By giving diazoxide intravenously and furosemide orally the diastolic blood pressure was kept under 110 mm Hg and the urinary output over 1 L/day for a 2-week period in 25 hypertensive patients with azotemia. During the first 2 weeks of treatment three patients died. Although the 40% decrease in mean arterial pressure in the remaining patients was associated with immediate improvement in the cardiovascular status, for example, clearing of congestive heart failure and papilledema, there was a 19% average increase in BUN and 17% average increase in serum creatinine values. Three months later, however, maintenance of the reduced arterial pressure was associated with average reductions of 24 mg/1100 ml in BUN and of 2.8 mg/100 ml in serum creatinine below control values. Each of the patients who remained on therapy continued to do well. Twenty-six months later six additional patients had died. In the remaining 16 patients the average mean arterial pressure was 117 mm Hg; papilledema had cleared; the average concentration of BUN was 22 mg/100 ml; the average serum creatinine was 1.8 mg/ 100 ml.
The immediate fall in arterial pressure following furosemide in the 17 hypertensive patients studied was asociated with a decrease in plasma volume, cardiac output, and extracellular fluid volume, and an increase in urinary sodium excretion. A glucose infusion administered at the trough of hypotension in an amount exceeding the urinary output resulted in the return of arterial pressure to control levels in each patient. Although an increase in plasma volume was noted in each patient, it was significantly below control levels. The central venous pressure, cardiac output, and state of negative sodium balance following the glucose infusion remained unchanged, but the extracellular fluid volume had re-expanded. It would seem that the changes in arterial pressure either after furosemide or during the glucose infusion were related to changes in extracellular fluid. The fact that a decreased pressor response to norepinephrine following furosemide was associated with a decrease in extracellular fluid and the fact that expansion of extracellular fluid with glucose restored the pressor response to normal further document the importance of the extracellular fluid in the regulation of arterial pressure.
accelerated hypertension has changed markedly in the past decade. As recently as the mid 1960's it was routinely taught that azotemic patients with hypertension should be treated conservatively and that if the blood urea nitrogen was greater than 60 mg/100 ml no antihypertensive therapy was indicated.' It was not until 1967 that Woods and Blythe2 hypothesized that patients with malignant hypertension and azotemia died before healing of the renal arteriolitis could occur. The pathogenesis of malignant nephrosclerosis in accelerated hypertension has been worked out in several experimental models3-6 and it has been adequately demonstrated that the renal lesions in malignant hypertension are the direct result of the elevated arterial blood &dquo; pressure and that sustained high levels of blood pressure cause a further deterioration of existing renal function.&dquo; The landmark study of Woods and Blythe demonstrated that intensive antihypertensive therapy of the azotemic patient with malignant hypertension could result in improved survival and some return of renal function.2 Scattered reports throughout the medical literature have documented that patients with malignant hypertension and severe functional renal impairment may have at least some return of renal function with medical control of the arterial pressure.'-11 Recent documentation with serial renal biopsies have also documented resolution of the acute pathologic changes associated with malignant hypertension.l2Previous studies from this laboratory have shown that intravenous administration of diazoxide and furosemide to patients with accelerated azotemic hypertension resulted in prompt and effective control of arterial blood pressure, clearing of congestive heart failure, and improvement in neuro-retinal status.&dquo; During or immediately after this aggressive therapy, the renal function deteriorated in most of the patients as witnessed by a rise in BUN and serum creatinine. After the acute phase of therapy with diazoxide and furosemide, the patients were maintained on standard oral antihypertensive agents and oral furosemide. The beneficial effects of a reduction in arterial pressure were noted to persist, however, the initial deleterious effects of the decreased renal function gradually improved and at the end of nearly five years of therapy there was significant improvement in renal function. The present report describes the longterm follow-up of these original 25 patients five years after their initial therapy for accelerated azotemic hypertension.
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