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The difficulty that nonnephrologists sometimes have with the differential diagnosis of hyponatremic patients often results from misinterpreting the significance of measured and calculated serum osmolalities, effective serum osmolalities (tonicities), and the influence of various normal (eg, serum urea nitrogen) and abnormal (eg, ethanol) solutes. Among the more commonly held misconceptions are that high serum urea or alcohol levels will, by analogy with glucose, cause hyponatremia, and that a normal (or elevated) measured serum osmolality in a hyponatremic patient excludes the possibility of hypotonicity. This article describes typical and deliberately comparative data of the serum levels of sodium, glucose, urea nitrogen, and mannitol and/or ethanol (if present); calculated and measured osmolality; effective osmolality; and the potential risk of hypotonicity-induced cerebral edema for each of 6 prototypical hyponatremic states. This provides a helpful educational tool for untangling these interrelationships and for clarifying the differences among various hyponatremic conditions.

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A patient with severe metabolic acidosis and an extremely elevated (57 mEq/L) serum anion gap (AG) is described, and the multiple factors that produced the patient's complex abnormalities are discussed in detail. These include renal failure, rhabdomyolysis, marked hyperphosphatemia, hemoconcentration, and an unidentified organic metabolic acidosis. A review of the literature indicates that the common thread observed in almost each instance of profoundly elevated AG values is a multifactorial pathogenesis that usually includes renal insufficiency, associated with a proven or likely cause of organic metabolic acidosis, or with exogenous phosphate intoxication.

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The management of patients with diabetes insipidus can be confusing because of the disorder's variable pathophysiology, the numerous medications used, and the possible complications related to their use. Nevertheless, the primary care physician, rather than the subspecialist, will increasingly be called on to manage patients with such relatively uncommon conditions in the future. If a few basic facts and principles are kept in mind, the care of most patients with diabetes insipidus can be successful. A comprehensive, practical review of the short- and long-term therapy for patients with diabetes insipidus, including central diabetes insipidus, nephrogenic diabetes insipidus, and the "excessive vasopressinase syndrome," is presented. The use of single and multidrug regimens, and of the newly marketed oral formulation of desmopressin acetate, is described for common clinical settings.

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Polyuria is an important symptom or sign because of its potential severity, diverse causes, and interesting pathophysiology. Whereas polyuria induced by water diuresis is reasonably well understood and easily recognized by clinicians, that produced by solute diuresis is more likely to cause confusion. In this article, we focus on solute diuresis as a cause of polyuria, review the classification and pathophysiology of polyuria, and describe the clinical and laboratory studies useful for the evaluation of the polyuric patient. A stepwise, logical approach is provided (1) to determine whether a patient has a water diuresis, a solute diuresis, or both (concurrently), and (2) if a solute diuresis is present, to determine if it is caused by electrolytes (eg, sodium chloride sodium bicarbonate), by nonelectrolytes (eg, glucose, urea), or by both. How to assess these possibilities and to determine the specific cause of the diuresis is discussed in detail. Three representative case examples are provided. Selected causes of a solute diuresis also are reviewed.

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A patient with a markedly elevated serum phosphorus level (23.9 mg/dL) is described, followed by a brief review of severe hyperphosphatemia. Elevated serum phosphorus levels may be artifactual or true. True hyperphosphatemia is usefully subdivided according to (a) whether phosphorus is added to the extracellular fluid from a variety of exogenous or endogenous sources, or (b) whether the urinary excretion of phosphorus is reduced from either decreased glomerular filtration or increased tubular reabsorption. Severe hyperphosphatemia, defined herein as levels of 14 mg/dL or higher, is almost invariably multifactorial--usually resulting from addition of phosphorus to the extracellular fluid together with decreased phosphorus excretion. The hyperphosphatemia of the patient described herein appeared to result from a combination of dietary phosphorus supplementation, acute renal failure, acute pancreatitis, and ischemic bowel disease, complicated by lactic acidosis.

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PURPOSE: To review the effects of heparin and heparinoid compounds on aldosterone physiology and associated induction of hyperkalemia. MATERIALS AND METHODS: A comprehensive literature search (of human and animal data) was carried out by computer and by using reference citations from primary sources. RESULTS: Heparin and its congeners are predictable, potent inhibitors of aldosterone production. This inhibitory effect is specific for the zona glomerulosa; other corticosteroids are not affected. Aldosterone suppression occurs within a few days of initiation of therapy, is reversible, and is independent of either anticoagulant effect or route of administration. Decreases in aldosterone levels may occur with heparin dosages as low as 5,000 U BID. The most important, but probably not the only mechanism of aldosterone inhibition appears to involve reduction in both the number and affinity of the angiotensin-II receptors in the zona glomerulosa. Prolonged use of heparin causes marked reduction in the width of the adrenal zona glomerulosa. CONCLUSIONS: Aldosterone suppression results in natriuresis and less predictably in decreased excretion of potassium. Greater than normal serum potassium levels occur in about 7% of patients, but marked hyperkalemia generally requires the presence of additional factors perturbing potassium balance (in particular, renal insufficiency, diabetes mellitus, or the use of certain medications). Heparin-induced increases in serum potassium need to be better anticipated by clinicians. Serum potassium levels should be monitored periodically in patients being given heparin for 3 or more days, and in patients at relatively high risk for hyperkalemia, the monitoring interval should probably be no greater than 4 days.

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Hyponatremia can be a serious medical problem, and severe hyponatremia can be a medical emergency. Nevertheless, considerable controversy remains with respect to the best way to avoid the important sequelae of hyponatremia, while minimizing the complications of its treatment. Unquestionably, severe hyponatremia may cause life-threatening and/or permanent neurologic abnormalities. The risk of these untoward events, however, is much greater with acute than with chronic hyponatremia. The adaptive changes in the brain that reduce the hazards of a low serum sodium concentration for patients with chronic hyponatremia increase the risk for therapy-induced central pontine myelinolysis. In general, acute, symptomatic hyponatremia should be corrected more rapidly than chronic hyponatremia, at least until severe symptoms abate. Detailed guidelines are provided for the management of acute and chronic hyponatremia. But regardless of guidelines, therapy must be individualized, with adjustments based on frequent assessments of clinical condition and laboratory data.

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The syndrome of hypercalcemia during the course of acute renal failure (usually associated with rhabdomyolysis) occurs most commonly in young men with very severe renal failure. Although fewer than 90 such patients have been reported, the prevalence of hypercalcemia in patients with rhabdomyolysis-associated renal failure averages 30%. Hypercalcemia occurs most commonly in the diuretic phase and resolves spontaneously. The mean duration of hypercalcemia is 14 days. The pathogenesis of this syndrome has not been clearly defined. In the rare instances where it has been measured, intact PTH is suppressed. In contrast, both elevated and suppressed values of plasma 1,25-dihydroxyvitamin D have been reported. The release of calcium from ectopic calcification in damaged muscle tissue provides a potential explanation for this syndrome. Therapy for the hypercalcemia should generally be conservative given its self-limited nature.

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Blood pressure declines in virtually all patients with severe congestive heart failure given an angiotensin-converting enzyme (ACE) inhibitor, but hypotension is of concern only if symptomatic. Acute renal insufficiency induced by an ACE inhibitor is due to reduced renal perfusion pressure together with blockade of angiotensin II-induced constriction of the efferent arteriole. Risk factors (or markers) for renal failure include hyponatremia, hypotension, volume contraction. Hyponatremia is an index of increased hemodynamic impairment, marked activation of the renin-angiotensin-aldosterone axis, and poor prognosis. Preventive measures for both ACE inhibitor-associated hypotension and renal insufficiency include withholding diuretics for a few days, initiating therapy with very small doses of ACE inhibitors, and cautious dose titration. Therapy for both hypotension and renal insufficiency involves increasing dietary sodium intake and reducing the dosage of, or temporarily discontinuing, the diuretic. The ACE inhibitor may have to be given at reduced dosage or discontinued for a time. If discontinuation is deemed necessary, administration of these survival-prolonging medications should be reinitiated after a brief respite whenever possible.

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We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.

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A patient with nephrotic syndrome secondary to renal amyloidosis was consistently observed to have serum anion gap levels as low as -1 mEq/L and averaging approximately 2 mEq/L. Neither multiple myeloma nor extreme hypertriglyceridemia was present, and the patient's serum albumin concentrations were not low enough to depress the anion gap to this degree. An increased serum bromide level (below the range expected to produce clinical toxicity) was the apparent cause of the low anion gap. The patient's parents, who live in the same apartment, also manifested low anion gaps and inexplicably elevated serum bromide levels. Despite detailed investigation, no environmental or pharmacologic source of bromide was uncovered. Although the source of the bromide in the present instance remains elusive, this report illustrates the necessity to measure serum bromide when a low anion gap cannot be explained by other factors, even when there is no history to suggest bromide exposure.

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Considerable evidence suggests that hyperactivity of the sympathetic nervous system is implicated not only in the pathogenesis of essential hypertension but also in several blood pressure-independent complications of essential hypertension. Even with the advent of newer antihypertensive agents, including angiotensin-converting enzyme inhibitors and calcium antagonists, the centrally acting sympatholytics (alpha 2-adrenoceptor agonists) remain a valuable group of medications for the management of hypertension of all grades of severity. Their advantages include efficacy; rarity of contraindication; absence of most metabolic and serious side effects; favorable effects on systemic hemodynamics; lack of true tolerance and infrequency of volume expansion-related pseudotolerance; suitability in the elderly, in isolated systolic hypertension, and in patients with various concomitant conditions, such as diabetes mellitus; ability to reverse left ventricular hypertrophy; and relative low cost. The long duration of action of guanfacine hydrochloride, the most recently marketed agent, and of the transdermal formulation of clonidine is an especially commendable feature. The principal disadvantages of this class of medications are an overlap between the therapeutic dosage and that producing sedation and dry mouth and the potential to cause the discontinuation syndrome and sexual dysfunction.

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First-of-the-month predialysis serum sulfate (SO4) and other blood chemistry values were measured prospectively for 5 to 7 months in 14 patients undergoing single pass chronic tri-weekly maintenance hemodialysis with bicarbonate dialysate. Blood was also obtained predialysis and again immediately postdialysis from seven patients (five of whom also participated in the chronic study). As expected, the patients manifested a high anion gap (AG) metabolic acidosis. Serum SO4 was only moderately stable from month to month (the average coefficient of variation was 0.30; correlation between the serum SO4 value of month one and months two and five were r = 0.59, p = 0.026; and r = 0.38, p = 0.182, respectively). The ratio of mean serum SO4 to mean AG (5.0 +/- 0.4 [SE] mEq/L divided by 19.1 +/- 0.5 mEq/L) was 0.26. Although there was a statistically significant correlation between the serum SO4 and the blood urea nitrogen (BUN), there was no such correlation between SO4 and AG. A single hemodialysis reduced serum SO4 by 54% (from 3.5 +/- 0.5 mEq/L to 1.6 +/- 0.1 mEq/L), but there was no correlation between the change in SO4 and the change in AG. The authors concluded that SO4 contributes importantly to the elevated AG in patients receiving chronic hemodialysis. Single pass bicarbonate hemodialysis temporarily reduces, but does not normalize, both the serum SO4 and the AG of such patients.

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The effect of hyperkalemia on insulin secretion remains undefined. We evaluated portal and peripheral insulin levels in anesthetized dogs after infusions of KCl. The mean maximal increase in peripheral plasma potassium at infusion rates of 0.2 mEq/kg/h was 0.68 +/- 0.20 mEq/l. There were no significant increases in either portal or peripheral insulin levels. In contrast, in six dogs whose plasma potassium concentration increased in each case by more than 2.0 mEq/l (infusion rate of 0.5 mEq/kg/h), portal insulin levels increased fivefold (p less than 0.05). We concluded that only marked increases in plasma potassium concentration stimulate pancreatic insulin secretion.

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The case is described of a 68-year-old man whose therapy induced tetany during each of two consecutive hospital admissions. On each occasion the patient had marked hypocalcemia and hypomagnesemia, presumably as a result of the hungry-bone syndrome associated with diffuse prostatic osteoblastic metastases. During the February 1991 admission, marked hypokalemia was the principal initial concern. It seems likely that the tetany associated with the administration of KCl, without sufficient calcium, resulted from attenuation of the protection against hypocalcemia-enhanced neuromuscular excitability conferred by coexisting hypokalemia. The admission in March 1991 was prompted by the finding (without symptoms) of very low levels of both serum Mg and serum Ca. Tetany occurred during the infusion of MgSO4, without calcium. An acute decrement in plasma ionized Ca resulting from complexing of Ca with sulfate ions together with augmented urinary excretion of Ca were likely pathogenic factors.

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The purpose of the study was to evaluate the potassium-lowering effect of hypertonic versus isotonic sodium bicarbonate (NaHCO3) in patients with end-stage renal disease (ESRD) receiving chronic maintenance hemodialysis. Immediately prior to dialysis, we infused isotonic (1.4%, 150 mEq/l) NaHCO3 in H2O (1 mEq/kg body weight over 2 h) to 10 patients with ESRD. Blood was drawn in heparinized tubes, without the use of a tourniquet, from the angioaccess for Na, K, pH, PCO2, HCO3, and osmolality at baseline (x 3) and after 10, 20, 40, 60, 90, 120, and 180 min of infusion. All patients were acidotic (HCO3 13-21 mEq/l, pH 7.25-7.38) prior to the study. In these patients, plasma HCO3 increased by an average of 3 mEq/l, and plasma K decreased by 0.35 mEq/l at 180 min. Plasma osmolality did not change. In 8 patients, a bolus of hypertonic (8.4%, 1,000 mEq/l) NaHCO3 (1 mEq/kg body weight over 5 min) tended to cause a transient increase in plasma HCO3, an increase in plasma osmolality, and minor changes in the K levels (an initial small and transient albeit significant decrease, followed by a tendency to increase). Finally, plasma K tended to increase in patients receiving infusions of either isotonic (n = 6) or hypertonic (n = 6) sodium chloride. Our data do not support the efficacy of the common practice of administering NaHCO3 for the emergency treatment of hyperkalemia in patients with ESRD receiving maintenance dialysis.

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The serum anion gap (AG) is usually calculated by the equation: AG = Na - (Cl + HCO3), reflecting the difference between the total level of unmeasured anions (all anions other than chloride and bicarbonate) and that of unmeasured cations (all cations other than sodium). Thus, several recent reviews have cited hypermagnesemia as a cause of a reduction in the AG. Whether this might occur depends in part on the nature of the accompanying anion (if the etiology of the hypermagnesemia is an exogenous load of magnesium), as well as on the presence of concomitant changes in endogenous unmeasured anions. In the present paper, we describe an unusual patient whose severe hypermagnesemia was not associated with AG reduction. Although multiple factors, including lactic acidosis, might have countervailed the effect of her hypermagnesemia on the AG, there is no actual substantiation in the literature of an association between increased serum Mg and AG lowering. In conclusion, the finding of a normal AG has no documented negative predictive value, and the finding of a low AG has no documented positive predictive value for the diagnosis of hypermagnesemia.

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