Biomedical subjects

J Work

Publications and source records attributed to J Work.

At least 37 records · Page 2Linked to original sources

PubMed1994

Transport of sodium and urea in outer medullary descending vasa recta.

We dissected and perfused outer medullary vasa recta (OMVR) from vascular bundles in the rat. Permeabilities of sodium (PNa) and urea (Pu) were simultaneously determined from the lumen-to-bath efflux of 22Na and [14C]urea. PNa and Pu were also measured by in vivo microperfusion of descending (DVR) and ascending vasa recta (AVR) at the papillary tip of Munich-Wistar rats. In some OMVR PNa was indistinguishable from zero. The mean +/- SE of PNa (x 10(-5), cm/s) in OMVR was 76 +/- 9. Pu in OMVR was always very high (x 10(-5), cm/s), 360 +/- 14. There was no correlation between OMVR PNa and Pu. Inner medullary AVR and DVR had PNa of 115 +/- 10 and 75 +/- 10, respectively, and Pu of 121 +/- 10 and 76 +/- 11, respectively. PNa and Pu in papillary vasa recta were always nearly identical and highly correlated. Transport of [14C] urea in OMVR was reversibly inhibited by addition of unlabeled urea or phloretin to the bath and lumen, providing evidence for carrier-mediated transport. These data suggest that sodium and urea might traverse the wall of inner medullary vasa recta by a paracellular pathway while urea also crosses by a transcellular route in OMVR. Electron microscopic examination of seven in vitro perfused OMVR revealed no fenestrations and exposure of these vessels to 10 microM calcium ionophore A23187 or 1 nM angiotensin II resulted in reversible contraction, suggesting that in vitro perfused OMVR are DVR only.

Angiotensin II↗

PubMed1994

Comparison of intramuscular versus subcutaneous erythropoietin for the treatment of anemia in CAPD patients.

Recombinant human erythropoietin (rHuEpo) can be administered to continuous ambulatory peritoneal dialysis (CAPD) patients subcutaneously (SC), intravenously (IV), and intraperitoneally (IP). Subcutaneous rHuEpo is preferred in CAPD patients because of its ease of administration and favorable pharmacokinetics. The longer half-life of SC rHuEpo allows for one or two doses per week. Since SC rHuEpo can cause pain and local irritation at the injection site, the efficacy and safety of intramuscular (IM) rHuEpo were compared to SC rHuEpo in 6 random stable CAPD patients. The protocol in each subject consisted of a single weekly injection of IM rHuEpo for 3-6 months (period 1), crossover to SC rHuEpo for 3-6 months (period 2), and crossover to IM rHuEpo for 3-6 months (period 3). The rHuEpo dose was adjusted by protocol to achieve a target hematocrit of 30%-33%. Pain at the injection site was graded on a scale of 0-3. All patients preferred IM rHuEpo to SC rHuEpo because of less pain at the injection site. One patient tolerated IM rHuEpo for six months (period 1), then left the study after one month of SC rHuEpo because of ecchymoses and pain at the SC injection sites. In all patients, there was no significant difference in the dose of rHuEpo (U/kg/wk) during the three study periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Tophaceous gout in patients with renal transplants treated with cyclosporine A.

Hyperuricemia and gout have been associated with cyclosporine A (CyA) therapy in transplant recipients. We describe 4 patients who developed severe tophaceous gout after renal transplantation. All of the patients received CyA, prednisone, and diuretic therapy. Three had episodes of allograft rejection. No patient had the diagnosis of gout before transplantation. All developed tophi within 5 years of the first attack of gout. Management of these patients has been difficult due to renal insufficiency, drug interactions and toxicity. Clinicians should be aware that tophaceous gout can occur rapidly in CyA treated transplant recipients.

Adult↗

PubMed1990

Total CO2 transport in rat cortical collecting duct in chloride-depletion alkalosis.

Previous studies in chloride-depletion metabolic alkalosis (CDA) generated by intraperitoneal dialysis have suggested major alterations in chloride and bicarbonate transport beyond the distal convoluted tubule. To investigate the possible role of the cortical collecting duct (CCD) in the pathophysiology of CDA, isolated CCD segments were perfused in vitro from either control (CON) rats dialyzed against Ringer-bicarbonate or those made alkalotic by peritoneal dialysis with 0.15 M NaHCO3. Tubules from CDA animals secreted CO2 for greater than or equal to 3 h after dissection (-22.4 +/- 7.2 pmol.mm-1.min-1) compared with CON tubules that absorbed CO2 (18.3 +/- 4.2 pmol.mm-1.min-1). Replacement of luminal chloride with gluconate in the perfusate abolished net total CO2 (tCO2) secretion in tubules from CDA animals (from -21.5 +/- 4.5 to -2.7 +/- 2.3 pmol.mm-1.min-1) but did not alter net tCO2 absorption in tubules from CON animals. In contrast, removal of bath chloride increased net tCO2 secretion (-12.1 +/- 2.9 to -26.1 +/- 3.6 pmol.mm-1.min-1) in CDA tubules, whereas net tCO2 flux was altered from absorption to secretion in CON tubules (15.5 +/- 4.0 to -13.6 +/- 9.2 pmol.mm-1.min-1). These results demonstrate that 1) CDA generated in vivo within 45 min results in stable net tCO2 secretion in vitro up to 240 min in the CCD; 2) luminal chloride is necessary for tCO2 secretion; 3) the shift of net tCO2 flux from absorption to secretion in CON tubules in vitro was not sustained in contrast to CDA tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗

PubMed1990

Resistance of descending vasa recta to the transport of water.

The effect of varying intracapillary oncotic pressure on the rate of transcapillary volume flux in microperfused descending vasa recta (DVR) was studied during furosemide diuresis in the Munich-Wistar rat. At the papillary base, plasma protein concentration and hydraulic pressure were 5.7 +/- 0.1 g/dl and 11.7 +/- 0.7 mmHg in nonperfused DVR, respectively, and 5.6 +/- 0.1 g/dl and 9.4 +/- 0.4 mmHg in nonperfused ascending vasa recta (AVR), respectively. These results demonstrate that the papillary microcirculation does not remove water from the interstitium during furosemide diuresis and defines Starling forces in the pericapillary interstitium. Osmolality and urea concentration were 380 +/- 11 mosmol/kgH2O and 56 +/- 5 mM in DVR plasma at the papillary base, respectively, and 386 +/- 10 mosmol/kgH2O and 62 +/- 5 mM in DVR plasma at the tip, respectively. These results demonstrate abolition of corticomedullary small solute gradients. DVR were perfused at a rate of 10 nl/min with a buffer solution containing small-solute concentrations that matched those of plasma in nonperfused DVR. The buffer solution also contained 2 x 10(6) mol wt fluorescein isothiocyanate-labeled dextran (FITC-Dx, 5 mg/ml) and either 0.1 or 5.0 g/dl albumin. Microperfused DVR were punctured a second time downstream of the perfusion site for sample collection or servo-nulling pressure measurement. The rate of transmembrane volume flux, determined from the change in FITC-Dx concentration from perfusate to collectate, was 0.99 +/- 0.29 nl.min-1.mm-1 when perfusate contained 0.1 g/dl albumin and 0.00 +/- 0.23 nl.min-1.mm-1 with 5.0 g/dl albumin (P less than 0.01). Intracapillary hydraulic pressures were 21.7 and 20.4 mmHg during microperfusion of DVR with 0.1 and 5.0 g/dl albumin, respectively. These results demonstrate that transcapillary driving forces of 20 mmHg (5 g/dl albumin) influence transcapillary water movement across the DVR endothelium. For an average capillary diameter of 12.9 microns, DVR hydraulic conductivity is calculated to be greater than 1.4 x 10(-6) cm.s-1.mmHg-1.

Animals↗

PubMed1987

Acute cryoglobulinemic renal failure after intravenous infusion of gamma globulin.

A 39-year-old woman had mixed IgM/IgG cryoglobulinemia, but was later found to have a lymphoma that produced an IgM kappa paraprotein with rheumatoid factor activity. With intermittent chlorambucil and prednisone therapy, the lymphoma was controlled for five years and she had no evidence of cryoglobulinemia. Because of the presence of intractable pulmonary infection and hypogammaglobulinemia G, she was given an intravenous infusion of gamma globulin. Within 72 hours, renal failure and a sustained decrease in serum concentrations of IgM and IgG began concurrently. A kidney biopsy specimen obtained five days after the infusion showed hyaline "thrombi" in numerous glomerular capillaries and glomerular necrosis, consistent with acute, severe mixed cryoglobulinemic nephropathy. Immunostaining showed strong positivity for IgM, IgG, and light chains in glomerular capillary lumina and subendothelial sites; immunostaining with a monoclonal antiidiotypic antibody specific for the patient's paraprotein established the presence of the rheumatoid factor paraprotein in the deposits. These observations strongly suggest that complexes consisting of IgM kappa rheumatoid factor, IgG, and complement initiated the renal damage. Therefore, demonstrable serum rheumatoid factor activity in patients with B cell neoplasms should be considered a contraindication to the administration of intravenous gamma globulin.

Acute Kidney Injury↗

PubMed1987

Effect of adrenalectomy on transport in the rat medullary thick ascending limb.

Previous studies in adrenalectomized (Adx) rats suggest that aldosterone may regulate ion transport in the ascending portion of Helen's loop. In order to examine directly the effect of adrenalectomy on transport, medullary thick ascending limb (Mtal) segments were isolated from Adx, Adx replaced with aldosterone (Adx + Ald, 0.5 micrograms X 100 g X body wt X d), and control Sprague-Dawley rats. Both net sodium and net chloride fluxes were significantly less in the Mtal segments from Adx rats compared with those in the control or Adx + Ald group. Physiologic levels of exogenous aldosterone increased net sodium chloride flux toward control values in the Adx + Ald group. Net potassium flux was not different among the three groups. We conclude that adrenalectomy impairs reabsorptive NaCl but not K transport in the Mtal, and that aldosterone restores this process. This reabsorptive defect may contribute to the urinary concentrating and diluting abnormality associated with adrenal insufficiency.

Adrenalectomy↗

PubMed1986

Ultrastructural immunolabeling in the diagnosis of light-chain-related renal disease.

Renal tissue from eight patients with light-chain deposition disease (LCDD) was immunolabeled for electron microscopy by a postembedding indirect immunogold staining procedure, using anti-kappa and anti-lambda antibodies. This technique provided an exact immunomorphological method to confirm the presence of monotypical light chains in glomeruli, tubules, and vessels. In two cases, it served to prove monotypical light-chain deposition which was not clear upon examination of sections stained for kappa and lambda light chains at the light microscopic level, using PAP or immunofluorescence methods. Three cases of amyloid nephropathy, in which the amyloid deposits stained for monospecific light chains and were immunolabeled ultrastructurally, are also described. LCDD manifests with a variety of morphological patterns in the kidney and the pathological definition of this entity has been difficult. Ultrastructural immunolabeling is a useful method to supplement existing techniques in the diagnosis of LCDD and related conditions. One outstanding feature of the postembedding technique is the ability to examine fixed and preserved renal tissue for the presence of light chains on a retrospective basis.

Adult↗

PubMed1986

The effect of assisted ventilation on creatinine clearance and hormonal control of electrolyte balance in very low birth weight infants.

Because renal function and electrolyte balance are commonly altered in premature infants, particularly those requiring ventilatory support, we studied the influence of assisted ventilation on renal electrolyte and water excretion in infants with birth weights less than 1501 g during the 2 days after birth. Twenty-two infants receiving assisted ventilation, either as intermittent mandatory ventilation or nasal continuous positive airway pressure, were compared with 21 spontaneously ventilating infants of similar birthweight and gestational age. Mean (and SEM) creatinine clearance was lower (p less than 0.05) in the assisted ventilation group on day 1 (2.9 +/- 0.4 versus 4.1 +/- 0.4 ml/min/1.73 m2) and on day 2 (4.1 +/- 1.0 versus 6.8 +/- 0.8 ml/min/1.73 m2, p = 0.05), and there was a correlation between creatinine clearance and mean blood pressure in both groups. Mean urine vasopressin was higher in the assisted ventilation group on the first day (360 +/- 86 versus 123 +/- 30 pg/mg creatinine; p less than 0.02) and correlated with higher urine osmolality. There were no differences in urine volume, in osmolar or free water clearances, or in the intake and urine excretion of sodium, potassium, and chloride. Plasma renin activity, urine aldosterone, and urine prostaglandin E2 were similar in both groups on both days. Neither the mode of assisted ventilation nor the cause of respiratory failure appeared to affect these results.

Creatinine↗

PubMed1985

Effect of reduced chloride reabsorption on renin release in the isolated rat kidney.

To investigate the relationship between tubular reabsorption of chloride and renal renin release in the isolated perfused rat kidney, perfusate renin activity was measured during substitution of either nitrate or thiocyanate for varying amounts of perfusate chloride but with maintained perfusate sodium concentration. Renin rose significantly as perfusate chloride fell; there was a sevenfold increase between perfusion with normal chloride and almost complete substitution of chloride by nitrate. With a normal perfusate chloride the addition of furosemide 10(-4) M to the perfusate also led to an increase in renin and a reduction in tubule chloride reabsorption. For all these experiments there was a significant negative correlation between renin and absolute tubular reabsorption of chloride (r = -0.68, P less than 0.001), but no such relationship with absolute sodium reabsorption. Renin release in a nonfiltering kidney, produced by elevating perfusate albumin concentration, increased approximately 40-fold. Thus increasing plasma oncotic pressure elevates renin by mechanisms additional to cessation of tubular chloride absorption. However, substitution of chloride in the perfusate by nitrate in this nonfiltering kidney did not further elevate renin release. We conclude that renin release is influenced by a signal dependent on, and inversely proportional to, chloride reabsorption in the thick ascending limb of the Loop of Henle.

Absorption↗

PubMed1985

Effects of chronic peripheral sympathectomy on plasma levels of, and the pressor response to, vasopressin.

The purpose of the present study was to assess the effect of chronic peripheral sympathectomy in rats on plasma vasopressin (basal and dehydrated) and on pressor sensitivity to vasopressin. Sympathectomy was produced in male Sprague-Dawley rats by daily injection of guanethidine (45 mg/kg) for 9 days. Control rats received saline over the same period. Plasma vasopressin was determined by radio-immunoassay, and pressor sensitivity was determined by monitoring mean arterial pressure response to graded injections of vasopressin (0.1-20 mU) in conscious rats. Sympathectomized rats showed ptosis and supersensitivity to norepinephrine, and had significantly greater basal and dehydrated plasma vasopressin levels than controls (10.3 +/- 1.5 versus 6.2 +/- 0.7, and 12.4 +/- 0.9 versus 8.6 +/- 1.0 pg/ml, s.e.m, respectively, P less than 0.05 for both). Sympathectomized rats also had an increased pressor sensitivity to vasopressin (dose response curve shifted to left, lower threshold, greater slope, P less than 0.001). Injection of a vasopressin pressor-antagonist, d (CH2)5 Me Tyr AVP, had no effect on blood pressure in control rats but caused a significant decrease of blood pressure in sympathectomized rats (15 +/- 1.0 mmHg, P less than 0.001). These results suggest that chronic peripheral sympathectomy in rats is associated with increased basal and dehydrated plasma vasopressin, and increased pressor sensitivity to vasopressin. The effect of the vasopressin antagonist suggests that vasopressin may play a role in blood pressure maintenance in sympathectomized rats.

Animals↗

PubMed1985

Diuresis and natriuresis following acute pneumothorax in very low birthweight infants.

Seven tension pneumothoraces developed in six very low birthweight infants receiving assisted ventilation for hyaline membrane disease. Mean values for blood pressure and creatinine clearance (Ccr) tended to increase following pneumothorax decompression, although neither increase was statistically significant. Urine volume, osmolar clearance and urine sodium excretion all increased significantly in the 8 h following diagnosis and decompression of pneumothoraces. However, when expressed as a percentage of Ccr, none of these variables changed significantly. Mean sodium balance changed from positive to negative despite a significant increase in urine aldosterone excretion. It is suggested that the increases in osmolar clearance and sodium excretion were consequences of the increase in Ccr following pneumothorax decompression. Developmental immaturity in the renal tubular response to aldosterone might also have contributed to development of negative sodium balance.

Acute Disease↗

PubMed1985

Prostaglandins in the sodium excretory response to altered renal arterial pressure in dogs.

Acute variations in renal arterial pressure are associated with corresponding alterations in absolute and fractional sodium excretion even under conditions of highly efficient autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). Since prostaglandins recently have been implicated in the regulation of sodium excretion, we investigated the hypothesis that the renal prostaglandin system participates in "pressure natriuresis." Anesthetized sodium-replete dogs were subjected to partial carotid artery constriction to elevate systemic arterial pressure. Under these control conditions, sodium excretion was 103 +/- 18 mueq/min (n = 17) and urinary prostaglandin E2 excretion averaged 4.6 +/- 1.5 ng/min (n = 8). Decreases in renal arterial pressure within the auto-regulatory range reduced sodium excretion (2.1%/mmHg) and prostaglandin E2 excretion (1.7%/mmHg), whereas GFR and RBF were not affected. There was a significant correlation between the changes in sodium and prostaglandin E2 excretion rates (r = 0.932, P less than 0.01). In nine dogs treated with indomethacin, sodium excretion was reduced by 70% while GFR and autoregulatory capability were unaffected. There was a marked attenuation of the effect of changes in arterial pressure on sodium excretion, with this parameter exhibiting changes averaging 0.6%/mmHg (P less than 0.001). These observations suggest that the renal prostaglandin system may exert an important influence on the pressure-natriuresis mechanism.

Animals↗

PubMed1985

Effect of 6-aminonicotinamide on renin release in isolated rat kidney: possible role for the pentose pathway.

To study the association between renal renin release and the pentose pathway, we perfused nonfiltering kidneys from Sprague-Dawley rats with Krebs-Ringer bicarbonate buffer containing 5 mM glucose and 14 g/100 ml bovine serum albumin in the presence or in the absence of 0.25 mM 6-aminonicotinamide (6AN), an inhibitor of glucose-6-phosphate dehydrogenase, the rate-limiting step of the pentose pathway. Eleven kidneys perfused in the absence of 6AN had a renin secretion rate of 7.4 +/- 2.2 ng ANG I X min-1 X ml-1. In six kidneys perfused in the presence of 6AN, renin release was depressed to 0.56 +/- 0.24 ng ANG I X min-1 X ml-1. The renal renin content for four control kidneys was 56 +/- 3.3 ng ANG I X mg-1 X h-1 while in four kidneys perfused with 6AN renal renin content was lower, 35 +/- 2.9 ng ANG I X mg-1 X h-1. In the presence of 5 mM lactate, the renin release of eight nonfiltering kidneys was 0.31 +/- 0.06 ng ANG I X min-1 X ml-1. The addition of 6AN did not further depress renin secretion in the presence of lactate. 6-Aminonicotinamide also completely blocked furosemide-stimulated renin release without having any effect on glomerular filtration rate or furosemide-induced natriuresis. However, 6AN did not inhibit stimulation of renin secretion by isoproterenol. We conclude that 6-aminonicotinamide interferes with renin release by nonfiltering kidneys and also inhibits furosemide-stimulated renin release but does not affect beta-adrenergic-stimulated renin secretion. Glucose but not lactate is important for maintaining augmented rates of renin secretion in nonfiltering kidneys. 6-Aminonicotinamide significantly reduced renal renin content in the presence of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗

PubMed1985

Effect of ADH on chloride reabsorption in the loop of Henle of the Brattleboro rat.

Both in vivo superficial loop segment microperfusion and in vitro perfusion of isolated medullary thick ascending limb segments were used to assess the effect of vasopressin on loop of Henle chloride absorption in the Brattleboro rat. Superficial loop segments were perfused between the latest proximal and earliest distal tubule in vivo at 19.2 +/- 0.4 nl/min (mean +/- SE) with an artificial tubule fluid. Under control conditions, absolute chloride reabsorption was 1,596 +/- 61 pmol/min and increased to 1,876 +/- 102 after intravenous infusion of vasopressin (P less than 0.005). Distal tubule fluid chloride concentration decreased 4.6 +/- 1.5 meq/liter (P less than 0.05), and fractional chloride reabsorption increased 4.8 +/- 2.0% (P less than 0.05). For in vitro perfusion, medullary thick ascending limb segments were bathed and perfused (9-15 nl/min) with phosphate-buffered solutions at 38 degrees C. Under control conditions, transepithelial voltage was +2.4 +/- 0.3 mV, lumen positive, and the net chloride flux was 147 +/- 24 pmol X min-1 X mm-1 in the absorptive direction. Addition of vasopressin to the bathing solution increased net chloride reabsorption to 342 +/- 56 pmol X min-1 X mm-1 (P less than 0.02) and transepithelial voltage to 3.0 +/- 0.3 mV (P less than 0.002). An additional group of tubules was examined under identical conditions; however, vasopressin was removed from the bathing medium during a subsequent recovery period. In these experiments, net chloride flux and transepithelial voltage significantly increased compared with the control period and returned to control values upon removal of vasopressin from the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1982

Transport of potassium in the rabbit pars recta.

Unidirectional fluxes of 42K+ and 86Rb+ were measured in isolated perfused segments of proximal straight tubules and no differences were found between the two isotopes for the same flux determination. In the three segments examined (the early and late superficial proximal straight tubule and the juxtamedullary proximal straight tubule) there was apparent net active K+ secretion as demonstrated by differences in the unidirectional fluxes of 2.6, 3.2, and 4.8 pmol.min-1.mm-1, respectively. However, in contrast to the expectations for active K+ secretion, the bath-to-lumen fluxes were unaffected by 0.1 mM ouabain added to the bathing solution, and in the early superficial and juxtamedullary segments these fluxes were directly proportional to the K+ concentration of the bathing solution over a range of concentrations. Apparent K+ permeability coefficients were calculated from lumen-to-bath fluxes to be 0.14 +/- 0.02, 0.10 +/- 0.02, and 0.52 +/- 0.07 micrometers.s-1 in the early and late superficial and juxtamedullary segments, respectively. Based on these data and on a mathematical analysis, we have concluded that active K+ secretion of the magnitude measured would have little importance in determining the K+ load delivered to the descending limb of the loop of Henle. However, the higher passive permeability of the juxtamedullary segment would allow significant net K+ secretion if the outer medullary interstitium had even a moderately elevated K+ concentration.

Animals↗

PubMed1982

New pathways for potassium transport in the kidney.

This review focuses on the hypothesis that potassium is recycled in the medulla by secretion into the pars recta or descending limb of long-looped nephrons and reabsorption from the ascending limb and/or medullary collecting duct. Evidence supporting the recycling hypothesis is summarized and the process is analyzed quantitatively by an examination of the mass flow of potassium reaching different sites along superficial and juxtamedullary nephrons and collecting tubules. From differences in potassium mass flow between sites, we have estimated the amount of potassium that must be secreted or absorbed by individual segments of the renal tubule. These rates of secretion and absorption are compared with the potassium transport characteristics of the respective segments, as assessed by isolated tubule perfusion in vitro and micropuncture in vivo. It is apparent that potassium secretion can occur passively in the pars recta and descending limb of long-looped nephrons as a consequence of the elevated potassium concentration in the medullary interstitium. At present, no active potassium absorptive mechanism has been demonstrated in any segment of the ascending limb. Due to the very high ionic permeability of the thin ascending segment and the lumen-positive transepithelial voltage in the thick ascending segment, however, considerable passive absorption likely occurs, although net potassium secretion has also been demonstrated in the cortical thick ascending limb. The high potassium concentration in the inner medullary interstitium and the difference in mass flow of potassium between the end of superficial nephrons in the cortex and the collecting ducts in the papilla, at least under certain circumstances, are best accounted for by net potassium reabsorption in the medullary collecting duct.

Animals↗

PubMed1980

Studies on the pathogenesis of Bartter's syndrome.

There is no agreement concerning the primary pathogenetic event leading to Bartter's syndrome. Free water clearance and distal fractional chloride reabsorption were abnormally low in our patient with Bartter's syndrome. This series of investigations in this patient with Bartter's syndrome and hypomagnesemia was undertaken to determine if the defect in chloride transport in the ascending limb and the associated renal potassium wasting was specifically related to potassium depletion, increased prostaglandin production or magnesium depletion. Neither potassium repletion, indomethacin administration nor magnesium repletion had an effect on the defect in free water clearance or in distal fractional chloride reabsorption. However, magnesium infusion eliminated renal potassium wasting. These observations suggest that the proximate cause of Bartter's syndrome in this patient is a primary defect in the reabsorption of sodium chloride in the ascending limb and not renal potassium wasting. however, hypomagnesemia may contribute to the renal potassium wasting seen in this syndrome.

Adult↗