Daniel S. Kushner

Familial hypogammaglobulinemia, splenomegaly and leukopenia. With a review of the etiological factors of the hypogammaglobulinemias.

Abstract The death from disseminated histoplasmosis of a patient with hypogammaglobulinemia, increased susceptibility to infection, splenomegaly and leukopenia led to an investigation of his family. Three of his six living children, a thirteen year old boy and six year old fraternal twin girls, were found to have a similar syndrome without evidence of infection with histoplasmosis. The patients father had splenomegaly but no other features of this syndrome. The other members of the family had none of these abnormalities. In the involved members the level of gamma globulins and the degree of immunologic responsiveness, while depressed, were greater than usually observed in other forms of hypogammaglobulinemia. The evidence suggests that this apparently new clinical entity is an hereditary disturbance transmitted possibly by an autosomal dominant gene. The etiological features of the known forms of hypogammaglobulinemia are reviewed and commented upon.

Diuretic action of benemid: Its effect upon the urinary excretion of sodium, chloride, potassium and water in edematous subjects

Abstract 1.1. In thirteen subjects with uncomplicated congestive heart failure benemid in dosage of 4 gm. daily produced a significant diuretic response. The mean increment of water excreted on the day of maximal response was 1,330 cc., of sodium 91 mEq. and of chloride 76 mEq./24 hours. A fourteenth subject with associated gout and renal disease showed a lesser but significant response. Diuresis occurred in most instances on either the first or second day of drug administration. 2.2. Water diuresis without enhancement of sodium or chloride excretion occurred in seven other subjects. Failure of diuresis to occur in the remaining five subjects was associated with the presence of hepatic disease, renal disease, hyponatremia and hyponatruria. 3.3. It is postulated that benemid-induced diuresis is the result of decreased tubular reabsorption of water, sodium and chloride.

Some aspects of the natural history and treatment of chronic glomerulonephritis.

Inapparent streptococcal infection may be complicated by equally inapparent (latent) glomerulonephritis which leads eventually to active chronic glomerulonephritis. Photomicrographs are presented illustrating the progression, in one year, from latent glomerulonephritis related to type 12 streptococci to an early nephrotic state with hypertension. The discouraging outlook of nephrotic glomerulonephritis in adults forces the consideration of heroic therapy with massive doses of corticosteroids, but it is not yet established whether or not such therapy is justified in latent chronic glomerulonephritis without the nephrotic state.