Milford Fulop

The Metabolic and Respiratory Acidosis of Acute Pulmonary Edema

Abstract Arterial blood gas tension and pH were measured in 50 consecutive patients with acute pulmonary edema due to left ventricular failure. In contrast to current belief that blood pH is typica...

Dialyzability, Protein Binding, and Renal Excretion of Plasma Conjugated Bilirubin*

Conjugated bilirubin is excreted in the urine, but unconjugated bilirubin is generally believed not to be excreted by the kidneys. The basis for this difference has not been resolved by past studies. Hoover and Blankenhorn reported that bilirubin was dialyzable only from the plasma of patients who had bilirubinuria, and that it was not dialyzable from the plasma of patients with acholuric jaundice (3). Most subsequent investigators, however, have maintained that neither conjugated nor unconjugated bilirubin was dialyzable or ultrafilterable from plasma (4-7). This led to the hypothesis that conjugated bilirubin was probably excreted in the urine by a process of renal tubular secretion (8). Studies that were performed in jaundiced dogs in this laboratory gave results consistent with a process of glomerular filtration of conjugated bilirubin (9). We therefore re-examined the question of the dialyzability of plasma bilirubin. A small fraction of plasma conjugated bilirubin in jaundiced humans and dogs was found to be dialyzable, and hence available for urinary excretion by glomerular filtration. The studies indicated that this dialyzable fraction was bound to low molecular weight carrier(s), which migrated in the alpha and beta globulin zones on paper electrophoresis and which sedimented on ultracentrifugation.

The phosphaturic effect of sodium bicarbonate and acetazolamide in dogs

Urinary inorganic phosphate excretion was studied before and during the administration of sodium bicarbonate and acetazolamide in dogs that were not given infusions of phosphate. The excretion fraction of filtered phosphate increased after sodium bicarbonate or acetazolamide was given. This phosphaturia was attributed to decreased tubular reabsorption of phosphate consequent to alkalinization of either tubular urine or cells.

Lactic Acidosis in Pulmonary Edema due to Left Ventricular Failure

Abstract Acidemia is common in severe pulmonary edema due to acute heart failure and is caused by metabolic and respiratory acidosis, in various combinations in different patients. The findings in ...

A Guide for Predicting Arterial CO2 Tension in Metabolic Acidosis

This presentation examines the relation of arterial CO2 tension to the severity of acidemia in three large groups of cases of diabetic ketoacidosis, totalling 405 episodes. In particular, it evaluates the previously reported anecdotal observation that PaCO2 (in torr) in such patients is usually numerically close to the two-digit number to the right of the pH decimal point, down to a pH of 7.10-7.15. The relations between measured arterial CO2 tension levels and calculated plasma bicarbonate concentration in the three groups were very similar to those previously reported by others and us, the regression equations approximating PaCO2 = 1.5 x [HCO3-] + 8. Further, in the 262 episodes with blood pH 7.10-7.37, down to a pH of 7.10-7.15, the average PaCO2 in torr often did approximate the two-digit number to the right of the decimal point in the pH value. This relation provides a quick and easily remembered alternative guide for predicting the approximate expected PaCO2 in patients with metabolic acidosis. The basis for this apparently fortuitous relation between PaCO2 and blood pH may be the closely similar correlation between PaCO2 and 1/cH+ (i.e., 10PH), which in turn derives from the physiologically significant relation of alveolar ventilation to blood pH, and the inverse relation between PaCO2 and alveolar ventilation.

Severe Hypertriglyceridemia in Diabetic Ketosis

In order to learn whether patients with diabetic ketosis who had very severe hypertriglyceridemia had underlying genetic hyperlipidemia, the authors measured plasma lipids in 211 episodes. They report the findings in the 15 patients who had initial plasma triglyceride concentrations above 11.3 mmol/L (1,000 mg/dL). These patients were detected during a prospective study of 155 episodes of ketoacidosis and 56 episodes of ketosis. Eleven of the 15 patients had definite or probable insulin-dependent diabetes mellitus (IDDM), but eight of the 15 were not acidemic despite their ketosis. Twelve of the 15 patients (80%) were men, a far higher percentage of men than the 53.6% in the base population of 211 episodes. Plasma triglyceride concentrations returned to normal levels either during the acute episode (seven cases) or well within a year (two more cases) in most of the patients. From that and other considerations, the authors infer that at least ten, and perhaps 12 of the 15 patients did not have an underlying genetic hyperlipidemia contributing to their original severe hypertriglyceridemia. That contrasts with the findings of others who reported that most patients with severe hypertriglyceridemia associated with noninsulin-dependent diabetes mellitus (NIDDM) (usually without ketosis) did have coexisting familial hypertriglyceridemia.

Increased ureteral back pressure enhances renal tubular sodium reabsorption

Moderate increases of ureteral back pressure usually cause decreases of glomerular filtration rate and even greater decreases of sodium excretion. It has been assumed previously that increased ureteral back pressure does not enhance renal tubular sodium reabsorption directly and that the decreases of sodium excretion are caused by the decreases of glomerular filtration rate. In the experiments reported here, the effect of increased ureteral back pressure on urinary sodium excretion was studied in dogs in which changes of filtration rate were minimized by infusing saline while ureteral back-pressure was increased. When ureteral back pressure was increased on one side by 10-23 cm of water, the inulin clearance of the experimental kidney decreased by only 3-12% in 21 experiments, did not change significantly (+/-2%) in eight experiments, and increased by 3-8% in seven experiments. The sodium excretion of the experimental kidney decreased in all experiments regardless of whether its inulin clearance increased, decreased, or was unchanged from control values. When the inulin clearance of the experimental kidney increased or remained unchanged during increased ureteral back pressure, its reabsorption of sodium increased more than could be accounted for by the increase of filtered sodium. When the inulin clearance of the experimental kidney decreased during increased ureteral back pressure, its reabsorption of sodium decreased less than could be accounted for by the decrease of filtered sodium.Therefore, the effect of increased ureteral back pressure to decrease urinary sodium excretion is caused in part by increased tubular reabsorption of sodium.

Defective Urinary Acidification in Wilson's Disease

Abstract Four of 12 patients with treated Wilsons disease had subnormal urinary acidifying capacity, and one of them had bilateral medullary nephrocalcinosis characteristic of distal renal tubular...

Case Report: Extensive Brain Calcification in Hypoparathyroidism

It is well known that most patients with hypoparathyroidism have radiologically detectable basal ganglia calcification. Not as well known is that the brain calcinosis may be more extensive. We describe a 55-year-old woman with a 44-year history of symptomatic idiopathic hypoparathyroidism who has extensive calcification of her cerebrum and cerebellum as well as her basal ganglia, evident on computed tomography of the head. When first evaluated here 32 years ago, plain radiography of the skull demonstrated calcification of both caudate and lentiform nuclei (basal ganglia). Despite fair control of her serum calcium level, she has developed focal seizures, possibly related to the calcinosis of her brain.

Recurrent diabetic ketoacidosis

This report presents and analyzes certain clinical and laboratory findings in 17 patients who were hospitalized repeatedly for diabetic ketoacidosis on a municipal hospital medical service during the early 1970s and the early 1980s. The 17 patients had a total of 92 hospitalizations for ketoacidosis during the survey periods. During the 1970s, most of the frequent recurrences occurred in young women, as has often been noted by others. In recent years, however, the number of patients with frequent recurrences hospitalized at Bronx Municipal Hospital Center has declined, and most of the patients have been young men. There is no obvious explanation for the latter trend. The laboratory findings were analyzed in order to learn whether they were similar in each patient during his or her recurrent admissions. In a few patients, blood pH, hemoglobin concentration, serum glucose level, anion gap, and osmolarity tended to be similar during their repeated hospitalizations. In the majority of the patients, however, there was significant variation in most of these laboratory indexes, except for the serum osmolarities and blood hemoglobin concentrations. The similarity of the serum osmolarities and hemoglobin concentrations in sequential episodes in most of the patients suggested that a certain severity of dehydration may have been the main factor that led them to seek hospitalization.