PubMed Health⌕ Search

Biomedical subjects

N A Kurtzman

Publications and source records attributed to N A Kurtzman.

At least 55 records · Page 3Linked to original sources
PubMed1990

A patient with hyperkalemia and metabolic acidosis.

Uptake of potassium by extrarenal tissues, primarily muscle and liver, represents a major defense mechanism in the maintenance of normokalemia following an acute elevation in the serum potassium concentration. Insulin, epinephrine, and aldosterone all play major roles in maintaining the normal distribution of potassium between the intracellular and extracellular environment. In addition to hormonal regulation, changes in blood pH and tonicity also exert a strong influence on extrarenal potassium metabolism. Last, the serum potassium concentration per se directly influences its own cellular uptake and this transport mechanism appears to be inhibited by uremia.

Acidosis↗
PubMed1990

Enzyme activity in obstructive uropathy: basis for salt wastage and the acidification defect.

Unilateral ureteral obstruction results in marked changes in renal function throughout the nephron, including impaired acid and potassium secretion and salt wastage. The nephron site believed responsible for the acidification defect is the collecting duct. It has been presumed, although not demonstrated, that the cellular mechanism for the acidification defect is both a decrease in transepithelial voltage and a decrease in activity of the proton pump located at the luminal membrane. The mechanism for the abnormalities in sodium handling are thought due to alterations in Na-K ATPase activity. Our laboratory has recently mapped the profile of the N-ethylmaleimide (NEM)-sensitive ATPase and Na-K ATPase in microdissected rat nephron, documenting their presence throughout much of the nephron. In animals with acute unilateral ureteral obstruction for 18 to 24 hours, we measured NEM-sensitive ATPase and Na-K ATPase activities in several nephron sites. In all nephron segments Na-K ATPase activity was markedly decreased. In the medullary collecting duct, NEM-sensitive ATPase activity was also markedly reduced in animals with acute ureteral obstruction; in the cortical collecting duct, activity fell significantly, but to a lesser degree than was observed in the medullary collecting duct. NEM-sensitive ATPase activity was unchanged from control in the proximal convoluted tubule and in the medullary thick ascending limb; in the cortical thick ascending limb enzyme activity increased. These results demonstrate a change in both Na-K ATPase and NEM-sensitive ATPase activities as a direct consequence of a defect known to result in salt wastage and an acidification defect in humans and animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1990

Collecting tubule adaptation to respiratory acidosis induced in vivo.

To examine the effects of respiratory acidosis in vivo on the adaptation of acidification in the collecting tubule, New Zealand White rabbits were exposed to a 6.7% CO2-93.3% O2 gas mixture in an environmental chamber for 0, 6, 24, or 48 h before obtaining collecting tubules for in vitro study. These collecting tubules were then perfused and bathed in vitro in identical Krebs-Ringer bicarbonate solutions. After 1 h equilibration total CO2 flux (JtCO2) was measured. The urine pH of the rabbits fell, whereas the blood bicarbonate rose as CO2 exposure time increased. In cortical collecting tubules, JtCO2 in vitro correlated with length of animal exposure to hypercarbia (y = 1.14174 + 0.1437x, r = 0.57, P = 0.002), and with the blood bicarbonate of the animal (y = 26.8471 + 0.0858x, r = 0.59, P less than 0.05). In vitro JtCO2 in medullary collecting tubules from rabbits that had been in hypercarbic atmosphere for 48 h (23.2 +/- 4.9 pmol.mm-1.min-1) did not differ from JtCO2 in control tubules (25.0 +/- 3.2 pmol.mm-1.min-1, not significant). Thus the cortical collecting tubule exhibits an adaptive increase in JtCO2 in response to hypercarbia, whereas the medullary collecting tubule does not.

Acidosis, Respiratory↗
PubMed1990

NEM-sensitive ATPase activity in rat nephron: effect of metabolic acidosis and alkalosis.

The present study was designed to quantitate the amount and to map the localization of N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) activity in microdissected segments of the rat nephron. After complete nephron mapping the effect of chronic metabolic acidosis and alkalosis on enzyme activity was determined. In control animals the highest enzyme activity was found in the early proximal convoluted tubule of juxtamedullary nephrons; superficial early proximal tubule as well as medullary and cortical thick ascending limbs and collecting ducts also contained substantial activity. Enzyme activity in the papillary collecting duct before entry into the ducts of Bellini was 329 +/- 93 pmol.mm-1.h-1 (n = 8); after entry, however, enzyme activity was approximately one-fourth that value (60 +/- 9 pmol.mm-1.h-1, n = 8, P less than 0.01). No NEM-sensitive ATPase activity was found in the thin limbs of the loop of Henle. Enzyme activity increased in both the medullary and cortical thick ascending limbs as well as in the cortical collecting tubule in response to NH4Cl-induced chronic metabolic acidosis; in the cortical collecting duct, metabolic acidosis increased maximum activity (Vmax) but did not change Michaelis-Menten constant (Km). In the proximal convoluted tubule, enzyme activity decreased with metabolic acidosis. Bicarbonate loading had no effect on enzyme activity except in the most distal portion of the collecting duct where it was stimulated. These results show that NEM-sensitive ATPase activity exists throughout much of the rat nephron. These data suggest that both the cortical collecting tubule and thick ascending limb are regulatory sites of distal urinary acidification during acid loading.

Acidosis↗
PubMed1989

Hypokalemia.

Explore the source record for details and available documents.

Humans↗
PubMed1989

Dimethyl sulfoxide affects water flow through a nonosmolar action.

Dimethyl sulfoxide (DMSO) is a dipolar organic compound commonly used as a solvent in studies of membrane transport. DMSO also has many effects on cell function and, although the precise mechanism of action is not known completely, it has been stated to exert its effect on transport solely through osmolality. The present study was designed to examine the effects of serosal DMSO at three osmolar concentrations on Basal Water Flow and vasopressin (AVP)- and cyclic AMP-stimulated water flow (Maximal Water Flow) in the toad bladder. The results obtained were compared to equi-osmolar concentrations of mannitol and NaCl. All three agents significantly enhanced Basal Water Flow after 60 min. The results obtained on Maximal Water Flow were different depending on the final osmolality. At 300 mOsm final concentration, all three agents increased AVP-stimulated water flow. When the serosal osmolality was 600 or 900 mOsm DMSO increased Maximal Water Flow, whereas mannitol and NaCl decreased it. When 300 mOsm DMSO plus 300 mOsm mannitol (600 mOsm total)-treated hemibladders were challenged with AVP, the water flow response was similar to that of 600 mOsm DMSO alone. In the presence of verapamil, AVP-stimulated water flow was decreased markedly; when DMSO was added to verapamil-pretreated hemibladders, and they were then challenged with AVP, water flow increased significantly. In similar experiments with mannitol, water flow remained inhibited. Dimethylsulfone did not enhance AVP-stimulated water flow as compared to the same concentration of DMSO. These results demonstrate that the effects of DMSO on water transport are not mediated solely by its osmolar action.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Site of the acidification defect in the perfused postobstructed collecting tubule.

The effect of prior urinary tract obstruction on total CO2 flux in cortical and medullary collecting tubules was examined using an unilateral ureteral obstruction model and isolated tubule in vitro microperfusion. Tubules were obtained from the control and obstructed kidneys after 1, 2, and 4 days of obstruction. Paired comparison of function of cortical or medullary tubules and urine pH was made. Medullary collecting tubules showed decreased acidification after 2 days of obstruction (7.7 +/- 8.5 vs. 29.9 +/- 6.6 pmol/mm/min). Cortical collecting tubules from the obstructed kidney showed high rates of acidification at all time periods examined, and rates from the postobstructed cortical collecting tubules exceeded levels from control tubules at the 24-hour period while barely missing significance (p less than 0.06) at the 48- and 96-hour periods. These data are not consistent with the hypothesis that the acidification defect in the postobstructed kidney occurs in the cortical collecting tubule by a voltage-dependent mechanism.

Acid-Base Imbalance↗
PubMed1989

Vanadate stimulates the N-ethylmaleimide-sensitive adenosine triphosphatase in rat nephron.

Vanadate has been used in many cellular systems to elucidate mechanisms of enzyme action. Vanadate inhibits Na-K adenosine triphosphatase (ATPase) activity in many tissues. In isolated collecting tubule it inhibits sodium transport and vasopressin-stimulated water flux, the latter presumably distal to cyclic AMP formation. Depending upon the tissue studied, vanadate also stimulates a variety of cellular reactions including adenylate cyclase, glucose oxidation and glycogen synthesis. We studied the effect of varying concentrations of vanadate on N-ethylmaleimide (NEM)-sensitive ATPase activity in microdissected segments of rat nephron. In proximal convoluted tubule and in cortical, medullary and papillary collecting ducts vanadate had no effect on enzyme activity. In medullary and cortical thick ascending limbs, however, vanadate significantly stimulated NEM-sensitive ATPase activity (medullary thick ascending limb, 241 +/- 14 pmol/mm/hr vs. 531 +/- 74 pmol/mm/hr; control vs. (1 mM) vanadate, respectively; n = 14, P less than 0.01). The stimulatory effect of vanadate on NEM-sensitive ATPase activity was present at 5 microM vanadate, a concentration that inhibited Na-K ATPase activity approximately 80%. Metabolic acidosis also stimulated enzyme activity in the thick ascending limb, and the effect of vanadate was not additive. Metabolic alkalosis had no effect on NEM-sensitive ATPase in the thick ascending limb, but the stimulatory effect of vanadate was still seen. These data document that the NEM-sensitive ATPase in thick ascending limb is different from that found in other nonmammalian proton secretory epithelia which are vanadate inhibitable. The results with vanadate plus metabolic acidosis suggest that both are acting via the same mechanism.

Acidosis↗
PubMed1989

Effect of phthalate acid esters on transport in toad bladder membrane.

Sclerosing peritonitis is a serious complication in patients on long-term peritoneal dialysis; it markedly decreases transport of water and solute across the peritoneal membrane. Although the precise mechanism is unknown, organic compounds (i.e., plasticizers) from plastic tubing and dialysis bags have been suggested to be a cause of the syndrome. The effects of three such compounds on water and sodium transport in vitro were studied in the toad bladder. The compounds studied were didodecylphthalate, dioctylphthalate, and benzylbutylphthalate. After 4 hr incubation in vitro, dioctylphthalate and benzylbutylphthalate significantly inhibited vasopressin-stimulated water flow in toad bladder. Basal water flow was not affected by any of the three compounds. Sodium transport, as measured using short-circuit current, was decreased to an equivalent degree by all compounds; inhibition of short-circuit current was dose dependent and was approximately 30% at 10(-3) M. The onset of action was between 3.5 and 4 hr, and the effect on short-circuit current was not reversible. These results demonstrate that the plasticizers (to which patients of all sorts are commonly exposed) inhibit transport across living membranes. In the toad bladder these compounds decrease sodium transport and maximal water flow. Although other evidence suggests that the cumulative toxic effects of these compounds may play a causal role in sclerosing peritonitis in patients on peritoneal dialysis, our study suggests that chronic exposure to the phthalate acid esters in patients with normal renal function may result in sodium wastage, polyuria, and a concentrating defect resistant to AVP.

Animals↗
PubMed1988

Assessment of collecting tubule hydrogen ion secretion in acute respiratory alkalosis using the urinary pCO2.

The use of the urine-blood (U-B) pCO2 difference as a marker of collecting tubule H+ secretion (CTH+S) faces serious interpretative pitfalls when applied to animals with respiratory acidosis. The present study was aimed to examine the use of this parameter in rats with acute respiratory alkalosis. During infusion of sodium bicarbonate, the U-B pCO2 was only slightly lower in hypocapnic than in eucapnic rats (30 +/- 2.2 and 39 +/- 3.3 mmHg, p less than 0.05) and this difference was no longer significant when this parameter was examined as a function of urine bicarbonate concentration. In contrast, the increment in urine pCO2 elicited by bicarbonate loading (i.e. the delta pCO2) was markedly reduced in hypocapnic as compared to eucapnic rats (22 +/- 3.0 and 38 +/- 4.5 mmHg, respectively, p less than 0.01). The infusion of carbonic anhydrase while the urine was highly alkaline and the blood pCO2 kept constant resulted in a decrement in urine pCO2 which was less in hypocapnic than in eucapnic rats (-23.9 +/- 1.9 vs -33 +/- 2.8 mmHg, p less than 0.02). These findings indicate that pCO2 generation from CTH+S and titration of bicarbonate is reduced in hypocapnic rats. The data are in accord with our proposal that the delta pCO2 is a better index of CTH+S than the U-B pCO2 is the assessment of respiratory acid-base disorders.

Alkalosis, Respiratory↗
PubMed1988

Humoral hypercalcemia due to squamous cell carcinoma of renal pelvis.

We describe an unusual and rare case of humoral hypercalcemia due to Stage D squamous cell carcinoma of the renal pelvis in a patient with no evidence of bony metastases. The literature on humorally mediated hypercalcemia associated with epithelial tumors of the renal pelvis is reviewed.

Adult↗
PubMed1988

Thiazides stimulate calcium absorption in the turtle bladder.

The mechanism of action of the thiazide diuretics on calcium transport is not completely understood. The present study was designed to examine the effect of hydrochlorothiazide (HTZ) on Na transport, proton secretion, and Ca45 flux in the turtle bladder, a high resistance membrane. When added to the mucosal solution, 1 mM HTZ had no effect on Na transport or proton secretion, but significantly increased mucosa-to-serosa Ca45 flux at 60 minutes (control 118.9 +/- 39.7 pmol/mg/60 min versus thiazide 286.0 +/- 64.9 pmol/mg/60 min, N = 16, P less than 0.02). In the presence of 5 X 10(-4) M ouabain, a maneuver which inhibits active Na transport, HTZ again significantly enhanced mucosa-to-serosa Ca45 flux. The increment of calcium transport under these conditions was 83.4 +/- 35.2 pmol/mg/60 min (N = 8, P less than 0.05). Mucosal HTZ had no effect on serosa-to-mucosa (that is, bath-to-lumen) Ca45 flux after a 60 minute incubation. Serosal addition of HTZ had no effect on either of the unidirectional Ca45 fluxes or on Na transport. Mucosal tissue Ca45 content was enhanced by HTZ (mucosal) in the presence or absence of ouabain. These results provide support for the view that thiazides have a direct stimulatory effect on calcium absorption at the luminal membrane, perhaps secondary to increased mucosal calcium permeability.

Animals↗
PubMed1988

Nephrotic syndrome and renal failure associated with a novel glycolipid storage disorder.

A 57-year-old Caucasian male presented with severe nephrotic syndrome and diffuse organomegaly; he subsequently developed renal failure and died. Intracellular, crystalloid material was identified by light and electron microscopy in bone marrow, liver, spleen, mesenteric lymph nodes, and kidneys. Tissue extraction analysis identified the material as glucocerebroside and its immediate precursor, ceramide lactoside. Although Gaucher's disease cannot be completely excluded, glycolipid profiles do not conform to those of known storage disorders. Additionally, electron-microscopic studies indicate that the structural features of the glycolipid deposits are different from those of previously described storage diseases. These findings suggest a unique crystalloid deposition as the probable cause of a multisystem process, which was associated with renal insufficiency and death.

Acute Kidney Injury↗
PubMed1988

On the mechanism of toluene-induced renal tubular acidosis.

This study was aimed to investigate the pathogenesis of toluene-induced renal tubular acidosis (RTA). In 5 individuals addicted to toluene sniffing we documented the occurrence of hypokalemia and hyperchloremic metabolic acidosis associated with inability to lower urine pH below 5.5 (6.06 +/- 0.24). Overall kidney bicarbonate reabsorption was normal or enhanced, a feature characteristic of the distal form of RTA (DRTA). These findings resemble those found during the administration of amphotericin B, a drug felt to cause DRTA by increasing hydrogen ion (H+) back-diffusion in the collecting tubule. In toluene sniffers, the urine pCO2 measured in a highly alkaline urine was reduced (47 +/- 8.8 mm Hg), suggesting a decrease in the rate of collecting tubule H+ secretion rather than H+ back-diffusion. To investigate these two mechanisms of altered distal acidification more directly we studied the effect of toluene on acidification by the urinary turtle bladder, an epithelial analogue of the mammalian collecting tubule. In this preparation, toluene resulted in a decrease in the rate of H+ secretion measured by either the pH stat technique or the reverse short circuit current. When mucosal pH was progressively lowered to examine H+ secretion against an H+ gradient, toluene-treated bladders displayed a significant decrease in proton conductance but the lowest mucosal pH required to nullify H+ secretion, (MpH) JH = O, was not different from that of control bladders (4.05 +/- 0.29 and 3.90 +/- 0.13, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1988

Metaauthorship.

Explore the source record for details and available documents.

Authorship↗