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Biomedical subjects

H A Koomans

Publications and source records attributed to H A Koomans.

At least 145 records · Page 8Linked to original sources
PubMed1993

Iso-oncotic volume expansion in the nephrotic syndrome.

1. In previous studies we found that albumin infusions caused only a modest natriuresis in the nephrotic syndrome, suggesting that hypovolaemia played no part in the sodium retention of these patients. However, this finding was inconclusive, since the hyperoncocity of the infused albumin probably opposed sodium excretion. 2. In the present study, we examined the effect of sustained (68 h) plasma volume expansion (+18%), by means of iso-oncotic albumin infusions, on renal function, blood pressure, humoral factors and sodium balance. 3. Plasma atrial natriuretic peptide levels increased almost threefold and renin-angiotensin system activity was suppressed. Glomerular filtration rate remained unchanged, whereas estimated renal plasma flow increased, resulting in a further decrease in filtration fraction. 4. The increase in plasma volume expansion was accompanied by a modest increase in sodium excretion, which, however, was less than the amount of sodium daily infused with the albumin solutions and consumed with the diet, so that net sodium was retained. 5. This observation supports the concept that an intrinsic renal defect causes the sodium retention in the nephrotic syndrome, and argues against the therapeutic use of albumin infusions.

Adult↗
PubMed1993

Natriuretic response to head-out immersion in humans with recent kidney transplants.

1. Recently implanted kidneys may have decreased flexibility to adjust sodium excretion to volume challenges, since modulation by renal sympathetic nerve activity is absent. To examine this hypothesis, we studied the natriuretic response to head-out water immersion in eight patients with well-functioning renal allografts of 37 days (range 24-56 days), at a time when renal re-innervation has probably not occurred. 2. By the third hour of head-out water immersion, sodium excretion had increased equally in the patients (from 120 +/- 21 to 204 +/- 37 mumol/min) and in eight healthy control subjects (from 105 +/- 9 to 191 +/- 19 mumol/min). 3. Glomerular filtration rate was 60 +/- 6 ml/min in the patients and 113 +/- 6 ml/min in the control subjects, and did not change upon head-out water immersion. Estimated renal plasma flow increased upon head-out water immersion in the control group but not in the patients. Blood pressure decreased similarly in both groups. The renal vascular resistance, calculated from these data, decreased in response to head-out water immersion in the control subjects but not in the renal transplant patients. 4. Head-out water immersion suppressed plasma renin activity only in the normal group, whereas the plasma aldosterone level was suppressed in both groups. The natriuretic response in patients was associated with about 3-fold elevated plasma levels of atrial natriuretic peptide. 5. Since renal re-innervation at 37 days after transplantation is very unlikely, these data suggest that inact renal innervation is not mandatory for a normal natriuretic response to head-out water immersion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Natriuretic and kaliuretic response to potassium load: modulation by sodium intake.

Potassium (K) loading is followed by a rapid increase in sodium (Na) and K excretion. To evaluate the influence of Na intake on this effect, we studied the acute natriuretic and kaliuretic response to a single oral K load (100 mmol) in six healthy volunteers equilibrated on a 10-, 100-, and 400-mmol Na intake. Compared to the 100-mmol Na intake, the 400-mmol Na intake greatly enhanced the natriuretic effect of the K load; during the 10-mmol Na intake no natriuresis but even some Na retention occurred. The kaliuretic effect was not significantly changed and occurred at similar values of plasma K. Plasma aldosterone was suppressed during the 400-mmol Na diet and stimulated during the 10-mmol Na diet, but the relative increments after the KCl load did not differ among the three diets. In conclusion, whereas the effect of a K load on kaliuresis is relatively independent of Na intake, its effect on Na excretion varies from marked natriuresis to slight Na retention. The Na retention is probably due to acute K-induced aldosterone stimulation, and the natriuresis to K-induced increase in distal Na delivery not utilized to promote K excretion. Apparently, the integration of renal Na and K handling after a K load is such that K balance is maintained at the cost of Na balance.

Adolescent↗
PubMed1993

Effects of enalapril on renal sodium handling in healthy subjects on low, intermediate, and high sodium intake.

Angiotensin-converting enzyme (ACE) inhibitors have a modest natriuretic effect, but the responsible changes in tubular sodium (Na) handling are not fully known. We therefore studied the effect of a single dose of 20 mg enalapril on Na excretion in 8 healthy subjects, using lithium clearance and maximal water diuresis to analyze tubular Na handling. Because the natriuretic effect may depend on the volume state, the same subjects were studied during low (20 mmol Na/day), medium (200 mmol Na/day), and high (400 mmol Na/day) salt intake. Enalapril caused natriuresis during the 20-mmol Na diet (from 51 +/- 9 to 81 +/- 14 mumol/min, p < 0.05) and the 200-mmol Na diet (from 190 +/- 24 to 230 +/- 31 mumol/min, p < 0.05), but not during the 400-mmol Na diet. The increase in Na excretion was not accompanied by consistent changes in glomerular filtration rate (GFR), free water clearance data, maximal urine flow, uric acid clearance, or lithium clearance. Instead, the increase in Na excretion was positively related to the increase in Na concentration in the maximally diluted urine (r = 0.75, p < 0.01). Regardless of diet, enalapril reduced the filtration fraction, but a significant increase in effective renal plasma flow was noted only during the 20-mmol Na diet. The data suggest that a decrease in Na reabsorption in the diluting segment, perhaps related to renal vasodilatation, participates in the natriuretic effect of ACE inhibition in humans.

Adult↗
PubMed1993

Effects of furosemide or acetazolamide infusion on renal handling of lithium: a micropuncture study in rats.

Renal lithium (Li) handling was studied by micropuncture at the late proximal (LPT) and early distal (EDT) tubules in control rats and rats infused with furosemide (FUR) or acetazolamide (ACTZ). In control rats, the tubular fluid-to-plasma Li concentration ratio [(T/P)Li] at the LPT exceeded unity (1.05 +/- 0.02, P < 0.05). Some 25% of the filtered load (FL) of Li and water was reabsorbed in proportion between the LPT and the EDT, and consequently the (T/P)Li at the EDT (1.03 +/- 0.03) did not change. FUR inhibited Li reabsorption in the proximal convoluted tubules (PCT), by approximately 7% of the FL. Reabsorption of Li and water in the loop segment was also inhibited, virtually in proportion, by approximately 10% of the FL. These data suggest that FUR-sensitive Li reabsorption in the loop mainly takes place in the pars recta. However, a small increase in the (T/P)Li at the EDT (to 1.10 +/- 0.01) suggested inhibition of some Li transport (approximately 2% of the filtered load of Li) without water, most likely in the thick ascending limb (TAL). In the PCT, ACTZ reduced Li reabsorption by approximately 16% of its FL. Although it is likely that ACTZ also inhibited the pars recta, net Li reabsorption in the loop was not reduced. This suggests that TAL Li reabsorption can compensate for increased delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1993

Plasma volume regulation: defences against edema formation (with special emphasis on hypoproteinemia).

In hypoproteinemia, increased interstitial hydrostatic and decreased interstitial colloid osmotic pressures, together with increases in lymph flow, prevent interstitial fluid volume expansion, thus forming the edema-preventing mechanisms. Transfer of a substantial portion of the interstitial protein pool into the vascular compartment by increased lymph flow is the major edema-preventing mechanism. The increase in interstitial pressure during progressive interstitial fluid volume expansion is limited by the high compliance of the interstitium in most tissues. During hypoproteinemia low interstitial colloid osmotic pressure and high interstitial compliance permit augmented changes in plasma volume in response to rapid increases (orthostasis, venous constriction) and decreases (hemorrhage) in capillary pressure. Nevertheless, these same forces are responsible for the finding that during the relatively slow changes in sodium balance that occur during volume retention or after treatment with diuretics, the change in plasma volume is relatively small. These phenomena are illustrated by observations gathered in experimental hypoproteinemia and in patients with the nephrotic syndrome.

Animals↗
PubMed1993

Natriuretic and hypotensive effect of adenosine-1 blockade in essential hypertension.

We studied the effects of a single dose (100 mg orally) and repeated administration (100 mg o.d. for 7 days) of FK453, a novel adenosine-1 receptor antagonist, on renal sodium handling and blood pressure in eight patients with essential hypertension. Within 60 minutes after administration of FK453, sodium excretion increased threefold. This occurred in the absence of a change in renal hemodynamics, assessed from inulin and para-aminohippurate clearance, and was accompanied by increased fractional excretion of lithium, phosphate, and uric acid and by increased excretion of calcium and magnesium. Maximal free water clearance data showed an increase in maximal urine flow and distal delivery term and a decrease in the diluting segment reabsorption term. FK453 also decreased blood pressure and increased heart rate, but this did not occur until about 3 hours after ingestion, that is, when the natriuresis was already over. The natriuretic effect of FK453 was short-lasting, and continued use of FK453 was in fact accompanied by some net sodium retention. Blood pressure on the seventh day before FK453 treatment was not different from blood pressure before administration of the first dose of FK453. Again an acute natriuretic response followed, although less than after the first dose. Changes in intrarenal sodium handling parameters, blood pressure, and heart rate were similar to those seen after the first dose. The natriuretic and hypotensive effects of FK453 indicate that adenosine-1 receptor activity plays a role in the regulation of blood pressure and renal sodium handling in patients with essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of acute mineralocorticoid and glucocorticoid receptor blockade on the excretion of an acute potassium load in healthy humans.

To examine the role of mineralocorticoid and glucocorticoid in potassium (K) tolerance in healthy humans, we studied the effects of canrenoate, a mineralocorticoid antagonist, and RU486, a glucocorticoid antagonist, on the excretion of a KCl load. Canrenoate (200 mg, iv) or RU486 (400 mg, orally) was administered 150 min before a KCl load (1 mmol/kg BW, orally) in seven healthy males undergoing maximal water diuresis. Clearance studies were extended for 5 h after the KCl load, and the data were compared with time control, KCl load alone, and canrenoate alone. KCl increased K excretion (from 18.8 +/- 2.4 to 63.3 +/- 3.9 mmol/5 h; P < 0.01) and sodium (Na) excretion (from 35.9 +/- 2.1 to 72.9 +/- 6.0 mmol/5 h; P < 0.01). Clearance calculations, based on maximal water diuresis, were compatible with increased distal Na and volume delivery. Canrenoate alone modestly increased basal cumulative NaCl excretion and had no effect on K excretion. However, canrenoate blunted the kaliuresis after the KCl load (51.9 +/- 4.4 mmol/5 h; P < 0.05 compared to KCl alone) and stimulated natriuresis in a complementary way. Clearance data were compatible with diminished distal Na reabsorption and K secretion in response to an undisturbed KCl-induced increase in distal Na delivery. RU486 did not influence the excretion of the KCl load or its effects on renal sodium handling parameters, although effective glucocorticoid receptor blockade was likely to be present in view of the increase in plasma cortisol. These data suggest that in healthy humans, mineralocorticoid activity, but not glucocorticoid activity, is involved in the elimination of a K load. The latter contrasts with data in adrenalectomized animals, in which situation glucocorticoid as well as aldosterone are indispensible for normal K tolerance.

Administration, Oral↗
PubMed1993

Relevance of the tubuloglomerular feedback mechanism in pathophysiology.

The balance between a high filtration rate and high reabsorption rate in the kidney is critical in the maintenance of extracellular fluid volume. One of the mechanisms that maintain this balance is the tubuloglomerular feedback (TGF) mechanism, which operates at the level of the macula densa assessing the load and/or solute concentration coming out of the loop of Henle and controlling this load by adjusting the GFR. This review discusses the potential role of the TGF system with respect to volume homeostasis in various conditions where GFR is maintained, decreased, or increased. In most of the states discussed, the TGF system seems to act appropriately regarding volume control; however, trade-off effects occasionally occur. After acetazolamide administration, during extracellular fluid volume contraction or expansion or acute hyperkalemia, the TGF mechanism responds appropriately with regard to volume balance. After a large reduction of renal mass, the system adjusts to function at a higher level of GFR and distal delivery. In chloride-depletion metabolic alkalosis, glomerulonephritis, diabetes mellitus, and acute renal failure, the adaptation of the TGF system appears to be appropriate with regard to volume control; however, it may lead to trade-off effects, such as maintenance of metabolic alkalosis, glomerular hypertension and sclerosis, or depression of GFR, respectively. Because the TGF mechanism often contributes to compensatory adjustments to or development of disease, it can be appreciated that any in-depth evaluation of the mechanisms responsible for various pathophysiologic conditions should include an assessment of the potential role of the TGF mechanism.

Acute Kidney Injury↗
PubMed1993

Plasma lipoproteins and renal apolipoproteins in rats with chronic adriamycin nephrosis.

The relation between plasma lipoprotein composition and renal apolipoprotein deposition was studied in nephrotic rats in which stable renal function had been monitored for 7 months after a single low dose of adriamycin (ADR, 3 mg/kg). Proteinuria was observed 3 weeks after ADR and increased progressively up to about 0.5 g/day (versus 0.07 g/day in controls; P < 0.001), while the creatinine clearance remained stable at about 80% of control values. Hypercholesterolaemia was observed 6 weeks after ADR, and increased progressively up to 7.0 +/- 1.0 mmol/l (versus 2.3 +/- 0.1 mmol/l in controls; P < 0.001). Cholesterol was primarily located in LDL2 and HDL2 lipoproteins. Plasma apolipoprotein (apo) A-I increased by more than 400% in the nephrotic rats (P < 0.001). Apo B and apo E increased by about 60% (P < 0.01), whereas apo A-IV remained unchanged. Focal sclerotic lesions in glomeruli had an incidence of 50 +/- 10% in ADR rats versus 2 +/- 1% in controls (P < 0.001). Immunohistochemistry revealed apo A-I and apo A-IV in the visceral epithelium. Apo E immunoreactivity and lipid deposits were observed in focal glomerular sclerotic lesions of ADR rats. Neither apolipoproteins nor lipids were detected in glomeruli of controls. Proximal tubular localization of apolipoproteins was extensive for apo A-I, apo A-IV and apo E, but no differences were observed in tubular deposition of apolipoproteins between ADR and control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Erysipelas: not always innocent.

The case histories of two patients with the "toxic-strep" syndrome are presented. This syndrome consists of a Streptococcus pyogenes group A infection, complicated by multi-organ failure. In our patients renal failure necessitating haemodialysis was present. General characteristics of the syndrome and long-term follow-up are presented.

Acute Kidney Injury↗
PubMed1993

Indomethacin- and desamino-8-D-arginine vasopressin-induced lithium reabsorption is not amiloride sensitive in humans.

This study was undertaken to analyze whether the mechanism of decreased fractional lithium excretion (FELi) induced in humans by the prostaglandin synthesis inhibitor indomethacin and the vasopressin analog desamino-8-D-arginine vasopressin (d-DAVP) is amiloride inhibitable. Eight sodium-restricted (10 mmol/day) healthy volunteers underwent clearance studies to evaluate the effects of indomethacin (50 mg tid for 6 days), amiloride (10 mg twice before the clearance study) and d-DAVP (4 micrograms, i.v.), and combinations of these drugs. Despite the sodium restriction, amiloride had no effect on FELi, although the dosage was sufficient to cause a 6-fold increase in sodium excretion, and potassium retention. Compared to a base-line value of 27.9 +/- 2.1%, FELi fell to 20.7 +/- 2.1% after indomethacin (P < .01) and to 22.4 +/- 1.5% after d-DAVP (P < .01). When d-DAVP was administered during indomethacin, the FELi fell to 18.0 +/- 1.4%. Compared to indomethacin alone, this represented no significant further change. Amiloride did not prevent the fall in FELi caused by indomethacin or d-DAVP or both. These data indicate that in humans, 1) sodium restriction does not cause amiloride-sensitive lithium reabsorption, and 2) the lithium reabsorption caused by d-DAVP and indomethacin is not amiloride sensitive.

Absorption↗
PubMed1992

Effects of acute NaCl, KCl and KHCO3 loads on renal electrolyte excretion in humans.

1. Potassium salts increase sodium excretion in humans. To define the role of the potassium ion in this effect, we compared the effects of equimolar single oral loads of 100 mmol of NaCl and KCl on renal electrolyte excretion in seven healthy subjects. In a second group (n = 7), we infused equimolar loads of NaCl or KCl (0.75 mmol/kg in 2 h). 2. In both experiments the KCl load quickly increased plasma potassium and aldosterone concentrations and potassium and sodium excretion to a maximum by 2 h after the load, whereas the NaCl load had no such effect. 3. In a third group (n = 7) we compared the effects of single oral loads of KCl and KHCO3 (1 mmol/kg), to assess the role of the anion in the natriuretic effect of potassium salts. 4. KCl and KHCO3 transiently stimulated urinary excretion of potassium and sodium in an identical manner. 5. We also followed the changes in acid excretion over time. Whereas both KCl and KHCO3 loading decreased acid excretion, this effect was greater after KHCO3 loading. Interestingly, acid excretion did not decrease further after the first collection hour after the potassium load, although the plasma potassium concentration was still increasing. 6. From these data we conclude (1) that increased excretion of sodium, potassium and chloride and decreased excretion of protons after administration of potassium salts are the specific effects of the potassium component; (2) that potassium also appears to have secondary, indirect effects on proton excretion, the mechanism of which remains to be clarified.

Administration, Oral↗
PubMed1992

Excessive cholesterolemic response in analbuminemic rats fed a cholesterol-rich diet containing casein.

Female Nagase analbuminemic rats and Sprague-Dawley rats were fed purified diets with or without 1% cholesterol and containing either soybean protein or casein. After consuming the cholesterol-free diets, the analbuminemic rats had significantly higher plasma cholesterol and triglyceride concentrations than the Sprague-Dawley rats. The higher plasma cholesterol levels were essentially in the low density and high density lipoproteins. Based on the fact that the analbuminemic rats excreted more bile acids in feces it is possible that the higher baseline plasma cholesterol concentrations in Nagase analbuminemic rats were partly caused by overproduction of cholesterol. The Nagase analbuminemic rats displayed a greater cholesterolemic response to cholesterol feeding than Sprague-Dawley rats, but only if casein was the protein source in the diet. Casein vs. soybean protein in either cholesterol-free or high cholesterol diets reduced bile acid excretion in Sprague-Dawley but not in Nagase analbuminemic rats. The increased sensitivity to casein plus cholesterol feeding in Nagase analbuminemic rats may be caused by a lack of inhibition of de novo cholesterol synthesis.

Animals↗
PubMed1992

Short-term indomethacin administration does not impair excretion of acute potassium load in humans.

Maintenance treatment with prostaglandin synthesis inhibitors often causes some degree of hyperkalemia, indicating impaired potassium (K) excretion. Hypoaldosteronism probably is a mediating factor, but it is unknown whether these drugs also impair renal K excretion directly. Indomethacin, for example, stimulates NaCl reabsorption in Henle's loop, and thus may impair K excretion by decreasing distal NaCl delivery. We therefore studied the effect of 1 day administration of indomethacin (50 mg tid) on the excretion of a single oral KCl (1 mmol kg-1 body weight) in six healthy volunteers taking a 40 mmol sodium diet. To allow analysis of renal sodium handling, clearance studies were performed during water loading. In this acute setting, indomethacin had no effect on plasma K, and did not decrease plasma aldosterone. However, indomethacin clearly reduced NaCl excretion. Nonetheless, the excretion of the K load was entirely normal. Excretion of the K load was accompanied by increased clearance of phosphate and uric acid, and natriuresis. Data derived from the maximal free water clearance were compatible with increased delivery to and decreased reabsorption from the diluting segment. Occurrence of these effects was not prevented by indomethacin, although overall NaCl excretion remained less than observed without indomethacin. Indomethacin reduced prostaglandin E2 excretion substantially. Apparently, in normal man indomethacin does not impair K excretion directly, even though it greatly reduces NaCl excretion. Moreover, the effects of K on renal NaCl handling, probably contributing to the excretion of a K load, are not dependent on renal prostaglandins.

Administration, Oral↗