophysiologic defect was an abnormality in proximal tubular sodium reabsorption which led to extracellular fluid volume depletion and consequent stimulation of the renin-angiotensin-aldosterone axis. After comparing the physiologic studies in this patient with those in other reported cases, we postulate that Bartter's syndrome may represent the end result of different pathophysiologic processes which share in common juxtaglomerular hyperplasia, increased renin release and secondary hyperaldosteronism. Therapy with B-adrenergic blocking agents produced adverse effects, but the patient responded well to more conventional measures.

Bartter Syndrome↗
PubMed1975

Factors influencing sodium and water excretion in uremic man.

Urinary excretion of sodium and water was investigated in patients with chronic end-stage renal disease before and after three different experimental manipulations: reduction in urea solute load by dialysis while extracellular fluid volume (ECFV) was maintained, dialysis without alteration in urea solute load or ECFV and reduction in ECFV without alteration in urea solute load. Sodium and water excretion significantly declined in association with a reduction in both urea solute load and ECFV, but not during a dialysis when reduction on both of these indexes was prevented. The excretory changes occurred in the absence of any alteration in creatinine clearance. The studies suggest that both solute load and the degree of extracellular fluid volume expansion contribute independently to the rate of sodium and water excretion in chronic renal disease. It is concluded that in any given patient the overall excretion of sodium and water is directly influenced by a number of factors including the solute load, the degree of ECFV and the glomerular filtration rate.

Adult↗
PubMed1975

Incomplete renal tubular acidosis: some clinical and physiological features.

17 patients with recurrent calcium-containing renal calculi were studied using the short NH4Cl test and one subject with 'incomplete renal tubular acidosis' was identified. In retrospect the only clue to this diagnosis was a fasting, morning urine pH exceeding 6.0 units. Fasting morning urine pH, which is usually less than 6.0 in subjects who acidify normally, is proposed as a simple screening test for 'incomplete RTA'. Modified high dose NH4Cl tests and Na2SO4 tests were performed in this subject and other patients with either complete or incomplete distal renal tubular acidosis. These studies suggest that the ability to lower urine pH is impaired less with the incomplete than with the complete form of the disease.

Acidosis, Renal Tubular↗