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PubMed1994

Restoration by corticosteroids of the hyperaldosteronism in hyponatraemic rats with panhypopituitarism.

1. In the syndrome of inappropriate secretion of antidiuretic hormone, hyponatraemia is associated with a normal bicarbonate concentration despite dilution. This normal bicarbonate concentration is related to the development of a hyperaldosteronism, which is attributed to a direct stimulation of the zona glomerulosa by the hyponatraemic state. Some workers have suggested that, to develop this hyperaldosteronism requires the presence of a pituitary factor. To determine whether the pituitary gland plays a role in this hyponatraemia-induced hyperaldosteronism, water intoxication was performed for 24 h in normal and in panhypopituitaric rats. 2. In normal rats, hyponatraemia (108 mmol/l), induced by the administration of 1-desamino-8-D-arginine vasopressin and 2.5% D-glucose-0.45% NaCl by gavage (15% body weight) was associated with a mild increase in bicarbonate concentration, and blood acid-base equilibrium showed a mixed metabolic and respiratory alkalosis (pH 7.57, partial pressure of CO2 29 mmHg, base excess +5.5 mmol/l), and aldosterone concentration was increased 3-fold as compared with the control value. When hyponatraemia (110 mmol/l) was induced in a similar manner in panhypopituitaric rats, we observed a very low aldosterone concentration (< 50 pg/ml) and a compensated respiratory alkalosis (pH 7.45, partial pressure of CO2 30 mmHg, base excess -2.6 mmol/l). The restoration of a hyperaldosteronaemic state in this group of rats was related essentially to corticosteroid intake. 3. These data suggest that corticosteroids play a critical role in the development of hyponatraemia-related hyperaldosteronism, a phenomenon not necessarily dependent on a pituitary factor.

Acid-Base Equilibrium↗

PubMed2002

Severe hypomagnesaemia-induced hypocalcaemia in a patient with Gitelman's syndrome.

Gitelman's syndrome (GS) is characterized by hyperreninaemic hyperaldosteronism, hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria and is due to a defect of the Na-Cl cotransporter at the distal tubule, which may appear in a sporadic or in a familial form. It is an autosomal recessive disorder associated with normal or reduced blood pressure. We report a case of severe hypomagnesaemia-induced hypocalcaemia in a 39-year-old Caucasian woman with GS. The patient had impaired parathormone (PTH) responsiveness to peripheral stimuli, as proved by the marked PTH increase and normalization of plasma calcium levels after acute and chronic administration of magnesium salts. Secondary normotensive hyperreninaemic hyperaldosteronism with hypokalaemia and metabolic alkalosis was also present. Normal plasma renin activity (PRA) and aldosterone levels were restored by administration of an inhibitor of prostaglandin synthesis. The electrolyte imbalance was successfully corrected with chronic treatment with magnesium and potassium salts. Genetic analysis identified a compound heterozygous mutation in the Na-Cl cotransporter gene (NCCT), confirming the diagnosis of GS. The striking feature of this case of GS was impaired PTH responsiveness to peripheral stimuli determined by hypomagnesaemia and the resulting severe hypocalcaemia, which had not previously been described in this syndrome.

Adult↗

PubMed2000

Marked hyperlactatemia associated with severe alkalemia in a patient with thrombotic thrombocytopenic purpura.

This report describes a case of severe alkalemia associated with a blood lactate level greater than 13 mEq/L in a patient without evidence of hypotension or hypoxemia. The patient, who had the clinical manifestations of thrombotic thrombocytopenic purpura (TTP), developed the alkalemia from an acute respiratory alkalosis superimposed on an existing metabolic alkalosis. Profound alkalemia may impair oxygen delivery because of stronger hemoglobin-oxygen affinity, vasoconstriction, and alterations in the redox potential of cytochrome c. We suggest that the synergistic effects of a sudden, extreme alkalemia and the localized tissue hypoxia that resulted from extensive microvascular thrombi secondary to TTP caused the patient's hyperlactatemia.

Adult↗

PubMed1988

Common mistakes in managing metabolic disorders.

Three mistakes are commonly made in managing metabolic disorders. 1. Oral fluids may be pushed to treat simple volume depletion. However, almost all fluids used for this purpose are sodium-poor and do not restore salt and water balance. 2. The physician may not be aware of common causes of hypophosphatemia, such as hyperventilation, sepsis, stress, use of antacids or diuretics, and alcoholism. If the patient is not monitored adequately, severe hypophosphatemia may develop with serious consequences. 3. Low serum bicarbonate levels may be attributed to metabolic acidosis only, when in actuality metabolic acidosis may coexist with respiratory alkalosis. Arterial blood gas studies differentiate the conditions and direct attention to the cause of respiratory alkalosis when present.

Aged↗

PubMed1991

Anaerobic work and power output during cycle ergometer exercise: effects of bicarbonate loading.

Eight trained male cyclists who competed regularly in track races, were studied under control, alkalotic (NaHCO3) and placebo (CaCO3) conditions in a laboratory setting to study the effect of orally induced metabolic alkalosis on 60 s anaerobic work and power output on a bicycle ergometer. Basal, pre- and post-exercise blood samples in the three conditions were analysed for pH, pCO2, pO2, bicarbonate, base excess and lactate. All blood gas measurements were within normal limits at basal levels. There were significant differences in the amount of work produced, and in the maximal power output produced by the cyclists in the experimental condition when compared to the control and placebo conditions (P less than 0.01). The post-exercise pH decreased in all three conditions (P less than 0.05) and post-exercise pCO2 increased significantly in the alkalosis trial (P less than 0.01). In the alkalotic condition, the pre-exercise base excess and HCO3- levels were both higher (P less than 0.05) than the basal levels, suggesting that the bicarbonate ingestion had a significant increase in the buffering ability of the blood. Post-exercise lactate levels were significantly higher (P less than 0.05) after the alkalotic trial when compared to the other two conditions, immediately post-exercise and for the next 3 min. Post-exercise lactate levels were higher than basal or pre-exercise levels (P less than 0.001). This was true immediately post-exercise and for the next 5 min. The results of this study suggest that NaHCO3 is an effective ergogenic aid when used for typically anaerobic exercise as used in this experiment. We feel that this ergogenic property is probably due to the accelerated efflux of H+ ions from the muscle tissue due to increased extracellular bicarbonate buffering.

Adult↗

PubMedDate not supplied

Alkaline pH-induced extracellular regulated protein kinase activation in brain microvascular endothelial cells: differential effects of Tris and lowered CO2.

As it was previously reported that Tris-elevated pH acutely activated extracellular regulated protein kinase (ERK) in rat aorta smooth muscle cells, this study tested whether this finding could be extended to endothelial cells and, moreover, the relevance of this finding in brain microvascular endothelial cells with respect to respiratory-induced hypocapnic alkalosis. Exposure of bovine brain microvascular endothelial cells to pH 7.90 due to Tris for 15 and 30 min activated ERK twofold. In contrast, pH elevated to 7.75 and 7.90 by lowered percent CO2 failed to activate ERK (15, 30, and 60 min). These results suggest that respiratory alkalosis due to hypocapnia does not activate ERK in brain microvascular endothelial cells. The ability of Tris to activate ERK suggests a novel pathway, possibly independent of pH elevation, whereby Tris activates ERK.

Alkalosis, Respiratory↗

PubMed1961

The effect of pH on growth, protein synthesis, and lipid-rich particles of cultured mammalian cells.

A simple procedure has been established for controlling and measuring the pH of media in which the bicarbonate-carbonic acid system is the predominant buffer. The HCO(-) (3) concentration was maintained at 22.5 mM and the H(2)CO(3) concentration was varied by equilibrating the media with 0.5 to 40 per cent CO(2) in air. The curve relating extracellular pH to 3 day cell growth was similar for glass-attached HeLa and Chang liver cells. Maximum growth occurred over a pH range of 7.38 to 7.87. Cell growth declined precipitously on the alkaline side and more gradually on the acid side of the optimal pH range. Comparable pH growth curves were also obtained with newly isolated cells from rat liver and skeletal muscle. It was shown that the effect of pH on growth was independent of the CO(2) concentration and that the essential nutrients in the medium were stable over the pH range studied. Although alkalosis depressed the 3 day cell population, cells exposed to a pH of 8.0 to 8.2 grew at the maximal rate for the first 12 to 24 hours. Growth then ceased abruptly and the cells entered a steady state with respect to net protein synthesis. This was followed by cytoplasmic retraction and cell death. Increasing the concentrations of calcium or magnesium in the medium failed to prevent the effects of alkalosis. Moreover, the increase in CO(-) (3) concentration of the media and the concomitant decrease in Ca(++) ion concentration that occur at high pH were eliminated as determining factors in the growth failure and death. While acidosis had a less pronounced effect on the 3 day cell population, its effect on the growth rate was immediate. The increase in cell generation time was proportional to the H(+) ion concentration. In each of the cell lines studied, acidosis was accompanied by a striking increase in the number of cytoplasmic perinuclear granules. These granules which stain supravitally with Janus green are extracted from fixed cells with lipid solvents. They maintain their identity in cell homogenates and may be isolated from the other subcellular structures by differential centrifugation; at 100,000 g they form a distinct layer at the top of the supernatant fraction. On the basis of their physical and chemical properties, these granules have been called lipid-rich particles. The accumulation of lipid-rich particles in acidosis was independent of the growth rate and the CO(2) concentration.

Acidosis↗

PubMedDate not supplied

Effects of plasma total ammonia content and pH on urea excretion in Nile tilapia.

Nile tilapia (Oreochromis niloticus) were infused with ammonium salts, acid, and base to investigate the effects of changes in arterial plasma total ammonia content (Tamm) and pH (pHa) on plasma urea-nitrogen (urea-N) levels and urea-N excretory fluxes (Jurea-N). The tilapia did not possess a functional hepatic ornithine urea-cycle (no significant carbamyl phosphate synthetase III activity). Infused substances were dissolved in a saline vehicle and injected twice (5 mL kg-1), the first infusion to "prime" the animal and promote a more marked response to the second infusion, given 2.5 h later. The results reported are those of the second infusion. Infusion of 200 mM NH4Cl increased Tamm, reduced pHa, and increased plasma urea-N and Jurea-N. Two hundred mM NH4HCO3 increased Tamm and arterial plasma total CO2 content (TaCO2), reduced pHa, and increased Jurea-N. Fifty mM HCl reduced pHa but had no effects on urea dynamics. Fifty mM NaOH increased pHa, plasma urea-N levels, and Jurea-N. Two hundred mM NaHCO3 increased pHa, TaCO2, plasma urea-N levels, and Jurea-N. Infusion of the saline vehicle was without effect. The results indicate that ammonia loading and plasma alkalosis both stimulate urea excretion in uricolytic fish. The responses to hyperammonemia or alkalosis were not modified when combined with elevated plasma bicarbonate levels.

Alkalosis↗

PubMed1977

Effect of the acute administration of sodium bicarbonate on respiration in the presence of hyperoxia.

The effects, on respiration, of the acute administration of sodium bicarbonate were studied in 10 normal subjects. Carbon dioxide responses curves and tidal volume v. PCO2 relationships were obtained under hyperoxic conditions using a closed-circuit breathing system. During alkalosis, a decrease in the slope, and a displacement of the response curves to the right, were observed. These findings indicate that metabolic alkalosis, induced acutely by the administration of sodium bicarbonate, alters the respiratory response to carbon dioxide and that sodium bicarbonate may have a depressant effect on respiration.

Adult↗

PubMed2000

Intracellular pH regulation in human preimplantation embryos.

We report here that intracellular pH (pH(i)) in cleavage-stage human embryos (2-8-cell) is regulated by at least two mechanisms: the HCO(3)(-)/Cl(-) exchanger (relieves alkalosis) and the Na(+)/H(+) antiporter (relieves acidosis). The mean pH(i) of cleavage-stage embryos was 7.12 +/- 0.008 (n = 199) with little variation between different stages. Embryos demonstrated robust recovery from alkalosis that was appropriately Cl(-)-dependent, indicating the presence of the HCO(3)(-)/Cl(-) exchanger. This was further confirmed by measuring the rate of intracellular alkalinization upon Cl(-) removal, which was markedly inhibited by the anion transport inhibitor, 4,4'-diisocyanatostilbene-2,2'-disulphonic acid, disodium salt. The set-point of the HCO(3)(-)/Cl(-) exchanger was between pH(i) 7.2 and 7.3. Embryos also exhibited Na(+)-dependent recovery from intracellular acidosis. Na(+)/H(+) antiporter activity appeared to regulate recovery up to about pH(i) 6.8; this recovery was HCO(3)(-)-independent and amiloride-sensitive, with a pH(i) set-point of approximately 6.8-6.9. A second system that was both Na(+)- and HCO(3)(-)-dependent appeared to mediate further recovery from acidosis up to about pH(i) 7.1. Thus, pH(i) of early human preimplantation embryos appears to be regulated by opposing mechanisms (HCO(3)(-)/Cl(-) exchanger, Na(+)/H(+) antiporter, and possibly a third acid-alleviating transporter that was both Na(+)- and HCO(3)(-)-dependent) resulting in the maintenance of pH(i) within a narrow range.

Acid-Base Equilibrium↗

PubMed2003

Unexpected haemodynamic instability associated with standard bicarbonate haemodialysis.

BACKGROUND: The bicarbonate concentration in dialysis fluids for intermittent haemodialysis usually is between 32 and 35 mmol/l. The severity of chronic metabolic acidosis secondary to end-stage renal failure is very variable, however, so that in some patients pre-dialysis acidosis is overcorrected. This study aimed to analyse haemodynamic tolerances to metabolic alkalosis during intermittent haemodialysis. METHODS: In this randomized controlled trial with a single blind, cross-over design, we used dialysis liquids with two different bicarbonate concentrations, 32 (modality A) and 26 (modality B) mmol/l, and in 26 patients, 468 dialysis sessions, compared blood pressure, heart rate, incidence of hypotension and the frequency of corrections required with saline or hypertonic glucose infusions. RESULTS: The results of intradialytic haemodynamic monitoring for modalities A and B, respectively, were: lowest systolic blood pressure 120.8+/-20.8 vs 124.3+/-20.6 mmHg (P < 0.01); mean systolic blood pressure 138.5+/-23.8 vs 144.6+/-24.8 mmHg (P < 0.001); and highest heart rate 73.5+/-12.0 vs 75.8 +/- 12.9 (NS); with modality A, patients had more dialysis sessions with hypotensive episodes (5.55 vs 1.7%, P < 0.05) and required more saline or hypertonic glucose infusions (20.9 vs 13.7% of the dialysis sessions, P < 0.05). CONCLUSIONS: Mild metabolic alkalosis resulting from standard bicarbonate haemodialysis (32 mmol/l) may induce symptomatic hypotension. While normalizing chronic metabolic acidosis is desirable, reducing bicarbonate concentrations should be considered in cases of significant alkalaemia or otherwise untreatable haemodynamic instability.

Adult↗

PubMed1975

Sodium bicarbonate and systemic hemodynamics in volunteers anesthetized with halothane.

The cardiovascular effects of acute metabolic alkalosis (NaHCO3) in normal male volunteers anesthetized with halothane were measured. Pure metabolic alkalosis was studied by maintaning the end-tidal carbon dioxide tension at 40 torr. In each subject, cardiac index increased and total peripheral resistance decreased after each dose of NaHCO3. The increased cardiac index was associated with increased central blood volume, left ventricular minute work index, stroke index, and heart rate. Systolic time intervals showed increased myocardial performance. NaHCO3 administered to volunteers whose hearts were depressed by halothane appeared to cause peripheral vasodilation, volume expansion, and myocardial stimulation. The authors conclude that NaHCO3 administered during halothane anesthesia decreases total peripheral resistance and may lead to severe hypotension.

Adult↗

PubMed1984

Blood pH and brain uptake of 14C-morphine.

14C-Morphine was injected iv in control awake rats or in rats subjected to metabolic alkalosis or acidosis. Ten minutes later, radioactivity was determined within each of seven brain regions, after correction was made for intravascular tracer. In each region, parenchymal radioactivity was correlated positively and significantly (P less than 0.05) with arterial blood pH. Brain radioactivity was twofold to threefold greater in alkalotic rats (mean pH = 7.62) than in acidotic rats (mean pH = 7.16). The results are consistent with the pH-partition hypothesis for drug entry into the brain and indicate that morphine uptake can be increased by elevating the fraction of lipid-soluble uncharged morphine base in blood, by means of alkalosis. The observations may account for an exaggerated morphine-induced analgesia in alkalotic patients.

Acidosis↗

PubMed1984

Effect of hyperventilation on total calcium, ionized calcium, and serum phosphorus in neonates.

The effect of alkalosis (pH greater than 7.55) on total calcium, ionized calcium, and serum phosphorus was studied in seven infants with persistent pulmonary hypertension (PPH) before, during, and after hyperventilation. Hyperventilation-induced alkalosis resulted in marked decreases in total calcium, phosphorus, and ionized calcium. There was an inverse correlation between plasma Ca+2 and pH; a 0.1-unit increase in blood pH decreased Ca+2 by 0.42 mg/dl. Two of the study infants had ionized calcium concentrations less than 2.5 mg/dl during hyperventilation. These disturbing changes in total calcium, ionized calcium, and serum phosphorus could have potentially detrimental effects on neonates with PPH.

Alkalosis↗

PubMed2000

Comparison of hyperventilation and inhaled nitric oxide for pulmonary hypertension after repair of congenital heart disease.

BACKGROUND: Pulmonary hypertension is associated with congenital heart lesions with increased pulmonary blood flow. Acute increases in pulmonary vascular resistance (PVR) occur in the postoperative period after repair of these defects. These increases in PVR can be ablated by inducing an alkalosis with hyperventilation (HV) or bicarbonate therapy. Studies have shown that these patients also respond to inhaled nitric oxide (iNO), but uncertainty exists over the relative merits and undesirable effects of HV and iNO. HYPOTHESIS: Alkalosis and iNO are equally effective in reducing PVR and pulmonary artery pressure (PAP) in children with pulmonary hypertension after open heart surgery. SETTING: Critical care unit of a tertiary care pediatric hospital. DESIGN: Prospective, randomized, crossover design. PATIENTS: Twelve children with a mean PAP > 25 mm Hg at normal pH after biventricular repair of congenital heart disease. INTERVENTIONS: Patients were assigned to receive iNO or HV (pH > 7.5) in random order, and the effect on hemodynamics was measured. Each treatment was administered for 30 mins with a 30-min washout period between treatments. Finally, both treatments were administered together to look for a possible additive effect. MEASUREMENTS AND MAIN RESULTS: Cardiac output and derived hemodynamic parameters using the dye dilution technique. Hyperventilation, achieved by an increase in ventilator rate without a change in mean airway pressure, decreased Pa(CO2) from a mean (SD) of 43.7+/-5.3 to 32.3+/-5.4 mm Hg and increased pH from 7.40+/-0.04 to 7.50+/-0.03. This significantly altered both pulmonary and systemic hemodynamics with a reduction in PAP, PVR, central venous pressure, and cardiac output and an increase in systemic vascular resistance. In comparison, iNO selectively reduced PAP and PVR only. The reduction in PVR was comparable between treatments, although addition of iNO to HV resulted in a small additional reduction in PVR. An additional decrease in PAP was seen when HV was added to iNO, attributable to a reduction in cardiac output rather than a further decrease in PVR. CONCLUSIONS: Inhaled NO and HV are both effective at lowering PAP and PVR in children with pulmonary hypertension after repair of congenital heart disease. The selective action of iNO on the pulmonary circulation offers advantages over HV because a decrease in cardiac output and an increase in SVR are undesirable in the postoperative period.

Administration, Inhalation↗

PubMed2001

Usefulness of plasma exchange plus continuous hemodiafiltration to reduce adverse effects associated with plasma exchange in patients with acute liver failure.

OBJECTIVE: To efficiently remove middle-molecular-weight substances such as hepatic toxins and minimize adverse effects associated with plasma exchange implementation, we have performed plasma exchange slowly in combination with continuous hemodiafiltration. This study was designed to determine the usefulness of plasma exchange with continuous hemodiafiltration in reducing the adverse effects associated with implementation of plasma exchange alone. DESIGN: A retrospective clinical study. SETTING: University teaching hospital. PATIENTS: The study involved 90 patients with liver failure who had been treated with plasma exchange in our department over the past 12 yrs. We examined these patients by dividing them into two groups (48 patients treated with plasma exchange alone and 42 patients treated with plasma exchange plus continuous hemodiafiltration at the time of plasma exchange implementation). MEASUREMENTS AND MAIN RESULTS: Baseline blood Na+ concentration, HCO3- concentration, and colloid osmotic pressure were followed after implementation of plasma exchange to compare the frequency of development of three adverse effects (hypernatremia, metabolic alkalosis, and sharp decrease in colloid osmotic pressure) in the two groups. Hypernatremia was found in 26.7% of treatments in the group with plasma exchange alone and 3.3% in the group of plasma exchange plus continuous hemodiafiltration, and metabolic alkalosis was found in 30.6% of treatments in the group with plasma exchange alone and 4.9% in the group of plasma exchange plus continuous hemodiafiltration; both percentages were significantly higher in the group with plasma exchange alone (p <.001). A sharp decrease in colloid osmotic pressure occurred in 13.3% of treatments in the group with plasma exchange alone but was not observed at all in the patients treated with plasma exchange plus continuous hemodiafiltration. CONCLUSIONS: We conclude that adverse effects associated with plasma exchange for artificial liver support for liver failure can be alleviated with use of plasma exchange plus continuous hemodiafiltration instead of plasma exchange alone.

Adolescent↗

PubMed2004

Altered renal distal tubule structure and renal Na(+) and Ca(2+) handling in a mouse model for Gitelman's syndrome.

Gitelman's syndrome, an autosomal recessive renal tubulopathy caused by loss-of-function mutations in the thiazide-sensitive NaCl co-transporter (NCC) of the distal convoluted tubule (DCT), is characterized by mild renal Na(+) wasting, hypocalciuria, hypomagnesemia, and hypokalemic alkalosis. For gaining further insights into the pathophysiology of Gitelman's syndrome, the impact of NCC ablation on the morphology of the distal tubule, on the distribution and abundance of ion transport proteins along its length, and on renal tubular Na(+) and Ca(2+) handling in a gene-targeted mouse model was studied. NCC-deficient mice had significantly elevated plasma aldosterone levels and exhibited hypocalciuria, hypomagnesemia, and compensated alkalosis. Immunofluorescent detection of distal tubule marker proteins and ultrastructural analysis revealed that the early DCT, which physiologically lacks epithelial Na(+) (ENaC) and Ca(2+) (TRPV5) channels, was virtually absent in NCC-deficient mice. In contrast, the late DCT seemed intact and retained expression of the apical ENaC and TRPV5 as well as basolateral Na(+)-Ca(2+) exchanger. The connecting tubule exhibited a marked epithelial hypertrophy accompanied by an increased apical abundance of ENaC. Ca(2+) reabsorption seemed unaltered in the distal convolution (i.e., the DCT and connecting tubule) as indicated by real-time reverse transcription-PCR, Western blotting, and immunohistochemistry for TRPV5 and Na(+)-Ca(2+) exchanger and micropuncture experiments. The last experiments further indicated that reduced glomerular filtration and enhanced fractional reabsorption of Na(+) and Ca(2+) upstream and of Na(+) downstream of the DCT provide some compensation for the Na(+) transport defect in the DCT and contribute to the hypocalciuria. Thus, loss of NCC leads to major structural remodeling of the renal distal tubule that goes along with marked changes in glomerular and tubular function, which may explain some of the clinical features of Gitelman's syndrome.

Alkalosis↗

PubMed1984

Apparent mineralocorticoid excess and deficient 11 beta-oxidation of cortisol in a young female.

A 19-year-old female, known to have had hypertension and hypokalemic alkalosis since the age of 9 months, was found to have suppressed renin, negligible plasma and urinary aldosterone and low plasma levels of other known sodium-retaining steroids. Despite the normal plasma cortisol the urinary excretion of 17-oxosteroids and 17-oxogenic steroids was low as was the cortisol secretion rate, suggesting a diminished metabolic clearance of cortisol. This was confirmed by the demonstration of a prolonged t 1/2 of 14C-cortisol. The abnormally high urinary excretion ratios of cortisol to cortisone, tetrahydracortisol to tetrahydrocortisone and 11-hydroxy-aetiocholanolone to 11-oxy-aetiocholanolone indicate that the diminished cortisol breakdown is the result of deficient 11 beta-oxidation. Moreover, the urinary excretion of free cortisol was elevated, probably due to diminished tubular reabsorption of cortisol. Hypokalemic alkalosis did not respond to spironolactone, but was partly corrected by amiloride. No response to dexamethasone was observed, but dexamethasone combined with aminogluthetimide normalized blood pressure and serum K. These findings support the involvement of a sodium-retaining, kaliuretic steroid in this rare syndrome.

Adrenocorticotropic Hormone↗

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