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Three patients with hemolytic uremic syndrome (HUS) developed peripheral gangrene. Bilateral carotid artery thromboses occurred in one of these patients after recovery from HUS. One patient had a long history of juvenile rheumatoid arthritis. In the second patient, a flu-like illness preceded the onset of HUS. The third was one of two sisters, with the HUS appearing more than 1 year apart. None had evidence of disseminated intravascular coagulation or infection with Streptococcus pneumoniae. The patient with rheumatoid arthritis had renal cortical necrosis but recovered moderate renal function after treatment with dialysis and plasmapheresis for 6 months. The child with a genetic form of HUS died of renal failure and had massive cortical necrosis and vascular thrombosis at autopsy. This is the first report of peripheral gangrene in children with idiopathic HUS and autosomal recessive HUS.

Secondary oxalosis is a complication of renal failure. Since oxalate is excreted by the kidney, the severity of oxalate deposition has been directly related to the duration of renal failure. We report a patient with acute renal failure on hemodialysis who received daily ascorbic acid (an oxalate precursor) via parenteral alimentation. He developed widespread secondary oxalosis, which was especially prominent in the kidneys and pancreas. This oxalate burden may have contributed to the complications seen during his hospital course. The provision of ascorbic acid to patients with renal failure should be carefully monitored to avoid accelerated development of secondary oxalosis.

Twenty-three women of ages 13 to 44 years were hospitalized with illnesses fulfilling the criteria of the case definition for the toxic-shock syndrome (TSS) associated with coagulase-positive staphylococci. Disease onset occurred during menses in 22, and all were oliguric when admitted. Prolonged hypotension and a reduced central venous pressure were common features. Measurements of urine volume and creatinine clearance in eight patients identified two types of acute renal failure, oliguric and nonoliguric, and prerenal azotemia related to intravascular volume depletion. Urinary sodium excretion and measurement of the renal index (UNa divided by U/PCr) provided further support for the presence of both prerenal and intrinsic renal failure. Hemodialysis was required in one patient in whom findings on renal nuclide scan were consistent with acute tubular necrosis. Pyuria was frequent, but proteinuria and more than five erythrocytes per high-power field were infrequent. Other features included initial hyponatremia and the combination of hypoproteinemia, hypoalbuminemia, hypocalcemia and hypophosphatemia of several days' duration. The hypoalbuminemia was believed to be due to exudation of protein from the intra- to the extravascular space. The hypoalbuminemia was believed to be due to exudation of protein from the intra- to the extravascular space. The hypocalcemia was probably related to the hypoalbuminemia. The pathogenesis of hypophosphatemia in the presence of acute renal failure is unclear. Following the intravenous administration of colloids, fluids and, in seven patients, dopamine, all recovered from the acute illness.

Elevated plasma antidiuretic hormone (ADH) levels were noted in seven patients with status asthmaticus during the acute illness. These values returned to normal with resolution of the disease. The mechanism of this release is not completely understood but is consistent with the hypothesis that bronchospasm leads to decreased pulmonary blood flow, decreased volume return to the left atrium, and stimulation of the atrial volume receptors regulating ADH release. Planning for fluid therapy in patients with status asthmaticus should take into account a high probability of increased plasma ADH concentration during the acute illness. Water intoxication as well as hypoxia and hypercarbia should be considered as a possible cause of an altered state of consciousness associated with status asthmaticus.

Known physiologic mechanisms explain the elevated blood ADH levels observed in most patients with the syndrome of inappropriate ADH. Therefore the word "inappropriate" is a misnomer. It implies that the mechanisms that regulate ADH release are not functioning normally--which is not true. The term misleads the physician who, ideally, should determine why a patient has an excessive blood ADH level and initiate appropriate treatment. Patients with ectopic production of ADH and hyponatremia should be so labeled: "Hyponatremia due to ectopic ADH production." The term SIADH, if used at all, should be reserved for the rare patient with CNS injury or disease that causes increased ADH release and in which the hypothalamic center does not respond normally to afferent peripheral stimuli.

An unusual case of systemic lupus erythematosus (SLE) in a young child is reported with sudden death from myocardial infarction. The diagnosis of lupus erythematosus in this patient was made by renal biopsy at the age of 3 years. Atherosclerosis of the coronary arteries and aorta was found at autopsy with occlusion of the anterior descending branch of the left coronary artery. It is suggested that the vascular changes in this case were related to hypertriglyceridemia and prolonged prednisone therapy superimposed on a hypersensitivity vasculitis related to SLE.

It has been postulated that alterations in the intravascular distribution of blood affect antidiuretic hormone (ADH) secretion in man. The studies reported here were designed to alter blood distribution by thermal and by positional change to test this thesis.HUMAN BLOOD ADH LEVELS HAVE BEEN SHOWN TO VARY WITH POSITION: a mean value of 0.4 +/- 0.6 (SD) muU/ml was obtained while the subject was supine, a value of 1.4 +/- 0.7 muU/ml while sitting, and 3.1 +/- 1.5 muU/ml while standing. In 79 control subjects, sitting comfortably for 30 min in a normal environment, a blood ADH level of 1.65 +/- 0.63 muU/ml was found. It is suggested that subjects assume this position during experiments in which blood is drawn for measurement of ADH levels.In eight seated subjects the ADH level rose from 1.6 +/- 0.4 to 5.2 +/- 0.8 muU/ml after a 2 hr exposure at 50 degrees C and fell to 1.0 +/- 0.26 muU/ml within 15 min at 26 degrees C.Six subjects with a mean ADH level of 2.2 +/- 0.58 muU/ml sat quietly in the cold (13 degrees C) for 1 hr, and the ADH level fell to 1.2 +/- 0.36 muU/ml. After 15 min at 26 degrees C, the level rose to 3.1 +/- 0.78 muU/ml. The serum sodium and osmolal concentrations remained constant during all studies.Water, sodium, and total solute excretion decreased during exposure to the heat, whereas the urine to plasma (U/P) osmolal ratio increased. During cold exposure, water, sodium, and total solute excretion increased, and there was a decrease in the U/P osmolal ratio.These data are interpreted as indicating that changes in activity of intrathoracic stretch receptors, in response to redistribution of blood, alter ADH secretion independently of changes in serum osmolality. The rapidity of change of blood ADH concentration indicates a great sensitivity and a prime functional role for the "volume receptors" in the regulation of ADH secretion.