696

microscopic features are necrosis of liver cells and infil-tration of the portal tracts with mononuolear cells, bilethrombi may be found, as in obstruction of the extra-hepatic ducts ; and with such obstruction focal necrosisof liver cells is occasionally as conspicuous as in hepatitis.Thus errors may arise in interpreting biopsy material,though these are rare and will become still rarer as

experience increases. Needle biopsy of the liver is

undoubtedly the most accurate of all means of assessinghepatic lesions, and it is fortunate that this invaluableprocedure is now proving so innocuous.

1. Rigas, D. A., Heller, C. G. J. clin. Invest. 1951, 30, 853.2. King, S. E., Gronbeck, C. Ann. intern. Med. 1952, 36,

765.3. Welty, J. W. Amer. J. med. Sci. 1937, 194, 70.4. Javitt, N. B., Miller, A. T. J. appl. Physiol. 1952, 4,

834.5. Ahronheim, J. H. War Med., Chicago, 1944, 5, 267.6. Raaschou, F. Nord. Med. 1945, 25, 457.7. King, S. E. J. Amer. med. Ass. 1954, 155, 1023.8. Bull, G. M. Clin. Sci. 1948, 7, 77.

SIGNIFICANCE OF PROTEINURIA

URINE normally contains a small amount of protein,but not enough to give a positive reaction in routineclinical tests. Rigas and Heller have shown, by ultra-filtration concentration, that healthy people excreteeach day 30-50 mg. of protein, about a third beingalbumin and two-thirds globulin. Electrophoreticseparation of the urinary globulin showed an excess ofx1, and x2 fractions, whereas in plasma B and y fractionspredominate.

Pathological proteinuria has been classified into thethree types of transitory, postural or orthostatic, andcontinuous.2 Transitory proteinuria occurs irregularlyand for short periods, and never indicates permanentrenal disease. Proteinuria due to contamination bysecretions from the lower urinary tract can readily beexcluded by examination of a catheter specimen. Febrileproteinuria is associated with many infectious diseasesand was found by Welty 3 in over 75% of patients treatedby artificial fever therapy with a pyrexia of 105°-106°Fmaintained for four to six hours.. Intense physicalexertion causes proteinuria which is greatest about fiveminutes after termination of the exercise.4 4 This iscorrelated both with the fall of plasma-pH producedby exercise and with simultaneous depression of theglomerular filtration-rate and renal blood-flow as a

result of renal vasoconstriction. Relatively insignificantemotional stresses, such as that from venepuncture,sometimes cause transitory proteinuria,5 s

Continuous proteinuria always betokens renal disease.Usually the cause is glomerulonephritis or pyelonephritis.The presence of many casts and red and white blood-cells in the urinary deposit, and in some cases hyper-tension or urea retention, is valuable confirmatoryevidence of nephritis. Occasionally, however, in provedchronic pyelonephritis the urine is normal for longperiods.6 In cases of constant proteinuria which are notdue to nephritis intravenous pyelography commonlyreveals a congenital or acquired renal defect. 7

Orthostatic or postural proteinuria is caused by thetwo separate factors of the erect posture and lumbarlordosis. Bull s demonstrated that such proteinuriacould be produced by lordosis with the patient recumbent,but was greatest in the erect lordotic posture. This

proteinuria is commonest in adolescence ; Bull found itin 77% of young people aged 14-16, but in only 12%of - people over 50. Usually, therefore, orthostatic

proteinuria which has been present in adolescence dis-appears with advancing age. Bull found that adoptionof the erect lordotic posture by patients with orthostaticproteinuria was associated with a fall of glomerularfiltration-rate, renal plasma-flow, and salt and waterexcretion ; but no control deterrninations with non-

proteinuric subjects were made. Other workers 9 founda greater fall in creatinine clearance and urine volumein persons with proteinuria than in normals. The pressurein the inferior vena cava and the foot-to-tongue circula.tion-time were increased by erect lordosis to a greaterextent in the proteinuric patients than in controls.Bull concluded that postural proteinuria was secondaryto increased pressure in the inferior vena cava andrenal veins due to rotation of the liver in the lordoticposition. This hypothesis is satisfactory where theproteinuria is derived from both kidneys, but does notexplain cases where the protein is derived only from theleft kidiiey.10 11 In such cases the anomaly may possiblybe due to compression of the left renal vein between theaorta and the origin of the superior mesenteric arteryPostural proteinuria is often accompanied by the passageof red and white blood-cells and of hyaline and granularcasts, roughly proportional in number to the degree ofproteinuria.8 8 The level of protein may be surprisinglyhigh. Wolman 13 records levels of up to 3 g. per 100 ml.urine, but the total daily loss is almost always muchless than that in glomerulonephritis. The excess proteinis predominantly albumin.1 About a third of all casesof continuous proteinuria include an orthostatic element,rthe rate of protein loss being greater in the ambulantthan in the recumbent position.The frequency of orthostatic proteinuria (compared

with the relative rarity of nephritis) and its disappearanceusually with increasing age suggest that it is hardlyever of pathological significance. Postural proteinuria.may occur during convalescence from acute glomerulo-nephritis,14 15 when it generally disappears after a.

few months. King has suggested that, if it persists, thismay indicate permanent renal damage from chronicglomerulonephritis. One patient who was allowed to pilota long-distance passenger aeroplane, despite persistentpostural proteinuria after acute glomerulonephritis,.five years later was found to have hypertension, constantproteinuria, and urea retention.16 The prognosis shouldbe guarded in cases of postural proteinuria where thereis a clear history of previous organic renal disease,especially if function tests confirm renal damage.

9. Gömöri, P., Greiner, A. Klin. Wschr. 1942, 21, 1061.10. Sonne, C. Z. klin Med. 1921, 90, 1.11. Beer, E. J. Mt Sinai Hosp. 1937, 3, 193.12. Kelling, G. Zbl. inn. Med. 1919, 40, 313.13. Wolman, I. J. Amer. J. med. Sci. 1944, 208, 767.14. Thorp, E. G., Wakefleld, E. G. Ann. intern. Med. 1933, 6,

1565.15. Derow, H. A. New Engl. J. Med. 1942, 227, 827.16. Milne, M. D. Personal communication.17. See Lancet, 1954, i, 1123.18. Quattlebaum, J. K. Ann. Surg. 1954, 139, 743.19. Mallory, H. R., Jason, R. S. Amer. J. Surg. 1942, 57, 359.

ANEURYSM OF THE HEPATIC ARTERY" WHAT do you do if you operate for massive gastro-

intestinal hoeiiiorrliage and fail to find the bleeding-point ? " " Blind gastrectomy " was one answer whenthis question was asked at this year’s meeting in Londonof the American College of Surgeons.I7 But blind gastrec-tomy can be contemplated only after full examinationat laparotomy, including a search for the rarer causesof haemorrhage. One such cause is aneurysm ofthe hepatic artery. Some may regard this as a.

collector’s piece, but Quattlebaum 18 has recorded 96cases.

Clinically this disorder may give rise to pain, haemor-rhage, and jaundice. Commonly the patient tells of painin the epigastrium or hypochondrium, passing throughto the back-a history that may easily lead to theerroneous diagnosis of bleeding duodenal ulcer. Haemor-

rhage was the first indication in 40 of the 85 reportedcases studied by Mallory and Jason.19 In some of thesecases the haemorrhage occurred into the peritoneal cavity