A new renal function test was developed based upon the pharmacologic effects of furosemide to quantify separately the rates of electrolyte and water reabsorption by different segments of the human nephron in vivo. Since furosemide impairs active NaCl transport to Henle's loop and the attendant hypertonicity of the interstitium, osmotic water reabsorption from collecting ducts decreases and the unreabsorbed volume is lost into the urine, causing a rise in flow rate. This volume is computed from the difference in urine flow rate during furosemide with respect to that previously measured during maximal water diuresis alone. Starting from this value, an appropriate set of equations allows the separate calculation of Na reabsorption by the loop of Henle and by the distal tubule. Studies to validate this hypothesis were performed by clearance techniques during maximal water diuresis in 58 normal controls, in 19 patients with liver cirrhosis and ascites, and in 11 patients with chronic renal failure. Measurements were performed before and after the intravenous administration of 50 mg furosemide. The quantitative measurements of segmental solute reabsorption in normal subjects were consistent with results obtained by different methods in man and experimental animals, fully validating this new method. In addition, the data allowed to establish that distal reabsorption is depressed because of reduced proximal delivery in cirrhosis, as a result of impaired transport along Henle's loop in chronic renal disease, while permeability of collecting ducts to water was normal in both conditions. Though still approximate, this new furosemide test represents a considerable improvement over current methods for measuring segmental transport by the human nephron.

A patient who had diffuse lymph node enlargement, fever, skin rashes, anemia and polyclonal hypergammaglobulinemia is described. Histologic examination of lymph nodes taken from different sites (cervical, axillary and inguinal) revealed the presence of giant lymph node hyperplasia. The liver and bone marrow showed a moderate lymphocytic and plasma cell infiltration. The clinical presentation of a multicentric variety of giant lymph node hyperplasia in the reported case is similar to the clinical features usually associated with angio-immunoblastic lymphadenopathy with dysproteinemia, indicating that these two disorders may be related and may affect the same organs and systems. Alternatively, this histologic reactive giant lymph node hyperplasia progressing with a rapid declivitous course can be considered distinctive of a separate entity.

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Experiments were performed on humans to study the blunting on the diuretic action of furosemide by prostaglandin synthetase inhibitors. Maximal water diuresis was instituted. At the peak of urine flow, clearance periods were performed during baseline conditions and repeated after the injection of aspirin and, subsequently, of furosemide. Control subjects did not receive aspirin. Urine flow rate (V), Cosm, and Na excretion (UNa) . V were significantly lower when the administration of the diuretic had been preceded by that of aspirin. In the absence of furosemide, however, aspirin did not influence renal hemodynamics nor Na and water reabsorption. Therefore, the same experimental protocol was repeated in paired experiments where each normal subject served as his own control, being studied twice, in the presence and absence of aspirin, respectively. The average changes in water and Na excretion induced by furosemide were not different when the patients were pretreated with aspirin as compared with those measured in the absence of prostaglandin inhibition. Changes occurring in individual experiments were significantly correlated (r = 0.95, P less than 0.01) with those in calculated furosemide clearance. Since aspirin, indomethacin, and meclophenamate are secreted by the organic acid transport system of the proximal tubule, competition for a common secretory mechanism, rather than prostaglandin inhibition, could mediate the blunting of furosemide diuresis.

The segment of the nephron where carbohydrate deprivation depresses Na transport leading to natriuresis was sought by a new clearance technique designed to measure segmental reabsorption in each portion of the human renal tubule. Experiments were performed during maximal water diuresis before and 4 days after carbohydrate withdrawal. Proximal reabsorption had fallen from 70 ± 4 to 60 + 5 ml ■ min^-1 p < 0.05, by the 4th day of sugar deprivation, accounting for the natriuresis and the associated weight loss of 1.8 kg. By the 4th day of fasting, when Na excretion had returned to control levels, GFR had fallen nonsignificantly from 99 ± 6 to 95 ± 5 ml · min^-1, while Na reabsorption along distal segments had risen. In fact, Na transport, expressed by the equivalent volumes of solute free-water generated, rose from 17.4 ± 3.4 to 23.6 ± 2.1 along the ascending limb of Henle’s loop, and from 8.1 ± 0.8 to 9.2 ± 1.3 ml · min^-1 · GFR^-1 · 100 along the distal tubule. Thus, analysis of segmental Na transport by this method discloses that starvation natriuresis is a proximal tubular event, progressively counterbalanced by enhanced Na reclamation in more distal sites. Volume contraction and the attendant fall in GFR concur to curb delivery out of the proximal tubule which is matched by enhanced distal Na reabsorption till a new steady-state excretion is attained.