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Biomedical subjects

R O Gans

Publications and source records attributed to R O Gans.

At least 55 records · Page 3Linked to original sources
PubMed1998

Comparison between the effects of amlodipine and lisinopril on proteinuria in nondiabetic renal failure: a double-blind, randomized prospective study.

Double-blind, randomized controlled studies of longer than 1 week in duration comparing the antiproteinuric potential of long-acting dihydropyridine calcium channel blockers with that of angiotensin converting enzyme (ACE) inhibitors are lacking. Therefore, we performed such a study in patients with nondiabetic renal disease and proteinuria. After a 4-week wash-out period in which patients did not use any medication known to affect proteinuria, 21 patients were randomized in a double-blind fashion to receive either the calcium channel blocker amlodipine (Amlo, 5 to 10 mg) or the ACE-inhibitor lisinopril (Lis, 5 to 10 mg). Throughout the 16-week study period, blood pressure, creatinine clearances, and proteinuria were measured every 2 weeks. In addition, device-measured blood pressure and renal hemodynamic studies were performed at the start and end of the study. Systolic blood pressure fell in the Lis group from 163+/-7 (SEM) to 140+/-8 mm Hg (P < .01) and from 157+/-10 to 147+/-6 mm Hg in the Amlo group; diastolic blood pressure fell from 101+/-3 to 86+/-7 mm Hg in the Lis group and from 98+/-3 to 91+/-2 mm Hg in the Amlo group. Renal hemodynamics were not affected by amlodipine treatment, whereas a fall in glomerular filtration rate (GFR) was seen in lisinopril-treated patients (from 55+/-11 to 50+/-10 mL/min; P < .01). Amlodipine did not significantly affect proteinuria. Lisinopril induced a decline in the protein-creatinine ratio with a maximal effect reached after 12 to 16 weeks of therapy (from 0.39+/-0.17 to 0.26 +/-0.11 g/mmol; P < .009). In conclusion, we could not demonstrate an antiproteinuric effect of the long-acting dihydropyridine calcium channel blocker amlodipine, whereas therapy with the ACE-inhibitor lisinopril resulted in a decrease in proteinuria. Amlodipine did not affect renal hemodynamics, whereas lisinopril induced a fall in GFR.

Adolescent↗
PubMed1998

Relationship between insulin's haemodynamic effects and insulin-mediated glucose uptake.

BACKGROUND: Insulin resistance and hyperinsulinaemia are associated with hypertension. The relationship between insulin's metabolic and haemodynamic actions has not been fully elucidated however. METHODS: We investigated, using the euglycaemic clamp technique, the relationship between insulin-mediated glucose uptake and insulin-induced changes in leg blood flow and cardiac index in 13 healthy subjects. As insulin's effects on blood flow are time dependent, studies were performed during a 4-h insulin (50 mU kg-1 h-1) infusion period. RESULTS: Mean arterial pressure during insulin infusion increased (82.9 +/- 6.7 to 89.8 +/- 7.7 mmHg; P < 0.001), whereas heart rate was unaltered. Leg blood flow gradually increased from 1.09 +/- 0.57 to 1.47 +/- 0.67 mL min-1 dL-1 during the second hour, and to 1.65 +/- 0.68 mL min-1 dL-1 during the fourth hour of the clamp (P = 0.01). Stroke volume index increased from 56.5 +/- 13.3 to 63.7 +/- 16.3 mL m-2 (P = 0.004) and cardiac index from 3.42 +/- 1.02 to 3.73 +/- 1.05 L min-1 m-2 (P = 0.04). The insulin-mediated glucose disposal and the increases in leg blood flow were not correlated during the second hour (r = 0.21, P = 0.51) but showed a strong correlation during the fourth hour of the clamp (r = 0.88, P < 0.001). Insulin-mediated glucose disposal was not correlated with the increases in cardiac index. CONCLUSION: Thus, insulin-mediated muscle blood flow may be an important contributor to glucose uptake during sustained exogenous hyperinsulinaemia aiming at physiological insulin levels.

Adult↗
PubMed1998

Hypertensive patients and diabetes: a high-risk population.

Rising worldwide rates of diabetes mellitus heighten the need to maintain adequate metabolic control in diabetic patients and to control for other cardiovascular risk factors, such as lipid profile disturbances, high blood pressure, and smoking habits. This is especially the case in diabetic patients who also present with hypertension, a co-morbid state that is present in at least 50% of Type 1 and Type 2 diabetic patients. Cardiovascular disease is present in 75% of all diabetes-related deaths, and the concomitant condition of diabetes and hypertension is believed to act synergistically on elevating the risk for cardiovascular disease. A number of trials have demonstrated a greater incidence of cardiovascular disease end points in diabetic hypertensive patients than in diabetic normotensive patients. Furthermore, hypertension is associated not only with an increased risk for cardiovascular mortality but also for microvascular complications in patients with diabetes. Adequate treatment of high blood pressure is imperative in these patients. The effectiveness of antihypertensive treatment can be measured not only by the degree of reduction in blood pressure but also by assessment of the effects on urinary albumin excretion rate. It is assumed that the greater the reduction in urinary albumin excretion rate, the greater the renoprotective effect. Treatment choices should be evidence-based, i.e., physicians should concentrate not only on the treatment of hypertension but also on improving glycemic control and lipid profile disorders, when necessary. When viewed in this regard, angiotensin-converting enzyme inhibitors, low-dose diuretics, and in some cases beta-blockers, should be considered agents of choice in hypertensive diabetic patients.

Diabetes Complications↗
PubMed1997

[Clinical thinking and decision making in practice. A patient with flank pain and anuria].

A 49-year-old man was admitted because of acute anuria. He had bilateral loin pain and was said to have been suffering from renal calculi seven years earlier. He used diclofenac as a pain killer. The renal pyela were mildly dilated. Eventually it became clear that the patient suffered from retroperitoneal fibrosis. This case illustrates (a) ureteral patency does not ensure actual urine flow; (b) non-steroidal anti-inflammatory drugs (NSAIDs) are a frequent cause of renal function loss, but only if there is an additional renal disease causing increased renal prostaglandin synthesis; (c) pattern recognition and verification are clinically relevant diagnostic tools.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

[Clinical application of albumin: a closer look at indications].

Albumin infusions are given far from always on the correct indications, and often there are alternatives that are cheaper and equally suitable. In septic or hypovolaemic shock, crystalline fluids are cheaper and equally efficacious for volume therapy. It is only in sporadic patients with a nephrotic syndrome that colloidal solutions such as albumin are indicated in hypovolaemia. Albumin infusion has no place in the combating of oedema. In decompensated hepatic cirrhosis with ascites, it appears useful to combine paracentesis with albumin infusion, to prevent renal insufficiency and hyponatraemia, but other colloidal fluids are probably equally suitable. Combating hypoalbuminemia as such is not useful in seriously ill patients; it is the underlying disease that should be treated.

Colloids↗
PubMed1997

[Clinical judgement and decision making in practice. A patient with hemoptysis].

A 43-year-old man was admitted because of severe and recurring haemoptysis, which was eventually ascribed to Goodpasture's syndrome. In case of an aspecific sign such as haemoptysis experienced clinicians will try to restrict the differential diagnosis by concentrating on other signs that are relevant to the main problem. In haemoptysis these other signs are general illness, fever, shortness of breath, painful respiration, chronic productive cough, and signs or a history of cardiac or pulmonary disease. If the differential diagnosis consists mainly of rare disorders or rare manifestations of common disorders, all possibilities should be considered. If Goodpasture's syndrome is suspected, further specific diagnostic tests should be done without delay.

Adult↗
PubMed1997

Renal handling of urate and sodium during acute physiological hyperinsulinaemia in healthy subjects.

1. The renal effects of insulin may play a central role in the association between insulin resistance, hypertension and hyperuricaemia. After a 2-h baseline period, we investigated the effects of exogenous insulin for 4 h (50 m-units h-1 kg-1) on fractional renal sodium and urate excretion in 13 healthy subjects, using the euglycaemic clamp and lithium clearance technique, and performed a control experiment in eight of the subjects. 2. Insulin caused a decline in both fractional renal sodium excretion, from 1.13 +/- 0.41% to 0.88 +/- 0.58% (control study: 0.81 +/- 0.35 to 1.35 +/- 0.49%; P < 0.001, insulin versus control), and fractional renal urate excretion, from 6.72 +/- 1.87% to 5.71 +/- 2.02% (control study: 7.03 +/- 2.06 to 7.05 +/- 1.94%; P = 0.085, insulin versus control). The changes in fractional renal sodium and urate excretion were positively correlated (r = 0.71, P < 0.01). Estimated fractional distal sodium reabsorption increased during insulin infusion from 93.7 +/- 2.8% to 96.7 +/- 1.9% (control study: 95.7 +/- 1.5% to 93.6 +/- 1.1%; P < 0.001, insulin versus control). Estimated fractional proximal tubular sodium reabsorption fell from 81.0 +/- 0.5% to 73.7 +/- 4.7% during insulin infusion, but less in the control study (81.5 +/- 4.3% to 79.3 +/- 4.8%; P = 0.056, insulin versus control). The changes in fractional proximal tubular sodium reabsorption and fractional distal sodium reabsorption during insulin infusion were inversely correlated (r = -0.59, P = 0.03). 3. During the course of the insulin infusion experiment an inverse correlation between the changes in fractional sodium and urate excretion, and the insulin-mediated glucose disposal, became gradually evident (r = -0.73, P < 0.01, and r = -0.71, P < 0.01, respectively; fourth hour of the insulin infusion period). 4. We conclude that exogenous insulin acutely decreases renal sodium and urate excretion, and that this effect is probably exerted at a site beyond the proximal tubule.

Adolescent↗
PubMed1997

Protection against cardiovascular collapse in an alcoholic patient with thiamine deficiency by concomitant alcoholic ketoacidosis.

Hyperlactataemia due to thiamine deficiency has so far only been reported in the setting of full-blown cardiovascular beriberi with congestive heart failure and systemic vasodilatation. Poor tissue oxygenation and impaired lactate clearance by the liver are generally accepted as underlying causes of the elevated lactate levels. We present an alcoholic patient with thiamine deficiency-induced hyperlactataemia and accompanying alcoholic ketoacidosis, who did not display the circulatory disturbances that are characteristic of cardiovascular beriberi. The hypothesis will be presented that the concomitant presence of alcoholic ketoacidosis has prevented haemodynamic deterioration. Putative mechanisms that could explain such an effect are discussed in detail, with special reference to the role of acetyl-CoA and adenosine.

Acidosis, Lactic↗
PubMed1997

Urinary albumin excretion rate during angiotensin II infusion in microalbuminuric patients with insulin and non-insulin-dependent diabetes mellitus.

As angiotensin-converting enzyme inhibition is accompanied by a marked decrease in glomerular protein loss, the hypothesis was tested that an increase of the glomerular transcapillary hydraulic pressure difference by exogenous angiotensin II would increase microalbuminuria in patients with insulin (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Acute effects of increasing doses of angiotensin II (1, 3 and 6 ng/kg/min) were studied on mean arterial pressure (MAP), glomerular filtration rate (GFR), effective renal plasma flow (ERPF), filtration fraction (FF), total renal vascular resistance (TRVR), and urinary albumin excretion rate (UAER) in 11 IDDM and 11 NIDDM microalbuminuric patients. Angiotensin II infusion changed MAP from 100 +/- 3 mmHg at baseline to 105 +/- 3, 111 +/- 3, and 116 +/- 3 mmHg (P < 0.001), ERPF from 542 +/- 29 to 478 +/- 24, 429 +/- 23, and 382 +/- 19 ml/min (P < 0.001), FF from 20.2 +/- 0.06 to 23.1 +/- 0.7, 27.1 +/- 1.1, and 29.8 +/- 1.2% (P < 0.001), and TRVR from 9454 +/- 809 to 11,158 +/- 930, 13,310 +/- 1206, and 15,538 +/- 1362 dyne s cm-5 (P < 0.001). GFR and UAER, however, did not change significantly. Therefore, during angiotensin II infusion ERPF decreased, while FF and TRVR increased. As UAER and GFR remained unchanged, the presumed rise in intraglomerular capillary pressure by exogenous angiotensin II did not increase UAER. We suggest that during manipulation of the renin-angiotensin system, as in other renal diseases with proteinuria, factors other than glomerular transcapillary hydraulic pressure determine the degree of urinary albumin loss in microalbuminuric IDDM and NIDDM patients.

Adult↗