3. ACUTE TUBULAR NECROSIS
• Destruction of renal TUBULAR epithelium
• Loss of renal function
• 50% of ACUTE renal failure
• Two types:
ISCHEMIC
NEPHROTOXIC
-AMINOGLYCOSIDES
-AMPHOTERICIN B
-CONTRAST AGENTS
20. FORMS OF PYELOPNEPHRITIS
• Chronic pyelonephritis can be divided into two forms:
→REFLUX NEUROPATHY
→CHRONIC OBSTRUCTIVE PYELONEPHRITIS
21. GROSS
• Shrunken , scarred kidneys.
• If both kidneys are involved - involvement is asymmetrical
(in constrast with chronic glomerulonephritis in which the
kidneys are symmetrically involved).
• Coarse , discrete cortico - medullary scarring overlying
blunted deformed calyces.
22.
23. MCIROSCOPY
• Tubules - Atrophy in some and Dilation & Hypertrophy in others.
• Dilated tubules filled with colloid casts – THYROIDIZATON.
• Neutrophils in tubules - if acute reinfection occurs
• Chronic Interstitial Inflammation - cortex and medulla.
• It is not uncommon to see lymphocytes accompany just about
any chronic renal disease: glomerulonephritis, nephrosclerosis,
pyelonephritis. However, the plasma cells are most
characteristic for chronic pyelonephritis.
• Fibrosis - Around calyceal mucosa.
24. … MCIROSCOPY
• Glomeruli - normal except for Periglomerular Fibrosis.
• Secondary Focal Segmental Glomerulosclerosis in patients with
chronic pyelonephritis and reflux nephropathy who develop
proteinuria in advanced stages. The mechanism is adaptive
glomerular alterations secondary to loss of renal mass caused
by pyelonephritic scarring (renal ablation nephropathy).
• Arcuate and interlobular vessels - Obliterative endarteritis.
• Other arteries - Hypertensive Hyaline Arteriolosclerosis.
25.
26.
27.
28.
29. DRUGS/TOXINS causing
INTERSTITIAL NEPHRITIS
• Synthetic penicillins (methicillin,
ampicillin), other synthetic antibiotics
(rifampin), diuretics (thiazides), NSAIDs,
and miscellaneous drugs (allopurinol,
cimetidine).
• 2 weeks later: Fever, eosinophilia, rash,
and an acute renal failure type of picture
32. URATE NEPHROPATHY
• Precipitation of Uric Acid Crystals in
the TUBULES, especially in a LOWER
than usual PH situation (mini-TOPHUS)
H & E alcohol fixed POLARIZED LIGHT MICROSCOPY
34. HYPERCALCEMIA
NEPHROCALCINOSIS
PRINCIPLE: In extreme or
uncontrolled or chronic
HYPERCALCEMIA, calcium stones form
in the tubulo-interstitium of the kidney,
which can eventually lead to tubular
obstruction and loss of function
36. Light Chain Cast Nephropathy
• Bence John Proteinuria and Cast
nephropathy
• Amyloidosis
• Light chain deposition disease
• Hypercalcemia and Hyperuricemia
37. • Acute Phosphate Nephropathy
– No hypercalcemia
– Ca Phosphate stones
• Bile cast Nephropathy
– Hepatorenal syndrome
– Analogous to myeloma protein
39. BENIGN NEPHROSCLEROSIS
• Sclerosis, i.e., “hyalinization” of arterioles
and small arteries, i.e., arterio-, arteriolo-
• Is this part of “routine” atherosclerosis????
• VERY VERY VERY common
40. MALIGNANT NEPHROSCLEROSIS
(i.e., malignant hypertension)
• NOT a part of “routine” atherosclerosis
• By definition, associated with rapidly
progressive hypertension (1-2% of HTN)
• VASCULAR DAMAGE
• FIBRINOID NECROSIS
• “ONION SKINNING”
• SIGNIFICANT LUMENAL NARROWING
42. Renal Artery Stenosis
• Rare cause of HTN
• SMALL Kidney
• 1) Plaque type is usual cause, yes
regular old atherosclerosis
• 2) Fibromuscular “dysplasia” type:
–INTIMAL HYPERPLASIA
–MEDIAL HYPERPLASIA
–ADVENTITIAL HYPERPLASIA
– In younger women
What percentage of these tubules are PROXIMAL convoluted tubules rather than DISTAL? Answer: 98%
The “necrotic” tubular cells are karryolytic.
Patterns of tubular damage in ischemic and toxic acute kidney injury. In the ischemic type, tubular necrosis is patchy, relatively short lengths of tubules are affected, and straight segments of proximal tubules (PST) and ascending limbs of Henle's loop (HL) are most vulnerable. In toxic acute kidney injury, extensive necrosis is present along the proximal convoluted tubule segments (PCT) with many toxins (e.g., mercury), but necrosis of the distal tubule, particularly ascending HL, also occurs. In both types, lumens of the distal convoluted tubules (DCT) and collecting ducts (CD) contain casts.
Acute kidney injury. Some of the tubular epithelial cells in the tubules are necrotic, and many have become detached (from their basement membranes) and been sloughed into the tubular lumens, whereas others are swollen, vacuolated, and regenerating.
Acute & Chronic
What are the 3 parts of the ureter which are most subject to obstruction or stones for anatomic reasons alone?
UPJ, pelvic brim, bladder inlet
Polyoma virus … transplant
Pitting geographic “scars” is the hallmark of chronic pyelonephritis.
“THYROIDIZATION” is another common hallmark of chronic pyelonephritis.
To my knowledge, this is one of 3 things which look like thyroid, but are not. What are the other two? 1) Pars intermedia of pituitary 2) lactation breast lobule
Is the primary inflammatory focus in the tubules or interstitium BETWEEN the tubules?
Drug-induced interstitial nephritis, with prominent eosinophilic and mononuclear cell infiltrate + tubulitis
What is “metastatic” calcification? Ans: The tissue calcification due to hypercalcemia
Differentiate Bence-Jones protein from amyloid
Is it fair to say just about all of the primary vascular diseases of the kidney might result in hypertension” Answer: YES
Does the name “malignant” imply, perhaps, EXTREME blood pressure elevations? Answer: YES
Could fibrin plugs in small vessels easily be missed if a fibrin stain is not done, thinking this is merely blood? Answer: YES
Is the CORTEX of a kidney MUCH more susceptible than a MEDULLA to ischemia? Answer: YES
What is an “anemic” infarct? Ans: It is an infarct which is grossly pale in the acute stage because of lack of collateral circulation.