Urinary Potassium Concentrations Research Articles

Hypokalaemia related to acute chloroquine ingestion

Summary Large doses of chloroquine can cause poisoning. Our aim was to determine the possible relation between the plasma potassium concentration on admission with the severity of acute chloroquine poisoning and to assess the mechanism of chloroquine-induced hypokalaemia. We conducted a retrospective study of 191 consecutive cases. The main data included the occurrence of vomiting before admission, plasma, and urinary potassium concentration at admission, whole blood chloroquine concentration on admission, haemodynamic parameters and ECG, administration of catecholamines and outcome. Mean blood chloroquine level was 20·1 μmol/L (SD 14·3) (therapeutic level ≤6 μmol/L). Mean plasma potassium concentration was 3·0 mmol/L (0·8) and was lower in the subjects who died than in those who survived (p=0·0003). Plasma potassium varied directly with the systolic blood pressure and inversely with the QRS and QT. Plasma potassium varied inversely with the blood chloroquine (p=0·0001; τ=-0·42). Acute chloroquine intoxication is responsible for a hypokalaemia which correlates with the gravity of the intoxication and may be due to a transport-dependent mechanism. Plasma potassium concentrations should be carefully observed, particularly among patients who also receive catecholamine infusions. We should keep in mind, however, that overzealous repletion invokes the risk of subsequent hyperkalaemia and thus should be avoided.

Chronic hypokalaemia of adults: Gitelman's syndrome is frequent but classical Bartter's syndrome is rare

We evaluated 27 adult patients with chronic hypokalaemia (K+ = 2.9 +/- 0.2 mmol/l), documented over at least 5 years, in whom the cause of the hypokalaemia had not been clarified in spite of previous testing. In 15 patients it was possible to establish a diagnosis by a thorough outpatient workup (diuretic abuse (n = 5), surreptitious vomiting (n = 8), laxative abuse (n = 1), renal tubular acidosis (n = 1)). Commonly utilized tests such as measurements of plasma renin activity, plasma aldosterone, and urinary potassium concentration proved not to be useful in the differential diagnosis of these patients. In contrast the following were diagnostically important: in surreptitious vomiting the hypochloraemia, the mild renal insufficiency, and the extremely low urinary chloride concentration; in diuretic abuse the high urinary concentration of chloride together with repeatedly positive toxicology screens for diuretics; in laxative abuse the high stool weight and extremely low urinary sodium concentration. In the remaining 12 patients none of these diagnoses applied and further tests for suspected Bartter's syndrome were done in the hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Association between the natriuretic action of angiotensin-(1-7) and selective stimulation of renal prostaglandin I2 release.

We previously reported that angiotensin-(1-7) [Ang-(1-7)], a heptapeptide derived from the metabolism of either Ang I or Ang II, was biologically active in the rat isolated kidney, producing a marked diuresis and natriuresis that could be dissociated from the modest increase in glomerular filtration rate. The natriuretic response was accompanied by an increase in sodium concentration and concomitant decrease in urinary potassium concentration. Ang-(1-7) has also been shown to stimulate arachidonic acid release from isolated proximal tubules and elicit prostaglandin release from a number of tissues. Therefore, in the present study we tested the hypothesis that prostaglandins participate in the renal actions of Ang-(1-7). Rat isolated kidneys were perfused at 37 degrees C with gassed (95% O2/5% CO2) Krebs-Henseleit buffer containing oncotic agents and amino acids for six 10-minute clearance periods at a constant pressure of 90 mm Hg. Ang-(1-7) was infused at a rate that achieved a final concentration of 3 pmol/mL in the presence and absence of 10 mumol/L indomethacin. Prostaglandin E2 (PGE2) and PGI2 released into ureteral and venous effluents were measured by enzyme-linked immunoassay. During Ang-(1-7) infusion there was a selective increase in 6-keto-PGF1 alpha, an index of PGI2, appearing in both urine and perfusate; PGE2 levels were unchanged. Inhibition of stimulated 6-keto-PGF1 alpha release with indomethacin halved the fourfold increase in urine flow and sevenfold increase in sodium excretion rate without altering the increase in urinary sodium concentration produced by Ang-(1-7).(ABSTRACT TRUNCATED AT 250 WORDS)

Urinary Oxalate Excretion in Premature Infants: Effect of Human Milk Versus Formula Feeding

Objective. To study urinary oxalate excretion in infants fed human milk versus formula, and to compare urinary calcium oxalate and calcium phosphate saturation in premature infants with term infants and adults. Methodology. We measured urinary oxalate-to-creatinine ratio and urinary oxalate concentration in 15 premature infants fed human milk compared to 16 formula-fed premature infants, and in eight human milk-fed term infants compared to 17 formula-fed term infants. We then studied urinary calcium oxalate and calcium phosphate saturations based on our observations of elevated urinary oxalate excretion in premature infants. Urinary calcium oxalate and calcium phosphate saturations were calculated from urinary concentrations of oxalate, calcium, sodium, potassium, chloride, uric acid, magnesium, phosphorus, and urinary pH. We calculated urinary calcium oxalate and calcium phosphate saturations in nine healthy adults and nine formula-fed term infants to establish control values for urinary saturation. Urinary calcium oxalate and calcium phosphate saturations were determined in nine premature infants receiving a glucose and electrolyte solution, 11 premature infants receiving parenteral nutrition, nine formula-fed premature infants, and 11 human milk-fed premature infants. Results. Urinary oxalate excretion was higher in formula-fed compared to human milk-fed premature infants whether expressed as oxalate-to-creatinine ratio (0.32 ± 0.04 versus 0.18 ± 0.03, P < .01) or urinary oxalate concentration (0.047 ± 0.007 versus 0.022 ± 0.002 mg/mL, P < .01). Urinary oxalate excretion was higher in formula-fed term infants than in human milk-fed term infants whether expressed as oxalate-to-creatinine ratio (0.14 ± 0.01 versus 0.07 ± 0.01, P < .01) or urinary oxalate concentration (0.022 ± 0.002 versus 0.012 ± 0.002 mg/mL, P < .01). The urinary calcium oxalate saturation in healthy adults was 2.84 ± 0.79; the value in formula-fed term infants was 2.12 ± 0.31. The urinary calcium oxalate saturation was significantly higher in premature infants receiving formula (15.68 ± 3.15), human milk (15.02 ± 2.27), or parenteral nutrition (11.38 ± 2.56) compared to adults or term infants (P < .01). Urinary calcium oxalate saturation in premature infants receiving a glucose and electrolyte solution (2.45 ± 0.36) was not significantly different from that in adults or term infants. In contrast, urinary calcium phosphate saturation in premature infants as well as term infants and adults was less than 1; precipitation of calcium phosphate is not likely to occur under these conditions. Conclusion. Formula-fed infants have higher urinary oxalate excretion than human milk-fed infants. Premature infants receiving standard nutritional regimens may have urinary calcium oxalate saturation levels at which dissolved calcium oxalate may form nuclei of its solid phase.

Renal complications of nonsteroidal anti-inflammatory drugs

A 63-year-old, hypertensive, nondiabetic man with a 4-year history of gout was hospitalized because of painful swelling of his right foot. His blood pressure had been treated with nifedipine, 20 mg orally, three times daily. On admission, the patient was normotensive (blood pressure, 140/85 mm Hg) and had no clinical signs of congestive heart failure or volume depletion. Physical examination revealed erythema and soft-tissue swelling of the dorsum of the right foot with metatarsal tenderness. Laboratory data showed mild azotemia with a BUN level of 23 mg/dl; serum creatinine, 1.8 mg/dl; creatinine clearance, 70 mllmin; serum potassium, 4.1 mEq/liter; serum bicarbonate, 24 mmol/liter; and serum uric acid, 13.2 mg/dl. Roentgenographic findings were consistent with erosive gout, and a diagnosis of acute gouty attack was made. Indomethacin, 50 mg orally three times daily, was begun. The patient's symptoms improved rapidly, but within 4 days, the BUN rose to 51 mg/dl; serum creatinine, 2.4 mg/dl; serum potassium, 6.6 mEq/liter; and serum bicarbonate, 27 mmollliter; the creatinine clearance decreased to 36 mI/mm, with a fractional excretion of sodium of 0.06% and a urinary potassium concentration of 21 mEq/liter. The urinary sediment was unremarkable. The patient's blood pressure ranged from 140/85 to 150/90 mm Hg and no major changes in urinary output were noted. Indomethacin treatment was discontinued and replaced by colchicine. The patient's renal function and serum potassium level returned to baseline values within 4 days.

Renal mechanism of trimethoprim-induced hyperkalemia.

1) To determine the incidence and severity of hyperkalemia during trimethoprim therapy. 2) To test the hypothesis that trimethoprim inhibits renal potassium excretion by blocking sodium channels in the mammalian distal nephron. Thirty consecutive patients who were treated with trimethoprim-containing drugs. All patients included in the study had the acquired immunodeficiency syndrome (AIDS). Thirty-nine male Sprague-Dawley rats receiving normal rat chow and tap water (allowed free access). Humans: high dose (20 mg/kg per day) of trimethoprim therapy. Rats: trimethoprim (9.6 mg/h per kg body weight) was infused intravenously or into the renal distal tubules (1 mmol/L). Humans: Serum and urine electrolyte levels, serum creatinine, renin, aldosterone, and cortisol levels were measured, and the transtubular potassium gradient was calculated. Rats: The effects of trimethoprim infusion on urinary sodium, chloride, and potassium concentration and urine volume were measured. Sodium, chloride, potassium, and inulin concentrations were measured in fluid samples obtained from kidney distal tubules. The voltage across the wall of the distal tubule was measured. Humans: Trimethoprim increased the serum potassium concentration by 0.6 mmol/L (95% Cl, 0.29 to 0.95 mmol/L) despite normal adrenocortical function and glomerular filtration rate. Serum potassium levels greater than 5 mmol/L were observed during trimethoprim treatment in 15 of 30 patients. Rats: Intravenous trimethoprim inhibited renal potassium excretion by 40% (Cl, 21% to 60%) and increased renal sodium excretion by 46% (Cl, 9% to 83%). Trimethoprim (1 mmol/L) in tubule fluid inhibited distal tubule potassium secretion by 59% (Cl, 26% to 92%) and depolarized the lumen-negative transepithelial voltage by 66% (Cl, 46% to 85%). Trimethoprim (an organic cation) acts like amiloride and blocks apical membrane sodium channels in the mammalian distal nephron. As a consequence, the transepithelial voltage is reduced and potassium secretion is inhibited. Decreased renal potassium excretion secondary to these direct effects on kidney tubules leads to hyperkalemia in a substantial number of patients being treated with trimethoprim-containing drugs.

Sodium and Potassium Concentrations in Urine can Influence Micturition Volume in Humans

Sodium and Potassium Concentrations in Urine can Influence Micturition Volume in Humans

Indomethacin-induced urinary flow rate reduction in the ovine fetus is associated with reduced free water clearance and elevated plasma arginine vasopressin levels

OBJECTIVE: The purpose of our study was to explore the urinary responses of the ovine fetus to indomethacin levels comparable with those used therapeutically in the human fetus.STUDY DESIGN: After a 1-hour control period, chronically catheterized ovine fetuses between 125 and 139 days of gestation were given an intravenous bolus of indomethacin (0.05 mg/kg estimated fetal weight) followed by a 0.0025 mg/kg/min continuous infusion for 5 hours. The experimental group (n = 9) was compared with a vehicle-only infusion group (n = 10).RESULTS: There was a sustained 55.7% ± 9.5% (mean ± SEM) decrease in urinary output by 2 hours of indomethacin infusion (p \\lt 0.00001, analysis of variance). Urinary osmolality, potassium, and chloride concentrations underwent sustained increases during the infusion period (p \\lt 0.005). Free water clearance decreased by 67.5% ± 12.0% (p \\lt 0.001). Fetal arterial pressure increased only transiently (p \\lt 0.05), and increases in venous pressure (p = 0.013) and heart rate (p \\lt 0.0001) were sustained. Fetal plasma arginine vasopressin concentration increased during indomethacin infusion (p \\lt 0.05) and was correlated with the fall in urinary flow rate and free water clearance (p = 0.002). During vehicle infusion no significant changes were observed in any of the variables.CONCLUSIONS: Our data indicate that the fetus undergoes antidiuresis when exposed to low levels of indomethacin and that the observed antidiuresis is mediated by a decrease in free water clearance. The reduction in free water clearance may be mediated by increases in plasma arginine vasopressin concentrations. (AM J OBSTET GYNECOL 1992;167:1723-31.)

Hypokalaemic episodic polymyopathy in cats fed a vegetarian diet.

A previously undocumented hypokalaemic condition with a cyclical nature, comprising acute bouts of polymyopathy followed by spontaneous recoveries, is described in the cat. Cats being fed a high protein vegetarian diet developed recurrent episodes of polymyopathy, characterised by ventroflexion of the head and neck, stiff forelimb gait, lateral head-resting and generalised muscle weakness. Plasma potassium concentrations (mean +/- standard deviation) were reduced from 3.28 +/- 0.33 mmol/l at the beginning of the experiment to 2.45 +/- 0.24 mmol/l during bouts of myopathy. This hypokalaemia was associated with increased creatine kinase activities indicative of muscle damage, and decreased urinary potassium concentrations, and was caused by insufficient dietary potassium. Cats that received the same diet supplemented with potassium did not develop hypokalaemic polymyopathy. Spontaneous recoveries of affected cats were not associated consistently with increases in plasma potassium concentrations. Plasma taurine concentrations decreased and glutamic acid increased markedly in all cats fed the experimental diet. There was no evidence of thiamin deficiency associated with the high glutamic acid intake. Veterinarians should be aware that hypokalaemic cats, and in particular those on potassium-deficient diets, may show cyclical disease with episodes of polymyopathy recurring after periods of spontaneous clinical recovery. This condition in cats may be a useful animal model for familial hypokalaemic periodic paralysis in humans.

Renal nerves contribute to salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits.

The objective of this study was to investigate the role of the renal nerves in the pathogenesis of salt-induced hypertension in sinoaortic-denervated uninephrectomized rabbits. Twelve rabbits were divided into two groups. Sinoaortic-denervated uninephrectomized rabbits with intact renal nerves (sham group: n = 6) and without renal nerves (RDN group; n = 6). In both groups, 2 days of 154 meq/l NaCl loading was followed by 10 days of 1,700 meq/l NaCl loading. We administered 154 meq/l or 1,700 meq/l NaCl intravenously at every 8 h. Serial changes in mean arterial pressure (MAP) and heart rate (HR) were recorded using a microcomputer system. We chronologically measured hematocrit, serum osmolality, serum sodium, potassium, and chloride concentration, serum creatinine, plasma renin activity, plasma aldosterone, plasma norepinephrine, plasma arginine vasopressin, and plasma atrial natriuretic peptide. Urine volume and body weight were recorded every day, as were urinary concentrations of sodium, potassium, and chloride. The basal value of MAP in the sham group was significantly higher than that in the RDN group (on day -2, 111 +/- 1 mmHg for sham, 99 +/- 2 for RDN, P less than 0.001). Hypertonic saline loading induced an elevation of blood pressure in the sham group (126 +/- 2 mmHg on day 4, 127 +/- 2 on day 7, 124 +/- 4 on day 10). There were no significant changes in the response to salt loading in the RDN group. In the sham group, the retention of sodium was significant compared with that in the RDN group on day 5, and this difference was maintained until the end of the experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal function and plasma arginine vasotocin during an acute salt load in feral chickens.

Renal clearance experiments were conducted on feral chickens descended from birds collected from a coral island off the coast of Queensland, Australia. Following a control period when 0.13 M NaCl was used as a vehicle for the renal function markers, a salt load was imposed by infusion of 1 M NaCl. The hypertonic NaCl infusion resulted in increases in glomerular filtration rate (GFR), effective renal blood flow (ERBF), and urine flow rate (V), whereas filtration fraction decreased. Haematocrit was reduced and plasma osmoality, sodium, chloride and potassium concentrations increased. Plasma arginine vasotocin (PAVT) levels increased from 31.4 +/- 2.3 pg.ml-1 during the control infusion to 56.0 +/- 1.7 pg.ml-1 following a salt load of 12 mmol NaCl.kg-1. The sensitivity of release of AVT was 0.69 +/- 0.11 pg.ml-1 per mosmol.kg-1. The concentrations of Na and Cl in urine increased, whereas urine osmolality and potassium concentration decreased. The expansion of the extracellular fluid volume induced by the salt loading would tend to suppress the release of AVT, whereas the osmotic stimulus would provide a stimulus for the release of AVT. In this study, GFR, ERBF and ERPF increased at the same time as PAVT increased.

Changes in Blood Pressure, Plasma Triglyceride and Aldosterone Concentration, and Red Cell Cation Concentration in Patients With Hyperinsulinemia

Blood pressure, plasma concentration of triglyceride, aldosterone, renin activity (PRA), and atrial naturietic peptide (ANP), and red blood cell, urine, and plasma sodium and potassium concentration were determined in 24 healthy individuals divided into two groups defined as being either hyperinsulinemic or normoinsulinemic. The results demonstrated that the hyperinsulinemic group had significantly higher values for both systolic (P less than .01) and diastolic (P less than .05) blood pressure. In addition, plasma concentrations of triglyceride (P less than .02), aldosterone (P less than .05) and potassium (P less than .05) were higher in hyperinsulinemic individuals as compared to those who were normoinsulinemic. Furthermore, red cell potassium was lower (P less than .01) and red cell sodium higher (P less than .01) in the hyperinsulinemic group. Finally, the magnitude of hyperinsulinemia correlated directly with systolic (r = 0.50, P less than .01) and diastolic (r = 0.44, P less than .05) blood pressure, concentration of plasma triglyceride (r = 0.55, P less than .01) and aldosterone (r = 0.46, p less than .05), and erythrocyte sodium concentration (r = 0.57, p less than .01). In contrast, plasma insulin response was negatively correlated with erythrocyte potassium concentration (r = 0.40, P less than 0.05). These observations provide further support for the view that hyperinsulinemia, presumably secondary to resistance to insulin-stimulated glucose uptake, is associated with a cluster of variables that may play important roles in the etiology and clinical course of hypertension.

Renal Excretory Actions of Furosemide, of Hydrochlorothiazide and of the Vasodilator Flosequinan in Healthy Subjects

The responses of urine and urinary solute outputs and flows to single doses of 80 mg furosemide, 25 mg hydrochlorothiazide, and 100 or 200 mg flosequinan were investigated in healthy subjects using a double-blind, randomized, crossover design. Treatment days were separated by 7 days. Volumes of urine passed between 0 and 3, 3 and 6, 6 and 9, 9 and 12, and 12 and 24 h after drug administration were determined and urinary concentrations of chloride, sodium, potassium, calcium, magnesium, phosphate, zinc, urate, urea and creatinine were measured. Venous blood was taken before and 6 and 24 h after dosing and the serum was analysed for the same solutes as urine. Excretions of urine and urinary solutes accumulated at the end of each collection period after each formulation were fitted by the UY function, whose derivative provided corresponding flows as functions of time. Instantaneous renal clearances of solutes 6 and 24 h after dosing were evaluated from the flows. This approach showed that 80 mg furosemide and 25 mg hydrochlorothiazide were equipotent 24-h natriuretics. Rapid urinary responses which then rebounded compared with the control responses were produced by 80 mg furosemide, whereas changes after 25 mg hydrochlorothiazide were smooth. Neither 100 or 200 mg flosequinan showed any important effect on urinary excretion.

Urine Electrolytes and Osmolality: When and How to Use Them

The purpose of this review is to provide an update on the use of the urine electrolyte and osmolality measurements in patients with disorders of fluid, electrolytes, and/or acid-base metabolism. It is critical to appreciate that there are no 'normal values' for these parameters, only 'expected values' relative to clinical situations. Pitfalls in the interpretation of each electrolyte in the urine are also provided. To detect a mild to moderate degree of reduction of the 'effective' intravascular volume, both urine sodium (Na) and chloride (Cl) concentrations should be measured. Pitfalls in this assessment are abnormal renal and adrenal function and the use of diuretics. Insights into the etiology of the low 'effective' intravascular volume can be deduced by comparing the urine Na, potassium (K), and Cl concentrations. The urine net charge (Cl vs. Na + K) is the most reliable way to estimate the urine ammonium concentration short of its direct measurement, an assay that is not provided by most laboratories. This measurement is important in the differential diagnosis of hyperchloremic metabolic acidosis. To examine the renal response to hypokalemia or hyperkalemia, the two components of K excretion (K secretion and urine flow rate) should be examined separately. The former is evaluated using the transtubular K, concentration gradient. The urine osmolality is used to assess antidiuretic hormone action and the osmolality of the renal medulla and to determine the etiology of polyuria and/or hypernatremia. The urine osmolality can also be used to assess the ammonium concentration, using the urine osmolal gap, and to detect unusual urine osmoles.

Is on-line monitoring of renal function possible?

Twenty patients who had undergone open heart surgery were studied in order to determine whether measurement of the combined urinary sodium and potassium concentration can be used to monitor renal function. The clearances of creatinine and the free water demonstrated a significant statistical correlation with the combined urinary sodium and potassium concentration. We conclude that measurement of the combined sodium and potassium concentration in the urine can be used as an indicator of renal function. Thus, measurement of the electrical conductivity in the urine might be suitable as an on-line monitor of renal function during surgery or in the intensive care unit.

Endocrines and osmoregulatory mechanisms in the Nile crocodile, Crocodylus niloticus

The changes in body fluid economy and endocrine status associated with exposure of the Nile crocodile, Crocodylus niloticus, to hypertonic media have been related to the responses to altered renin-angiotensin system (RAS) activity observed in fresh water (FW) animals. Animals held in hypertonic media for 7 days showed a 18.2% body weight loss and raised plasma and urinary sodium, potassium, chloride, and osmotic concentrations. Within 6 hr of return to FW rapid imbibition had largely restored body weight and produced significant plasma dilution. Although plasma sodium, chloride, and osmotic concentrations remained higher than in FW controls, plasma levels of corticosterone, aldosterone, and arginine vasotocin were not significantly altered. Angiotensin I (AI) administration in FW crocodiles stimulated drinking and raised plasma aldosterone levels by comparison with animals given the converting enzyme inhibitor, Captopril, together with AI. The compensatory drinking behaviour exhibited by the Nile crocodile may thus involve the RAS. The RAS also appears to influence interrenal steroidogenesis and thus may afford an integrative role in crocodile fluid management as it does in homeotherms.

Effects of urinary potassium and sodium ion concentrations and pH on N-butyl-N(4-hydroxybutyl)nitrosamine-induced urinary bladder carcinogenesis in rats

The promoting activities of low and high sodium or potassium ion concentrations, under conditions of neutral as well as elevated urinary pH, in urinary bladder carcinogenesis, were investigated in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). Male Wistar rats were given 0.05% BBN in their drinking water for 4 weeks and then treated for 32 weeks with either control diet (group 1) or this diet supplemented with equimolar amounts of the following minerals: 2.34% NaCl (group 2), 2.98% KCl (group 3), 3.36% NaHCO3 (group 4), 1.68% NaHCO3 + 2% KHCO3 (group 5), or 4% KHCO3 (group 6). The alkalizing salts NaHCO3 and KHCO3 induced comparable increases in urinary pH and elevated urinary sodium or potassium ion concentrations respectively. The combination of NaHCO3 + KHCO3 similarly caused an elevation of the urinary pH and less increased sodium and potassium ion concentrations. In the groups fed NaHCO3 and KHCO3 either alone or in combination, the incidences of papillary/nodular hyperplasia, papillomas and carcinomas in the urinary bladder had increased as compared to controls. NaCl and KCl also induced high urinary sodium or potassium ion concentrations without alteration of urinary pH. This was accompanied by increased incidences of simple hyperplasia, papillary/nodular hyperplasia, and/or papillomas but no carcinomas. The present results indicate that the potassium ion is as potent as the sodium ion in promoting urinary bladder carcinogenesis under conditions of elevated urinary pH, and that both the sodium and potassium ions may exert weak promoting activity under conditions of neutral urinary pH.

Total body water, total exchangeable sodium and potassium in patients with convalescent acute myocardial infarction one to two months after onset.

Total exchangeable sodium (Nae), potassium (Ke), and total body water (TBW) were measured by the multiple isotope dilution method, in 10 healthy subjects (normal), 10 patients with congestive heart failure (CHF), and 47 patients with acute myocardial infarction (AMI), 1-2 months after onset. According to Killip's classification, 29 patients with AMI were classified as class I, and 18 patients were classified as class II and III (referred to as class II & III). No differences were found in plasma and urine sodium and potassium concentrations. By the multiple isotope dilution method, significant elevations in Nae/BSA (body surface area) were observed in the following order: normal, class I, class II & III and patients with CHF. Compared with normal subjects, Nae/BSA and Nae/Ke were elevated in class I patients. Elevations of Nae/Ke and TBW/BSA in both class II & III patients with AMI and patients with CHF indicated severe cardiac impairment. Both Nae/BSA (p = -0.60) and Ke/BSA (p = 0.71) had negative and positive correlations with the left ventricular ejection fractions (EF) measured by catheterization in 20 patients with AMI. This indicates a major sodium and water retention mechanism due to impaired cardiac function in AMI. It is worth noting that conspicuous abnormalities in body fluid compositions, particularly in class I patients with AMI as well as class II & III, remained despite no evidence of cardiac failure.

In vivo hypotensive activity of Pistacia lentiscus L

AbstractThe present studies were undertaken to explain the mechanism of action of the hypothesive effect of Pistacia lentiscus L. aqueous extract. The potassium, calcium and magnesium content of the aqueous extract was determined and synthetic mixtures of salts evaluated in rats. The urinary excretion volume and the sodium and potassium concentrations in urine were also determined. In an effort to explain the effects of the extract, in vivo pharmacological experiments were conducted.

Renal Injury in Sick Newborn Infants: A Prospective Evaluation Using Urinary β2-Microglobulin Concentrations

Urinary concentrations of β2-microglobulin and creatinine were measured serially in 140 sick infants, of whom 109 were asphyxiated, and in 35 healthy preterm and term infants. First voided urines and samples from days 3 and 7 postpartum were studied. Urinary β2-microglobulin concentrations in healthy infants averaged 1.34 ± 1.34 mg/L (mean ± SD) in first voided specimens and 1.32 ± 0.98 mg/L in day 3 samples; the calculated upper limit of normal (95% confidence limit) was 4.00 mg/L. Elevated values (those exceeding the 95% confidence limit) occurred most often in the sick asphyxiated patients (56%); the first voided sample value in these patients was 10.0 ± 10.4 mg/L. The equivalent value in the sick nonasphyxiated infants was 8.32 ± 7.27 mg/L. Values were significantly and persistently elevated in the sick infants on days 3 and 7. Factoring β2-microglobulin levels by urinary creatinine concentration did not affect the significance of the findings. The increased urinary β2-microglobulin levels were not (1) related to gestational age; low β2-microglobulin values occurred at all gestational ages for both healthy and sick infants; (2) a consequence of urine flow rate; urinary β2-microglobulin did not correlate with urinary creatinine concentration or with urine to plasma creatinine ratio; and (3) a consequence of increased production of β2-microglobulin; urinary and serum β2-microglobulin values did not correlate (r = .03). Thus, we propose that the elevated levels of urinary β2-microglobulin in the sick infants were the consequence of tubular injury. This was associated with hematuria but not with a high incidence of azotemia or oliguria. In the most premature infants (<32 weeks), elevated urinary β2-microglobulin concentrations were associated with significantly increased urinary concentrations of sodium and potassium. These data suggest a higher prevalence of acute tubular injury in sick newborn infants than has been reported in previous studies in which more traditional indices of renal injury were used.