Gastrointestinal and renal excretion of potassium in African-Americans and White Americans.

OBJECTIVE: Several studies have confirmed the remarkable observation that cumulative urinary potassium (K(+)) excretion is less in African-Americans than White Americans even when identical amounts of potassium are provided in the diet. This study was designed to examine whether this decrease in urinary potassium could be compensatory to an increase in gastrointestinal excretion of potassium in African-Americans. METHODS: Twenty-three young, healthy, normotensive participants of both sexes and races were placed on a fixed diet of 100 mEq per day of K(+) and 180 mEq per day of sodium (Na(+)) for 9 days. All urine and stool were collected daily and analyzed for electrolytes. Blood was obtained for determination of electrolytes, blood urea nitrogen (BUN), creatinine, glucose, insulin, renin, and aldosterone at the beginning and at the end of the study period. RESULTS: Cumulative urinary excretion of K(+) was significantly less in African-Americans (609 ± 31 mEq) compared with White Americans (713 ± 22 mEq, P = 0.015). There was no significant racial difference, however, in the cumulative gastrointestinal excretion of K (105 ± 11 versus 95 ± 9 mEq, P = 0.28) in African-Americans versus White Americans, respectively. CONCLUSION: The racial difference in urinary K(+) handling manifested by decreased excretion of K(+) in African-Americans cannot be attributed to an increase in net gastrointestinal excretion of this cation.

Racial differences in potassium disposal.

BACKGROUND: African Americans appear relatively potassium (K(+))-deficient compared with Caucasian Americans whether on unregulated diets or on diets controlled for K(+) content. METHODS: To determine whether extrarenal K(+) disposal was affected by race, KCl (0.5 mEq/kg in 0.9% saline) was infused over 48 minutes to 12 African American and 12 Caucasian American normotensive, healthy subjects. Identical infusions were administered before and after 10 days of fixed electrolyte intake. In addition to serum K(+), glucose, insulin, renin, and aldosterone were measured in blood, and K(+) and sodium (Na(+)) in urine voided spontaneously during the infusions. Data were analyzed using a two-factor analysis of variance (ANOVA) with repeated measures. RESULTS: Basal serum K(+) did not differ between races (African American 3.97 +/- 0.06 mEq/L and Caucasian American 3.98 +/- 0.05, P= NS). The rise in serum K(+) during the infusion and the area under the curve of serum K(+) over the 3.5 hours of observation were both greater in African American (African American +0.82 +/- 0.07 mEq/L and Caucasian American +0.61 +/- 0.06, P= 0.001; and African American 6.9 +/- 0.5 units and Caucasian American 5.1 +/- 0.6, P= 0.0012). The 10-day period of controlled intake did not abolish these differences. Aldosterone at baseline was lower and insulin was higher in African Americans at the end of the infusion. Urinary K(+), plasma glucose, and renin levels did not differ between African Americans and Caucasian Americans. CONCLUSION: Disposal of an intravenous (iv) K(+) load is decreased in African Americans compared with Caucasian Americans, which may reflect decreased Na(+),K(+)-ATPase activity in African Americans in vivo.

Juxtaglomerular apparatus tumor: a rare, surgically correctable cause of hypertension.

Although uncommon, presentation of juxtaglomerular cell tumor is distinct and should allow a correct preoperative diagnosis in most patients. Typical clinical presentations include headaches, polyuria, or isolated, asymptomatic, severe hypertension. The diagnosis of a juxtaglomerular apparatus (JGA) tumor typically results from identification of plasma renin levels two- to sevenfold greater than the normal value. Although JGA tumors are considered benign, with no reports of metastases or recurrence, they are potentially lethal if left untreated. Surgical excision is curative.