B. Nephritis

Embolic suppurative nephritis may occur after any septicaemia or bacteriemia when bacteria lodge in renal tissue but is most commonly associated with valvular endocarditis.

Localization of single bacterial cells or bacteria in small clumps in renal tissue causes the development of embolic sup­purative lesions.

Emboli which block vessels larger than capillaries cause in­farction in which portions of kidney, the size varying with the caliber of the vessel which is occluded, are rendered acutely ischemic. These infarcts are not usually so large that the residual renal tissue cannot compensate fully and they usually cause no clinical signs. If the urine is checked repeatedly for the presence of protein and erythrocytes, the sudden appearance of proteinuria, casts and microscopic hematuria without other signs of renal disease suggests the occurrence of a renal infarct. The gradual enlargement of focal embolic lesions leads to the development of toxemia and gradual loss of renal function. Clinical signs usually develop only when the emboli are multiple and destroy much of the renal parenchyma.

Enlargement of the kidney may be palpable on rectal examina­tion. If the causative bacteria can be isolated and their sen­sitivity to standard antibiotics and sulphonamides determined, control of early cases of embolic nephritis can usually be effective.

Bacteriological examination of the urine is advisable at intervals after treatment is completed to ensure that the in­fection has been completely controlled.