[Serum antibodies before and after vaccination of hemodialyzed children. Preliminary results].
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Biomedical subjects
Publications and source records attributed to C Kleinknecht.
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In order to evaluate the role of calorie and protein intake in growth impairment due to chronic renal failure (CRF), a subtotal nephrectomy was performed in weanling Wistar rats. A two-thirds reduction of renal function was obtained, which induced a marked growth retardation. Growth retardation was identical in nephrectomized and in pair-fed controls, and thus appeared to be entirely due to a deficient food intake. Using low protein diets, administration of a supplement with small amounts of essential amino acids (EAA) resulted in accelerated growth associated with a higher calorie intake, a better utilization of ingested calories for growth and a greater fall of blood urea nitrogen concentration.
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The effects of chronic metabolic acidosis (CMA) on zinc (Zn) bone content and urinary excretion were examined in the presence of normal or reduced renal function together with some aspects of calcium (Ca) metabolism. Four groups of rats were compared. All were fed a 30% protein and 9 mg Zn/100 g diet. Two were uremic (U): The first developed acidosis (UA), which was suppressed in the other (UNA) by NaHCO3 supplement. Two other groups had normal renal function: One was normal (CNA), and the other had NH4Cl in the drinking water and acidosis (CA). Femur total Zn and Ca content was markedly reduced by CMA and was not affected by uremia. Zn urinary excretion was increased by CMA and unaltered by uremia. Ca urinary excretion was markedly reduced in uremic rats, but was enhanced in both acidotic conditions. Urinary Ca and Zn showed a strong correlation in uremic and in control rats. Plasma parathormone and 1,25(OH)2D3 were unchanged by CMA. These data are in agreement with a direct primary effect of CMA on bone in releasing buffers. CMA induces bone resorption and a parallel decrease of mineral bone components, such as Ca and Zn, with little or no role of PTH, 1,25(OH)2D3 and of uremia itself.
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Systematic clinical ocular examinations completed by electrophysiological studies were performed on fifty-five children with nephronophthisis. Twenty children, all under ten years of age, had tapetoretinal degeneration, either pure in fourteen cases (Senior-Löken syndrome), either associated with extra-oculorenal abnormalities in six cases (bones, liver, neurology). Twelve older children had a normal examination. Twenty-three children had a normal clinical examination, but non evolutive alterations of ERG.
The effects of intravenous Nitrogen Mustard (NM), given with a total cumulative dose of 0.8 mg/kg BW, were studied in 60 children with idiopathic nephrotic syndrome (INS). Thirty patients were frequent relapser with corticosteroid dependence. In this group the actuarial remission rate was 43, 30 and 15% after 1, 2 and 3 years respectively. The relapse rate per year was decreased from 2.76 +/- 1.56 to 0.88 +/- 0.79 after NM. Ten of the 17 patients showing a partial response to steroids went into complete remission after NM but 6 of them relapsed. Of the 13 patients who did not respond to steroids only 3 went into remission for a short time. Vomiting and leukopenia were noted in one third of cases. The data indicate that NM may improve the course of corticosteroid dependent INS, being less effective in partial responders and probably without effect in non responders.
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