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Biomedical subjects

G Castillo

Publications and source records attributed to G Castillo.

At least 55 records · Page 3Linked to original sources
PubMed1986

Hyperkalemic distal renal tubular acidosis in salt-losing congenital adrenal hyperplasia.

Functional indices of distal urinary acidification were assessed in two male infants, aged 1 and 3 months, with salt-losing congenital adrenal hyperplasia. In both cases the diagnosis was sustained by the presence of elevated plasma levels of 17-hydroxyprogesterone, hyponatremia, hyperkalemia, metabolic acidosis and increased plasma renin activity. Both patients were unable to lower urinary pH below 5.9 either during acute ammonium chloride-induced acidosis or after i.v. administration of furosemide. One patient also failed to decrease urine pH below 5.5 and to increase urinary potassium excretion during sodium sulfate infusion. Oral sodium bicarbonate loading was given to both patients but failed to induce a significant increase in the urine minus blood PCO2 gradient. This gradient remained low also after neutral phosphate administration. Repeated studies after acute administration of fludrocortisone in one case or after prolonged administration of hydrocortisone in the other resulted in complete normalization of all functional studies. We conclude that salt-losing congenital adrenal hyperplasia can lead to hyperkalemic distal renal tubular acidosis in early infancy. The defective renal secretion of hydrogen ion and potassium is probably related to the abolishment of the negative potential difference in the cortical collecting tubule induced by the impaired reabsorption of sodium.

Acidosis, Renal Tubular↗
PubMed1984

Production of soluble and cell-associated fibronectin by cultured keratinocytes.

Fibronectin has been demonstrated in epithelial cell types in culture, but published studies of keratinocytes have shown patterns of fibronectin produced by cells grown in medium with serum, which contains fibronectin. Since plasma fibronectin can bind to cells in vitro, cells grown in serum-supplemented media could show artifactual patterns of cell-associated fibronectin. To study insoluble fibronectin produced by keratinocytes, we plated cells in the absence of feeder layers in medium lacking fibronectin. Medium conditioned by metabolically labeled keratinocytes was studied by immunoprecipitation and by extraction with gelatin-Sepharose. Cells grown in fibronectin-free medium were labeled using affinity-purified anti-fibronectin antibody and fluorescein-conjugated antirabbit IgG. Keratinocytes produced soluble fibronectin, since both immunoprecipitation and adsorption to gelatin-Sepharose detected 35S-methionine-labeled material which comigrated with human plasma fibronectin on sodium dodecyl sulfate polyacrylamide gels. Demonstration of insoluble, cell-associated fibronectin was enhanced in Triton X-100-extracted cells and was seen in subcellular fibrillar arrays at both physiologic and reduced Ca++ concentrations, but in intracellular locations only at physiologic Ca++ concentrations. When cells grown in 1.1 mM Ca++ were removed with Triton X-100, diffusely distributed fibrillar fibronectin remained on the surface of the coverslip. Asymmetric "tracks" of fibronectin left by sparsely plated cells suggested movement. Fibronectin is deposited by keratinocytes on the culture surface and may be modulated by culture conditions.

Animals↗
PubMed1983

Biochemical features of dietary chloride deficiency syndrome: a comparative study of 30 cases.

The diagnosis in one infant of a severe state of chloride deficiency after ingesting a diet consisting exclusively of a modified cow milk formula containing only 0.5 mEq/100 kcal chloride ion led to the identification of 30 additional infants (age 2.6 +/- 0.7 months) fed the same commercial formula. The total absence of chloride in the urine was used as a biochemical index of subclinical dietary chloride deficiency. Serum and urine values were studied at diagnosis and 10 to 12 days after chloride replenishment, and compared statistically with the values obtained in a control group of 40 infants (age 2.8 +/- 1.2 months) fed exclusively a different modified formula containing an adequate chloride concentration. The outstanding laboratory abnormalities noted in the infants ingesting a low chloride formula were hypochloremia and metabolic alkalosis. Mean serum concentrations of potassium, urea, creatinine, and uric acid were in the normal range, but group values were statistically different from normal. A previously unreported finding was the demonstration of a significant elevation in the serum concentrations of calcium and phosphate and in the urinary excretions of calcium and magnesium, which persisted after almost complete recovery of the remaining biochemical disturbances. These results indicate the potential risk of nephrocalcinosis after dietary chloride deficiency.

Calcium↗
PubMed1983

Transient pseudohypoaldosteronism secondary to obstructive uropathy in infancy.

A syndrome of renal tubular resistance to aldosterone has been identified in infants with obstructive uropathy and urinary tract infection. Six infants (ages 9 days to 7 months) were seen with fever, vomiting, polyuria, dehydration, or failure to thrive. Urine cultures were positive for Escherichia coli. Radiologic studies demonstrated bilateral ureterohydronephrosis (four patients), left ureteral duplication with upper pole hydronephrosis (one), and left vesicoureteral reflux (one). The infants had hyponatremia, hyperkalemia, and metabolic acidosis. Plasma aldosterone concentration was markedly elevated, and plasma renin activity was similar to or higher than that reported in normal infants of comparable age. Fractional excretion of potassium was not significantly different from control values, both in absolute terms or when related to glomerular filtration rate, but fractional sodium excretion was significantly increased. The UK/UNa ratio was significantly lower in the patients. After medical or surgical therapy (when appropriate), all blood and urine determinations returned to normal, except for UK/UNa values, which although higher, remained significantly diminished. Our data indicate that a hyperkalemic salt-losing state can arise in infants with obstructive uropathy and urinary tract infection as a consequence of tubular unresponsiveness to aldosterone, and that the clinician should rule out such cause before establishing the diagnosis of primary pseudohypoaldosteronism.

Aldosterone↗
PubMed1983

Renal handling of sodium in premature and full-term neonates: a study using clearance methods during water diuresis.

A study using fractional clearances during orally induced water diuresis was designed to delineate the mechanism underlying defective tubular reabsorption of sodium in very low-birth-weight neonates. The use of clearance methodology during maximal water diuresis may give an indirect estimate of distal sodium delivery [urine volume (V), CH2O + CNa + K], sodium reabsorption at the diluting segments (CH2O), and proportion of the distal load reabsorbed distally (CH2O/CH2O + CNa + K), when all values are corrected to 100 ml glomerular filtration rate. The study was carried out in 28 healthy newborn infants who were grouped according to conceptual age (CA): 13 infants with mean birth weight of 1370 +/- 330 g and mean CA of 31.8 wk (range, 28-34 wk), and 15 infants with mean birth weight of 2330 +/- 550 g and mean CA of 37.9 wk (range, 35-41 wk). All studies were performed at 6-7 days of age. It was demonstrated that higher urinary osmolality (67.5 +/- 23.2 versus 52.9 +/- 9.4 mOsm/kg, P less than 0.0025) and higher fractional sodium excretion (2.3 +/- 1.8 versus 0.9 +/- 0.5 ml/dl glomerular filtration, P less than 0.01) observed in the group of very preterm infants resulted from significantly decreased proximal (V: 18.7 +/- 6.0 versus 13.3 +/- 3.6 ml/dl glomerular filtration, P less than 0.005; CH2O + CNa + K: 17.1 +/- 5.2 versus 11.9 +/- 3.3 ml/dl glomerular filtration, P less than 0.005) and distal (CH2O/CH2O + CNa + K X 100: 81.9 +/- 8.2 versus 88.2 +/- 4.5%, P less than 0.01) tubular sodium reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Diuresis↗
PubMed1982

Natural history of primary distal renal tubular acidosis treated since infancy.

Clinical and pathophysiologic studies were performed in five unrelated children with primary distal renal tubular acidosis who were diagnosed during infancy and followed for 3 to 9 1/2 years. All patients had permanent defects in hydrogen ion secretion, sodium reabsorption, and concentrating capacity. A transient, age-related, proximal tubular defect in sodium and bicarbonate reabsorption was also present. Renal bicarbonate wasting was mainly observed during the first years of life and progressively decreased with advancing age. Glomerular filtration rate remained within normal limits. Following sustained therapy with sodium and potassium bicarbonate, the patients had optimal growth, arrest of progression of nephrocalcinosis, and lack of other characteristic features of the disease with the exception of polyuria. Dosage of alkali was mainly determined by the magnitude of the renal bicarbonate loss and decreased progressively from a maximum of 3.9 to 10.0 mEq/kg/day during the first year of life to about 3 mEq/kg/day at or beyond 6 years of age. The total dosage of alkali required could be derived by the sum of the urinary excretion of bicarbonate plus 2 mEq/kg/day, which represents mean endogenous acid production. Although calciuria was normal when metabolic acidosis was corrected, patients with higher urinary sodium excretion had higher urinary excretion of calcium and thus were at greater risk of developing nephrocalcinosis if therapy was not carefully controlled.

Acidosis, Renal Tubular↗
PubMed1982

Defect in urinary acidification in nephrotic syndrome and its correction by furosemide.

6 children with idiopathic nephrotic syndrome were investigated during clinical relapse to examine the interrelation between distal urinary acidification and urinary sodium excretion. Blood and urine studies were initiated 4 h after completion of ammonium chloride loading, prior to and following the intravenous administration of furosemide. Values for plasma bicarbonate before and after furosemide administration were not significantly different. In the control periods, when urinary sodium excretion was very low, a defect in urinary acidification was demonstrated (UPH: 6.09 +/- (SD) 0.27; UTAV and UNH4V: 12.6 +/- 3.1 and 36.4 +/- 15.8 mumol/min/1.73 m2, respectively.) Following furosemide-induced natriuresis UPH fell to 4.81 +/- 0.25 (p less than 0.0005), and UTA2V and UNH4V increased to 46.3 +/- 15.8 and 125.6 +/- 49.5 mumol/min/1.73 m2, respectively (p less than 0.002). No overall correlation existed between urinary acidity, both considered as hydrogen ion concentration and as hydrogen ion excretion, and rate of urinary sodium excretion; but significant correlations were present between hydrogen ion concentration in the urine and both UC1V-UNAV (r = 0.38, p less than 0.05), and UC1V - (UNaV + UKV) (r = 0.64, p less than 0.01). These results indicate that the defect in distal urinary acidification observed in nephrotic syndrome is probably due to decreased delivery of sodium to the distal nephron. The enhanced secretion of hydrogen ion observed after furosemide administration may be related both to increased sodium delivery and to greater sodium than chloride reabsorption in the collecting duct.

Child↗
PubMed1982

Different functional characteristics of residual nephrons in infantile vs adult diffuse cortical necrosis.

In this report we study the functional characteristics of residual nephrons in a 37 year-old woman, 7 months after diffuse bilateral cortical necrosis (CN) of unknown etiology, and in two infants, aged 13 and 15 months, who suffered CN in early infancy after surgical shock and acute dehydration, respectively. In the three cases CN was proven histologically by renal biopsy but undamaged nephrons were only present in the juxtamedullary area in the adult patient whereas in the two infants they were located in the outer part of the cortex. At the time of the study all patients presented a similar degree of renal insufficiency (creatinine clearance: 17-23 ml/min/1.37 m2). The adult patient showed a partly conserved ability to concentrate the urine, a marked free water formation in relation to the degree of distal sodium delivery and an unimpaired capacity to acidify the urine after an acid load. Both infants, by the contrary, were unable to concentrate the urine, had lower free water formation at similar rates of distal sodium delivery and presented a clear incapacity to acidify the urine. These results confirm previous finding indicating the sparing of juxtamedullary nephrons after CN in the adult subject but favor the existence of a surviving population of superficial nephron when CN occurs in early infancy. These differences are probably in relation with associated damage of deep cortex and medulla infancy due to the specific characteristics of blood flow distribution present at that age.

Acute Kidney Injury↗
PubMed1980

Renal handling of water and sodium in children with proximal and distal renal tabular acidosis.

Renal sodium wasting has been observed in both proximal and distal renal tubular acidosis (RTA), although few studies have been reported indicating the tubular localization of such a defect. The use of clearance methodology during hypotonic saline diuresis may give an indirect estimate of proximal tubular reabsorption of sodium, sodium reabsorption at the diluting segments and proportion of sodium load reabsorbed distally. This study was carried out in 17 normal children, in 9 children with proximal RTA, associated in all but one with the Fanconi syndrome, and in 5 children with primary distal RTA. Patients with proximal RTA presented mainly an impaired reabsorption of sodium in the proximal tubule, which was in great part but not completely compensated by an absolute increase in distal sodium reabsorption. Patients with distal RTA showed normal reabsorption of sodium in the proximal tubule but they were unable to reabsorb completely the load of sodium escaping proximal reabsorption due to a defect of sodium reabsorption in the distal diluting segments. These results indicate that the classification of RTA in proximal and distal types is also valid according to the differences found in the tubular handling of water and sodium.

Acidosis, Renal Tubular↗
PubMed1978

Proximal renal tubular acidosis in metachromatic leukodystrophy.

A 2-year-old girl affected with the late infantile form of metachromatic leukodystrophy had a persistent and moderate metabolic acidosis. Renal functional studies demonstrated the presence of decreased tubular reabsorption of sodium, bicarbonate and some amino acids. Other tubular functions, including distal urinary acidification and concentrating mechanism were normal. Glomerular filtration rate was moderately decreased. Metachromatic inclusions were demonstrated along the nephron by histochemistry and electron microscopy. Tubular dysfunction in metachromatic leukodystrophy could have been overlooked until now given the severity of the neurological picture.

Acidosis, Renal Tubular↗
PubMed1975

Proximal renal tubular acidosis in the tetralogy of fallot.

A 9-year-old girl presented with tetralogy of Fallot and moderate metabolic acidosis. Despite a Blalock's fistula there was evidence of chronic hypoxia with cyanosis, clubbing of fingers and toes and very elevated blood hematocrit values. Renal acidification and bicarbonate titration demonstrated the existence of proximal renal tubular acidosis: renal bicarbonate threshold was low (18 mmoles/1) and normal urinary acidificaiton was present at subthreshold serum bicarbonate levels. Following corrective heart surgery, blood acid-base values and renal reabsorption of bicarbonate became normal. A causal relationship between extracellular fluid volume expansion dependent on the high hematocrit and proximal renal tubular acidosis is suggested.

Acidosis, Renal Tubular↗
PubMedDate not supplied

[Environmental contamination with Toxocara sp. eggs in public squares and parks from Santiago, Chile, 1999].

Most of cases of visceral larva migrans syndrome are caused by Toxocara canis larvae. Man acquires the infection by accidental ingestion of ripe eggs of the helminth. In order to find out the frequency of the presence of Toxocara sp. eggs in dog fecal specimens from public places of Santiago city in 1999 july-september a study was carried out in 84 squares and 12 parks from 32 counties. Three fecal samples were collected in each of these places, making a total of 288. Each sample was processed according to a modified Telemann method and three smears of each were microscopically examined. Toxocara sp. eggs were found in 39 (13.5%) fecal specimens. In 28/84 (33.3%) squares and in 8/12 (66.7%) parks these eggs were detected. These results make necessary the control of dogs and cats populations with the aim of reduce the presence of animals without responsible owners. It should be advisable to prevent dogs and cats defecation in public areas grounds, trying to exclude these animals from recreation areas.

Animals↗
PubMedDate not supplied

Pathophysiology of primary distal renal tubular acidosis.

Functional indices of distal acidification were assessed in five unrelated children with primary distal renal tubular acidosis. All patients were unable to lower urinary pH below 6.0 both during ammonium chloride-induced acidosis or after acute i.v. administration of furosemide. In these patients the urine minus blood Pco2 gradient failed to increase normally during acute sodium bicarbonate loading (mean +/- SEM: 5.8 +/- 2.0 mmHg), or after neutral phosphate administration (13 +/- 2.7 mmHg), despite adequate urinary concentrations or bicarbonate (72.2 +/- 14.6 mmol/L) and phosphate (25 +/- 2.3 mmol/L), respectively. They also failed to decrease urine pH below 5.5 with sodium sulfate (7.17 +/- 0.08), but urinary potassium excretion increased significantly. These results strongly suggest that the mechanism responsible for defective distal acidification is a failure of hydrogen ion secretion ("secretory' defect) and not an inability to establish a steep hydrogen ion gradient, as it was formerly believed.

Acidosis, Renal Tubular↗