Effect of alterations of sodium intake in patients with hyporeninemic hypoaldosteronism.

The effect of changes of sodium intake on serum and urinary electrolytes, plasma renin activity (PRA) and plasma aldosterone concentration (PA) was studied in five hyperkalemic patients with the syndrome of hyporeninemic hypoaldosteronism (SHH). The patients were evaluated during 8 days on a 10-mEq sodium and 50-mEq potassium diet plus furosemide, followed by 8 days on a 150-mEq sodium and 50-mEq potassium diet. After sodium depletion, both PRA and PA were substantially higher than after a previous 4-day period of simple dietary sodium restriction and an increase in serum potassium concentration occurred in only one subject.

Use of banding techniques for zygosity diagnosis in twins.

Detailed comparison of human variant chromosomes found by Q- and C-banding technique is performed in a pair of twins to show that these variants can be used for zygosity diagnosis.

Hyporeninemic hypoaldosteronism after chronic sodium bicarbonate abuse.

We describe a 52-year-old man who, following the discontinuation of massive intake of sodium bicarbonate, in the absence of renal insufficiency, developed progressive hyperkalemia and hyponatremia in association with hyporeninemic hypoaldosteronism. The mechanism of this syndrome is not known, but may involve suppression of the renin-angiotensin-aldosterone axis by chronic volume expansion.

Renal acidification in hypothyroid man.

The role of thyroid hormone in renal hydrogen ion secretion remains largely unknown, and there is only limited information on renal acidification in hypothyroid patients. In the present study two of five adult male patients with untreated primary hypothyroidism and without clinical evidence of systemic autoimmune disease were unable to lower their urine pH appropriately after short duration acid-loading. Since, prior to acid-loading, their arterial blood gas values were within the normal range and urinary bicarbonate excretion was trival, the findings are consistent with the incomplete syndrome of distal renal tubular acidosis.

Renal acidification in sickle-cell disease.

Renal acidification was evaluated in patients with sickle-cell disease (HvSS) with both oral NH4CI and NaHC03 and the results were compared to those of subjects with sickle-cell trait (HbAS) and controls. The pH of arterial blood was normal in HbSS subjects but their PC02 and [HC03] were lower than those of controls. In response to NH4CI, six of 20 HbSS subjects had an abnormal minimal urine pH (greater than 5.

Antihypertensive effects of oxprenolol and propranolol.

The antihypertensive effects of the beta blockers oxprenolol and propranolol were compared in a randomized double-blind study of patients with standing diastolic pressures (SDP) exceeding 99 mm Hg when receiving hydrochlorothiazide alone. After 3 wk of hydrochlorthiazide with placebo, the latter was replaced with oxprenolol (n= 12) or propranolol (n = 14), 20 mg three times daily. Beta blocker was increased subsequently to 40 and 80 mg three times daily if SDP exceeded 89 mm Hg.

Hepatorenal syndrome following hemihepatectomy.

The hepatorenal syndrome following right hemiphepatectomy is reported in a previously healthy patient who sustained a shotgun wound in the abdomen. In spite of the development of severe oliguric renal insufficiency and the administration of massive amounts of volume expanders and furosemide, the urine sodium concentration remained very low, therby excluding the diagnosis of acute tubular necrosis. Although severe hyperbilirubinemia developed, the prothrombin time was only slightly abnormal and the liver doubled in size in the 2 weeks after surgery.

Antihypertensive effectiveness of oxprenolol administered twice daily.

Oxprenolol, a beta-blocker, is an effective antihypertensive when administered 3 or 4 times daily. We evaluated the antihypertensive effect of oxprenololgiven twice daily (bid). The subjects were 15 ambulatory men whose standing diastolic blood pressure (BP) was at least 100 mm Hg after 3 wk of treatment with hydrochlorothiazide and oxprenolol placebo.

Impaired renal concentrating ability in hypothyroid man.

The renal concentrating ability was studied in ten patients with hypothyroidism and in 15 euthyroid controls. Solute-free water reabsorption was reduced in the patients with myxedema (4.2 +/- 0.

The G syndrome. A four-generation family study.

A male infant with hypertelorism, hypospadias, swallowing difficulties with tendency to regurgitation and cough, high arched palate, and a delicate voice, consistent with the G syndrome, is reported. In the family the same symptoms in addition to cleft lip and palate were known in several family members through four generations. In the females only slight manifestations of the syndrome were found, and in the males variable expression of symptoms was observed.

Renal acidification in patients with mineralocorticoid deficiency.

Renal acidification was studied in eight patients with Addison's disease or bilateral adrenalectomy receiving glucocorticoid replacement only and without renal insufficiency (group I); in five patients with hyporeninemic hypoaldosteronism and moderate chronic renal insufficiency (group II), and in nine control subjects (group III). During acidosis minimal urine pH was 5.4 or less in all subjects, but excretion of ammonium and titratable acid was moderately reduced in group I and markedly reduced in group II.

Renal acidification in sickle cell trait.

Nine sickle cell trait and nine control subjects underwent six-hour ammonium chloride acid loading. Maximal urine osmolality and renal hemodynamics were studied separately. Base line arterial pH, carbon dioxide pressure (Pco2), and [HCO3] were normal and comparable in the two groups.

The effect of dexamethasone on urinary acidification.

Although it is well recognized that mineralocorticoids enhance renal acid excretion, the effect of glucocorticoids on renal acidification is unclear. Oral administration of dexamethasone to six healthy volunteers for 1 week at a daily dose of 4.5 mg was associated with mild respiratory alkalosis and a small but statistically significant increase in baseline urine pH.

Incomplete syndrome of renal tubular acidosis induced by lithium carbonate.

Renal acidification was studied in 10 control subjects and 15 lithium carbonate-treated psychiatric patients of similar age. Seven lithium-treated patients were unable to lower urine pH normally after short duration acid-loading (Li-1:5.35 to 6.

Abnormal renal acidification in alcoholic liver disease.

After ingestion of 150 mEq. of calcium chloride (CaCl-2), urinary acidification was studied for 6 hours in 22 normokalemic patients with alcoholic liver disease (L) of varying severity, and in 7 control (C) subjects during 10 studies. The degree of the induced systemic acidosis was similar in all groups.

A 21-year psycho-social follow-up of 524 unselected cases of down's syndrome and their families.

The death rate was followed, and a life table has been constructed. Three crucial events were examined: 1. the period of diagnosis, 2.

Mortality and life-table in Down's syndrome.

The causes of death in 130 patients with Down's Syndrome and mortality rates from a material of 524 patients were tabulated; a life-table for the ages over 5 years was constructed. An overall death rate of 5-7 times the general population rate was found. No sex difference was observed.

A girl with karyotype 46,XX,del(7)(qter-p 15:).

A girl with partial deletion of the short arms of one chromosome 7 is described. Among many other symptoms she has craniosynostoses. Early closure of cranio-sutures has previously been described in 2 of 3 patients with partial deletion 7.