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PubMed1978

Ultrastructural changes of colonic mucosa in patients with chronic laxative misuse.

Laxatives are amongst the most widely used and misused drugs. Especially the "irritant chathartics" are associated with severe cell poisoning. Electrolyte disturbances like potassium deficiency may occur as a result of enhanced potassium secretion into the colon. Ultrastructural studies of patients with chronic laxative misuse demonstrate, that this functional disorder is correlated with damage of the colonic epithelial cells consisting in stereotyped lesions as changes in microvilli, reduction and structural defects of cytoplasmic organelles and an increase of lysosomes and dense bodies. The lesions have a focal distribution and may explain the potassium loss from a morphological point of view.

Cathartics↗
PubMed1987

Effect of magnesium salt anions on potassium balance in normal and magnesium-depleted rats.

Potassium depletion often accompanies clinically significant magnesium depletion, and magnesium replacement is most frequently undertaken with magnesium sulfate. However, inorganic sulfate acts as a nonreabsorbable anion in the distal nephron, an effect that could potentially interfere with the correction of any associated potassium deficiency. We have investigated the effect of a variety of magnesium salts, including sulfate and nonsulfate forms, on cation balance and skeletal muscle ion composition in normal and magnesium-depleted rats. Even modest amounts of dietary sulfate increased the urinary excretion of potassium in both normal and magnesium-depleted rats. During a 7-day feeding period, diets containing MgSO4 or MgO with an equivalent amount of Na2SO4 resulted in significantly greater urinary excretion of potassium than diets without sulfate. In normal animals, this kaliuresis did not produce hypokalemia or muscle potassium depletion. Magnesium-deficient feeding produced magnesium depletion, kaliuresis, and a decline in both plasma and muscle potassium content. When magnesium was restored to the diet without sulfate, urinary potassium excretion decreased, and both magnesium and potassium deficits were corrected. However, when magnesium refeeding included sulfate salts, magnesium stores returned to normal, whereas the kaliuresis and potassium depletion persisted. When accompanied by a high sodium intake, the kaliuretic effect of sulfate was increased.

Animals↗
PubMed1990

Protective effect of KCl loading in gentamicin nephrotoxicity.

Aminoglycoside nephrotoxicity in experimental animals can be reduced by calcium loading, inducing diabetes, and giving thyroid hormone, while a potassium deficient diet enhances aminoglycoside nephrotoxicity. This study investigated whether potassium loading protects against gentamicin nephrotoxicity in the rat. In part I, group GK ate a diet containing 3.5% potassium and drank 0.2 mol/L KCl. Pair-fed rats eating a standard diet, group G, ate a 1% potassium diet and drank water. After 10 days, each group received gentamicin subcutaneously, 60 mg/kg twice daily for 8 days. The control groups, K and C, received the high or normal potassium diet, respectively. To control for a protective effect from a high solute load, the effect of equimolar NaCl loading was studied in group GNa and Na. At the end of the 8 days of gentamicin, inulin clearance was significantly higher in GK compared with G(0.6 +/- 0.1 v 0.3 +/- 0.1 mL/min per 100 g body weight [BW], P less than 0.05), but group GNa (0.4 +/- 0.1 mL/min per 100 g BW) was not different from group G. Morphological studies demonstrated that potassium-loaded rats (group GK) had significantly less proximal tubular necrosis compared with rats on a standard potassium diet, group G. Sodium loading did not protect against cellular necrosis. Part II studied renal function, cortical Na,K-adenosine triphosphatase (ATPase) and gentamicin accumulation after 2 days of gentamicin to determine the early functional and biochemical effects of potassium loading before overt renal functional impairment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Response of spring rape (Brassica napus var. oleifera L.) to inoculation with plant growth promoting rhizobacteria containing 1-aminocyclopropane-1-carboxylate deaminase depends on nutrient status of the plant.

Responses of rape (Brassica napus var. oleifera L.) to inoculation with plant growth promoting rhizobacteria, Pseudomonas putida Am2, Pseudomonas putida Bm3, Alcaligenes xylosoxidans Cm4, and Pseudomonas sp. Dp2, containing 1-aminocyclopropane-l-carboxylate (ACC) deaminase were studied using growth pouch and soil cultures. In growth pouch culture, the bacteria significantly increased root elongation of phosphorus-sufficient seedlings, whereas root elongation of phosphorus-deficient seedlings was not affected or was even inhibited by the bacteria. Bacterial stimulation of root elongation of phosphorus-sufficient seedlings was eliminated in the presence of a high ammonia concentration (1 mM) in the nutrient solution. Bacterial effects on root elongation of potassium-deficient and potassium-sufficient seedlings were similar. The bacteria also decreased inorganic phosphate content in shoots of potassium- and phosphorus-sufficient seedlings, reduced ethylene production by phosphorus-sufficient seedlings, and inhibited development of root hairs. The effects of treatment with Ag+, a chemical inhibitor of plant ethylene production, on root elongation, ethylene evolution, and root hair formation were similar to bacterial treatments. The number of bacteria on the roots of phosphorus-deficient seedlings was not limited by phosphorus deficiency. In pot experiments with soil culture, inoculation of seeds with bacteria and treatment with aminoethoxyvinylglycine, an inhibitor of ethylene biosynthesis in plants, increased root and (or) shoot biomass of rape plants. Stimulation of plant growth caused by the bacteria was often associated with a decrease in the content of nutrients, such as P, K, S, Mo, and Ba, in shoots, depending on the strain used. The results obtained show that the growth-promoting effects of ACC-utilizing rhizobacteria depend significantly on the nutrient status of the plant.

Alcaligenes↗
PubMed1981

Effect of restricted potassium intake on its excretion and on physiological responses during heat stress.

The effect of low potassium (K+) intake on its excretion, concentration in sweat and on physiological responses during heat stress was evaluated on eight Indian male soldiers in winter months at Delhi. After a stabilization period of 3 days on each diet, i.e., 85 mEq of K+/d (diet I, normal), 55 mEq of K+/d (diet II), and 45 mEq of K+/d (diet III), the physiological responses and the sodium and potassium concentrations in sweat, plasma, RBC, and urine were measured when the subjects were exposed to heat for 3 h daily in a climatic chamber maintained at 40 degrees C DB and 32 degrees C WB. The subjects worked in the chamber at the rate of 465 W/h for 20 min periods with 40 min rest between each period of exercise. The whole body sweat was collected after the spell of work and was analysed for sodium and potassium levels. Throughout the study the subjects remained on positive sodium balance except on day 4 in diet III. Fluid balance also remained positive while potassium balance was negative in subjects on diet II and diet III. There was no significant change in heart rate, sweat volume, oral temperature, sodium, and potassium concentrations in plasma and RBC during the entire period of the study. Even in the subjects with negative potassium balance there was no change in the sodium and potassium concentrations in sweat during exercise in heat. The only evidence of potassium conservation was a reduced excretion in urine. Out of the eight subjects, in one subject there was a flattening of the 'T' wave in the ECG and reduction in amplitude of the 'T' wave in two more subjects. As there is no reduction in sweat potassium concentration and the urine volume is low, the marginal level of reduced excretion of potassium in urine with a high rate of sweating (7-81) in subjects doing work in the tropics, there is every likelihood of potassium deficiency if a liberal intake is not ensured. In our earlier studies (Malhotra et al. 1976) we found that the concentration of potassium (K+) in sweat is much higher than in plasma even in acclimatised subjects. A large amount of K+ is therefore likely to be lost in sweat during exposure to heat. In that study there was no evidence of a reduction in K+ concentration in the sweat or urine upon repeated exposure of the subjects to heat, indicative of a compensatory mechanism for conservation of K+ losses. However, these earlier studies were done on subjects who were on a normal diet which contained 75-80 mEq of K+ per day. Since a compensatory mechanism may be triggered only when the body K+ becomes dificient and not earlier, as is the case with sodium (Malhotra et al. 1959), we have now investigated the effects of a sequential reduction of reduced dietary K+ on the dermal and urinary losses of K+. The effects of K+ deficiency on the physiological responses to heat have also been studied. The results of these studies are reported here.

Adult↗
PubMed1978

Fetomaternal potassium relations in the rat on the twentieth day of gestation. II. Effects of maternal hypokalemia.

Time-corrected measurements of transplacental and transamniotic electrical potentials were made in potassium-deficient rats on the 20th day of gestation. These averaged 6.4 mV and 2.0 mV, respectively, in the deficient group as compared with 14.3 and 18.4, respectively, in the controls. The measured maternal potassium concentrations were 2.8 mEq/liter in the K+-restricted animals and 4.8 mEq/liter in the controls. These figures were substituted into the Nernst equation in order to predict fetal concentrations in plasma. Similar predictions were made for amniotic fluid assuming equilibrium with fetal plasma. Predicted concentrations in fetal plasma were 2.3 mEq/liter in the deficient animals and 2.8 mEq/liter in the controls. By contrast, observed time-corrected potassium concentrations in fetal plasma were 4.0 mEq/liter in deficient animals and 2.9 mEq/liter in controls. Amniotic fluid values were predicted to be 4.7 mEq/liter in deficient and 2.5 mEq/liter in control animals. These values were compared with the observed averages in amniotic fluid of 4.7 and 4.6 mEq/liter in the deficient and control groups, respectively.

Amniotic Fluid↗
PubMed1979

The syndrome of inappropriate antidiuretic hormone secretion (SIADH): pathophysiologic mechanisms in solute and volume regulation.

1. Studies on eight patients were performed to clarify the mechanism(s) of altered sodium metabolism and volume regulation in SIADH. The mechanism controlling water excretion was also studied to determine whether there is evidence that altered osmoregulation may be the basis for inappropriate ADH secretion in some patients. 2. These studies show that cumulative sodium balance and aldosterone secretion rates in patients with SIADH are negatively correlated with water intake. There is also a negative correlation between aldosterone secretion and urinary sodium excretion. In the absence of normal urine diluting ability, this increased excretion of sodium becomes a mechanism that allows an increased quantity of water to be excreted despite the persistence of an ADH effect on the renal tubules. 3. Within the range of hyponatremia observed in our studies, changes in serum sodium concentration were accounted for by changes in solute and water balance. One patient, who was potassium deficient during the studies, retained large quantities of sodium and potassium that could not be accounted for by an increase in either serum osmolality or body weight. These observations suggest that intracellular osmotically active solute is either lost or "inactivated" in some manner as intracellular potassium is replenished. 4. Marked impairment of urine diluting ability was demonstrated in all patients. However, two patients with SIADH associated with pulmonary tuberculosis exhibited graded responses to water loading, which suggests that ADH secretion may have been suppressed as serum osmolality was progressively reduced. Whether this can be attributed to a basic alteration or "re-setting" or osmoreceptor function, or is merely an indication that greater than normal reductions of serum osmolality are required to inhibit potent nonosmotic stimuli, remains to be determined.

Adult↗
PubMed1984

Effects of potassium supplementation on insulin binding and insulin action in human obesity: protein-modified fast and refeeding.

To investigate the role of potassium deficiency in the development of glucose intolerance during caloric deprivation, potassium balance was maintained within normality with oral potassium supplementation in a group of obese subjects who underwent protein-modified fast and the results of the study of carbohydrate metabolism (oral glucose test, insulin receptors on monocytes and peripheral glucose utilization as assessed by euglycaemic clamp) were compared with those obtained in a group of obese subjects admitted to protein-modified fast without potassium supplementation. Caloric deprivation without oral potassium supplementation was followed by a negative potassium balance and a decrease of serum potassium levels; a decrease of the peripheral levels of insulin along with an increase in insulin receptors and a striking reduction of peripheral glucose utilization were also observed. The maintenance of normal potassium balance and normal serum potassium levels with oral potassium-chloride supplementation was associated with higher peripheral levels of insulin (P less than 0.01) and improvement of peripheral glucose utilization (P less than 0.01) whereas the binding of insulin to monocytes was unchanged. The data suggest that potassium depletion during protein-modified fast causes a decrease of the peripheral levels of insulin and a resistance to insulin action at the postreceptors sites which is reversed by potassium supply.

Adult↗
PubMed1992

Heart failure and electrolyte disturbances.

Electrolyte abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. Magnesium and potassium deficiencies play an important role in the development of cardiac arrhythmias. Magnesium is essential for the maintenance of intracellular potassium concentration. Although there are conflicting data regarding the prevalence of hypomagnesemia in patients with chronic heart failure (the values range from 7-37%), multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal controls. As magnesium and potassium are mainly intracellular ions, measurements in serum or plasma are of limited value to assess magnesium status. There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for mononuclear cells or erythrocytes or for myocardial and skeletal muscle. Loop diuretics (e.g. furosemide) are supposed to cause a substantial loss of both magnesium and potassium in the plasma and intracellular space. The potassium-sparing diuretics amiloride and triamterene are reported to also exert magnesium-sparing effects. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion. Low magnesium and potassium concentrations increase cardiac glycoside toxicity. In contrast, elevated levels of magnesium decrease the sensitivity of human myocardium to antiarrhythmogenic actions of cardiac glycosides, without affecting maximally developed tension. Moreover, magnesium increases binding affinity of cardiac glycosides to the receptor. The antiarrhythmic action of magnesium is suspected to be mediated by a reduced sensitivity to electrophysiological changes induced by Ca2+, thus indicating Ca2+ antagonistic properties of magnesium. Magnesium deficiency has also been implicated in sudden death, notably in patients with congestive heart failure. Therefore, when treating congestive heart failure, one must consider how to prevent depletion of electrolytes or how to replete potassium and magnesium in deficiency states.

Arrhythmias, Cardiac↗
PubMed1976

Asymptomatic chronic hypomagnesemia and hypokalemia in a child: Cell membrane disease.

An 8-year-old boy was followed for four years because of chronic hypomagnesemia and hypokalemia. THe clinical manifestations were episodic and characterized by spontaneous carpopedal spasm. There were no other signs of magnesium or potassium deficiency. Metabolic studies revealed that the urinary exceretion of magnesium and potassium was elevated in relation to the serum level, but appropriate for a normal boy of that age. No abnormality was detected in the renin-angiotensin-aldosterone system, and the renal functions were normal. Various therapeutic attempts (oral magnesium and/or potassium supplements, spironolactone) failed to correct the abnormal serum concentrations of magnesium and potassium. This disease may represent a defect in the maintenance of a normal gradient between intra-and extracellular magnesium and potassium.

Aldosterone↗
PubMed1985

In vivo and in vitro studies of urinary concentrating ability in potassium-depleted rabbits.

The factors responsible for the urinary concentrating defect associated with the potassium-depleted (KD) state are uncertain. The present studies were designed to, first, determine whether a urinary concentrating defect exists in potassium-depleted rabbits and, second, to use the technique of in vitro perfusion to evaluate directly the antidiuretic hormone (ADH) responsiveness of cortical collecting tubules (CCT) in this setting. Feeding female New Zealand White rabbits a potassium-deficient diet for 2 wk caused a significant fall in plasma potassium levels in both the ad-libitum and controlled water intake groups (P less than 0.001). Muscle potassium content after 2 wk of potassium restriction fell from 45.6 +/- 0.9 to 29.0 +/- 1.2 meq/100 g fat-free dry solids (P less than 0.001). Renal papillary sodium content fell significantly from a control value of 234.6 +/- 8.0 to 182.46 +/- 10.0 meq/kg H2O after 2 wk of potassium restriction. Maximal urinary osmolality measured after 12 h of dehydration and 1.25 U pitressin IM was significantly decreased in rabbits after 2 wk of potassium restriction in both the ad-libitum and controlled water intake groups (P less than 0.001). The relationship between plasma potassium concentration and maximum urinary osmolality was significantly correlated in both the ad-libitum and controlled water intake groups, r = 0.73 and 0.68 (P less than 0.001), respectively. In addition, refeeding KD rabbits with normal chow for 1 wk resulted in normalization of both plasma potassium levels and urinary concentrating ability. CCT from control and KD rabbits were perfused in vitro at 25 degrees C. The hydraulic conductivity coefficient, Lp, was significantly reduced at all doses of ADH tested in tubules from KD rabbits when compared with control tubules. In addition, the maximal hydraulic conductivity in tubules from KD rabbits when tested with 200 microU/ml ADH at 37.5 degrees C was only 23% of control values (P less than 0.05). Furthermore, this reduced ADH responsiveness persisted when the bath potassium was elevated from 5 to 20 mM. The reflection coefficient for NaCl when compared with raffinose was 0.91 in tubules from KD animals. Thus, these data suggest that the ADH-resistant urinary concentrating defect associated with potassium depletion is due, at least in part, to a diminished responsiveness of the CCT to ADH. Therefore, further studies were designed to investigate the cellular steps involved in this abnormal response. There was no difference in the 8-para-chlorophenylthio cyclic AMP induced hydroosmotic response between CCT from KD and control rabbits. Since the cAMP-induced hydroosmotic response was similar between KD and control CCT, experiments were performed to evaluate the contribution of phosphodiesterase (PDIE) activity by using the potent PDIE inhibitor isobutylmethylxanthine (10(-4) and 10(-3)M) in the presence of ADH (200 U/ml). Although Lp was increased by PDIE inhibition in CCT from both control and KD animals, the overall hydroosmotic response in CCT from KD rabbits was still significantly reduced when compared with controls. The final experiments used forskolin to evaluate further the adenylate cyclase complex. The resulting hydroosmotic response in CCT from KD rabbits was almost identical to that obtained in controls. In conclusion, these data suggest that the decreased responsiveness of CCT from KD rabbits to ADH involves a step at or proximal to the stimulation of the catalytic subunit of adenylate cyclase, and that PDIE activity makes no contribution to this abnormal hydroosmotic response.

Animals↗
PubMed1982

Aspects of hypertension among blacks.

The universal prevalence of arterial hypertension among Blacks is no longer disputed, although there still remain unanswered questions. Hypertension among Blacks is nearly always primary (85% of cases), while the secondary form is synonymous with some type of renal disorder. A few 'associations' of hypertension exist. Diet may be significant, especially potassium deficiency as a result of high starch intake, low intake of potassium and other practices. Enigmatic clinical aspects include: (i) the absence of symptoms generally, especially in the presence of established severe clinical disease with and without target organ damage; (ii) the clinically apparent selective target organ damage; (iii) labile blood pressure readings at any stage; (iv) cerebral thrombosis and frequent blood pressure normalization; (v) cardiomyopathy in relation to hypertension; (vi) the discordance of morbid events; (vii) dramatic isolated morbid events, which suggest special vulnerability.

Black or African American↗
PubMed1982

Captopril in renovascular hypertension: long-term use in predicting surgical outcome.

The angiotensin converting-enzyme inhibitor captopril was used as long-term preoperative treatment in a series of hypertensive patients with unilateral renal arterial disease. There were immediate and sustained falls in plasma angiotensin II and aldosterone concentrations, with converse increases in circulating renin and angiotensin I. In patients with sodium and potassium deficiency and secondary aldosterone excess before treatment captopril corrected the sodium and potassium deficits; in these cases the initial hypotensive response was profound but the later effect was less pronounced. When sodium and potassium state was initially normal it remained unchanged during captopril treatment, while the full hypotensive effect took up to three weeks to be attained. The immediate, but not long-term, falls in arterial pressure with captopril were proportional to the immediate decrements of plasma angiotensin II. Nevertheless, while the immediate blood-pressure reduction with captopril variously overestimated and underestimated the eventual surgical response, the absolute blood-pressure values during long-term captopril related well with those after operation. Pretreatment plasma renin and angiotensin II concentrations, while closely predicting the immediate captopril response, are fallible guides to surgical prognosis. In contrast, long-term treatment with converting-enzyme inhibitors may provide an accurate indication of surgical outcome.

Adolescent↗
PubMed2004

Mechanisms of acute myocardial infarction study (MAMIS).

Acute myocardial infarction (AMI) is a highly dynamic event, which is associated with marked neuroendocrinological dysfunction in addition to cardiac damage. The immediate trigger for AMI is not precisely known. Studies conducted by Lown, Braunwald, Halberg, Otsuka and our group have demonstrated a marked increase in sympathetic activity, oxidative stress, and magnesium and potassium deficiency during AMI. Clinical studies have reported an increased incidence of AMI, sudden death and ischemia during first quarter of the day when there is a rapid withdrawal of vagal activity and increase in sympathetic tone. In one case-control study of 202 patients with AMI, there was a significant (P < 0.02) increase in cardiac events in the second quarter of the day compared to other quarters, respectively (16.8%, 41.0%, 13.8%, 28.2% per quarter). This characteristic remained prevalent in both men and women and among patients with and without known AMI (n = 52), diabetes (n = 53) or hypertension (n = 75). Triggers of AMI were noted among 162 (82.2%) of the patients. Neuropsychological mechanisms were observed as follows: emotional stress (45.5%), sleep deprivation (27.7%), cold climate (29.2%), hot climate (24.7%), large meals (47.5%) and physical exertion (31.2%). These triggering factors are known to enhance sympathetic activity and decrease vagal tone, resulting in an increased secretion of plasma cortisol, noradrenaline, aldosterone, angiotension-converting enzyme (ACE), interleukin (IL)-1, -2, -6, -18, and tumor necrosis factor-alpha (TNF-alpha), all of which are are proinflammatory agents. There is also a deficiency in the serum levels of vitamin A, E, and C and magnesium, potassium, melatonin, and IL-10 (an anti-inflammatory agent). In our study, we found a decrease in magnesium, potassium, vitamin A, E, C and beta carotene combined with an increase in thiobarbituric acid-reactive substances (TBARS), MDA and diene conjugates, TNF-alpha and IL-6, all of which are indicators of oxidative damage and proinflammatory activity, respectively.

Activity Cycles↗
PubMed1998

Effect of an increase in the plasma potassium concentration on renal magnesium handling in healthy volunteers.

BACKGROUND: Lower plasma magnesium concentrations are associated with clinical problems such as arrhythmias and hypertension. Plasma magnesium concentration is tightly controlled by the kidney. Modifying renal magnesium threshold may provide a means to increase the plasma magnesium concentration. Since evidence has been presented that potassium deficiency by itself may increase renal magnesium loss, the hypothesis that elevating plasma potassium would result in an increase in plasma magnesium concentration was tested in healthy volunteers. METHODS: Plasma potassium was raised in nine healthy volunteers by oral administration of 20 mg amiloride daily during 3 weeks. Magnesium metabolism was assessed before and after this period by plasma levels, urinary magnesium excretion and fractional magnesium excretion, and magnesium loading test (MLT). This MLT allows calculation of renal retention of a magnesium load. RESULTS: Basal plasma magnesium levels (0.84 +/- 0.07 vs 0.84 +/- 0.05 mmol/l) as well as urinary magnesium excretion (4.37 +/- 1.73 vs 3.67 +/- 1.37 mmol/day) and erythrocyte magnesium levels (1.72 +/- 0.16 vs 1.76 +/- 0.14 mmol Mg/l red blood cells) were similar before and on amiloride. Plasma potassium rose significantly on amiloride (3.64 +/- 0.24 vs 4.07 +/- 0.54 mmol/l, P < 0.05). No change was observed in magnesium retention with the MLT: 22.7 +/- 26.7 vs 29.2 +/- 20.6% (P = 0.5). CONCLUSIONS: Despite an increased plasma potassium concentration, no change was observed in plasma magnesium levels, urinary magnesium excretion or renal magnesium retention of an intravenously administered magnesium load. This indicates that increasing plasma potassium within the normal range does not modify the renal magnesium threshold.

Adult↗
PubMed2006

Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge.

CONTEXT: The aim of this article was to review the clinical presentation, pathogenesis, and management of thyrotoxic periodic paralysis (TPP). EVIDENCE ACQUISITION: A MEDLINE search was conducted for articles published during the last 40 yr based on the key words thyrotoxic periodic paralysis and hypokalemic periodic paralysis. A total of 281 primary articles and 168 references of the retrieved articles were also reviewed. EVIDENCE SYNTHESIS: TPP is a common complication of hyperthyroidism in Asian men but is increasingly seen in Western countries. Hypokalemia and muscle paralysis results from a sudden intracellular shift of potassium and is not due to potassium deficiency. Clinical features of hyperthyroidism in patients with TPP may be subtle. Immediate potassium supplementation prevents serious cardiopulmonary complications and may hasten the recovery of muscle weakness. Nonselective beta-adrenergic blockers can ameliorate and prevent recurrence of the paralytic attacks. This episodic paralysis will remit with definitive control of hyperthyroidism. Increased sodium-potassium ATPase pump activity and enhanced insulin response in patients with TPP is postulated to contribute to the hypokalemia. The genetic predisposition for TPP is not entirely clear. Association of polymorphisms of the calcium channel alpha1-subunit gene with TPP has been noted. CONCLUSIONS: Due to population mobility, TPP is increasingly common in Western countries. Early diagnosis and prompt treatment prevent life-threatening complications associated with hypokalemia and muscle weakness. Assaying of thyroid function in patients with hypokalemic paralysis distinguishes TPP from other forms of hypokalemic periodic paralysis.

Antithyroid Agents↗
PubMed1991

Role of potassium in the pathogenesis of acute renal failure.

Potassium depletion can potentiate several experimental models of acute renal failure. It causes renal vasoconstriction, probably under the influence of vasoconstrictor prostaglandins and angiotensin II, and causes a reduction in vasodilatory prostaglandins. Aminoglycoside nephrotoxicity in experimental animals and in man causes a reduction in serum potassium and in animals it enhances the functional and histological damage produced by aminoglycosides. Chronic potassium loading protects against mercuric chloride, uranyl nitrate, and gentamicin models of acute renal failure. In the gentamicin model, protection is associated with a stimulation of renal cortical Na-K-ATPase activity and a reduction in the level of gentamicin accumulated in cortical tissue. In the clinical setting, potassium deficiency should be avoided in patients at risk for acute renal failure. However, potassium loading should also be avoided, since a falling glomerular filtration rate in the presence of a potassium load could result in potentially serious hyperkalemia.

Acute Kidney Injury↗