Nicolaos E. Madias

Captopril-Induced Functional Renal Insufficiency in Patients with Bilateral Renal-Artery Stenoses or Renal-Artery Stenosis in a Solitary Kidney

ACUTE renal failure occasionally complicates therapy with the oral angiotensin-converting-enzyme inhibitor captopril.1 2 3 4 5 A variety of mechanisms have been postulated to account for captopril-...

Impact of Hospital-Associated Hyponatremia on Selected Outcomes

BACKGROUND Hyponatremia is the most common electrolyte disorder encountered in hospitalized patients. METHODS We evaluated whether hospital-associated hyponatremia has an independent effect on all-cause mortality, hospital length of stay (LOS), and patient disposition. This cohort study included all adult hospitalizations at an academic medical center occurring between 2000-2007 for which an admission serum sodium concentration ([Na(+)]) was available (N = 53 236). We examined community-acquired hyponatremia (admission serum [Na(+)], <138 mEq/L [to convert to millimoles per liter, multiply by 1.0]), hospital-aggravated hyponatremia (community-acquired hyponatremia complicated by worsening in serum [Na(+)]), and hospital-acquired hyponatremia (nadir serum [Na(+)], <138 mEq/L with a normal admission serum [Na(+)]). The independent associations of these hyponatremic presentations with in-hospital mortality, LOS, and patient disposition were evaluated using generalized estimating equations adjusted for age, sex, race, admission service, and Deyo-Charlson Comorbidity Index score. RESULTS Community-acquired hyponatremia occurred in 37.9% of hospitalizations and was associated with adjusted odds ratios (ORs) of 1.52 (95% confidence interval [CI], 1.36-1.69) for in-hospital mortality and 1.12 (95% CI, 1.08-1.17) for discharge to a short- or long-term care facility and a 14% (95% CI, 11%-16%) adjusted increase in LOS. Hospital-acquired hyponatremia developed in 38.2% of hospitalizations longer than 1 day in which initial serum [Na(+)] was 138 to 142 mEq/L. Hospital-acquired hyponatremia was associated with adjusted ORs of 1.66 (95% CI, 1.39-1.98) for in-hospital mortality and 1.64 (95% CI, 1.55-1.74) for discharge to a facility and a 64% (95% CI, 60%-68%) adjusted increase in LOS. The strength of these associations tended to increase with hyponatremia severity. CONCLUSIONS Hospital-associated hyponatremia is a common occurrence. All forms of hyponatremia are independently associated with in-hospital mortality and heightened resource consumption.

Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood.

Abstract To assess arteriovenous differences in acid-base status, we measured the pH and partial pressure of carbon dioxide (PCO2) in blood drawn simultaneously from the arterial and central venous circulations in 26 patients with normal cardiac output, 36 patients with moderate and 5 patients with severe circulatory failure, and 38 patients with cardiac or cardiorespiratory arrest. The patients with normal cardiac output had the expected arteriovenous differences: venous pH was lower by 0.03 unit, and venous PCO2 was higher by 0.8 kPa (5.7 mm Hg). These differences widened only slightly in those with moderate cardiac failure. Additional simultaneous determinations in mixed venous blood from pulmonary arterial catheters were nearly identical to those in central venous blood. In the five hypotensive patients with severe circulatory failure there were substantial differences between the mean arterial and central venous pH (7.31 vs. 7.21) and PCO2 (5.8 vs. 9.0 kPa [44 vs. 68 mm Hg]). Large arteriovenous diff...

Changes in plasma potassium concentration during acute acid-base disturbances☆

Abstract It has been widely held that the changes in plasma potassium concentration observed during acute acid-base disorders are solely determined by the associated changes in blood acidity. However, a critical examination of the literature uncovers wide differences among the four cardinal acid-base disorders with respect to the associated changes in plasma potassium concentration. In fact, the data suggest that a host of factors other than the attendant changes in plasma hydrogen ion concentration may well modulate the intercompartmental distribution of body potassium during acid-base disorders. In this study we review the qualitative, quantitative and mechanistic aspects of the plasma potassium response to acute alterations in blood acidity.

Serum Anion Gap: Its Uses and Limitations in Clinical Medicine

The serum anion gap, calculated from the electrolytes measured in the chemical laboratory, is defined as the sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration. This entity is used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication. The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability. Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide. Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently. A presumed 1:1 stoichiometry between change in the serum anion gap (DeltaAG) and change in the serum bicarbonate concentration (DeltaHCO(3)(-)) has been used to uncover the concurrence of mixed metabolic acid-base disorders in patients with high anion gap acidosis. However, recent studies indicate variability in the DeltaAG/DeltaHCO(3)(-) in this disorder. This observation undercuts the ability to use this ratio alone to detect complex acid-base disorders, thus emphasizing the need to consider additional information to obtain the appropriate diagnosis. Despite these caveats, calculation of the serum anion gap remains an inexpensive and effective tool that aids detection of various acid-base disorders, hematologic malignancies, and intoxications.

Percutaneous transluminal renal angioplasty in management of atherosclerotic renovascular hypertension: results in 100 patients.

The long-term effect of percutaneous transluminal renal angioplasty (PTRA) on blood pressure and renal function was assessed in 100 consecutive patients with atherosclerotic renovascular hypertension. Technical success rates (complete plus partial) of a first PTRA averaged 76.2%, 74.1%, and 67.7% for the unilateral (n=42), bilateral (n=27), and solitary (n=31) groups, respectively. Of the technical successes, 59% (43/73) experienced sustained blood pressure benefit (mostly amelioration) during a mean follow-up period of 29 months. Rates of blood pressure benefit were similar in the three groups. Ostial lesions comprised the majority of blood pressure benefit failures. Repeat angioplasty in 14 patients resulted in a 71% technical success rate and a 50% blood pressure benefit rate during a mean follow-up period of 22 months. Long-term stability of mean serum creatinine level was observed after technically successful angioplasty in all three groups. Acute renal insufficiency, which was reversible in all but one patient, complicated 26% of the procedures. Mechanical complications occurred in 14% (20/145) of the arteries acted on; surgical intervention was required in five patients. The mortality rate was 2%. These results suggest that angioplasty is effective in both the long-term management of renovascular hypertension and the preservation of renal function hi a large fraction of patients with atherosclerotic renovascular hypertension.

Metabolic acidosis: pathophysiology, diagnosis and management

Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3−) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of ∼1 mmHg for every 1 mmol/l fall in serum HCO3− concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum anion gap, calculated as [Na+] – ([HCO3−] + [Cl−]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for the treatment of chronic metabolic acidosis is associated with improved cellular function and few complications.

Epidemiology of Hyponatremia

Hyponatremia is the most common electrolyte abnormality encountered in clinical practice with wide-ranging prognostic implications in a variety of conditions. This review summarizes the available literature on the epidemiology of hyponatremia in both hospitalized and ambulatory-based patients. Particular attention is given to hyponatremia in the geriatric population, drug-induced hyponatremia, exercise-associated hyponatremia, and the medical costs of hyponatremia. The frequency and outcomes of hyponatremia in congestive heart failure, cirrhosis, pneumonia, and human immunodeficiency virus infection also are reviewed. Although the knowledge on hyponatremia has expanded in the past few decades, the disorder largely remains an underdiagnosed condition. Substantial additional work is needed to improve the awareness of hyponatremia among medical professionals. The advent of vasopressin-receptor antagonists as a plausible treatment option for some forms of euvolemic and hypervolemic hyponatremia now offers the opportunity to gain further insights into the prognostic impact of hyponatremia and its management in various clinical settings.

Pregnancy in women with renal disease and moderate renal insufficiency

Data were gathered on 25 pregnancies in 23 women with moderate renal insufficiency as defined by a serum creatinine level of 1.4 mg/dl or greater prior to or at the onset of pregnancy. Twelve of the women had primary glomerular diseases, five (accounting for seven pregnancies) had interstitial diseases, and six had other renal diseases. In seven women with baseline serum creatinine levels ranging from 1.7 to 2.7 mg/dl, pregnancy was accompanied by a decline in renal function that was believed to be greater than expected from the natural history of the disease. The change ranged from a rise in serum creatinine level of 1.2 mg/dl to a functional decline that required dialysis. In 14 women (16 pregnancies), renal function either remained stable or declined to a degree consistent with the natural history of the disease. In two, the follow-up period was not long enough to judge the effect on the natural history of the disease. In 14 pregnancies, development or worsening of hypertension occurred. In nine, the diastolic blood pressure rose to 110 mm Hg or greater, and delivery was required because of hypertension. Twenty-three of 25 pregnancies ended in live births (92 percent) and 21 babies survived (84 percent). Fourteen of the 23 live births were premature. It is concluded that, in a substantial fraction of women with moderate renal insufficiency, pregnancy is accompanied by a decline in renal function; however, the fetal survival is much better than previously reported.

Precordial ST-segment mapping. 2. Effects of oxygen inhalation on ischemic injury in patients with acute myocardial infarction.

Precordial ST-segment mapping was serially applied in the Coronary Care Unit for the study of the effect of oxygen inhalation on the ischemic injury in 17 patients with acute anterior transmural myocardial infarction. A 49-lead ECG system was used. The sum of all ST elevations (ZST) recorded was taken as an index of magnitude of ischemic injury and the number of recording sites showing ST elevation (NST) was taken as an index of extent of ischemic damage. Stability of the precordial maps was observed over a period of one hour while the patients were on ambient air. Oxygen inhalation for a mean of 66 min resulted in a fourfold increase of PaO, and a mean of 16% reduction of both EST and NST. When the patients were returned to ambient air breathing, a mean of 13% increase of 2ST and 19% of NST from the levels recorded during oxygen inhalation were observed. Levels of 25ST and NST on ambient air following discontinuation of oxygen inhalation were not significantly different from the corresponding values from maps recorded before onset of oxygen breathing. Blood pressure and heart rate remained unchanged throughout the study. Clinical status of the patients was unchanged during the study period save for two patients who showed changes in intensity of their chest pain.