Gibt es die ?Febrile Proteinurie??

Abstract

The significance of proteinuria during febrile infectious diseases is widely underestimated, although the more marked proteinuria probably signalizes a parainfectious nephropathy rather than a functional disorder. This study shows that mild proteinuria of less than 0.65 g/24 h (normal range less than 0.3 g/24 h using the sensitive tannine-FeCl3-technique) might be caused by the elevated body temperature alone. 9 out of 18 volunteers without renal disease undergoing experimental hyperthermia of 40-41 degrees C for 1-2 h did not develop a proteinuria according to quantitative and qualitative (SDS-PAGE) measurements. In 6/18 the amount and composition of urinary proteins changed giving a glomerular type of proteinuria, possibly caused by temperature related transient glomerular alterations. In 3/18 a mild glomerulopathy existed before hyperthermia, as deduced from a glomerular pattern despite a quantitatively physiological proteinuria, leading in all 3 to pathological proteinuria during hyperthermia. In all 18 volunteers alterations reversed to normal within 12 h. Therefore, the degree of proteinuria during febrile diseases should be considered. Proteinuria of less than 0.5-1 g/24 h in adults might be explained by an altered glomerular function alone. Proteinurias exceeding this value, with a slow regressing tendency will indicate glomerular or tubulo-interstitial diseases, caused possibly by immunologic or toxic products resulting from underlying infectious disease.

Renal disease in lymphatic filariasis: evidence for tubular and glomerular disorders at various stages of the infection

“…Several aspects must be taken into consideration in these patients: Fever itself is often accompanied by increased proteinuria, usually of the glomerulo-tubular type (Boesken et al 1983); in W bancrofti patients undergoing filarial fever there seems to be a temporarily increased metabolic activity of adult worms, evidenced by increased numbers of mf and increased levels of circulating antigen in the blood of these individuals (Kar et al 1993); the levels of circulating immune complexes seem to rise significantly during the filarial fever episode (Kar et al 1993). Possibly, parainfectious immunmediated or toxic acute tubulointerstitial nephritis is the predominating renal disorder in this group of patients and the additional occurrence of glomerular proteinuria is due to fever (Boesken et al 1983) or glomerular involvement in primary tubulointerstitial disease (Alt et al 1983). sequela in Brugia filarias.…”

Nephrotoxicity of ifosfamide, carboplatin and etoposide (ICE) alone or combined with extracorporeal or radiant-heat-induced whole-body hyperthermia

“…The induction of transient, mild proteinuria by an increase in body temperature has been reported in children (Hemmingsen and Skaarup 1987), healthy adults (Boesken et al 1983) and animals (Elkon et al 1982). Other investigators studied the eects of WBH combined with chemotherapy in animals.…”