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Shih-Hua Lin

Publications and source records attributed to Shih-Hua Lin.

63 records · Page 4Linked to original sources
PubMed2002

Hypercalcaemia and metabolic alkalosis with betel nut chewing: emphasis on its integrative pathophysiology.

BACKGROUND: Events in the gastrointestinal tract that might contribute to a high absorption of calcium were simulated in vitro to evaluate why only a small proportion of individuals who ingest alkaline calcium salts develop hypercalcaemia, hypokalaemia and metabolic alkalosis. METHODS: A patient who chewed and swallowed around 40 betel nuts daily developed hypercalcaemia, metabolic alkalosis, hypokalaemia with renal potassium wasting, and renal insufficiency. The quantities of calcium and alkali per betel nut preparation were measured. Factors that might increase intestinal absorption of calcium were evaluated. RESULTS: Hypercalcaemia in the index case was accompanied by a high daily calcium excretion (248 mg, 6.2 mmol). Circulating levels of 1,25-dihydroxyvitamin D(3) and parathyroid hormone were low. Hypokalaemia with a high transtubular K(+) concentration gradient, metabolic alkalosis, a low excretion of phosphate and a very low glomerular filtration rate were prominent features. CONCLUSIONS: Possible explanations for the pathophysiology of metabolic alkalosis and hypokalaemia are provided. We speculate that a relatively greater availability of ionized calcium than inorganic phosphate in the lumen of the intestinal tract could have enhanced dietary calcium absorption.

Alkalosis↗
PubMed2002

Osmotic demyelination syndrome after correction of chronic hyponatremia with normal saline.

Rapid correction of severe chronic hyponatremia with hypertonic saline has been known to cause osmotic demyelination syndrome (ODS). Less recognized are the dangers of rapid correction with normal saline. A 60-year-old woman on thiazide diuretics for hypertension presented with profound hyponatremia (94 mmol/L) and hypokalemia (1.9 mmol/L) associated with volume depletion. Normal saline (2 L/day) and (KCl 40 mmol/day) were given for 5 days. Serum Na+ concentration rose to 106 mmol/L within 18 hours. With improvement of her hyponatremia, she became more alert although the hypokalemia persisted. However, she developed progressive obtundation, quadriplegia, and respiratory failure 6 days later. Magnetic resonance imaging of the brain clearly showed typical features of pontine and extrapontine myelinolysis. We suggest that the aggressive KCl supplement would have been the first-line therapy for this patient presenting with chronic hyponatremia and hypokalemia associated with volume depletion.

Benzothiadiazines↗
PubMed2002

Mechanisms used to dispose of progressively increasing alkali load in rats.

Our objective was to describe the process of alkali disposal in rats. Balance studies were performed while incremental loads of alkali were given to rats fed a low-alkali diet or their usual alkaline ash diet. Control groups received equimolar NaCl or KCl. Virtually all of the alkali was eliminated within 24 h when the dose exceeded 750 micromol. The most sensitive response to alkali input was a decline in the excretion of NH(4)(+). The next level of response was to increase the excretion of unmeasured anions; this rise was quantitatively the most important process in eliminating alkali. The maximum excretion of citrate was approximately 70% of its filtered load. An even higher alkali load augmented the excretion of 2-oxoglutarate to >400% of its filtered load. Only with the largest alkali load did bicarbonaturia become quantitatively important. We conclude that renal mechanisms eliminate alkali while minimizing bicarbonaturia. This provides a way of limiting changes in urine pH without sacrificing acid-base balance, a process that might lessen the risk of kidney stone formation.

Acid-Base Equilibrium↗
PubMed2002

Two novel aquaporin-2 mutations responsible for congenital nephrogenic diabetes insipidus in Chinese families.

Mutations in the aquaporin-2 gene (AQP2), encoding the vasopressin-regulated water channel of the renal collecting duct, are responsible for the autosomal recessive or dominant forms of congenital nephrogenic diabetes insipidus. We describe two new families with normal hypotensive and coagulation responses following the administration of desamino-8-D-arginine AVP, a clinical suggestion of normal vasopressin-2 receptors. The patients were compound heterozygotes for point mutations at nucleotide position 170 (CAG to CCG; Q57P) and at position 299 (GGA to GTA; G100V) in exon 1 of the AQP2 gene. Expression of the G57P and G100V AQP2 proteins in Xenopus oocytes showed only 1.3-fold and 1.2-fold increase, respectively, in the water permeability in contrast to 8.0-fold increase in oocytes injected with wild-type cRNA. Immunoblots of oocyte lysate revealed the intensities of the 29-kDa bands were comparable among oocytes injected with wild-type and mutant cRNAs. Immunocytochemistry showed the plasma membrane was not stained in oocytes injected with cRNA of Q57P and of G100V. These results provide evidence that the Q57P and G100V mutations in congenital nephrogenic diabetes insipidus are attributable to the misrouting of AQP2.

Adult↗
PubMedDate not supplied

Attenuation of mouse mesangial cell contractility by high glucose and mannitol: involvement of protein kinase C and focal adhesion kinase.

Hyperglycemia and mannitol activate protein kinase C (PKC) and induce mesangial cell hypocontractility that subsequently may modulate renal function. Since focal adhesion kinase (FAK) activation is known to be linked with PKC activity, FAK may also be involved in mesangial cell contraction. To facilitate our understanding of the PKC- and FAK-modulating mechanism, we developed an in vitro model of mouse mesangial cell hypocontractility induced by hyperglycemia or mannitol. Mouse mesangial cells (CRL-1927) were exposed to: normal D-glucose (group N), high D-glucose (group H), and control groups at the same osmolality as H plus L-glucose (group L) and mannitol (group M). Changes in the planar surface area of cells in response to 1 microM phorbol 12-myristate 13-acetate (PMA) were determined. Western blot analyses for PKC, phosphorylated (p)-PKC, tyrosine phosphorylation, FAK, and p-FAK were done on each of these four groups. The effects of mannitol in various doses on cell contraction and activation of PKC and FAK were also assayed. The planar surface areas of groups H and M both showed an attenuated change in response to PMA stimulation. Before PMA stimulation, the baseline PKC expression of groups H and M showed a higher expression of p-PKC alpha and delta than that seen in group N (p < 0.05). Results of tyrosine phosphorylation and immunoprecipitation showed that FAK may be involved in this contraction process. The total amount of FAK showed no significant difference among the four experimental groups; however, p-FAK was found to have significantly increased in group M (p < 0.05). The use of PKC and tyrosine kinase inhibitors reduced PMA-induced mesangial cell contraction in all four groups. Activation of PKC alpha, delta, and FAK with the resultant inhibition of mesangial cell contraction by mannitol was found to be dose-dependent. These results may provide a correlation between increased expression of several PKC isoforms and, in particular, increased phosphorylation levels of PKC alpha and delta and hypocontractility induced by high glucose and mannitol treatment. Furthermore, the mannitol-induced hypocontractility involving PKC and FAK occurred in a dose-dependent manner.

Animals↗
PubMedDate not supplied

Acute hyperkalemic paralysis in a uremic patient.

Hyperkalemia is a less-recognized life-threatening cause of paralysis. We describe a 38-year-old uremic man on regular hemodialysis (HD) without interruption who suffered from muscle weakness progressing to ascending symmetric paralysis, and inability to masticate. Physical examination revealed flaccid paralysis with areflexia of the four limbs. Computed tomography of the brain and cervical spine did not demonstrate any organic lesions. Laboratory investigations revealed serum K+ 8.1 mmol/L, urea nitrogen 32 mmol/L, creatinine 919 micromol/L. Of note, electrocardiography (ECG) did not show typical features of hyperkalemia. Emergent HD with low K+ dialysate (1.0 mmol/L) rapidly normalized serum K+ (4.7 mmol/L) and reversed all neuromuscular symptoms within one hour. Upon reviewing his food and medication history, he admitted drinking 750 ml of raw coconut juice per day (K+ concentration 44.3 mmol/L) to quench his thirst for three consecutive days. Hyperkalemia should be born in mind in the differential diagnosis of acute paralysis despite no ECG changes. Hidden sources of K+ intake, such as coconut juice, should not be overlooked, especially in patients with impaired renal function.

Adult↗
PubMedDate not supplied

Recurrent hyponatremia in a patient with chronic kidney disease.

Hyponatremia, albeit common in chronic renal insufficiency, necessitates a detailed search of the underlying hidden causes. We report on a 67-year-old woman with chronic kidney disease (creatinine 230 micromol/L) and hypertension who suffered from general fatigue, dizziness, nausea, vomiting and abdominal fullness off and on for 6 months. Hyponatremia (plasma Na(+) 106-125 mmol/L) on 4 occasions during the past 6 months was noticed. Her extracellular volume status was apparently normal. Plasma Na(+) concentration 110 mmol/L was the most striking laboratory abnormality with mild metabolic acidosis (HCO(3)- 19.8 mmol/L). Her urine Na(+) concentration and osmolality were inappropriately high. Her hyponatremia was refractory to normal saline, hypertonic NaHCO(3) and 0.1-microg 9 alfa-fludrocortisone. Despite normal plasma cortisol and thyroid hormone concentrations, a provocation test with cosyntropin (250 microg) showed a blunted cortisol (<579 nmol/L) but intact aldosterone response. Magnetic resonance imaging of her brain displayed a normal pituitary gland and hypothalamus. A history of intermittent intravenous steroid therapy to treat her allergic rhinitis for 3 years was uncovered. Steroid supplements induced water diuresis and corrected hyponatremia to 135 mmol/L in 5 days. With nonspecific clinical symptoms, glucocorticoid insufficiency must be kept in mind as a cause of hyponatremia even in patients with impaired renal function and normal plasma cortisol concentration.

Aged↗