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Biomedical subjects

G Boner

Publications and source records attributed to G Boner.

At least 145 records · Page 8Linked to original sources
PubMed1979

Occult progressive renal damage in the elderly male due to benign prostatic hypertrophy.

A review of the case histories of 345 patients who underwent protatectomy showed that 1.7 percent (6 patients) had "occult and progessive renal damage" secondary to prostatic hypertrophy. All these men were over the age of 60 and the disturbances in micturition were so mild that the patients were unaware of, or chose to ignore them. The presenting symptoms were nonspecific and included generalized weakness, anorexia, nausea, constipation, and weight loss. Investigation revealed impaired renal function of varying degrees. Prostatectomy was associated with a dramatic improvement in all 6 patients. Physicians should be aware of the clinical entity of occult and progressive renal damage secondary to obstruction of the bladder outlet, especially in the elderly male. Uremia can develop with minimal urinary symptoms. Elderly men often suppress or deny their symptoms because of the fear of operation.

Age Factors↗
PubMed1977

Dacron arterio-venous interposition graft: an access to circulation in patients on chronic hemodialysis.

In a small percentage of cases, conventional a-v fistulae of the Brescia-Cimino type fail to provide long-term access facilities for chronic hemodialysis. When homologous venous interposition grafts are not available, the surgeon is forced to seek foreign interposition material. In three instances woven dacron arterio-venous interposition grafts were successfully constructed in the thigh, and uneventful hemodialysis was accomplished in all 3 patients.

Arteriovenous Shunt, Surgical↗
PubMed1975

Diuretics, urate excretion and sodium reabsorption: effect of acetazolamide and urinary alkalinization.

The uricosuric properties of acetazolamide were investigated in order to elucidate the relationship between changes in proximal tubular sodium reabsorption and urate excretion in man. Acetazolamide produced a modest uricosuric response which was not suppressible by pyrazinamide. Alkalinization of the urine with sodium bicarbonate elicited an even smaller increment in the urate clearance. If urinary alkalinization does play a role in the uricosuric response to acetazolamide, it probably decreases urate reabsorption within the distal nephron. The present studies, when taken together with previous work, suggest that alterations in proximal tubular sodium and water reabsorption probably do not play an important role in the normal control of urate excretion or in the pathogenesis of hyperuricemic states. Diuretic-induced hyperuricemia occurring during extracellular fluid volume depletion probably results from either diminished tubular secretion of urate, accelerated postsecretory urate reabsorption, or both.

Acetazolamide↗
PubMed1973

Origins of the uricosuric response.

The acute effects of intravenous (i.v.) probenecid and chlorothiazide on renal urate handling were investigated in paired studies in normal men. Uricosuric responses to these agents were compared in the same subjects, both without and with pyrazinamide (PZA) pretreatment. Assuming that PZA selectively inhibits the tubular secretion of urate and that uricosuric agents act by increasing the excretion of filtered urate, then the uricosuric responses (the increment in urate excretion or clearance) should have been unaffected by PZA. Defined in this manner, however, uricosuric responses to probenecid and chlorothiazide were significantly decreased after PZA pretreatment. In order to determine whether PZA diminished other renal actions of chlorothiazide, changes in sodium and inorganic phosphorus excretion were examined. Chlorothiazide produced equivalent natriuretic and phosphaturic responses after PZA pretreatment, indicating that PZA does not interfere with at least some of the renal actions of chlorothiazide. In separate studies, PZA depressed urate excretion by at least 68% during the maintenance of chlorothiazide-induced natriuresis and phosphaturia, suggesting that chlorothiazide does not diminish the anti-secretory action of PZA. The results suggest that probenecid and chlorothiazide may derive their uricosuric properties by facilitating the excretion of both filtered and secreted urate. Possibly, increased excretion of secreted urate might occur through modulation of urate reabsorption at a site distal to tubular secretion, rather than by the direct acceleration of secretory transport. However, PZA-induced interference with the actions of probenecid and chlorothiazide on renal urate transport mechanisms cannot be excluded as a possible explanation for the present results.

Adult↗