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Biomedical subjects

L H Beck

Publications and source records attributed to L H Beck.

At least 19 recordsLinked to original sources
PubMed1990

Perioperative renal, fluid, and electrolyte management.

Normal physiologic changes of aging increase the likelihood of renal-electrolyte disorders in the elderly surgical patient. The most important of these changes are a decrease in the GFR, decreased urinary concentrating ability, and narrowed limits for the excretion of water, sodium, potassium, and acid. Because of the decrease in GFR, the elderly surgical patient is at increased risk for virtually every cause of acute renal failure, an outcome associated with a mortality of greater than 50%. Certain types of surgery, especially cardiac, aortic, and biliary tract operations, are associated with a higher risk of acute renal failure than are others. The most important principles of prevention in the elderly surgical patient are to maintain normal intravascular volume and avoid hypovolemia. Meticulous attention must be paid to salt and water balance and to drug dosing. Should perioperative renal insufficiency occur, evaluation and management in the elderly patient are similar to usual practices in a younger individual.

Acute Kidney Injury↗
PubMed1988

Maintaining health with renal disease or dysfunction.

A decline in renal function, similar to mild chronic renal insufficiency, normally occurs in the elderly concomitantly with various anatomic and histologic changes in the kidney. These morphologic and physiologic changes result in diminished ability to respond to body fluid or solute stresses. Superimposition of chronic renal insufficiency upon these age-related physiologic changes can accelerate renal functional decline. However, with proper management, most elderly patients with renal disease can remain highly functional.

Aged↗
PubMed1979

Acute massive hydrothorax complicating peritoneal dialysis, report of 2 cases and a review of the literature.

Acute massive right-sided hydrothorax is a relatively rare but serious complication of peritoneal dialysis and may be responsible for the development of dyspnea during peritoneal dialysis. The pleural fluid appears to arise from the peritoneal dialyzate based on the time of its appearance and its chemical composition. It should be included in the differential diagnosis when a patient becomes dyspneic during peritoneal dialysis along with exaccerbation of congestive heart failure, pneumonia, atelectasis, and purulent bronchitis. Its occurrence is an indication to stop the peritoneal dialysis and contraindicates further use of this form of dialysis. Treatment may be conservative or aggressive (thoracentesis) depending on the clinical condition of the patient. Etiology is poorly understood. In some cases, there may be traumatic diaphragmatic fenestrations, but the majority of cases appear to be due to less well defined communications between the peritoneal and pleural spaces.

Dyspnea↗
PubMed1978

Dissociation of tubular sites of action of saline, PTH and DbCAMP on renal phosphate reabsorption.

The effects of saline expansion, parathyroid hormone (PTH) administration and dibutyryl cyclic 3'5'-adenosine monophosphate (DbCAMP) infusion on renal phosphate reabsorption were examined in acutely thyroparathyroidectomized (TPTX), phosphate infused dogs by the recollection micropuncture technique. Saline expansion reduced whole kidney phosphate reabsorption from a mean of 66.1 to 50.4% of filtered load. This response was entirely accounted for by an inhibition of proximal tubular phosphate reabsorption which fell from a mean of 35 to 21% of the filtered phosphate load. Both PTH and DbCAMP produced a fall in whole kidney phosphate reabsorption comparable to saline. However, this effect was the sum of inhibition of both proximal tubular and distal nephron phosphate reabsorption. These studies demonstrate the important role of the distal nephron in modulating urinary phosphate excretion.

Animals↗
PubMed1973

Sodium-independent active potassium reabsorption in proximal tubule of the dog.

Prior studies of proximal tubule reabsorption have failed to distinguish conclusively between a separate active K+ transport system and K+ movement linked to Na+ reabsorption. To attempt to dissociate movement of K+ from Na+ and Ca++, recollection micropuncture experiments were performed in proximal tubules of intact and thyroparathyroidectomized (TPTX) dogs under two different conditions known to inhibit Na+ reabsorption: saline expansion to 5% body wt, and 5 mg/kg acetazolamide. A control hydropenic group was also studied. Tubular concentrations of K+, Na+, and Ca++ were measured by electron probe analysis. During initial collections, mean+/-SEM tubular fluid/plasma (TF/P)(K+) was 1.07 +/-0.05, 1.05+/-0.05, and 1.00+/-0.03 in intact hydropenic (n = 7), saline (n = 6), and acetazolamide (n = 8) groups; fractional reabsorption (FR) of K+ in proximal tubules was 0.35, 0.39, and 0.31 respectively. After saline, (TF/P)(Inul in) fell from 1.81 to 1.34 (P < 0.01); (TF/P)(K+), (TF/P)(Na+), and tubular fluid/ultrafiltrate, (TF/UF)(Ca++) did not change, so that FR of all three ions fell proportionately. After acetazolamide, however, despite a 24% inhibition of FR of Na+ and Ca++, (TF/P)(K+) fell to 0.85+/-0.04 (P < 0.005) so that FR of K+ was unchanged at 0.34. In three corresponding groups of TPTX dogs, similar results were obtained. Acetazolamide (n = 7) inhibited FR of Na+ and Ca++ by 41%, but (TF/P)(K+) fell from 1.03+/-0.03 to 0.89+/-0.04 (P < 0.005) so that FR of K+ was unchanged (0.36-0.34).A separate uphill transport system for K+ in proximal tubules is therefore unmasked by acetazolamide, a drug which selectively inhibits Na+ (and Ca++) reabsorption. Saline, on the other hand, inhibits net reabsorption of all three ions, probably by increasing passive backflux via intercellular channels.

Acetazolamide↗