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Biomedical subjects

N Gretz

Publications and source records attributed to N Gretz.

At least 91 records · Page 5Linked to original sources
PubMed1993

Treatment of renal anemia by subcutaneous erythropoietin in children with preterminal chronic renal failure.

Eleven children aged 0.6-17 years with preterminal chronic renal failure and anemia (mean serum creatinine concentration 4.8 mg/dl; mean hemoglobin concentration 7.9 g/dl) were treated with sc injections of recombinant human erythropoietin (EPO, initial dose 150 U/kg/week) over a mean period of 13 months. When a target hemoglobin concentration of 11.5-13.5 g/dl was reached, the dose was adapted. Iron deficiency was corrected. Hemoglobin concentration increased by > 2 g/dl in all patients within 14-119 (mean 45) days. The last maintenance dose ranged between 75 and 300 (mean 133) U/kg/week. No major adverse effects were observed, except for hypertension which occurred in about half of the patients and necessitated interruption of EPO in one child with advanced renal failure. Additional antihypertensive drugs were given to five patients. Body height increased in two patients by 0.6 and 1.3 SDS/year, respectively. In six patients with a mean observation period of 14 months before and 16 months after the start of EPO, the mean slope of the reciprocal serum creatinine concentration curve improved slightly (p = 0.05). The proposed schedule appears to be safe for the treatment of renal anemia in most pre-dialysis patients. Frequent monitoring of hemoglobin, blood pressure, serum creatinine and ferritin is required.

Adolescent↗
PubMed1992

Growth hormone treatment in children with preterminal chronic renal failure: no adverse effect on glomerular filtration rate.

Impaired growth and stunting remains a major therapeutic problem in children with chronic renal failure (CRF). Recombinant human growth hormone (rhGH) treatment may be beneficial, but concern has been raised about possible side-effects, i.e. deterioration of renal function and glucose intolerance. We have treated 10 prepubertal children with CRF (median age 7.5 [1.7-10.0] years) with 4 IU rhGH/m2 per day s.c. over a period of 1 year. Height velocity increased significantly (P less than 0.03) from basal 4.6 (2.0-14.0) cm/year to 9.7 (6.8-17.6) cm/year. Height velocity SDS for chronological age and for bone age increased in all children from basal median -2.3 to +3.8 (P less than 0.005). Median glomerular filtration rate (GFR) measured by single injection inulin clearance at onset was 18 (11-66) ml/min per 1.73 m2 and did not change significantly during the treatment year. The loss of GFR as estimated by creatinine clearance was similar during the treatment year (median loss 1.3 ml/min per 1.73 m2) compared to the year before treatment (median loss 3.7 ml/min per 1.73 m2). Serum glucose levels during an oral glucose tolerance test did not change, but fasting as well as stimulated insulin levels increased significantly with time during the study period. It is concluded that the rhGH regimen employed was remarkably effective in improving growth velocity in children with CRF without adversely affecting GFR. Glucose homeostasis remained stable, but at the expense of increased serum insulin levels.

Blood Glucose↗
PubMed1992

Reduced capillary density in the myocardium of uremic rats--a stereological study.

Using stereological techniques capillaries, interstitium and myocardial fibers were analyzed in perfusion-fixed hearts of subtotally nephrectomized male Sprague-Dawley rats with uremia of 14 months duration (or their sham-operated controls). Uremic rats had higher systolic blood pressure (140 +/- 20.3 mm Hg vs. 119 +/- 6.61 mm Hg) and left ventricular weight/body weight ratio (3.37 +/- 0.09 mg/kg vs. 2.01 +/- 0.12 mg/kg) than controls, and had slight anemia (Hct 35.0 +/- 3.16% vs. 40.4 +/- 3.3%). Length density (Lv) of capillaries, that is, capillary length per unit myocardial volume, was significantly (P < 0.001) decreased in uremia (2485 +/- 264 mm/mm3 vs. 3329 +/- 194 mm/mm3) versus controls. In parallel, surface density and volume density of the capillary lumina were also reduced (7.95 +/- 1.69 cm3/cm3 vs. 11.4 +/- 1.8 cm3/cm3) in the uremic rats. We conclude that in experimental uremia, cardiac hypertrophy is not accompanied by a commensurate increase in capillaries.

Animals↗
PubMed1991

Effect of low-protein diet on renal function: are there definite conclusions from adult studies?

Low-protein diets have been used for roughly a century in order to alleviate uraemic symptoms and to delay progression of chronic renal failure (CRF). Currently a number of different low-protein diets are used, supplying either 0.6 g protein/kg body weight or 0.3-0.4 g supplemented with amino-acids or keto-acids. Single centre trials have attempted to demonstrate the efficacy of these diets in slowing down the progression of CRF. The results from these trials are, however, sometimes inconclusive, showing either a high efficiency of the low-protein diet or no efficiency at all. Conclusive data from multicentre trials, however, are not yet available. A crucial point in analysing the efficacy of low-protein diets is the degree of compliance with the protein restriction. Today, the data available indicate that sometimes only a poor degree of compliance is achieved both in single and in multicentre trials.

Dietary Proteins↗
PubMed1991

Muzolimine-induced severe neuromyeloencephalopathy: report of seven cases.

We report on 7 patients (2 women, 5 men) with chronic renal failure, who developed under a high dosage of the new diuretic muzolimine (range 240 to 1440 mg per day) fatal neuromyeloencephalopathy. Clinical neurophysiological and neuroradiological findings and finally neuropathological studies in 2 patients resembled those found in vitamin-B12-deficiency-syndrome with a predominant affection of the spinal posterior column and the corticospinal tracts. The first neurological symptoms like paraesthesia, severe hyperpathia of the legs and mild to heavy spinal ataxia occurred after an average time of treatment of 78 days and a mean dosage of 52 g. The most progressive neurological deficits like severe tetraspastic paresis, were seen only in the nondialytic renal insufficient group (3 patients), while the others had a more benign course of the disease. This lead to the hypothesis of a partially dialysable toxic metabolite of muzolimine. After a follow-up of more than 2 1/2 years no significant recovery was seen in these cases.

Adult↗
PubMed1990

[Neuromyeloencephalopathy caused by high-dose muzolimine medication in patients with renal failure].

We report on 7 patients suffering from chronic renal failure (2 females, 5 males; aged 35-75 (phi 53.5) years) who showed severe neuromyeloencephalopathy (NME) after high doses of a new Henle's loop diuretic, Muzolimine. The temporal and phenomenological development of these systems was strikingly parallel. The neurological deficit was revealed on neurophysiological, neuroradiological and in 2 cases on neuropathological tests (gross demyelinisation of the posterior column, mainly of the fasciculus gracilis, less in the lateral corticospinal tract and in some spinal roots). The critical drug dose for first neurological impairment was 52 g on average; at this point the patients had been treated for 78 days. The maximal daily dose was 1.440 mg. Dominant clinical features were pallhypaesthesia, ataxia, signs of peripheral neuropathy in combination with hyperreflexia and progressive para- to tetraspastic paresis. Constellation of symptoms, course of disease and findings of additional investigations, especially those of neuropathology, very much resemble Vitamin B12 deficiency and SMON-(Subacute Myelo Optic Neuropathy) syndrome. The rare entity of Muzolimine-NME is discussed in respect to other endogenous and exotoxic neuromyelopathies. We present the hypothesis of a toxic, partially dialysable metabolite of Muzolimine.

Adult↗
PubMed1990

A low-protein diet protects uremic rats against the negative sequelae of metabolic acidosis.

Metabolic acidosis is a common finding in uremia. The metabolic consequences, however, are poorly understood. Thus, the aim of our study was to assess the effect of chronic metabolic acidosis in 5/6-nephrectomized male Sprague-Dawley rats given a normal (18%; n = 19) and a low-protein diet (8%; n = 23). Each of these groups was sequentially given CaCO3 and CaCl2 in the drinking water for a fortnight each. The animals were randomly assigned to start either with CaCO3 or CaCl2 (random cross-over design). The blood pH decreased significantly in both CaCl2 groups (18% protein: CaCO3 7.18 vs. CaCl2 7.11; 8% protein: CaCO3 7.26 vs. CaCl2 7.09) as did standardized base excess (18% protein: CaCO3-5.9 vs. CaCl2-9.7; 8% protein: CaCO3-3.6 vs. CaCl2-12.6). Food intake declined during acidosis in both groups, but more in the 18% protein group. The same occurred with body weight (g) in the 18% group, which decreased dramatically (8% protein: CaCO3 389 vs. CaCl2 390; 18% protein: CaCO3 413 vs. CaCl2 366). The change in body weight was reflected in the urinary urea excretion (mg/24 h/g food) (8% protein: CaCO3 0.9 vs. CaCl2 1.0; 18% protein: CaCO3 2.2 vs. CaCl2 30.8). There was a significant increase in proteinuria (mg/24 h) in the 8% group (CaCO3 10 vs. CaCl2 15), while in the 18% group no real change occurred (CaCO3 24 vs. CaCl2 18). Factoring the proteinuria for food intake, however, also resulted in a tendency towards an increased proteinuria in the 18% group.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗