The peculiarities presented by the urine differ somewhat from those which we are accustomed to find in other infectious diseases, yet they are not sufficiently definite to be considered characteristic.

As to the amount, the great majority of cases manifest a not inconsiderable polyuria, and this increased excretion is usually observed on days when paroxysms take place. Two to four liters are not rare. This is the more striking on account of the organism losing so large an amount of water by the profuse sweating. A postmalarial polyuria is even more frequent, and it may develop to such a degree as to be appropriately designated a postmalarial diabetes insipidus.

This postmalarial diabetes was recognized by Sydenham. It was recently studied by Mosse. Among 100 cases of malaria , he found an increase in the amount of urine 11 times. The polyuria began three to six days after the last paroxysm, quickly increased to its acme, then rapidly diminished, although it continued in a lessened degree for a long time. The patients usually left the hospital still showing it. The largest daily amount observed by Mosse was eight liters. The daily excretion of urea during the polyuria was normal, but the chlorids were considerably increased, usually about double. In one case 65 gm. were excreted within twenty four hours.

Some observers affirm that during the cold stage the urine is light in color and profuse; during the hot stage, scanty, and during the sweating stage, highly concentrated and especially large in amount. This may be true for some cases, but it is by no means constant. The old physicians laid great diagnostic value, especially in latent cases, on the lateritious sediment.

The specific gravity varies, and in pronounced polyuria is not always correspondingly low. As was first demonstrated by Traube and Jochmann, the percentage of urea and chlorids increases with the paroxysm and falls after it. Sydney Ringer, Hirtz, and Jaccoud found that the increased excretion of urea began several hours before the paroxysm, reached its acme toward the end of the cold stage, and then fell, though it continued over the normal.

According to Ringer, the increase in urea is in proportion to the rise of temperature. Redtenbacher found in ten cases the amount of urea and urine increased (even to three and one fifth times the normal) during the paroxysm, and diminished during the apyrexia. Uric acid appears to show no noticeable deviations from the normal.

Rem picci, Caccini, and Bernasconi recently found, among 37 cases, the chlorids increased in 22, normal in 6, diminished in 9. The amount of chlorids was proportional to the amount of urine. The chlorids were found diminished by Hammond and Uhle. According to Gee, Rosenstein, and others, the phosphates are decreased during the paroxysms and increased during the defervescence. Rem picci, Caccini, and Bernasconi found the phosphates diminished during the entire paroxysm and increased during the apyrexia.

The amount of iron in the urine was found increased by Colasanti and Jacoangeli.

Among the abnormal constituents, serum albumin is not uncommon. It is found during the paroxysm in larger or smaller amounts. Martin Solon reported its presence in one fourth of the severe cases,

Osier 133 times in 333 cases, Marchoux 39 times in 40 cases. The albuminuria disappears in the majority of cases with the cessation of the paroxysms, yet there are not a few cases in which the albuminuria continued two to three weeks or ever longer. (For further details see section on Complications and Sequelae.)

I have repeatedly found nucleo albumin in traces or more evident amounts during or shortly after the paroxysm. Peptone was found regularly during the paroxysm and for a few days after by Dubujadoux.

Acetone and diacetic acid have been occasionally observed in severe cases during the paroxysm.

Glycosuria has been frequently reported. Burdel speaks of it as a common symptom. The largest amount of sugar which he met with was 12 per cent. In 60 cases Range found in no instance a marked reduction of the copper solution; a slight reduction in 24. In 72 cases Sorel observed a fleeting excretion of small amounts of sugar in only a few. Mosse saw transitory glycosuria twice in 100 cases, and even these two are not above suspicion, since one was a midwife, the other a patient suffering simultaneously from arthritis. Laveran, Kelsch and Kiener, and others were also unable to confirm Burdel's assertion. In my cases I found only one: a ten year old girl with double tertian, whose urine, passed during the paroxysm, showed nucleo albumin, albumin, considerable acetone, and a marked reducing substance. The urine responded also to the phenylhydrazin test, but showed no rotatory power in the polariscope; the reducing substance was, therefore, not sugar. It appeared again with every paroxysm.

Bilirubin is rarely observed, while urobilin is almost constant and often in considerable quantities. Indican is frequently increased. Ehrlich's diazo reaction responds in a few cases. (For hemoglobinuria see the section devoted to it.)

Microscopically we often find in the albuminous urine of the paroxysm isolated hyaline or granular casts, red and white blood corpuscles, and kidney epithelium.

According to the experimental investigations of Roque and Lemoine, the urine passed after a paroxysm possesses markedly toxic properties. They found, for instance, that the hypertoxic coefficient before a severe paroxysm = 0.130; after it, 0.684; and once, 0.752. Following the administration of quinin, the coefficient increased for twelve hours to 1.276 and then fell.