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Accidental hypothermia is defined as a spontaneous decrease in core temperature to 35°C or below. Several techniques of active core rewarming have been described. We present the case of a 34-year-old man with severe hypothermia (27 °C) caused by cold environment exposure and barbiturate intoxication treated with general supportive measures and active core rewarming with hemodialysis. Core temperature increased by 2.15^¤C/h with hemodialysis and became normal in 4 h. The clinical situation clearly improved during the hemodialysis session and the patient recovered without any defect. Hemodialysis is a rapid and effective treatment for accidental hypothermia.

Proximal glomerulotubular balance was examined in hydropenic rats and rats undergoing saline diuresis. Three experimental procedures were used to lower GFR: aortic constriction, ureteral obstruction and renal venous occlusion. During hydropenia all three manipulations lowered total GFR and nephron GFR, and prolonged transit-time, but did not significantly alter TF/P inulin ratios. Absolute reabsorption decreased proportionately to GFR and glomerulotubular balance was well maintained. Calculated tubular volume increased with ureteral obstruction and venous occlusion, but did not change with aortic constriction. The ratio of reabsorption to tubular volume (C/πr²) decreased in all the experiments. During saline diuresis all three experimental maneuvers lowered total GFR and nephron GFR. Aortic constriction did not change absolute reabsorption and glomerulotubular balance was disrupted. Venous occlusion reduced reabsorption but not proportionately to the fall in GFR; glomerulotubular balance occurred but was incomplete. Ureteral obstruction reduced reabsorption proportionately to GFR and balance was well maintained. C/πr² increased with aortic constriction, did not change with venous occlusion and fell with ureteral obstruction. The changes in reabsorption occurring during glomerulotubular balance were not related to changes in tubular volume. It is concluded that some factor(s) other than tubular geometry, possibly hydrostatic and oncotic pressures in the peritubular capillaries are responsible for linking tubular reabsorption to the rate of glomerular filtration.

Although some cases of tubular dysfunction (TD) associated with nephrotic syndrome have been described, the incidence and the characteristics of this complication remain unknown. We investigated the presence of TD (renal glycosuria, aminoaciduria, metabolic acidosis with normal anion gap, hypouricaemia, and throughout hypophosphataemia) in 36 patients with nephrotic syndrome. Ten patients (group 1) showed glycosuria at some time during the course of their illness, ranging from 2.5 to 11.2 g/24 h. In addition, seven of them had metabolic acidosis with normal anion gap, five aminoaciduria, and two hypouricaemia. Membranous glomerulonephritis was the most frequent aetiology in group 1 patients (7 of 10). Proteinuria and serum creatinine (SCr) were significantly higher in group 1 patients than in the 26 remaining patients without TD (group 2): 10.2 +/- 3.7 versus 6.7 +/- 2.9 g/24 h (P less than 0.01) and 3.2 +/- 1.9 versus 1.6 +/- 0.9 mg/dl (P less than 0.05) respectively. The appearance of TD coincided with a clear worsening of renal function in most of group 1 patients. In addition, at the end of follow-up, SCr had increased from 3.2 +/- 1.9 to 5.6 +/- 3.3 mg/dl (P less than 0.05) in this group. In contrast, SCr did not show significant changes in group 2 (1.6 +/- 0.9 versus 2.1 +/- 2.2 mg/dl). In conclusion, a significant proportion (27.7%) of patients with nephrotic syndrome present TD data at some moment of their course; the appearance of this complication appears to be a sign of poor prognosis.

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