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Biomedical subjects

S F Wen

Publications and source records attributed to S F Wen.

At least 37 records · Page 2Linked to original sources
PubMed1992

Acute renal failure following binge drinking and nonsteroidal antiinflammatory drugs.

Two college students who developed reversible acute deterioration in renal function following binge drinking of beer and the use of nonsteroidal antiinflammatory drugs (NSAIDs) are reported. Both patients presented with back and flank pain with muscle tenderness, but showed no evidence of overt rhabdomyolysis. The first case had marked renal failure, with a peak serum creatinine reaching 575 mumol/L (6.5 mg/dL), and acute tubular necrosis was documented by renal biopsy. The second case had only modest elevation in serum creatinine, and renal function rapidly improved on rehydration. The contribution of the potential muscle damage associated with alcohol ingestion to the changes in renal function in these two cases is not clear. However, the major mechanism for the acute renal failure was thought to be related to inhibition of renal prostaglandin synthesis in the face of compromised renal hemodynamics secondary to alcohol-induced volume depletion.

Acute Kidney Injury↗
PubMed1991

Effects of endogenous and exogenous hyperglycemia on renal glucose transport in the rat.

As acute renal glucose loading requires intravenous infusion of a large quantity of hypertonic glucose solution, we performed free-flow micropuncture studies in nine streptozotocin diabetic rats to evaluate renal tubule glucose transport in hyperglycemic state and the results were compared with those of 10 normal rats in which comparable hyperglycemia was induced by exogenous glucose loading. Despite hyperglycemia with a mean plasma glucose concentration at 19.2 mmol/l, glomerulotubular balance in the proximal tubule of the diabetic rats was well maintained with a mean proximal tubule fluid-to-plasma inulin ratio at 2.08 +/- 0.15 as compared with that of the normal control at 2.16 +/- 0.11. Acute glucose loading in the normal rats raised plasma glucose to a similar mean of 19.6 mmol/l, significantly inhibited proximal fluid and glucose reabsorption, increased their reabsorption in the intermediate segment (between late proximal tubule and early distal tubule) and led to natriuresis and exaggerated glycosuria (fractional sodium excretion 1.32% and fractional glucose excretion 14.8% compared with 0.47% and 7.3%, respectively, for the diabetic control). Administration of insulin to normalize plasma glucose in the diabetic rats also inhibited proximal fluid and glucose reabsorption and resulted in modest natriuresis. This observation is consistent with the existence of sodium-glucose cotransport in the proximal tubule with sodium transport being reduced along with glucose transport following insulin administration. It is concluded that acute glucose loading, as performed in the conventional glucose titration study, leads to artifactual inhibition of proximal sodium and glucose transport.

Animals↗
PubMed1990

Ionophores for monovalent cations inhibit angiotensin-stimulated aldosteronogenesis.

We examined the effects of monensin (a sodium ionophore), valinomycin (a potassium ionophore), and nigericin (a nonspecific ionophore) on steroid production and its stimulation in bovine adrenal glomerulosa and fasciculata cells. All three ionophores at nanomolar concentrations inhibited angiotensin (AII)-stimulated aldosterone production; potassium-stimulated aldosteronogenesis was more sensitive, and cortisol synthesis by fasciculata cells was much less sensitive. Ionophores completely inhibited the early pathway of aldosteronogenesis and partially inhibited conversion of progesterone to aldosterone. Ionophores had no effect on pregnenolone production by isolated glomerulosa mitochondria. Monensin had no effect on AII binding, calcium flux, calcium transient, protein phosphorylation, or protein synthesis; valinomycin slightly inhibited these processes. Valinomycin lowered cell potassium and raised cell sodium, but its inhibition of aldosteronogenesis was not overcome by increasing extracellular potassium. Monensin and nigericin had no effect on cell potassium or sodium. Cellular ATP was decreased by valinomycin, but not by monensin or nigericin. Our results show that stimulation of aldosteronogenesis by AII and potassium is highly sensitive to ionophores of monovalent cations. Monensin and nigericin inhibit steroidogenesis at concentrations that have no other observed deleterious effects on glomeulosa cells. These results identify a distinguishing characteristic of adrenal glomerulosa cells and suggest a new pharmacologic approach to inhibition of aldosteronogenesis.

Adenosine Triphosphate↗
PubMed1989

Two case studies from a family with primary Fanconi syndrome.

We report two cases from a family with primary Fanconi syndrome. A 39-year-old white woman with a history of frequent bone fractures developed hypophosphatemia, hypouricemia, hypokalemia, metabolic acidosis, and renal glycosuria. Her 15-year-old son had renal glycosuria without metabolic acidosis. Both had mildly to moderately impaired renal function. Determination of amino acids in 24-hour urine specimens confirmed the generalized nature of aminoaciduria. Acid-loading, bicarbonate-loading, and phosphate-loading tests revealed that the mother had proximal (type II) renal tubular acidosis and excessive renal loss of phosphate for her level of renal function. These tests for the son were normal or within normal limits of his renal function. Known causes of Fanconi syndrome, such as cystinosis and Wilson's disease, were excluded by slit-lamp eye examination and leukocyte cystine level determination. One unexpected finding in the son was the preseNce of nephrocalcinosis on x-rays; a percutaneous needle biopsy of the kidney showed tubular atrophy, interstitial fibrosis, and calcium oxalate crystal deposits. The two cases presented here represent a familial variety of the primary Fanconi syndrome, a rare entity with a limited number of cases reported in the literature.

Adolescent↗
PubMed1988

An impedance method for blood pressure measurement in awake rats without preheating.

The tail-cuff methods for measuring systolic blood pressure in the rat usually require preheating of the animal to obtain recordable pulse signals. To find a more sensitive method, we applied the principle of differentiated impedance (dZ/dt) to the tail-cuff measurement of systolic blood pressure. We obtained clear pulse signals from the tail in awake rats without preheating the animals, and the systolic blood pressure obtained by this method had an excellent correlation with the directly measured femoral artery pressure (correlation coefficient = 0.98). Heating the animals at 40 degrees C for 5 minutes increased systolic blood pressure by a mean of 6 mm Hg as compared with that determined at the ambient temperature of 21 to 24 degrees C. Mean systolic blood pressure in young female diabetic rats was 122 +/- 3 mm Hg, which was significantly higher than the 111 +/- 2 mm Hg of normal rats. It is concluded that the technique of electrical impedance as applied to the tail-cuff method is simple and highly sensitive and is suitable for measurement of tail systolic blood pressure in awake rats without preheating.

Animals↗
PubMed1985

Effects of low-protein diet on experimental diabetic nephropathy in the rat.

To evaluate the role of glomerular hyperfiltration in the development and progression of diabetic nephropathy, we performed clearance and histopathologic studies in 24 rats with streptozocin-induced diabetes after 3 months of diets with different protein compositions. Calcium phosphate was added to an 8% protein diet in group I (nine rats), and calcium carbonate to a 24% protein diet in group II (nine rats) to equalize calcium and phosphate contents in these diets. Group I and II rats also received small doses of insulin to reduce the excessive hyperglycemia induced by the high sucrose content of the diets. In group III, six rats given an 8% protein diet, no calcium, phosphate, or insulin was added. In groups I and III, low dietary protein significantly reduced glomerular filtration rate and renal plasma flow per gram of kidney weight as compared with rates observed in group II rats with a higher protein intake. Features of diabetic glomerulopathy including mesangial hypercellularity and mesangial matrix expansion were also significantly milder in the groups with a low protein diet. On the other hand, medullary calcification and interstitial changes were most prominent in group I, given calcium phosphate supplement; the increase in the kidney weight was greater in groups I and II, which received insulin, than in group III, which did not. It was concluded that low protein diet significantly ameliorates diabetic glomerulopathy but that supplementation with inorganic phosphate in an amount equal to organic phosphate contained in the higher protein diet causes medullary calcification and interstitial nephritis. Also, administration of suboptimal doses of insulin in diabetic animals greatly enhances renal growth, more than that induced by diabetes alone.

Animals↗
PubMed1984

Segmental analysis of renal glucose transport in young female rats.

Free-flow micropuncture studies were performed on twenty-seven young female Sprague-Dawley rats before and after 10% extracellular volume expansion to evaluate glucose reabsorption at the accessible sites of both surface and papillary nephrons. In the distal nephron segments no significant glucose reabsorption was observed for the distal tubule and papillary collecting duct but significant difference in fractional glucose delivery was demonstrated between the bend of the Henle's loop and early distal tubule and between the late distal tubule and the base of the collecting duct. Comparison of the fractional glucose delivery within the same nephron group for both superficial and juxtamedullary nephrons indicated that glucose reabsorption occurred at some sites beyond the bend of the Henle's loop. Volume expansion inhibited glucose reabsorption in the proximal convoluted tubule, enhanced it in the segment between the late proximal and early distal tubules, but had no effect on glucose transport at further distal sites. It is concluded that, in addition to the proximal tubule, the ascending loop of Henle or cortical collecting tubule may play a role in maintaining glucose-free urine under physiological conditions.

Absorption↗
PubMed1983

A case of IgA nephropathy with an unusual response to corticosteroid and immunosuppressive therapy.

We report a case of IgA nephropathy that presented with nephrotic syndrome without hematuria. Renal biopsy revealed typical features of IgA nephropathy on light microscopy, immunofluorescence microscopy, and electron microscopy. A dramatic response occurred on corticosteroid and immunosuppressive therapy, characterized by clearance of proteinuria and a fall of serum IgA level to normal. The absence of hematuria and a response to therapy are distinctly unusual features of IgA nephropathy. This case represents a variant of IgA nephropathy associated with a nephrotic syndrome that resembles nephrotic syndrome with minimal change lesion in its responsiveness to immunosuppressive therapy.

Adult↗
PubMed1983

Mechanism of glycosuria during volume expansion superimposed on subthreshold glucose loading.

In order to elucidate the mechanism of glycosuria, clearance and micropuncture studies were performed in 19 dogs before and after subthreshold glucose loading and again after superimposition of extracellular volume expansion. Subthreshold glucose loading inhibited proximal sodium reabsorption and increased proximal glucose reabsorption, demonstrating dissociation between net sodium and glucose transport. Glucose delivery out of the proximal convoluted tubule was greatly increased by the combined effect of increased filtered load of glucose and reduced fractional proximal fluid reabsorption. There was a remarkable compensatory increase in glucose reabsorption in the segment between late proximal tubule and distal tubule (intermediate segment) and glycosuria did not occur. When 10% extracellular volume expansion was superimposed on the ongoing subthreshold glucose loading, absolute proximal glucose reabsorption was inhibited. This led to an additional increase in glucose delivery to the intermediate segment, but glucose reabsorption in this segment failed to increase further and overt glycosuria eventually developed. Thus the intermediate segment possesses some capacity to reabsorb glucose when glucose load is increased, and glycosuria develops only when the glucose reabsorptive capacity of this segment is exceeded. We conclude that the intermediate segment serves as the "buffer zone" of renal glucose transport and plays an important role in the regulation of urinary glucose excretion.

Absorption↗
PubMed1981

Renal phosphate adaptation in uraemic dogs with a remnant kidney.

1. Clearance and micropuncture studies were performed in 27 dogs made uraemic by segmental infarction to examine the factors responsible for phosphate adaptation in chronic renal failure. 2. The animals were studied before and after extracellular volume expansion to 10% of body weight in the presence and absence of parathyroid glands. The results were compared with 19 normal dogs studied under similar experimental conditions. 3. In the dogs with a remnant kidney and intact parathyroids adaptation of phosphate transport was evident, with a high fractional excretion of phosphate. Thyroparathyroidectomy 3 days before study in the dogs with a remnant kidney and moderate renal failure reduced fractional excretion of phosphate to near normal values, indicating a major role of parathyroid hormone in phosphate adaptation. Extracellular volume expansion in these thyroparathyroidectomized uraemic dogs led to an exaggerated phosphaturic response with fractional excretion of phosphate returning towards the value in the uraemic dogs with intact parathyroid glands. Thus acute extracellular volume expansion could also contribute to the increase in fractional phosphate excretion, but extracellular volume probably plays a relative minor role in the adaptation of phosphate excretion. 4. With more advanced renal failure fractional excretion of phosphate remained high, even after thyroparathyroidectomized, indicating that parathyroid hormone-independent factors become important for phosphate adaptation in the advanced stage of renal failure. The nature of parathyroid hormone-independent changes in fractional phosphate reabsorption in chronic renal failure remains unknown. 5. Proximal tubular fluid/plasma ultrafiltrate phosphate ratios were high in all groups of dogs with a remnant kidney regardless of thyroparathyroidectomy or the degree of renal failure. The non-specific nature of the proximal tubule pattern of phosphate transport indicates that phosphate adaptation is primarily determined by alterations in phosphate transport at a site distal to the proximal convoluted tubule. Alternatively, deep nephrons may play a greater role in determination of the overall phosphate adaptation in the chronically diseased kidney.

Adaptation, Physiological↗
PubMed1979

Effect of volume expansion on renal glucose transport in normal and uremic dogs.

Proximal and distal tubule micropuncture studies were performed in normal and uremic remnant-kidney dogs to examine the tubule mechanism of glucose reabsorption before and after 10% extracellular volume expansion. In normal dogs volume expansion markedly inhibited glucose reabsorption in the proximal convoluted tubule, but the ensuing increase in further distal glucose delivery was nearly completely reabsorbed in the intermediate segment (between late proximal tubule and distal tubule). In the uremic, remnant-kidney dogs, glomerulotubular balance for glucose was well maintained in the proximal convoluted tubule despite an adaptive increase in nephron filtration rate. Volume expansion markedly increased glucose delivery out of the proximal convoluted tubule and an incomplete glucose reabsorption in the intermediate segment led to glycosuria. When glucose delivery to the intermediate segment was increased to a comparable degree by subthreshold glucose loading in hydropenic normal dogs, glucose reabsorption in this segment was virtually complete, suggesting that in the volume-expanded uremic dogs glucose reabsorptive capacity in the intermediate segment was reduced. Thus, the intermediate segment appears to play a significant role in the fine regulation of urinary glucose excretion.

Animals↗
PubMed1978

Effect of phosphate deprivation on renal phosphate transport in the dog.

In order to examine the role of dietary intake of phosphate in regulating renal phosphate transport, clearance and micropuncture studies were performed in 25 dogs with various duration of phosphate deprivation induced by low phosphate diet and aluminum hydroxide gel. In phosphate deprivation of 17-41 days duration, the phosphaturic response to extracellular volume expansion (ECVE) was blunted in the intact group and was virtually abolished in the acutely thyroparathyroidectomized (TPTX) group. With longer phosphate deprivation of 53-110 days, no phosphaturia occurred after ECVE or administration of parathyroid hormone (PTH), even with intact parathyroids. These alterations in phosphaturic responses did not correlate with the plasma phosphate but rather with the duration of phosphate deprivation. Fractional proximal tubule phosphate reabsorption was enhanced in phosphate deprivation and the proximal tubule fluid-to-ultrafilterable phosphate ratio appeared to be a good index for the degree of phosphate deprivation. Acute infusion of phosphate to raise plasma phosphate slightly above normal did not completely restore the responsiveness to ECVE. It is concluded that the adaptive response to phosphate deprivation occurs in both proximal and distal nephron segments and that factors other than plasma phosphate are primarily responsible for such an adaptation.

Animals↗