Renal insufficiency in treated essential hypertension.

We analyzed the clinical courses of 94 patients with treated primary hypertension and initially normal serum creatinine concentrations (less than or equal to 133 mumol per liter [less than or equal to 1.5 mg per deciliter]) who were followed for a mean (+/- SD) of 58 +/- 34 months (range, 12 to 174) to determine the frequency with which renal function deteriorated and the factors associated with deterioration. Fourteen patients (15 percent) had an increase in serum creatinine concentrations (greater than or equal to 35 mumol per liter [greater than or equal to 0.4 mg per deciliter]); in 16 percent of the 61 patients with apparently good control of blood pressure, the serum creatinine concentration rose 59 +/- 33 mumol per liter (0.67 +/- 0.38 mg per deciliter). Despite good control of diastolic blood pressure (less than or equal to 90 mm Hg), black patients were twice as likely as white patients to have elevations in serum creatinine (23 percent vs. 11 percent). Stepwise discriminant function analysis showed that a significant rise in the serum creatinine concentration was most likely to occur in association with older age, black race, a higher number of missed office visits, and employment as a laborer. We conclude that although renal function was preserved in 85 percent of patients with treated hypertension, it may deteriorate in some patients despite good blood-pressure control. Our observations may partly explain why hypertension, particularly among black persons, remains a leading cause of renal disease in the United States.

[1]  R. Prineas,et al.  All-cause mortality in the Hypertension Detection and Follow-up Program: findings for the whole cohort and for persons with less severe hypertension, with and without other traits related to risk of mortality. , 1986, Progress in cardiovascular diseases.

[2]  E. Roccella,et al.  Epidemiologic considerations in defining hypertension. , 1987, The Medical clinics of North America.

[3]  S. Rostand,et al.  Racial differences in the incidence of treatment for end-stage renal disease. , 1982, The New England journal of medicine.

[4]  T. Strasser,et al.  MORTALITY AND MORBIDITY RESULTS FROM THE EUROPEAN WORKING PARTY ON HIGH BLOOD PRESSURE IN THE ELDERLY TRIAL , 1985, The Lancet.

[5]  J. E. Woods Renal function in essential hypertension , 1983 .

[6]  J. Cutler,et al.  The 1984 Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. , 1984, Archives of internal medicine.

[7]  F. Luft,et al.  Sodium sensitivity and resistance in normotensive humans. , 1982, The American journal of medicine.

[8]  W. Pettinger,et al.  Renal function during long-term treatment of hypertension with minoxidil: comparison of benign and malignant hypertension. , 1980, Annals of internal medicine.

[9]  F. Dunn,et al.  Greater renal vascular involvement in the black patient with essential hypertension. A comparison of systemic and renal hemodynamics in black and white patients. , 1984, Mineral and electrolyte metabolism.

[10]  Easterling Re Racial factors in the incidence and causation of end-stage renal disease (ESRD). , 1977 .

[11]  A. H. Norris,et al.  The effect of age on creatinine clearance in men: a cross-sectional and longitudinal study. , 1976, Journal of gerontology.

[12]  P. Eggers,et al.  Effect of transplantation on the Medicare end-stage renal disease program. , 1988, The New England journal of medicine.

[13]  D. Richardson,et al.  CHANGES IN RENAL FUNCTION ASSOCIATED WITH DRUG OR PLACEBO THERAPY OF HUMAN HYPERTENSION. , 1964, The American journal of medicine.

[14]  W. Mroczek,et al.  The Value of Aggressive Therapy in the Hypertensive Patient with Azotemia , 1969, Circulation.

[15]  M. Blaufox,et al.  The effect of treatment on mortality in "mild" hypertension: results of the hypertension detection and follow-up program. , 1982, The New England journal of medicine.

[16]  B. Brenner,et al.  Therapeutic advantage of converting enzyme inhibitors in arresting progressive renal disease associated with systemic hypertension in the rat. , 1986, The Journal of clinical investigation.

[17]  R. Winickoff,et al.  The persistent problem of poor blood pressure control. , 1987, Archives of internal medicine.

[18]  R. A. Norman,et al.  Arterial pressure regulation. Overriding dominance of the kidneys in long-term regulation and in hypertension. , 1972, The American journal of medicine.

[19]  J. Brentjens,et al.  Renal lesions and proteinuria in the spontaneously hypertensive rat made normotensive by treatment. , 1981, Kidney international.

[20]  N. Shulman,et al.  Financial cost as an obstacle to hypertension therapy. , 1986, American journal of public health.

[21]  D. Sackett,et al.  Persistence of reduction in blood pressure and mortality of participants in the Hypertension Detection and Follow-up Program. Hypertension Detection and Follow-up Program Cooperative Group. , 1988, JAMA.

[22]  W. Kannel,et al.  Downward trend in cardiovascular mortality. , 1981, Annual review of medicine.

[23]  Effects of treatment on morbidity in hypertension. Results in patients with diastolic blood pressures averaging 115 through 129 mm Hg. , 1967, JAMA.

[24]  D F DAVIES,et al.  Age changes in glomerular filtration rate, effective renal plasma flow, and tubular excretory capacity in adult males. , 1950, The Journal of clinical investigation.

[25]  K Hirschhorn,et al.  Letter: Immunotherapy for colorectal cancer. , 1976, Lancet.