1/284. Renal tubular acidosis, hypokalemic paralysis, rhabdomyolysis, and acute renal failure--a rare presentation of Chinese herbal nephropathy.We encountered a 66-year-old Chinese man presented with hypokalemic paralysis, rhabdomyolysis and acute renal failure after administration of mixed Chinese herbs. Proximal renal tubular acidosis and selective glucosuria were the main tubular dysfunctions. The renal failure recovered smoothly and rapidly after resuscitation and the tubular function abnormalities regained spontaneously after medicine withdrawal. It should be recognized that renal tubular acidosis with hypokalemic paralysis, rhabdomyolysis and subsequent acute renal failure may develop after taking Chinese mixed herbal medicine.- - - - - - - - - - ranking = 1keywords = hypokalemic (Clic here for more details about this article) |
2/284. Hypokalemic myopathy due to chronic alcoholism.A patient with hypokalemic myopathy occurring in the context of chronic alcoholism was reported. A 56-year-old male patient, heavy drinker for 20 years, complained of marked weakness and acutely developing pains in his limbs. The principal clinical findings were weakness and tenderness of the proximal limbs and girdle muscle. He was unable to lift his head or any extremities from the bed. Deep tendon reflexes were diminished, but not absent. There was no sensory disturbance except for muscle tenderness. These clinical manifestations disappeared gradually by abstinence from drinking, and potassium administration therapy, and the patient recovered completely on the 26th day after onset. On the day after admission (8th day), serum potassium value was 2.2mEq/L, and serum CPK activity was 4270IU. The ECG pattern was consistent with a diagnosis of low potassium content in serum, and the EMG pattern was consistent with a diagnosis of myopathy. These electrophysiological findings had a tendency to recover from this pattern to normal range correspondingly with clinical improvement. The repeated muscle biopsies showed that vacuolation, hyaline degeneration and significant phagocyte infiltration were observed in the muscle on the 9th day after the onset of muscle weakness, and that these pathological findings disappeared almost completely three weeks later. The frequently repeated examinations of potassium content and CPK activity in sera showed that there was a close correlation between these biochemical abnormalities and clinical improvememt. The pathogenesis of alcoholic myopathy and significance of CPK abnormality in chronic alcoholism were discussed.- - - - - - - - - - ranking = 0.16666666666667keywords = hypokalemic (Clic here for more details about this article) |
3/284. Hypokalemic myopathy due to chronic alcoholism.A patient with hypokalemic myopathy occurring in the context of chronic alcoholism was reported. A 56-year-old male patient, heavy drinker for 20 years, complained of marked weakness and acutely developing pains in his limbs. The principal clinical findings were weakness and tenderness of the proximal limbs and girdle muscle. He was unable to lift his head or any extremities from the bed. Deep tendon reflexes were diminished, but not absent. There was no sensory disturbance except for muscle tenderness. These clinical manifestations disappeared gradually by abstinence from drinking, and potassium administration therapy, and the patient recovered completely on the 26th day after onset. On the day after admission (8th day), serum potassium value was 2.2 mEq/L, and serum CPK activity was 4270 IU. The ECG pattern was consistent with a diagnosis of low potassium content in serum, and the EMG pattern was consistent with a diagnosis of myopathy. These electrophysiological findings had a tendency to recover from this pattern to normal range correspondingly with clinical improvement. The repeated muscle biopsies showed that vacuolation, hyaline degeneration and significant phagocyte infiltration were observed in the muscle on the 9th day after the onset of muscle weakness, and that these pathological findings disappeared almost completely three weeks later. The frequently repeated examinations of potassium content and CPK activity in sera showed that there was a close correlation between these biochemical abnormalities and clinical improvement. The pathogenesis of alcoholic myopathy and significance of CPK abnormality in chronic alcoholism were discussed.- - - - - - - - - - ranking = 0.16666666666667keywords = hypokalemic (Clic here for more details about this article) |
4/284. Licorice-induced hypokalemic myopathy and hypokalemic renal tubular damage in anorexia nervosa.A patient with a history of anorexia nervosa developed licorice-induced hypokalemic myopathy. With potassium replacement, high CPK blood level and myopathic signs returned to normal. However, the patient manifested persistent hypokalemia and impaired renal function to concentrate and acidify the urine. Renal biopsy demonstrated intense degeneration and vacuolation of tubules with a normal glomerus which was consistent with hypokalemic nephropathy. Prolonged hypokalemia in anorexia nervosa is sometimes attributed to surreptitious purging or taking diuretics, but it is necessary to check the urine pH, the urine-specific gravity, and the urine potassium level in order to find underlying renal damage even after hypokalemic myopathy is treated successfully.- - - - - - - - - - ranking = 1.8333333333333keywords = hypokalemic (Clic here for more details about this article) |
5/284. hypokalemic periodic paralysis associated with hypophosphatemia in a patient with hyperinsulinemia.A 34-year-old man was admitted to the hospital because of acute quadriplegia. On admission, serum potassium was 2.1 mEq/L and serum inorganic phosphate was 1.4 mg/dL. Thyroid function was normal. serum levels of aldosterone, cortisol, and intact parathyroid hormone were normal. fasting plasma glucose was 109 mg/dL, and fasting serum insulin was 25.0 U/mL. Shortly after intravenous supplementation of potassium, muscle strength was normalized. Oral glucose tolerance test revealed impaired glucose tolerance and hyperresponse of insulin. During the oral glucose tolerance test, serum potassium and phosphate decreased significantly. These findings suggest that hyperinsulinemia and insulin-induced transmembrane shift of extracellular potassium and phosphate may have been involved in the abnormalities of serum electrolytes and development of hypokalemic periodic paralysis in the present patient.- - - - - - - - - - ranking = 0.16666666666667keywords = hypokalemic (Clic here for more details about this article) |
6/284. Prominent bifid T waves observed in the QT prolongation caused by complete atrioventricular blockade in a hypokalemic diabetic patient.A 63-year-old diabetic man was admitted with general fatigue. Electrocardiogram (ECG) on admission showed complete atrioventricular (AV) blockade associated with prominent bifid T waves. The second component of the bifid T waves was distinguished from U waves by the beat-to-beat varying bifidity and the nadir between the two components located at > or = 1 mm above the isoelectric line. Range of absolute QT interval was 535 to 650 ms. hypokalemia (3.6 mEq/L) was noted at admission. Partial restoration of the potassium level (3.9 mEq/L) prior to temporary ventricular demand pacing obscured the bifid T waves and attenuated the QT prolongation and dispersion to some extent (absolute QT interval ranging 520 to 620 ms). It was concluded that marked bradycardia caused by complete AV blockade (ie, a junctional escaped rhythm at a rate of 42 beats/min), hypokalemia, and underlying diabetes mellitus contributed in concert to the QT prolongation and dispersion leading to the prominent bifid T waves.- - - - - - - - - - ranking = 0.66666666666667keywords = hypokalemic (Clic here for more details about this article) |
7/284. Chronic microscopic enterocolitis with severe hypokalemia responding to subtotal colectomy.The authors present the first case report of a 50-year-old woman with a 33-year history of severe, chronic watery diarrhea and hypokalemia secondary to chronic active microscopic enterocolitis with patterns similar to lymphocytic colitis but with acute cryptitis and terminal ileum involvement microscopically. The progressive nature of her illness resulted in multiple hospital admissions secondary to hypokalemia with subsequent chronic renal failure. High continuous doses of oral potassium supplements failed to correct the hypokalemic episodes. After subtotal colon resection, the patient made a marked clinical improvement with normal serum potassium levels without receiving potassium supplementation.- - - - - - - - - - ranking = 0.18866164755034keywords = hypokalemic, watery diarrhea, diarrhea (Clic here for more details about this article) |
8/284. Gitelman's syndrome: report of a 19-year old woman with intractable hypomagnesemia and hypokalemia, and a review of the syndrome.A case of refractory hypomagnesemia associated with hypokalemic alkalosis and hypocalciuria (Gitelman's syndrome) is described. The genetic mutations discovered to cause the hypokalemic alkalotic syndromes are described (the thiazide-sensitive sodium chloride co-transporter gene or TSC mutations in Gitelman's syndrome, and the sodium-potassium-chloride co-transporter gene or NKCC2 mutations in Bartter's syndrome). The molecular, electrolyte, and volume abnormalities are described, and the implications for diagnosis, therapy, and future research discussed.- - - - - - - - - - ranking = 0.57774342106197keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
9/284. Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman.The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.- - - - - - - - - - ranking = 0.67462464585264keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
10/284. Influence of severe potassium depletion and subsequent repletion with potassium on muscle electrolytes, metabolites and amino acids in man.1. Two women with severe hypokalaemic alkalosis were investigated by means of muscle biopsy before and at the end of 2 and 3 weeks respectively of intense therapy with potassium chloride. 2. The muscle biopsy material was analysed for water, electrolytes, adenine nucleotides, phosphocreatine, free creatine, pyruvate, lactate, glycogen and free amino acids. The extra- and intra-cellular distribution of water, electrolytes and amino acids was calculated by the chloride method. 3. Both patients showed a marked loss of intracellular potassium and an increase in intracellular sodium concentration. The muscle magnesium content was also slightly decreased. After repletion with potassium chloride, muscle sodium and potassium became normal. 4. The contents of creatine phosphate, ATP, ADP, AMP, lactate and pyruvate were within normal limits, but the phosphocreatine/total creatine ratio was reduced. After repletion, a small change in the apparent creatine-phosphokinase equilibrium had occurred, suggesting a minor increase in intracellular pH. 5. The concentrations of the basic amino acids, lysine, arginine and ornithine were increased far above normal. The intracellular accumulation of arginine was much higher than the increase in lysine concentration and histidine concentration was normal. This differs from findings in potassium-depleted rats, where the intracellular lysine concentration is much higher than arginine concentration and histidine is high as well. After potassium repletion the intracellular concentration of ornithine, lysine and arginine became normal in one case and decreased considerable in the other. An increased intracellular concentration of glutamate and glutamine was also observed after potassium repletion.- - - - - - - - - - ranking = 0.016146870798445keywords = alkalosis (Clic here for more details about this article) |
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