Page 494 - Concise Pathology for Exam Preparation ( PDFDrive )

16 Diseases of the Kidney and Lower Urinary Tract 479

2. Diffuse glomerulosclerosis:
(a) Overall thickening of GBM
(b) Diffuse increase in mesangial matrix with proliferation of mesangial cells
(c) Exudative lesions
(i) Capsular hyaline drops (eosinophilic hyaline thickening of the parietal layer of
Bowman’s capsule, which bulges into glomerular space).
(ii) Fibrin caps (homogenous, brightly eosinophilic material in the wall of a
peripheral capillary of a lobule).
3. Nodular glomerulosclerosis (Kimmelstiel–Wilson lesions/intercapillary glomer-
ulosclerosis):
(a) These lesions are specific for juvenile onset DM or islet cell antibodies-positive DM.
(b) One or more nodules are seen in glomeruli accompanied by thickening of
basement membrane of surrounding capillaries.
(c) Nodules are ovoid, spherical, laminated, hyaline, acellular and PAS-positive
masses, which contain lipid and fibrin and compress capillaries to obliterate
glomerular tufts leading to tubular atrophy and interstitial fibrosis.
4. Vascular lesions
(a) Atheromas in renal arteries.
(b) Hyaline arteriosclerosis of afferent and efferent arterioles.
(c) These vascular lesions are responsible for renal ischaemia, which results in tubular
atrophy and interstitial fibrosis.
(d) The above-mentioned changes may result in a small contracted kidney.
5. Diabetic pyelonephritis: Poorly controlled diabetics are susceptible to bacterial infection
and acute pyelonephritis. Papillary necrosis is an important complication.
6. Tubular lesions (Armanni–Ebstein lesions): In untreated diabetics, who have high
blood sugar levels, the epithelial cells of PCT develop extensive glycogen deposits
appearing as vacuoles.

Pathogenesis of Diabetic Glomerulosclerosis
• Metabolic defects: Insulin deficiency and recurrent hyperglycaemia.
• Biochemical changes in GBM: Increased collagen and fibronectin, decreased pro-
teoglycans and heparin sulphate.
• Nonenzymatic glycosylation of haemoglobin and other proteins (collagen and BM
material), resulting in thickening of BM.
h
• Haemodynamic changes: GFR associated with glomerular hypertrophy.

Q. Describe the aetiopathogenesis, clinical features and morphology
of acute tubular injury (ATI) or acute kidney injury (AKI).
Ans. ATI is a reversible disorder characterized by destruction of tubular epithelial cells
and acute suppression of renal function. It is the most common cause of acute renal failure.
Other causes of acute renal failure besides ATI include
• Severe glomerular disease, eg, RPGN
• Diffuse renal vascular disease, eg, microscopic polyangiitis and thrombotic microan-
giopathies
• Acute papillary necrosis associated with acute pyelonephritis
• Acute drug-induced interstitial nephritis
• Urinary obstruction due to tumours, NHP, blood clots, etc.

Types

1. Ischaemic ATI
2. Nephrotoxic ATI

mebooksfree.com