A number of renal function tests were combined into one 7-hour day in the rat, using urinary tests only to allow sequential measurements in individual animals, and involving 18 measurements for each one-day test. The use of 1.42% sterile sodium sulphate solution containing 3 mg% phenolsulphonphthalein (20 ml/kg) and a mineralocorticoid drug (Florinef, 9-α-fluorohydrocortisone, 0.2 mg/kg) by intraperitoneal injection was found to overcome the difficulty of achieving reproducible values for minimum urinary pH in the rat. Pitressin (antidiuretic hormone) was observed to interfere with minimum urinary pH, and its administration (0.4 units/kg i.p.) was delayed for 2 h. Normal values (mean ± SD) obtained in 64 one-day tests in 40 animals (involving over 1,000 measurements) were as follows: urinary protein (Albustix), 30 ± 15mg%; urinary phenolsulphonphthalein excretion in first hour, 27 ± 5 (males) and 37 ± 7 (females), as percent of injected dose; maximum sodium excretion after sodium load, 1,300 (range 700–2,200) µEq/mg creatinine; minimum sodium excretion after mineralocorticoid load, 10 ± 7 µEq/mg creatinine; maximum sodium excretion/conservation ratio 130 (range 40–1,100); maximum urinary creatinine concentration after Pitressin, 150 ± 35 mg%; and minimum urinary pH in second hour after sulphate load, 5.1 ± 0.2 units. In a 6-week illustrative study of cases of acute experimentally-induced renal disease, the administration of analgesic powders (42% aspirin, 42% phenacetin and 16% caffeine citrate) to 2 cases (8 one-day tests) or acetazoleamide to 3 cases (9 one-day tests) was found to induce defects in urinary concentrating ability after Pitressin and in minimum sodium excretion after a mineralocorticoid load, suggesting specific tubular or vasa recta lesions. Analgesic powders possibly affected the urinary acidification mechanism as well. On the other hand, dosage with puromycin aminonucleoside or human serum albumin in 4 cases (16 one-day tests) produced mainly decreased glomerular function and proteinuria typical of the nephrotic syndrome, with decreased flexibility of urinary sodium excretion.