Tubulointerstitial disorders Flashcards

1
Q

Rapid reduction of renal function and urine flow to <400 ml/day within 24 hrs

A

Acute tubular injury/necrosis

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2
Q

Pre-renal causes of acute tubular injury/necrosis

A

Ischemia –> malignant HTN, microscopic polyangiitis, DIC, HUS, TTP, severe trauma, acute pancreatitis, etc

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3
Q

Renal causes of acute tubular injury/necrosis

A

Direct toxic injury –> drugs, contrast dyes, poisons, heavy metals, organic solvents (CCL4)

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4
Q

Combined ischemic and toxic causes of acute tubular necrosis/injury

A

Hemolytic crises –> hemoglobinuria
Skeletal muscle injuries –> myoglobinuria

Iron is toxic to kidney

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5
Q

Characteristic urine findings in combined causes of acute tubular necrosis/injury

A

Hemoglobin and myoglobin tubular casts

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6
Q

Acute tubular injury type characterized by focal involvement of the tubules at multiple points, tubulorrhexis, and tubular lumen casts. Regeneration is complete

A

Ischemic

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7
Q

Tubular lumen casts seen in ischemic acute tubular injury

A

Hyaline
Pigmented brown granular casts (Tamm-Horsfall protein)

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8
Q

Acute tubular injury type characterized by continuous involvement of the tubule, usually proximal descending, without BM rupture.

A

Toxic

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9
Q

Features of initiation phase of acute tubular injury

A

36 hrs
Dominated by cause
Slight decrease in renal output with increased BUN

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10
Q

Features of maintenance phase of acute tubular injury

A

Sustained oliguria
Salt and water overload
Hyperkalemia
Metabolic acidosis
Increased BUN concentration
Uremia

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11
Q

Treatment of maintenance phase of acute tubular injury

A

Maintain water and electrolyte balance (crucial)
Dialysis

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12
Q

Features of recovery phase of acute tubular injury

A

Steady increase in urine volume
Loss of water and electrolytes in urine
Hypokalemia
Eventually tubular concentrating ability returns

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13
Q

Reason for loss of water and electrolytes in urine in recovery phase in acute tubular injury

A

Tubular damage

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14
Q

Causes of pre-renal acute tubular injury due to decreased effective arterial volume

A

CHF
Hypovolemia
Systemic vasodilation (sepsis)

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15
Q

Causes of pre-renal acute tubular injury due to renal vasoconstriction

A

NSAIDs
ACE inhibitors

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16
Q

Intra-renal manifestations of acute tubular injury

A

Acute interstitial nephritis
Glomerulonephritis
Thrombotic microangiopathy

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17
Q

Post-renal causes of acute tubular injury

A

Kidney stones
BPH
Neurogenic bladder
Neoplasia

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18
Q

When does a post-renal acute tubular injury occur?

A

Bilateral outflow obstruction

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19
Q

Characteristics of acute pyelonephritis

A

Renal lesion associated with UTI caused by bacteria

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20
Q

Parts of kidney affected by pyelonephritis

A

Renal tubules
Interstitium
Renal pelvis

Glomeruli are relatively resistant to infection

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21
Q

Possible causes of chronic pyelonephritis

A

Bacterial infection
Vesicourethral reflux
Obstruction

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22
Q

Reasons that DM predisposes to pyelonephritis

A

Increased susceptibility to infection
Neurogenic bladder dysfunction
More frequent instrumentation

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23
Q

Discrete focal abscesses involving one or both kidneys with haphazard distribution that can extend to form large wedge-shaped areas of suppuration.

A

Acute pyelonephritis

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24
Q

Areas of the kidney most commonly affected in reflux associated pyelonephritis

A

Lower and upper poles

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25
Q

Biopsy of kidney shows patchy suppurative interstitial inflammation, intratubular aggregates of neutrophils, and tubular necrosis.

A

Acute pyelonephritis

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26
Q

Complications of pyelonephritis

A

Papillary necrosis
Pyonephrosis
Perinephric abscess

27
Q

Conditions associated with papillary necrosis

A

DM
Urinary tract obstruction
Analgesic nephropathy
Sickle cell disease

28
Q

Gray-white or yellowish areas of coagulative necrosis in distal renal pyramids

A

Papillary necrosis

29
Q

Changes in surface of kidney in papillary necrosis

A

Depressed areas that overly necrotic papillae

30
Q

Complication of papillary necrosis

A

Transitional cell carcinoma of renal pelvis

31
Q

Post-pyelonephritis finding almost always associated with inflammation, fibrosis, and deformation of the underlying calyx and pelvis

A

Pyelonephritic scar

32
Q

Chronic tubulointerstitial inflammation and scarring with pathologic involvement of the renal calyces and pelvis.

A

Chronic pyelonephritis

33
Q

Important cause of kidney destruction in children with severe LUT abnormalities

A

Chronic pyelonephritis

34
Q

Two types of chronic pyelonephritis

A

Reflux nephropathy
Chronic obstructive pyelonephritis

35
Q

Coarse, discrete corticomedullary scars overlaying dilated blunted calyces with flattening of papillae, mostly in the upper and lower poles. Results in asymmetric, irregular, scarred kidneys.

A

Chronic pyelonephritis

36
Q

Microscopy shows atrophic or dilated tubules filled with colloid casts (thyroidization of tubules) with variable amounts of inflammatory cells in the interstitium. Normal glomeruli with periglomerular fibrosis or fibrous glomeruli can be seen.

A

Chronic pyelonephritis

37
Q

Possible complication of chronic pyelonephritis

A

FSGS

38
Q

Rare variant of chronic pyelonephritis characterized by presence of foamy macrophages, plasma cells, lymphocytes, PMN, and giant cells. Often associated with Proteus.

A

Xanthogranulomatous pyelonephritis

39
Q

Gross appearance of kidney in xanthogranulomatous pyelonephritis

A

Yellowish-orange nodules

40
Q

Differential diagnosis with same gross appearance as xanthogranulomatous pyelonephritis

A

Renal cell carcinoma

41
Q

Urine finding in chronic pyelonephritis that affects the tubules and why

A

Polyuria and nocturia –> loss of concentrating ability

42
Q

Poor prognostic sign in chronic pyelonephritis

A

Proteinuria and FSGS

43
Q

Causes of acute drug induced interstitial nephritis

A

Sulfonamides
Methicillin and ampicillin
Rifampicin
Thiazide diuretics
NSAIDs
Allopurinol
Cimetidine

44
Q

Clinical features of acute drug induced interstitial nephritis

A

Fever
Skin rash
Eosinophilia
Hematuria, proteinuria, and WBCs in urine
Rising serum creatinine or ARF with oliguria (50%)

45
Q

Analgesics that can cause nephropathy when used in combination

A

Phenacetin, aspirin, caffeine, and codeine

46
Q

How does acetominophen injure cells?

A

Depletes glutathione –> injury occurs by generation of oxidative metabolites

47
Q

AKI due to decreased synthesis of vasodilatory prostaglandins 2/2 COX-2 inhibition

A

NSAID associated nephropathy

48
Q

Precipitation of uric acid crystals in the tubules due to acidic pH in the collecting ducts leading to obstruction of nephrons and renal failures.

A

Acute uric acid nephropathy

49
Q

3 types of urate nephropathy

A

Acute uric acid nephropathy
Chronic urate (gouty) nephropathy with hyperuricemia
Nephrolithiasis

50
Q

Deposition of monosodium urate crystals in the acidic distal tubules and collecting ducts leading to giant cell reaction and fibrosis (gouty tophus). Birefringent needle-like crystals in tubular lumen or interstitium.

A

Chronic urate (gouty) nephropathy with hyperuricemia

51
Q

Another name for light-chain cast nephropathy

A

Myeloma kidney

52
Q

Factors that contribute to kidney damage in light-chain cause nephropathy

A

Bence Jones proteinuria and cast nephropathy
Amyloidosis (AL type)
Light chains deposits
Hypercalcemia and hyperuricemia

53
Q

Tubular casts seen in light-chain cast nephropathy

A

Bence Jones protein and Tamm-Horsfall protein combine and obstruct tubular lumina

54
Q

Pink to blue amorphous masses that fill and distend the lumen in light-chain neuropathy

A

Casts

55
Q

Earliest functional defect in nephrocalcinosis

A

Inability to concentrate urine (hyposthenuria)

56
Q

Pt present with renal insufficiency several weeks after colonoscopy

A

Acute phosphate nephropathy

57
Q

Features of type 1 (distal) renal tubular acidosis

A

Distal acidification
Serum bicarbonate <10
Serum potassium reduced
Urine pH >5.3

58
Q

Features of type 2 (proximal) renal tubular acidosis

A

Proximal bicarbonate reabsorption
Serum bicarbonate 12-20
Serum potassium reduced
Urine pH can be <5.3

59
Q

Features of type 4 (hypoaldosteronism) acute tubular acidosis

A

Decrease in or resistance to aldosterone
Serum bicarbonate >17 (varies)
Serum potassium increased
Urine pH can be <5.3

60
Q

Type of hypersensitivity in hyperacute transplant rejection

A

Type II –> recipient antibodies

61
Q

Type of hypersensitivity in acute transplant rejection

A

IV –> recipient T-cells

62
Q

Type of hypersensitivity in chronic transplant rejection

A

III and IV –> T-cell and deposition

63
Q

Transplant rejection mediated by donor T-cells

A

GVHD

64
Q
A