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Biomedical subjects

R Krapf

Publications and source records attributed to R Krapf.

At least 55 records · Page 3Linked to original sources
PubMed1993

[3 dangerous electrolyte disturbances: hyponatremia, hyperkalemia and hypomagnesemia].

Three cases of acute and potentially dangerous electrolyte disturbances provide a basis for discussion of selected aspects of pathogenesis, clinical manifestation and correction of certain electrolyte disorders (hyponatremia, hyperkalemia, hypomagnesemia). A case of diuretic-induced hyponatremia illustrates the controversy surrounding correction of this disorder. The regulatory mechanisms of transcellular potassium equilibrium are discussed with the help of a case of exercise-induced hyperkalemia. A separate case is dedicated to the discussion of the multiple causes and symptoms of magnesium depletion.

Acute Disease↗
PubMed1993

Determining peritoneal dialysis prescriptions by employing a patient-specific protocol.

OBJECTIVE: To develop a formula that would permit a rapid and simple calculation of required dialysate volume needed to provide a predetermined daily creatinine clearance. DESIGN: Prospective study of peritoneal dialysis patients followed for 6 months. SETTING: A primary care teaching hospital in New York. PATIENTS: Twenty-six patients beginning peritoneal dialysis entered and completed the study. INTERVENTION: By employing each patient's measured peritoneal equilibration test (PET) and a standard clearance formula, a patient-specific treatment protocol (PSP) was calculated. The PET 2-hour D/Pcreat was used for continuous cycling peritoneal dialysis (CCPD) and the 4-hour D/Pcreat was used for patients on continuous ambulatory peritoneal dialysis (CAPD) to determine a PSP that would provide a minimum of 6 L of creatinine clearance daily. MAIN OUTCOME MEASURES: Patients were followed for 6 months to assess the ability of this approach of maintaining acceptable levels of blood urea nitrogen, creatinine, albumin, and hematocrit over the 6-month period of observation. RESULTS: Our study of 26 patients revealed that only 6 patients (23%) could be treated with the standard prescription of 8 L/day on CAPD. The remaining 77% of our patients required 9-13 L/day for CAPD and 12-21 L/day for CCPD. All patients were free of uremic symptoms and demonstrated acceptable biochemical parameters over a 3-6 month period of observation. CONCLUSIONS: A patient-specific protocol utilizing individually derived PET data provides an acceptable and easy to calculate initial treatment prescription for each patient that avoids the necessity for trial and error that has heretofore been employed.

Adult↗
PubMed1992

Chronic respiratory alkalosis induces renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans.

The effects of chronic respiratory alkalosis on divalent ion homeostasis have not been reported in any species. We studied four normal male subjects during a four-day control period (residence at 500 m), during six days of chronic respiratory alkalosis induced by hypobaric hypoxia (residence at 3450 m), followed by a six-day eucapnic recovery period (500 m) under metabolic balance conditions. Chronic respiratory alkalosis (delta PaCO2, -8.4 mm Hg, delta[H+] -3.2 nmol/liter) resulted in a sustained decrement in plasma ionized calcium concentration (delta[IoCa++]p, -0.10 mmol/liter, P less than 0.05) and a sustained increment in plasma phosphate concentration (delta[PO4]p, +0.14 mmol/liter, P less than 0.005) associated with increased fractional excretion of Ca++ (+0.5%, P less than 0.005), decreased phosphate clearance (-6.1 ml/min, P less than 0.025) and decreased excretion of nephrogenous cAMP (-1.5 nmol/100 ml GFR, P less than 0.0025). Urinary phosphate excretion decreased by 15.4 mmol/24 hr on day 1 of chronic respiratory alkalosis (P less than 0.0025), but returned to control values by day 6 despite hyperphosphatemia. Serum intact [PTH] did not change. Sustained hypomagnesuria (-0.8 mmol/24 hr, P less than 0.05) occurred during chronic respiratory alkalosis and was accounted for, at least in part, by decreased fractional excretion of Mg++ (-0.7%, P less than 0.05) in the absence of change in plasma magnesium concentration. Serum 1,25(OH)2D levels were unchanged by chronic respiratory alkalosis. In conclusion, the decrease in nephrogenous cAMP generation despite unchanged serum intact PTH concentration suggests that chronic respiratory alkalosis results in impaired renal responsiveness to PTH as manifested by alterations in PTH-dependent renal calcium and phosphate transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Abuse of germanium associated with fatal lactic acidosis.

Germanium compounds are marketed as nonprescription drugs in Europe and are recommended by the suppliers for AIDS and metastatic cancer disease. We observed a patient with nonmetastatic breast cancer who died because of severe lactic acidosis (plasma lactate concentration = 27 mmol/l) after ingestion of 25 g of elemental germanium over a 2-months period. Renal failure and hepatotoxicity had newly developed during germanium intake. Postmortem examination revealed severe hydropic vacuolation of tubule cells and the presence of inclusion bodies predominantly in straight proximal tubule cells with normal appearance of renal interstitium and glomeruli. The liver showed panlobular steatosis. Urine, blood and tissue (kidney, liver, muscle, pancreas) levels of germanium were high. Lactic acidosis may have been caused by the combined, germanium-induced renal and hepatic failure (underutilization), but it remains to be seen whether germanium can affect lactate production and/or metabolism directly.

Acidosis↗
PubMed1992

Chronic metabolic acidosis increases the serum concentration of 1,25-dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia.

Chronic metabolic acidosis results in metabolic bone disease, calcium nephrolithiasis, and growth retardation. The pathogenesis of each of these sequelae is poorly understood in humans. We therefore investigated the effects of chronic extrarenal metabolic acidosis on the regulation of 1,25-(OH)2D, parathyroid hormone, calcium, and phosphate metabolism in normal humans. Chronic extrarenal metabolic acidosis was induced by administering two different doses of NH4Cl [2.1 (low dose) and 4.2 (high dose) mmol/kg body wt per d, respectively] to four male volunteers each during metabolic balance conditions. Plasma [HCO3-] decreased by 4.5 +/- 0.4 mmol/liter in the low dose and by 9.1 +/- 0.3 mmol/liter (P < 0.001) in the high dose group. Metabolic acidosis induced renal hypophosphatemia, which strongly correlated with the severity of acidosis (Plasma [PO4] on plasma [HCO3-]; r = 0.721, P < 0.001). Both metabolic clearance and production rates of 1,25-(OH)2D increased in both groups. In the high dose group, the percentage increase in production rate was much greater than the percentage increase in metabolic clearance rate, resulting in a significantly increased serum 1,25-(OH)2D concentration. A strong inverse correlation was observed for serum 1,25-(OH)2D concentration on both plasma [PO4] (r = -0.711, P < 0.001) and plasma [HCO3-] (r = -0.725, P < 0.001). Plasma ionized calcium concentration did not change in either group whereas intact serum parathyroid hormone concentration decreased significantly in the high dose group. In conclusion, metabolic acidosis results in graded increases in serum 1,25-(OH)2D concentration by stimulating its production rate in humans. The increased production rate is explained by acidosis-induced hypophosphatemia/cellular phosphate depletion resulting at least in part from decreased renal tubular phosphate reabsorption. The decreased serum intact parathyroid hormone levels in more severe acidosis may be the consequence of hypophosphatemia and/or increased serum 1,25-(OH)2D concentrations.

Acidosis↗
PubMed1992

Ventilatory support during magnetic resonance imaging.

Ventilatory support during magnetic resonance imaging is difficult because metallic objects on ventilatory support devices can interfere with the imaging field and/or become magnetized and move inside the patient or become flying projectiles. We report the successful MRI examination of an intubated respirator-dependent pediatric patient. Ventilatory support was carried out with a plastic ambu bag, exhalation valve circuit, and tubing.

Equipment Design↗
PubMed1991

[Hypo- and hyperventilation: consequences for acid-base balance].

Deviations of the alveolar ventilation rate from normality induce respiratory acid-base disturbances. Alveolar hyperventilation leads to hypocapnia and thus respiratory alkalosis whereas alveolar hypoventilation induces hypercapnia leading to respiratory acidosis. The changes in CO2 induce compensatory alterations of renal bicarbonate transport: Hypercapnia stimulates renal reabsorption of bicarbonate whereas hypocapnia enhances urinary bicarbonates. The plasma bicarbonate concentration rises in response to hypercapnia and falls following hypocapnia. Renal regulation of plasma bicarbonate results in a characteristic dependence on systemic PCO2 permitting the formation of diagnostic criteria for respiratory imbalance of acid-base homeostasis. In chronic respiratory acidosis plasma bicarbonate should rise by 0.35 mmol/l per mmHg increase in PCO2. In chronic respiratory alkalosis, on the other hand, plasma bicarbonate should fall by 0.4 mmol/l for every mmHg decrease in PCO2. If the measured bicarbonate values do not fall into this expected range, acute respiratory or mixed (respiratory and metabolic) acid-base disturbances should be suspected. The clinical significance and application of these diagnostic criteria are illustrated by examples.

Acid-Base Equilibrium↗
PubMed1991

Chronic respiratory alkalosis. The effect of sustained hyperventilation on renal regulation of acid-base equilibrium.

BACKGROUND: In normal subjects, chronic hyperventilation lowers plasma bicarbonate concentration, primarily by inhibiting the urinary excretion of net acid. The quantitative relation between reduced arterial carbon dioxide tension (PaCO2) and the plasma bicarbonate concentration in the chronic steady state has not been studied in humans, however, and the laboratory criteria for the diagnosis of chronic respiratory alkalosis therefore remain undefined. We wished to provide such reference data for clinical use. Moreover, because chronic hyperventilation paradoxically lowers blood pH still further in dogs with metabolic acidosis, we desired to study the effect of chronic hypocapnia on the plasma bicarbonate concentration (and blood pH) in normal human subjects in whom acidosis had been induced with ammonium chloride. METHODS: Under metabolic-balance conditions, we used altitude-induced hypobaric hypoxia to produce chronic hypocapnia in nine normal young men, five of whom received ammonium chloride daily to cause metabolic acidosis (the mean [+/- SE] steady-state plasma bicarbonate level in these five was 12.0 +/- 0.5 mmol per liter). RESULTS: For each decrease of 1 mm Hg (0.13 kPa) in the PaCO2, the plasma bicarbonate concentration decreased by 0.41 mmol per liter in the subjects who started with a normal plasma bicarbonate concentration and by 0.42 mmol per liter in the subjects with acidosis. In contrast to the findings in previous studies of dogs, hypocapnia increased blood pH similarly in both groups; the blood hydrogen ion concentration decreased by about 0.4 nmol per liter for every decrease of 1 mm Hg (0.13 kPa) in PaCO2. CONCLUSIONS: These results provide reference data for the diagnosis of chronic respiratory alkalosis in humans. Although chronic hypocapnia decreased plasma bicarbonate levels similarly in normal subjects with acidosis and without acidosis, the percent reduction in PaCO2 was always greater than the corresponding percent reduction in the plasma bicarbonate concentration. Therefore, as was not true of the response in dogs, the subjects' blood pH always increased with hyperventilation, regardless of the initial plasma bicarbonate concentration.

Acid-Base Equilibrium↗
PubMed1991

[Aplastic anemia in carbamazepine therapy].

We report a case of carbamazepine-induced aplastic anemia. After an initial treatment period of 10 days (600 mg/day), moderate, persisting pancytopenia was observed. Three years later, carbamazepine treatment was resumed at 400 mg/day for 120 days. Subsequently, more severe, irreversible pancytopenia due to bone marrow aplasia was diagnosed. History, course, bone marrow findings and the extensive, negative work-up for other causes of aplastic anemia strongly indicate that carbamazepine was etiologically responsible. Aplastic anemia secondary to carbamazepine treatment is rarely reported. Information on the dose and time of exposure are only available from anecdotal case reports. Based on a literature survey we analyze the risk of this potentially lethal hematological side-effect and make recommendations for routine blood checks.

Aged↗
PubMed1991

Studies on the kinetics of Na+/H+ exchange in OK cells: introduction of a new device for the analysis of polarized transport in cultured epithelia.

The present study describes a new perfusion technique--based on the use of a routine spectrofluorometer--which enables fluorometric evaluation of polarity, regulation and kinetics of Na+/H+ exchange at the level of an intact monolayer. Na+/H+ exchange was evaluated in bicarbonate-free solutions in OK (opossum kidney) cells, a renal epithelial cell line. Na+/H+ exchange activity was measured by monitoring changes in intracellular pH (pHi) after an acid load, using the pH-sensitive dye 2'7'-bis (carboxyethyl) 5-6-carboxy-fluorescein (BCECF). Initial experiments indicated that OK cells grown on a permeable support had access to apical and basolateral perfusion media. They also demonstrate that OK cells express an apical pHi recovery mechanism, which is Na+ dependent, ethylisopropylamiloride (EIPA) sensitive and regulated by PTH. Compared to resting conditions (pHi = 7.68; pHo = 7.4) where Na+/H+ exchange is not detectable, transport rate increased as pHi decreased. A positive cooperativity characterized the interaction of internal H+ with the exchanger, and suggests multiple H+ binding sites. In contrast, extracellular [Na+] increased transport with simple Michaelis-Menten kinetics. The apparent affinity of the exchanger for Na+ was 19 mM at an intracellular pH of 7.1 and 60 mM at an intracellular pH of 6.6. Inhibition of Na+/H+ exchange activity by EIPA was competitive with respect to extracellular [Na+] and the Ki was 3.4 microM. In conclusion, the technique used in the present study is well suited for determination of mechanisms involved in control of epithelial cell pHi and processes associated with their polarized expression and regulation.

Amiloride↗
PubMed1991

Expression of rat renal Na/H antiporter mRNA levels in response to respiratory and metabolic acidosis.

The mammalian proximal tubule is an important mediator of the renal adaptive response to systemic acidosis. In chronic metabolic and respiratory acidosis the bicarbonate reabsorptive (or proton secretory) capacity is increased. This increase is mediated, at least in part, by an increase in Vmax of the luminal Na/H antiporter. To determine whether this adaptation involves increased mRNA expression, Na/H antiporter mRNA levels were measured by Northern analysis in renal cortex of rats with metabolic (6 mmol/kg body wt NH4Cl for 2 or 5 d) and respiratory (10% CO2/air balanced for 2 or 5 d) acidosis and of normal, pair-fed rats. Na/H antiporter mRNA levels were unchanged after 2 d of both metabolic and respiratory acidosis. After 5 d, however, Na/H antiporter mRNA expression was increased 1.76 +/- 0.12-fold in response to metabolic acidosis (P less than 0.005, n = 8), but was not different from normal in response to respiratory acidosis: 1.1 +/- 0.2 (NS, n = 8). Thus, the renal adaptive response to metabolic acidosis involves increased cortical Na/H antiporter mRNA levels. In contrast, the enhanced proximal tubule Na/H antiporter activity and bicarbonate reabsorption in respiratory acidosis seem to involve mechanisms other than increased Na/H antiporter gene expression.

Acidosis↗
PubMed1991

Na/H antiporter mRNA expression in single nephron segments of rat kidney cortex.

Renal cortical tubules consist of polarized epithelial cells where Na/H antiport activity has been demonstrated on the apical and/or basolateral membrane. Apical Na/H antiport activity plays an important role in transcellular bicarbonate (HCO3-) reabsorption, whereas basolateral Na/H antiport activity could be involved in transcellular HCO3- secretion as well as cell volume and pH control. To determine whether this heterogeneity in both localization and function is due to the existence of more than one Na/H antiporter, we studied the tissue distribution of Na/H antiporter mRNA by use of reverse transcription (RT) and polymerase chain reaction (PCR) in isolated nephron segments from rat renal cortex. The primers used were directed against the rat renal cortical Na/H antiporter cDNA which is homologous to the human growth factor-activatable Na/H antiporter. RT/PCR of beta-actin mRNA were performed as positive controls. Na/H antiporter mRNA expression in the proximal tubule was not detectable in S1 and S2 segments from superficial and most midcortical nephrons, which exhibit exclusively luminal Na/H antiport activity. It was expressed in S1 and S2 segments from juxtamedullary nephrons which have also basolateral Na/H antiport activity. Beta-actin mRNA was expressed uniformly in all segments of the proximal tubule. Na/H antiporter mRNA was also expressed in cortical thick ascending limb and cortical collecting duct, segments with basolateral Na/H antiport activity as well as in the glomeruli. In conclusion, at least two different Na/H antiporters exist in the renal cortex, i.e., the proximal tubule. The close correlation between functional localization of basolateral Na/H antiport activity and mRNA expression suggests that the rat kidney Na/H antiporter DNA homologous to the human growth factor activatable Na/H antiporter encodes a basolateral exchanger. The observed expression in a minority of midcortical proximal tubules could reflect a certain heterogeneity in these nephron segments.

Animals↗
PubMed1990

[Atherosclerotic nephropathy. Clinical manifestations of chronic arterial circulatory insufficiency of the kidneys].

Atherosclerotic nephropathy is defined as renal insufficiency due to atheromatous disease of the main renal arteries and/or their branches. This disease essentially is characterized by atheromatous lesions in the renal arteries which compromise arterial renal blood flow. Clinically, patients with atherosclerotic nephropathy can present with refractory hypertension and renal insufficiency, acute renal failure after treatment with antihypertensive drugs and unexplained, slowly progressive renal failure with or without hypertension (elderly patients). Observations from uncontrolled studies indicate that both the progression of renal insufficiency and the control of hypertension can be influenced favorably in about 80% of the cases by a revascularization procedure (arterial anastomosis, percutaneous arterial dilatation). Patients with suspected atherosclerotic nephropathy should probably be evaluated invasively and considered candidates for a revascularization procedure. The benefits of these therapies compared to conservative management need, however, evaluation in a controlled, prospective clinical trial.

Antihypertensive Agents↗
PubMed1990

Normal diet NaCl variation can affect the renal set-point for plasma pH-(HCO3-) maintenance.

In humans who are ingesting abundant NaCl, blood pH (pHb) and plasma bicarbonate concentration [HCO3-)p) change little or imperceptibly in response to the ingestion of alkali salts. We tested the hypothesis that such tight homeostatic regulation is an artifact of eating a culturally imposed NaCl-enriched diet, not a fundamental physiological trait of humans. In five normal men ingesting a constant acid-producing diet with a low intrinsic NaCl content (0.15 mEq/kg of body weight per day), we measured plasma and urine acid-base composition during four 7-day periods in which the diet was supplemented as follows: no supplements----NaHCO3 only----NaHCO3 plus NaCl----NaCl only. Each sodium supplement was 2.0 mmol/kg body weight per day. With no supplements, pHb was 7.43 +/- 0.005 and (HCO3-)p was 25.0 +/- 0.4 mEq/L. When NaHCO3 only was added, pHb rose 0.02 (to 7.45 +/- 0.004; P less than 0.01) and (HCO3-)p rose nearly 4 mEq/L (to 28.9 +/- 0.6 mEq/L, P less than 0.001). The rise in (HCO3-)p was sustained predominantly by an increased rate of renal bicarbonate reabsorption. When NaCl was added, (HCO3-)p returned to the earlier level, despite continued NaHCO3 supplementation (24.9 +/- 0.6 mEq/L), and remained there when NaHCO3 supplementation was subsequently stopped (24.1 +/- 0.5 mEq/L). Thus, tight homeostatic regulation of plasma acid-base composition in response to a change in dietary base occurred only when dietary NaCl was abundant. To our knowledge, this is the first study in normal humans that demonstrates that diet NaCl variations within the normal range significantly influence plasma acid-base composition.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗