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Medline ® Abstracts for References 91-93

of 'Causes and evaluation of hyperkalemia in adults'

91
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Impaired renal tubular potassium secretion in sickle cell disease.
AU
DeFronzo RA, Taufield PA, Black H, McPhedran P, Cooke CR
SO
Ann Intern Med. 1979;90(3):310.
 
We examined renal tubular function in six patients with sickle cell hemoglobin. All had normal inulin and para-aminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (U,V) was significantly lower in sickle cell patients than in control subjects, and the percentage of potassium load excreted in 5 h was markedly reduced. Urinary potassium excretion after sodium sulfate infusion was also markedly reduced in sickle cell patients compared to control subjects. After 40 mg of oral furosemide, U,V was also diminished in sickle cell patients. Plasma aldosterone response to ACTH and intravenous potassium was similar to that of control subjects. Plasma renin activity increased normally after volume contraction. We conclude that sickle cell patients have a defect in their ability to excrete an acute potassium load that cannot be attributed to abnormal renin or aldosterone secretion. Overall potassium homeostasis is maintained by extrarenal mechanisms during acute potassium loading.
AD
PMID
92
TI
Pathophysiology of potassium absorption and secretion by the human intestine.
AU
Agarwal R, Afzalpurkar R, Fordtran JS
SO
Gastroenterology. 1994;107(2):548.
 
When normal people ingest 90 mEq/day of K+ in their diet, they absorb about 90% of intake (81 mEq) and excrete an equivalent amount of K+ in the urine. Normal fecal K+ excretion averages about 9 mEq/day. The vast majority of intestinal K+ absorption occurs in the small intestine; the contribution of the normal colon to net K+ absorption and secretion is trivial. K+ is absorbed or secreted mainly by passive mechanisms; the rectum and perhaps the sigmoid colon have the capacity to actively secrete K+, but the quantitative and physiological significance of this active secretion is uncertain. Hyperaldosteronism increases fecal K+ excretion by about 3 mEq/day in people with otherwise normal intestinal tracts. Cation exchange resin by mouth can increase fecal K+ excretion to 40 mEq/day. The absorptive mechanisms of K+ are not disturbed by diarrhea per se, but fecal K+ losses are increased in diarrheal diseases by unabsorbed anions (which obligate K+), by electrochemical gradients secondary to active chloride secretion, and probably by secondary hyperaldosteronism. In diarrhea, total body K+ can be reduced by two mechanisms: loss of muscle mass because of malnutrition and reduced net absorption of K+; only the latter causes hypokalemia. Balance studies in patients with diarrhea are exceedingly rare, but available data emphasize an important role for dietary K+ intake, renal K+ excretion, and fecal K+ losses in determining whether or not a patient develops hypokalemia. The paradoxical negative K+ balance induced by ureterosigmoid anastomosis is described. The concept that fecal K+ excretion is markedly elevated in patients with uremia as an intestinal adaptation to prevent hyperkalemia is analyzed; we conclude that the data do not convincingly show the existence of a major intestinal adaptive response to chronic renal failure.
AD
Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas.
PMID
93
TI
New clinical approach to evaluate disorders of potassium excretion.
AU
West ML, Marsden PA, Richardson RM, Zettle RM, Halperin ML
SO
Miner Electrolyte Metab. 1986;12(4):234.
 
A new clinical approach to patients with disorders of potassium excretion is reported. This approach uses a urinary index, the ratio of potassium concentrations in the urine to vein after adjusting the urine potassium concentration for medullary water abstraction. This index provides a semiquantitative assessment of the apparent transtubular potassium concentration gradient (TTKG) in the major distal nephron segment where potassium is secreted. Three clinical situations are presented where the use of this index provided a better indication of the renal action of mineralocorticoids than did the traditional approach; in each case, the presence of mineralocorticoids was known as drugs with this action were administered. We emphasize that use of this index is restricted to situations where the urine is not hypotonic and distal nephron sodium delivery is not limiting for potassium secretion (greater than 25 mM, twice the sodium concentration required for maximum potassium transport at this nephron site).
AD
PMID