Page 696 - Textbook of Pathology, 6th Edition

680 ETIOLOGY. The toxic agents causing toxic ATN are as
under:
1. General poisons such as mercuric chloride, carbon
tetrachloride, ethylene glycol, mushroom poisoning and
insecticides.
2. Heavy metals (mercury, lead, arsenic, phosphorus and
gold).
3. Drugs such as sulfonamides, certain antibiotics (genta-
mycin, cephalosporin), anaesthetic agents (methoxyflurane,
halothane), barbiturates, salicylates.
4. Radiographic contrast material.
MORPHOLOGIC FEATURES. Poisoning with mercuric
chloride provides the classic example that produces
widespread and readily discernible tubular necrosis (acute
mercury nephropathy).
Grossly, the kidneys are enlarged and swollen. On cut
Figure 22.27 Ischaemic ATN. There is focal necrosis along the section, the cortex is pale and swollen, while the medulla
nephron involving proximal convoluted tubule (PCT) as well as distal is slightly darker than normal.
convoluted tubule (DCT). The affected tubules are dilated, their lumina Histologically, the appearance varies according to the
contain casts (hyaline or pigmented haem) and the affected regions are cause of toxic ATN but, in general, involves the segment
lined by regenerating thin and flat epithelium.
of tubule diffusely (unlike ischaemic ATN where the
involvement of nephron is focal). In mercuric chloride
Prognosis of ischaemic ATN depends upon the underlying poisoning, the features are as follows (Fig. 22.28):
etiology. In general, cases that follow severe trauma, surgical 1. Epithelial cells of mainly proximal convoluted tubules
procedures, extensive burns and sepsis have much worse are necrotic and desquamated into the tubular lumina.
outlook than the others. 2. The desquamated cells may undergo dystrophic
calcification.
3. Tubular basement membrane is generally intact.
Toxic ATN
SECTION III
4. The regenerating epithelium, which is flat and thin
Toxic ATN, also called nephrotoxic ATN or toxic nephrosis with few mitoses, may be seen lining the tubular basement
or upper (proximal) nephron nephrosis, occurs as a result membrane.
of direct damage to tubules, more marked in proximal
portions, by ingestion, injection or inhalation of a number of Prognosis of toxic ATN is good if there is no serious
toxic agents. damage to other organs such as heart and liver.
The contrasting features of the two forms of ATN are
presented in Table 22.12.

TUBULOINTERSTITIAL DISEASES
The term tubulointerstitial nephritis is used for inflammatory
Systemic Pathology
process that predominantly involves the renal interstitial
tissue and is usually accompanied by some degree of tubular
damage. A number of primary glomerular, tubular, vascular
and obstructive diseases are secondarily associated with
interstitial reaction. However, the term interstitial nephritis is
reserved for those cases where there is no primary
involvement of glomeruli, tubules or blood vessels. The older
nomenclature, interstitial nephritis, is currently used syno-
nymously with tubulointerstitial nephritis or tubulointerstitial
nephropathy.
A number of bacterial and non-bacterial, acute and
chronic conditions may produce tubulointerstitial nephritis
and are listed in Table 22.13. The important and common
examples among these are discussed below.
Figure 22.28 Toxic ATN. There is extensive necrosis of epithelial
cells involving predominantly proximal convoluted tubule (PCT) diffusely. Acute Pyelonephritis
The necrosed cells are desquamated into the tubular lumina and may
undergo dystrophic calcification. The tubular lumina cont ain casts Acute pyelonephritis is an acute suppurative inflammation
(granular) and the regenerating flat epithelium lines the necrosed tubule. of the kidney caused by pyogenic bacteria.