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TUBULOINTERSTITIAL DISEASES
Morphologically
ACUTE
Interstitial edemacortical
and medullary infiltration
of both mononuclear and
PMN leukocytespatchy
areas of tubular necrosis
PRIMARY
histologic and functional
abnormalities that
involve the tubules and
insterstitium
CHRONIC
interstitial fibrosis
inflammatory cells are
typically mononuclear
tubular atrophy,
luminal dilatation and
thickening of tubular
basement membrane
SECONDARY
occurs as a
consequence of
progressive glomerular
and vascular injury
DIAGNOSIS:
History
Associated symptoms
Imaging studies
Classification of the Causes
I.
Acute Tubulointerstital disorders
1. Acute Interstitial Nephritis
o
Therapeutic agents
Antibiotics
NSAIDS
Diuretics
Anticonvulsants, Misc.
o
Infection
Syogrens syndrome
SLE
Granulomatous IN (IgG4-related
systemic disease)
Metabolic Disturbances
1. Hypercalcemia and /or Nephrocacinosis
2. Hyperuricemia
3. Prolonged Hypokalemia
4. Hyperoxaluria
5. Cystinosis
Cystic and Hereditary Disorders
1. Polycystic Kidney Disease
2. Nephronopthisis
3. Adult Medullary cystic disease
4. Medullary Sponge Kidney
Miscellaneous
1.
2.
3.
4.
5.
Dr. PINLAC
Aging
CGN
Chronic Urinary tract obstruction
Ischemia and Vascular disease
Radiation Nephritis
Renal biopsy
o
show features of minimal change nephrosis in addition
to the characteristic findings of interstitial nephritis.
Antibiotic-induced acute tubulointerstitial nephritis
renal biopsy
o
eosinophils can be a component of the interstitial
nephritis.
o
Occasionally, ill-defined granulomas are present.
In HIV disease
o
acute interstitial nephritis is usually observed in
conjunction with glomerular disease (ie, focal
segmental glomerulosclerosis). Parenchymal invasion
by the virus is not always present, and other
TUBULOINTERSTITIAL DISEASES
Analgesic nephropathy
Dr. PINLAC
The mechanism appears to be dependent largely on the potent
vasoconstrictive effects of these drugs.
However, this condition is rare in bone marrow transplant
recipients, because these individuals receive the drugs for a short
time and generally at lower doses.
In renal transplant recipients, cyclosporine- or tacrolimus-induced
chronic interstitial nephritis is similar to chronic rejection.
Because the pathophysiology of both is poorly understood, these
conditions tend to be included under the generic term of chronic
transplant nephropathy. Most kidney transplant patients have a
stable course with mild impairment of renal function.
o
However, up to 10% of heart transplant recipients
develop progressive renal insufficiency and eventually
require dialysis.
Both cyclosporine and tacrolimus frequently cause hypertension
and hyperkalemia.
Hypomagnesemia caused by renal magnesium wasting is also
common in cyclosporine-treated patients.
Concomitant use of calcium channel blockers reduces
nephrotoxicity. Long-term use of cyclosporine has been
associated with patchy interstitial fibrosis, usually in a striped
pattern and with tubular atrophy.
Thrombotic microangiopathy might further contribute to both
acute and chronic nephrotoxicity.
Lead nephropathy
TUBULOINTERSTITIAL DISEASES
Dr. PINLAC
Sjgren syndrome
Treatment
o
Steroids with maintenance therapy with azaor
mycophenolate mofetil to prevent relapse
Balkan endemic nephropathy
However, most experts agree that the evidence for its role in this
endemic nephropathy is weak.
Hypercalcemia
o
is the most common cause.
o
Chronic hypercalcemia can occur in
primary hyperparathyroidism
sarcoidosis
multiple myeloma, and other neoplasms
(particularly with bone metastases)
vitamin D intoxication.
o
Even transient hypercalcemia can lead to chronic renal
insufficiency; renal involvement is mostly confined to
the distal tubular structures.
Clinically, polyuria and concentrating defect are common.
o
During acute hypercalcemia, urinary concentrating
defect can lead to dehydration and may aggravate
acute renal failure.
Radiologic examinations
o
may reveal nephrocalcinosis, and renal stone
formation can be a complicating factor in
hypercalcemia.
DIAGNOSTICS
CBC With Differential
Eosinophilia
o
very helpful in the evaluation of tubulointerstitial
nephritis.
o
However, this finding is neither specific nor sensitive
enough to establish the diagnosis.
o
Although the true incidence of eosinophilia in acute
tubulointerstitial nephritis is unknown, it is estimated
to be present in approximately half of patients.
o
Typically, eosinophilia is absent in acute
tubulointerstitial nephritis that is induced by NSAIDs.
Chemistry Panel
Beta-2 microglobulinuria
TUBULOINTERSTITIAL DISEASES
o
Dr. PINLAC
and atrophy are also present (eg, Renal biopsies have shown
severe interstitial fibrosis in patients with Chinese
herb/aristolochic acid nephropathy).
HISTOPATH!!!!!!!!!!!!!!!!!!!!!!!
ACUTE INTERSTITIAL NEPHRITIS
TUBULOINTERSTITIAL DISEASES
Dr. PINLAC
CHOLESTEROL MICROEMBOLISM
The arteriole in the center of the field has a thickened wall. The
lumen is occluded by elongated spaces, corresponding to
dissolved crystals surrounded by cellular reaction. The 2 glomeruli
flanking the arteriole are sclerotic and hardly recognizable
(hematoxylin and eosin, 40 X).
MANAGEMENT
Management of Acute Tubulointerstitial Nephritis
Analgesic nephropathy
TUBULOINTERSTITIAL DISEASES
and increased incidence of uroepithelial cancers is also
observed in patients with analgesic nephropathy.
Cyclosporine/tacrolimusinduced renal failure
Extended therapy with this agent to reduce body lead stores may
be of possible benefit.
Atherosclerotic kidney disease and cholesterol microembolic disease
Dr. PINLAC
RALPH COSUE