Tubulointerstitial disorders Flashcards
Rapid reduction of renal function and urine flow to <400 ml/day within 24 hrs
Acute tubular injury/necrosis
Pre-renal causes of acute tubular injury/necrosis
Ischemia –> malignant HTN, microscopic polyangiitis, DIC, HUS, TTP, severe trauma, acute pancreatitis, etc
Renal causes of acute tubular injury/necrosis
Direct toxic injury –> drugs, contrast dyes, poisons, heavy metals, organic solvents (CCL4)
Combined ischemic and toxic causes of acute tubular necrosis/injury
Hemolytic crises –> hemoglobinuria
Skeletal muscle injuries –> myoglobinuria
Iron is toxic to kidney
Characteristic urine findings in combined causes of acute tubular necrosis/injury
Hemoglobin and myoglobin tubular casts
Acute tubular injury type characterized by focal involvement of the tubules at multiple points, tubulorrhexis, and tubular lumen casts. Regeneration is complete
Ischemic
Tubular lumen casts seen in ischemic acute tubular injury
Hyaline
Pigmented brown granular casts (Tamm-Horsfall protein)
Acute tubular injury type characterized by continuous involvement of the tubule, usually proximal descending, without BM rupture.
Toxic
Features of initiation phase of acute tubular injury
36 hrs
Dominated by cause
Slight decrease in renal output with increased BUN
Features of maintenance phase of acute tubular injury
Sustained oliguria
Salt and water overload
Hyperkalemia
Metabolic acidosis
Increased BUN concentration
Uremia
Treatment of maintenance phase of acute tubular injury
Maintain water and electrolyte balance (crucial)
Dialysis
Features of recovery phase of acute tubular injury
Steady increase in urine volume
Loss of water and electrolytes in urine
Hypokalemia
Eventually tubular concentrating ability returns
Reason for loss of water and electrolytes in urine in recovery phase in acute tubular injury
Tubular damage
Causes of pre-renal acute tubular injury due to decreased effective arterial volume
CHF
Hypovolemia
Systemic vasodilation (sepsis)
Causes of pre-renal acute tubular injury due to renal vasoconstriction
NSAIDs
ACE inhibitors
Intra-renal manifestations of acute tubular injury
Acute interstitial nephritis
Glomerulonephritis
Thrombotic microangiopathy
Post-renal causes of acute tubular injury
Kidney stones
BPH
Neurogenic bladder
Neoplasia
When does a post-renal acute tubular injury occur?
Bilateral outflow obstruction
Characteristics of acute pyelonephritis
Renal lesion associated with UTI caused by bacteria
Parts of kidney affected by pyelonephritis
Renal tubules
Interstitium
Renal pelvis
Glomeruli are relatively resistant to infection
Possible causes of chronic pyelonephritis
Bacterial infection
Vesicourethral reflux
Obstruction
Reasons that DM predisposes to pyelonephritis
Increased susceptibility to infection
Neurogenic bladder dysfunction
More frequent instrumentation
Discrete focal abscesses involving one or both kidneys with haphazard distribution that can extend to form large wedge-shaped areas of suppuration.
Acute pyelonephritis
Areas of the kidney most commonly affected in reflux associated pyelonephritis
Lower and upper poles
Biopsy of kidney shows patchy suppurative interstitial inflammation, intratubular aggregates of neutrophils, and tubular necrosis.
Acute pyelonephritis
Complications of pyelonephritis
Papillary necrosis
Pyonephrosis
Perinephric abscess
Conditions associated with papillary necrosis
DM
Urinary tract obstruction
Analgesic nephropathy
Sickle cell disease
Gray-white or yellowish areas of coagulative necrosis in distal renal pyramids
Papillary necrosis
Changes in surface of kidney in papillary necrosis
Depressed areas that overly necrotic papillae
Complication of papillary necrosis
Transitional cell carcinoma of renal pelvis
Post-pyelonephritis finding almost always associated with inflammation, fibrosis, and deformation of the underlying calyx and pelvis
Pyelonephritic scar
Chronic tubulointerstitial inflammation and scarring with pathologic involvement of the renal calyces and pelvis.
Chronic pyelonephritis
Important cause of kidney destruction in children with severe LUT abnormalities
Chronic pyelonephritis
Two types of chronic pyelonephritis
Reflux nephropathy
Chronic obstructive pyelonephritis
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.
Chronic pyelonephritis
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.
Chronic pyelonephritis
Possible complication of chronic pyelonephritis
FSGS
Rare variant of chronic pyelonephritis characterized by presence of foamy macrophages, plasma cells, lymphocytes, PMN, and giant cells. Often associated with Proteus.
Xanthogranulomatous pyelonephritis
Gross appearance of kidney in xanthogranulomatous pyelonephritis
Yellowish-orange nodules
Differential diagnosis with same gross appearance as xanthogranulomatous pyelonephritis
Renal cell carcinoma
Urine finding in chronic pyelonephritis that affects the tubules and why
Polyuria and nocturia –> loss of concentrating ability
Poor prognostic sign in chronic pyelonephritis
Proteinuria and FSGS
Causes of acute drug induced interstitial nephritis
Sulfonamides
Methicillin and ampicillin
Rifampicin
Thiazide diuretics
NSAIDs
Allopurinol
Cimetidine
Clinical features of acute drug induced interstitial nephritis
Fever
Skin rash
Eosinophilia
Hematuria, proteinuria, and WBCs in urine
Rising serum creatinine or ARF with oliguria (50%)
Analgesics that can cause nephropathy when used in combination
Phenacetin, aspirin, caffeine, and codeine
How does acetominophen injure cells?
Depletes glutathione –> injury occurs by generation of oxidative metabolites
AKI due to decreased synthesis of vasodilatory prostaglandins 2/2 COX-2 inhibition
NSAID associated nephropathy
Precipitation of uric acid crystals in the tubules due to acidic pH in the collecting ducts leading to obstruction of nephrons and renal failures.
Acute uric acid nephropathy
3 types of urate nephropathy
Acute uric acid nephropathy
Chronic urate (gouty) nephropathy with hyperuricemia
Nephrolithiasis
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.
Chronic urate (gouty) nephropathy with hyperuricemia
Another name for light-chain cast nephropathy
Myeloma kidney
Factors that contribute to kidney damage in light-chain cause nephropathy
Bence Jones proteinuria and cast nephropathy
Amyloidosis (AL type)
Light chains deposits
Hypercalcemia and hyperuricemia
Tubular casts seen in light-chain cast nephropathy
Bence Jones protein and Tamm-Horsfall protein combine and obstruct tubular lumina
Pink to blue amorphous masses that fill and distend the lumen in light-chain neuropathy
Casts
Earliest functional defect in nephrocalcinosis
Inability to concentrate urine (hyposthenuria)
Pt present with renal insufficiency several weeks after colonoscopy
Acute phosphate nephropathy
Features of type 1 (distal) renal tubular acidosis
Distal acidification
Serum bicarbonate <10
Serum potassium reduced
Urine pH >5.3
Features of type 2 (proximal) renal tubular acidosis
Proximal bicarbonate reabsorption
Serum bicarbonate 12-20
Serum potassium reduced
Urine pH can be <5.3
Features of type 4 (hypoaldosteronism) acute tubular acidosis
Decrease in or resistance to aldosterone
Serum bicarbonate >17 (varies)
Serum potassium increased
Urine pH can be <5.3
Type of hypersensitivity in hyperacute transplant rejection
Type II –> recipient antibodies
Type of hypersensitivity in acute transplant rejection
IV –> recipient T-cells
Type of hypersensitivity in chronic transplant rejection
III and IV –> T-cell and deposition
Transplant rejection mediated by donor T-cells
GVHD
