Page 496 - Concise Pathology for Exam Preparation ( PDFDrive )

16 Diseases of the Kidney and Lower Urinary Tract 481

TABLE 16.8. Differences between ischaemic and nephrotoxic ATI
Features Ischaemic AKI Nephrotoxic AKI
Definition ATI caused by renal ischaemia ATI caused by toxic agents
Causes Shock, mismatched blood transfusion, Nephrotoxins like heavy metals, eg, mercu-
haemolytic crises, myoglobinuria, ric organic solvents, gentamycin and am-
acute pancreatitis and septicaemia photericin B, cisplatin and radiographic
contrast media
Distribution of lesions Straight portion of proximal tubule and Proximal convoluted tubules
ascending thick loop of Henle
Pathology Blebbing and sloughing of brush border, Tubular basement membrane is spared.
detachment of tubular cells from their Mercury salts cause coagulative necrosis,
basement membrane and their slough- CCL4 causes lipoid degeneration and
ing in the urine ethylene glycol causes hydropic degen-
eration of the PCT
Oliguria Present Typically nonoliguric
Casts Eosinophilic and pigmented granular Nonspecific; dependent on the causative
casts consisting of Tamm–Horsfall agents, eg, lipid casts are present in CCl4
protein, haemoglobin, myoglobin and poisoning
other plasma proteins are present

Q. Differentiate between benign and malignant nephrosclerosis.

Ans. Differences between benign and malignant nephrosclerosis are listed in Table 16.9.

TABLE 16.9. Differences between benign and malignant nephrosclerosis

Features Benign nephrosclerosis Malignant nephrosclerosis
Cause Benign hypertension, DM, increasing age Malignant hypertension
Gross Leather grain appearance Flea-bitten appearance due to tiny petechial
haemorrhages
Microscopy • Narrowing of the lumen of arterioles caused by • Hyperplastic arteriolitis (onion-skinning)
thickening and hyalinization of the walls due to proliferation and elongation of
(hyaline arteriosclerosis) smooth muscle cells
• Fibroelastic hyperplasia of arteries and • Necrotizing glomerulitis (neutrophilic
arterioles infiltration and thrombosis of capillaries)
• Fibrinoid necrosis of arterioles (necrotiz-
ing arteriolitis)
Clinical features • Hypertension • Accelerated hypertension with renal im-
• Microscopic haematuria pairment, encephalopathy and retinopathy
• Contracted kidney • Enlarged kidneys
• Trace proteinuria • Marked proteinuria

Q. Describe the aetiopathogenesis, gross appearance and complications
of renal calculi/urolithiasis.

Ans. The clinicopathological features of various renal calculi/urolithiasis are summarized
in Table 16.10.

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