A female neonate, born by cesarean section at 37 weeks of gestation, presented with respiratory distress syndrome, right pneumothorax and anuria. A sonogram showed increased echogenicity, with neither hydronephrosis nor macroscopic cysts. Peritoneal dialysis was started on the 14th day because of renal insufficiency, but the newborn died on the 33rd day. Family history was unremarkable, except that the mother received piroxicam at about the 26th week of gestation. A sonogram at the 28th week showed oligohydramnios. Histopathological study of the kidneys revealed crowded glomeruli and only few differentiated proximal convoluted tubules in the inner cortex, abnormally differentiated microcystic tubules and microcystic glomeruli in the outer cortex. Periodic acid-Schiff staining showed only traces of brush border in the dilated tubules of the outer cortex. Immunoperoxidase staining for epithelial membrane antigen was positive in the luminal border of all tubules. Electron microscopy confirmed the presence of brush border remnants and other proximal tubular characteristics in some segments. The renal abnormality bears some similarities to that found in familiar renal tubular dysgenesis, but it fits better with those described after maternal use of angiotensin converting enzyme inhibitors and nonsteroidal anti-inflammatory drugs. The lesion in this case appears to have resulted from fetal exposure to piroxicam. Recently, a second pregnancy ended in a completely normal female newborn.
Forty-nine patients with a diagnosis of idiopathic haemolytic uraemic syndrome (HUS) were investigated to determine evidence of infection by verotoxin-producing Escherichia coli (VTEC). Free faecal cytotoxin active on Vero cells (VT) was detected in 15 out of 49 patients (31%). Seroconversion or high titres of VT-neutralizing antibodies were detected in 11 out of 18 patients (61%). The results of the present study suggest an association between HUS and infection by VTEC.
Summary. The effects of maleic acid on the gluconeogenic capacity and energy metabolism of rat kidney cortex were studied. In vitro maleic acid inhibits glucose production from various substrates by rat kidney cortex slices. Of the substrates tested, inhibition of gluconeogenesis was much greater with pyruvate, lactate and a-ketoglutarate than with glycerol, succinate, fumarate and malate. Subcutaneous injection of maleic acid produced a dose-dependent effect on aminoaciduria in vivo and on gluconeogenic capacity of slices prepared from the kidney cortices. The content of adenine nucleotides and adenylate kinase activity of kidney cortex of the maleic acid injected rats were significantly decreased.While no ultrastructural alteration of the glomeruli was demonstrable with any of the doses of maleic acid injected, electron microscopic changes of the tubules were dose-dependent, and correlated well with the degree of aminoaciduria and inhibition of gluconeogenic capacity of kidney cortex slices. Vesieulation of mitochondrial cristae found in the proximal, as well as distal convoluted tubular cells, may be associated with impairment of energy metabolism and, in turn, the reduced renal glueoneogenic capacity of the kidney cortex and the amino aciduria of maleic acid nephropathy.Key words: Kidney, Metabolism --Gluconeogenesis --Maleic acid --Adenosintriphosphate --Fanconi syndrome.Maleic acid has been reported to impair the function of the renal tubular epithelium in the dog [7], rabbit [4] and rat [4,15,27,29,36] with minimal evidence of structural damage. Dilatation of the proximal tubules with shortening of the brush border, vacuolization of the apical and compression of the basal parts of the cells, and thickening of the basal infoldings, have been described. These are reversible abnormalities and neither glomerular lesions nor structural changes of the distal tubular cells were noted [36].
The determination of urinary bicarbonate with the Henderson-Hasselbalch equation was compared using two methods: (1) correcting the pK in every urine sample according to ionic strength and using the solubility constant of CO2 in urine (alpha=0.0309) and (2) using a fixed pK value (6.1) and a CO2 solubility constant of 0.0301, which we use to calculate blood bicarbonate. Nine patients were studied and 29 determinations were performed. A high correlation was found between the methods (r=0.99). Bicarbonate calculated with corrected pK was 24.3+/-6.6 mEq/l (95% confidence interval 11.4-37.2) and bicarbonate calculated with pK fixed at 6.1 was 25.6+/-6.6 mEq/l (95% confidence interval 12.7-38.5). For each urine sample, the delta bicarbonate was calculated as the difference between the bicarbonate obtained with pK at 6.1 minus that obtained with the corrected pK (mean 1.25, standard error 0.83, P=0.15). This indicates that the difference between the methods was not significant. No difference was found whether pK was corrected or fixed (6.1). Therefore, our results suggest that it is valid to take the value shown by the equipment for blood gas determination as the urinary bicarbonate value. This would allow the rapid and accurate determination of urinary bicarbonate in patients with hyperchloremic acidosis, especially those with renal tubular acidosis.
We studied the function of phagocytes and the distribution of lymphocyte subpopulations in 23 patients with Idiopathic Minimal Change Nephrotic Syndrome. All the patients were in relapse at the time of the study. The latter was performed before specific therapy was started. Our control group consisted of 26 normal children who were studied while undergoing routine analysis prior to plastic surgery. Polymorphonuclear leukocytes from the patients showed no alterations in their ability to ingest and to kill candidas. On the contrary, peripheral blood monocytes had a normal phagocytic function with a decreased candidacidal activity when compared to normal controls (p less than 0.001). No correlation was found between serum immunoglobulin levels and the monocyte lytic function. The absolute number of B lymphocytes was significantly increased (p less than 0.05), whereas the absolute number of total lymphocytes, T lymphocytes and T4+ and T8+ cell subsets did not differ from those of the age-matched normal controls. Natural killer cells were functionally normal.
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