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K Lau

Publications and source records attributed to K Lau.

102 records · Page 6Linked to original sources
PubMed1982

Effects of phosphate administration on tubular calcium transport.

To evaluate the mode and tubular sites of action of PO4 administration on renal Ca reabsorption, micropuncture and clearance experiments were performed on acutely parathyroidectomized rats: (1) control (n=7), 2.5% saline expansion + furosemide infusion (0.5 mg/kg/hr); (2) PO4 infusion (n=6), treated as were the controls plus intravenous neutral PO4 (25 mg/kg/hr). CaCI2 was infused to keep plasma UF Ca comparable in both groups [2.68 +/- 0.08 mEq/l (mean +/- S.E.) vs 2.52 +/- 0.10, N.S.]. Po4 infusion increased plasma PO4 (14.0 vs 8.4 mg/dl, p less than 0.001) and FE PO4 (9.03% vs. 0.09%, p less than 0.001) but decreased FE Ca (1.83% vs. 5.95%, p less than 0.02) while GFR and FE Na were similar. FD of Na, PO4 and Ca were similar in late proximal and ED tubule punctures. In the LD tubule, PO4 infusion increased FD PO4 (18.5% vs. 7.9%, p less than 0.005) and reduced FD Ca (3.51% vs. 6.66%, p less than 0.01) and (TF/UF) Ca/Na (0.69 vs. 1.40, p less than 0.001). LD tubule FD Ca (y) was inversely related to TF/P PO4 concentration (X) in LD tubules: (y=7.2 - 0.12x, r=0.68, p less than 0.02). Significant Ca reabsorption (1.68% of filtered load) was observed beyond the superficial LD tubule only during PO4 infusion. These data indicate that phosphate infusion enhances Ca reabsorption independently of PTH, plasma Ca, and renal Na handling at a site within and possible beyond the distal convoluted tubule of the superficial nephron. (J Lab Clin Med 99:317, 1982).

Animals↗
PubMed1979

Differing effects of acid versus neutral phosphate therapy of hypercalciuria.

Studies were performed on 12 patients with idiopathic hypercalciuria to evaluate the hypothesis that the acid load accompanying potassium acid phosphate would adversely affect renal calcium reabsorption and citrate excretion compared to the neutral form of the phosphate salt. During acute clearance studies, neutral phosphate (NP) led to a fall in FECa (2.2 +/- 0.6% to 0.8 +/- 0.1%, P less than 0.02) and no change in titratable acidity (TA) or net acid excretion (NAE). Acid phosphate (AP) did not reduce FECa acutely, and led to a rise in TA (22 +/- 4 to 62 +/- 6 muEq/min, P less than 0.02) and NAE (46 +/- 6 to 6 89 +/- 7 muEq/min, P less than 0.02). During chronic administration, AP resulted in higher urinary calcium excretion in both absorptive (187 +/- 29 vs. 141 +/- 18 mg/day, P less than 0.02) and renal hypercalciuric patients (233 +/- 24 vs. 173 +/- 190.02 mg/day, P less than 0.02). Also, TA and NAE were higher following AP, whereas citrate excretion was lower (375.4 +/- 64.6 vs. 633.4 +/- 28.8 mg/day, P less than 0.01). These data suggest that the reported ineffectiveness of AP in the therapy of nephrolithiasis may be related to the deleterious effects of the acid load on calcium and citrate metabolism.

Acid-Base Equilibrium↗
PubMed1979

Evidence for an intrinsic renal tubular defect in mice with genetic hypophosphatemic rickets.

To investigate the role of parathyroid hormone (PTH) and(or) an intrinsic renal tubular reabsorptive defect for phosphate in mice with hereditary hypophosphatemic rickets, we performed clearance and micropuncture studies in hypophosphatemic mutants and nonaffected littermate controls. Increased fractional excretion of phosphate in mutants (47.2+/-4 vs. 30.8+/-2% in controls) was associated with reduced fractional and absolute reabsorption in the proximal convoluted tubule and more distal sites. Acute thyropara-thyroidectomy (TPTX) increased phosphate reabsorption in both mutants and controls with a fall in fractional phosphate excretion to congruent with7.5% in both groups indicating that PTH modified the degree of phosphaturia in the intact mutants. Absolute reabsorption in the proximal tubule and beyond remained reduced in the mutants, however, possibly because of the reduced filtered load. Serum PTH levels were the same in intact mutants and normals as was renal cortical adenylate cyclase activity both before and after PTH stimulation. To evaluate the possibility that the phosphate wasting was caused by an intrinsic tubular defect that was masked by TPTX, glomerular fluid phosphate concentration was raised by phosphate infusion in TPTX mutants to levels approaching those of control mice. Phosphate excretion rose markedly and fractional reabsorption fell, but there was no change in absolute phosphate reabsorption in either the proximal tubule or beyond, indicating a persistent reabsorptive defect in the absence of PTH. We conclude that hereditary hypophosphatemia in the mouse is associated with a renal tubular defect in phosphate reabsorption, which is independent of PTH and therefore represents a specific intrinsic abnormality of phosphate transport.

Animals↗
PubMed1979

Renal tubular sites of altered calcium transport in phosphate-depleted rats.

Increased calcium (Ca) excretion is characteristic of chronic phosphate (PO(4)) depletion (PD). To study the changes in tubular transport and the site of the hypocalciuric effect of PO(4) administration, clearance and micropuncture experiments were performed in intact rats pair fed either a control diet (0.5% PO(4)) or a PO(4)-depleted (PD) diet (0.01% PO(4)) plus Al(OH(3)) and in parathyroidectomized (PTX) PD rats, infused either with saline or with neutral sodium PO(4). Intact PD rats, compared with intact rats on a control diet, exhibited a lower plasma ultrafiltrable (UF) PO(4) (5.8+/-0.5 vs. 7.8+/-0.3 mg/dl), higher fractional excretion (FE) of Ca (4.1+/-1.2 vs. 0.6+/-0.1%), and reduced FE PO(4) (0.1+/-0.01 vs. 10.2+/-1.8%). Tubular fluid/plasma inulin was lower in the late proximal tubule of PD rats, associated with increases in fractional delivery (FD) from the proximal tubule of Na and Ca.The%FD of Ca to the early distal tubule of PD rats was increased (20+/-3 vs. 11+/-2%), but this difference was abolished by the late distal tubule (5.1+/-1.2 vs. 3.3+/-0.9%). In PTX-PD rats, PO(4) infusion increased plasma UF PO(4) (13.8+/-0.7 vs. 7.8+/-0.7 mg/dl). FE of Ca was reduced (1.08+/-0.35 vs. 4.59+/-1.57%) without correcting the increased Ca delivery to the late distal tubule. These data indicate that PD impairs Ca reabsorption in tubular segments before but not within the distal convoluted tubule, so that hypercalciuria is ultimately a result of decreased Ca transport either in the terminal nephron or in deeper nephrons where PO(4) infusion stimulates Ca transport independent of parathyroid hormone or changes in the filtered load of Ca.

Animals↗
PubMed1978

Mechanism of lithium-induced hypercalciuria in rats.

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.

Animals↗
PubMed1976

Effectiveness of bumetanide in nephrotic syndrome: a double-blind crossover study with furosemide.

A double-blind crossover study was undertaken to delineate the renal tubular sites of action of bumetanide and to compare its effects upon electrolyte excretion to that of furosemide in six nephrotic patients with various degrees of renal insufficiency. Bumetanide was found to be a potent oral natriuretic agent without producing changes in either GFR or effective renal plasma flow. The natriuresis was associated with inhibition of proximal tubular transport as evidenced by an increased distal delivery (CH2O+CNA+K) and inhibition of sodium transport in the loop of Henle as shown by a fall in CH2O/CH2O+CC1 during sustained water diuresis and an unchanged TCH2O with continued hydropenia. The increases in free-water clearance induced by furosemide and bumetanide were equivalent, but bumetanide produced significantly higher flow rate, greater solute delivery from the proximal tubule, and a greater natriuresis. The data indicate that at the dosages used, bumetanide has a proportionately greater inhibitory effect than furosemide in both the proximal tubule and the ascending limb of the loop of Henle.

Adolescent↗
PubMedDate not supplied

Effects of pressure on vesicle size, density, and distribution in the canine carotid arterial endothelium.

The purpose of the present experiment was to study the effects of internal hydrostatic pressure on vesicle size, density, and distribution in the canine carotid arterial endothelium by transmission electron microscopy. The pressures applied in this study were 0 (control), 40, 60, 80, 100, and 150 mm Hg. The results of transmission electron microscopy and computer analysis on the plasmalemmal vesicles of aortic endothelium showed that luminal, abluminal, and junctional vesicles all increased their diameter as the pressure was raised from 0 mm Hg, reaching a maximum at 80 mm Hg, and then decreased in size with further increases in pressure to 150 mm Hg. There was a significant difference in diameter among vesicles in different regions of the endothelium, with the diameter of luminal vesicles larger than those of abluminal and junctional vesicles. The densities of vesicles showed very little change from 0 to 80 mm Hg; but they increased markedly as the pressure was further raised from 80 to 150 mm Hg. These results indicate that pressure is an important mechanical factor governing the size and density of plasmalemmal vesicles in aortic endothelium.

Animals↗
PubMedDate not supplied

L-myc genotypes in Hong Kong Chinese colorectal carcinoma patients.

L-myc genotypes have been correlated with prognosis in different human tumors. Its role in colorectal carcinoma (CRC) is still unclear. This study aimed to assess the L-myc genotypes in 99 Hong Kong Chinese CRC patients by PCR-RFLP techniques. The results obtained were correlated with clinical, histological and pathological parameters and genetic alterations. The observed frequency of L-myc genotypes (LL:LS:SS) was 27:46:26. The ratio of S to L alleles was 0.51:0.49. Distribution of L-myc genotypes and alleles in Hong Kong Chinese CRC was similar to that of healthy Chinese and CRC patients of other ethnic origins. The homozygous SS genotype was significantly associated with Dukes' stages C versus B. Other parameters including sex, differentiation status and survival, and genetic alterations such as p53 and Ki-ras mutations and Dcc LOH had no significant association with L-myc SS genotype.

Asian People↗