TY - JOUR
T1 - Disorders of Potassium Homeostasis
T2 - An Approach Based on Pathophysiology
AU - Kamel, K. S.
AU - Quaggin, S.
AU - Scheich, A.
AU - Halperin, M. L.
PY - 1994
Y1 - 1994
N2 - Disorders of potassium (K+) homeostasis are frequently encountered in clinical medicine and may have serious sequelae, particularly cardiac arrhythmias. Since long-term K+ balance depends on regulation of renal excretion of K+, the focus of this paper is to provide a novel way to analyze the K+ excretory process at the bedside in a noninvasive fashion. A fundamental aim was to incorporate recent new advances in K+ physiology to the clinical analysis of K+ disorders. In so doing, we have tried to replace eponyms and largely descriptive terms with more specific, but hypothetical pathophysiologic diagnoses. The approach we used focuses on an assessment of the components of K+ excretion in vivo. If the rate of excretion of K+ differs from the “expected” value for the stimulus of hypokalemia or hyperkalemia, one should determine whether the fault is with the flow rate and/or the [K+] in the terminal cortical collecting duct. The former is influenced primarily by the rate of excretion of osmoles when antidiuretic hormone acts, whereas the [K+] in the cortical collecting duct is determined by factors that modulate rate of electrogenic reabsorption of Na+ in that segment and its conductance for K+. By examining the extracellular fluid (ECF) volume status, the plasma renin activity, and the renal response to the induction of ECF volume contraction, we attempted to deduce whether the change in electrogenic reabsorption of Na+ was due to an altered Na+ transport or apparent permeability to chloride in the cortical collecting duct. We believe that an approach which draws heavily on pathophysiology can be of practical use at the bedside and, in addition, indicate areas in which more research could be fruitful. To illustrate these points, two clinical cases with hypokalemia and two with hyperkalemia were analyzed. Nevertheless, it is important to emphasize that the approach provided is speculative.
AB - Disorders of potassium (K+) homeostasis are frequently encountered in clinical medicine and may have serious sequelae, particularly cardiac arrhythmias. Since long-term K+ balance depends on regulation of renal excretion of K+, the focus of this paper is to provide a novel way to analyze the K+ excretory process at the bedside in a noninvasive fashion. A fundamental aim was to incorporate recent new advances in K+ physiology to the clinical analysis of K+ disorders. In so doing, we have tried to replace eponyms and largely descriptive terms with more specific, but hypothetical pathophysiologic diagnoses. The approach we used focuses on an assessment of the components of K+ excretion in vivo. If the rate of excretion of K+ differs from the “expected” value for the stimulus of hypokalemia or hyperkalemia, one should determine whether the fault is with the flow rate and/or the [K+] in the terminal cortical collecting duct. The former is influenced primarily by the rate of excretion of osmoles when antidiuretic hormone acts, whereas the [K+] in the cortical collecting duct is determined by factors that modulate rate of electrogenic reabsorption of Na+ in that segment and its conductance for K+. By examining the extracellular fluid (ECF) volume status, the plasma renin activity, and the renal response to the induction of ECF volume contraction, we attempted to deduce whether the change in electrogenic reabsorption of Na+ was due to an altered Na+ transport or apparent permeability to chloride in the cortical collecting duct. We believe that an approach which draws heavily on pathophysiology can be of practical use at the bedside and, in addition, indicate areas in which more research could be fruitful. To illustrate these points, two clinical cases with hypokalemia and two with hyperkalemia were analyzed. Nevertheless, it is important to emphasize that the approach provided is speculative.
KW - Bicarbonaturia
KW - extracellular fluid (ECF) volume
KW - hypertension
KW - potassium
KW - renin
KW - transtubular [K] gradient
KW - urine electrolytes
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U2 - 10.1016/S0272-6386(12)80220-4
DO - 10.1016/S0272-6386(12)80220-4
M3 - Article
C2 - 7942818
AN - SCOPUS:0028081349
SN - 0272-6386
VL - 24
SP - 597
EP - 613
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
IS - 4
ER -