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Biomedical subjects

V M Buckalew

Publications and source records attributed to V M Buckalew.

At least 73 records · Page 4Linked to original sources
PubMed1981

Chronic renal failure and end-stage renal disease in northwest North Carolina. Importance of analgesic-associated nephropathy.

A retrospective study was undertaken to determine the extent to which analgesic-associated nephropathy (AAN) causes chronic renal failure (CRF) and end-stage renal disease (ESRD). Of 363 cases of CRF diagnosed between 1974 and 1976, 48 were caused by AAN; 14 of 140 cases of ESRD were caused by AAN. Of the 14 patients with ESRD from AAN, 12 initially had ESRD and two progressed to ESRD while continuing consumption of analgesics. The remaining 34 patients who had AAN with CRF discontinued using analgesics and have not progressed to ESRD. Thus, 34 of 36 patients with AAN-CRF who initially did not have ESRD discontinued use of analgesics and have not progressed to ESRD. We conclude that AAN causes a large percentage of CRF and ESRD in our patient population. Early recognition of this entity can prevent progression to ESRD if analgesic consumption is discontinued.

Female↗
PubMed1980

Headache.

Explore the source record for details and available documents.

Analgesics↗
PubMed1980

Analgesic-associated nephropathy and transitional cell carcinoma of the urinary tract.

Epidemiologic studies from Europe suggest that patients with analgesic-associated nephropathy have an increased risk of developing transitional cell carcinoma of the urinary tract. We did a similar epidemiologic study supporting this association. Six of 115 cases of transitional cell carcinoma diagnosed over 3 years had analgesic-associated nephropathy. The patients were predominantly female, younger, and had renal pelvis tumors instead of bladder tumors (P < 0.002), an mortality rate was higher (P < 0.05). In a historical prospective study, 146 patients with interstitial nephritis diagnosed between 1974 and 1976 were divided into those with and those without analgesic-associated nephropathy. In 4 of 84 patients with analgesic-associated nephropathy transitional cell carcinoma has developed. None of the 98 patients without analgesic associated nephropathy have developed transitional cell carcinoma (P < 0.001). These data strongly incriminate analgesic abuse as a risk factor for the development of transitional cell carcinoma.

Adult↗
PubMed1979

Improvement of hypercalciuria, potassium wasting and hyperreninemia in incomplete distal renal tubular acidosis by indomethacin.

A patient with incomplete distal renal tubular acidosis (RTA) demonstrated hypercalciuria, potassium wasting and hyperreninemia. Indomethacin administration resulted in sustained improvement of these abnormalities. The results suggest that overproduction of prostaglandins contributes to hypercalciuria, potassium wasting and hyperreninemia in some patients with RTA and that indomethacin may be useful in treating patients with this disorder.

Acidosis, Renal Tubular↗
PubMed1979

Techniques of renal biopsy.

The diagnostic information obtained by renal biopsy has both diagnostic and therapeutic value in patients with symptoms and signs suggestive of renal parenchymal disease. The clinician must be familiar with the indications and contraindications for the procedure, and is responsible for choosing the most appropriate technique and approach from the various methods available.

Biopsy↗
PubMed1976

Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog.

Vasopressin (VP) was administered for 1 h intravenously to hydropenic, anesthetized dogs in doses of 1.0-1.25 mU/kg per min. In 14 experiments, sodium excretion (UNA V) increased from a mean of 13 +/- 5 to a peak of 96 +/- 21 mueq/min 40 min after beginning infusion (P less than .001). Urine flow and potassium excretion increased from 0.18 +/-.04 ml/min and 20 +/- 2 meuq/min to peak values of 0.6 +/- .08 ml/min and 61 +/- 9 mueq/min, respectively (P less than .001), with no significant increase in glomerular filtration rate. No significant changes in UNA V occurred in eight sham control experiments of in six experiments in which VP was given at 75 muU/kf per min. To test the hypothesis that VP might be natriuretic indirectly by releasing a natriuretic substance, plasms ultrafiltrates were tested for toad bladder antinatriferic activity(AA). During steady-state control, AA was -10 +/- 3%. Thirty and sixty minutes after beginning VP, AA increased to -24 +/- 3% (P less than .05) and -26 +/- 2% (P less than .001), respectiviely. No significant change in plasma AA occurred in either sham controls or in animals given the subnatriuretic VP dose. Incubation of plasma with 1,000 muU/ml VP caused no increase in AA. The data show that VP natriuresis is accompanied by an increase in plasms AA. The results suggest that vasopressin natriuresis in hydropenic dogs at least in part to the release of a humoral inhibitor of renal tubular sodium transport.

Animals↗
PubMed1976

Renin response and angiotensinogen control during graded hemorrhage and shock in the dog.

Hemorrhage and hemorrhagic hypotension have been shown to be potent stimulators of renin release. However, the relationship between angiotensinogen consumption and angiotensinogen production has yet to be completely defined during this type of circulatory stress. Peripheral renin activity increased progressively as the blood pressure was decreased stepwise by hemorrhage to 50 mmHg and remained elevated throughout the shock phase of the experiment. Angiotensinogen did not change from control (809 ng/ml) throughout hemorrhabic hypotension and shock. During hemorrhagic hypotension, with the infusion of the angiotensin antagonist, [1-sarcosine, 8-alanine]angiotensin II, angiotensinogen concentration fell progressively from 693 to 208 ng/ml at 50 mmHg. Intravenous angiotensin II infused continuously after the mean blood pressure reached 50 mmHg significantly elevated plasma angiotensinogen concentration. In conclusion, during hemorrhagic hypotension and shock, the kidney and the liver appeared capable of maintaining elevated plasma renin activity and adequate plasma renin substrate, angiotensinogen, respectively. The mechanism responsible for the maintenance of plasma angiotensinogen is suggested to involve a positive-feedback effect of angiotensin II on the liver.

Angiotensin II↗