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TUBULOINTERSTITIAL DISEASES

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

Drug or Toxin exposure

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

Bacteria, viruses, Misc.


o
Autoimmune

TINU (Tubulointerstitial nephritis and


uveitis)

Syogrens syndrome

SLE

Granulomatous IN (IgG4-related
systemic disease)

IAIN (allergic interstitial nephritis)


o
Acute Obstructive disorders

Light chain cast nephropathy

Acute PO4 nephropathy

Acute Urate nephropathy


II.
1.
2.
3.
4.
5.
6.
7.
8.

Chronic Tubulointerstitial disorders


Vesicoureteral reflux/ reflux Nephropathy
Sickle cell disease
Chronic exposure to toxins of therapeutic agents
Analgesics-Phenacetin
Lithium
Heavy metals (Lead, Cadmium)
Aristolochicacid(Chinese herbal and Balkan
endemicNephropathy)
Calcineurin inhibitors (Cyclosporine, tacrolimus)

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

Acute tubulointerstitial nephritis (general features)


Typically, acute tubulointerstitial nephritis begins abruptly, manifesting as
acute kidney injury.

In most instances, acute tubulointerstitial nephritis occurs within


days of exposure to the offending drug.

In some instances (particularly with NSAIDs), acute


tubulointerstitial nephritis begins after several months of
exposure.
Acute tubulointerstitial nephritis caused by NSAIDS

Acute tubulointerstitial nephritis due to NSAIDs is more common


in elderly people, perhaps because of the higher incidence of
arthritic disorders in this population.

Acute allergic interstitial nephritis should not be confused with


the acute vasomotor renal insufficiency that can occur in patients
with preexisting underperfusion of the kidney.

A unique feature of allergic interstitial nephritis caused by NSAIDs


is that patients may present with nephrotic syndrome.
o
massive proteinuria with hypoalbuminemia and
edema are present in addition to the typical features
of acute interstitial nephritis.

Renal biopsy
o
show features of minimal change nephrosis in addition
to the characteristic findings of interstitial nephritis.
Antibiotic-induced acute tubulointerstitial nephritis

usually observed in the hospital setting during treatment of


serious infections, within several days to weeks of initiation of
antibiotic therapy

Rash, eosinophilia, and eosinophiluria, as well as pyuria(sterile),


hematuria, and modest proteinuria (usually < 1 g/d) are common

However, unlike in NSAID-induced allergic interstitial nephritis,


nephrotic-range proteinuria is very rare.

renal biopsy
o
eosinophils can be a component of the interstitial
nephritis.
o
Occasionally, ill-defined granulomas are present.

Among antibiotics, rifampin is unique in that the interstitial


nephritis generally occurs when the antibiotic is reintroduced
after an interval.
o
The interstitial nephritis associated with it does not
manifest with eosinophilia
o
In some cases, rifampin-associated interstitial nephritis
has been reported to show casts containing
immunoglobulin light chains in tubular lumens
without any evidence of myeloma in the patient.

Flulike symptoms, flank pain, hypertension, and oliguric acute


renal failure are common.

In some patients, circulating anti-rifampin antibodies and


immunoglobulin G (IgG) deposits along the tubular basement
membranes have been reported.
Acute tubulointerstitial nephritis caused by miscellaneous agents

Infections with viral agents, bacteria, and fungi are occasionally


associated with acute interstitial nephritis.
o
Hantavirus, cytomegalovirus (CMV), and human
immunodeficiency virus (HIV) are common among the
infectious agents associated with acute interstitial
nephritis.

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

characteristic features, such as eosinophilia and fever,


are usually absent.
Bacterial infection with renal parenchymal invasion is sometimes
responsible for acute interstitial nephritis, but this is exceedingly
rare in the absence of obstruction.
Other infections such as tuberculosis and histoplasmosis are also
among the rare causes of acute tubulointerstitial nephritis and
may be diagnostic challenges.

Chronic tubulointerstitial nephritis (general features)

The chronic form of tubulointerstitial nephritis is an insidious


disease and most probably represents the common final
response pattern of the kidney to a variety of insults and agents
o
Important causes include drugs (eg, analgesics,
cyclosporine, cisplatin, and lithium); lead; and
metabolic disorders, notably hypercalcemia,
potassium depletion, and hyperoxaluria.

Because of its insidious nature, chronic tubulointerstitial nephritis


is often diagnosed incidentally on routine laboratory screening or
evaluation of hypertension. Patients are usually asymptomatic.
Hypertension is common but not universal, and it is conspicuously
absent in Balkan endemic nephropathy.

Analgesic nephropathy

is the most common category of chronic interstitial nephritis


worldwide.

occurs with long-term ingestion of combinations of phenacetin,


aspirin, and caffeine or phenacetin-acetaminophen or NSAIDs
and acetaminophen.
o
In its most severe form, analgesic nephropathy is
associated with papillary necrosis.

The amount of phenacetin-acetaminophen combination required


to cause chronic interstitial nephritis has been estimated to be at
least 2-3 kg over many years.
o
Although initially thought to be exclusively associated
with phenacetin-containing combinations, all
analgesics, including acetaminophen, aspirin, and
NSAIDs, can cause analgesic-induced chronic
tubulointerstitial nephritis.

Analgesic nephropathy is most common in women in the sixth


and seventh decades of life who have a history of low back pain,
migraine headaches, or other chronic musculoskeletal pain.
o
In some patients, a history can be elicited of episodes
of papillary necrosis (ie, gross hematuria with flank
pain occasionally accompanied by obstruction and
infection).

Clinically, patients with analgesic nephropathy present with renal


insufficiency, modest proteinuria, sterile pyuria, and anemia.

Diagnosis of this condition can be supported by a history of heavy


analgesic use
o
Computed tomography (CT) scans may reveal
microcalcifications at the papillary tips.
Lithium nephropathy

Distal tubular dysfunction (ie, polyuria, concentrating defect,


downregulation of aquaporin-2)
o
occurs in up to 50% of patients receiving lithium.

Chronic interstitial nephritis


o
occurs in a small subset of patients receiving long-term
lithium therapy who have had repeated episodes of
lithium toxicity with high serum levels.
Cyclosporine- and tacrolimus-induced nephropathy

Although indispensable in the management of solid organ


transplantation, cyclosporine and tacrolimus can cause acute and
chronic nephrotoxicity.
o
Chronic tubulointerstitial nephritis induced by
cyclosporine or tacrolimus is common among patients
receiving kidney, heart, liver, and pancreas
transplants.

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

Environmental and occupational exposure to lead can cause


chronic tubulointerstitial nephritis.
o
Occupations in welding, smelting, the battery industry,
and mining have all been responsible for lead
nephropathy cases.
o
Environmental exposure from leaded gasoline is
decreasing, because the use of leaded gasoline has
ceased in the United States; however, sporadic
exposure is still observed, particularly among children
living in deteriorating housing in urban areas.

Rarely, lead poisoning can be observed among individuals who


consume moonshine whiskey and those who drink beverages
from imported ceramics painted with leaded glaze.

Children with severe lead poisoning can present with


o
Encephalopathy
o
acute renal failure with Fanconi syndrome.

Because lead has a biologic half-life of several decades, if


untreated by chelation,
o
both intermittent acute poisoning and low-level
environmental exposure result in chronic cumulative
lead poisoning.

The major consequence of chronic lead


poisoning is chronic tubulointerstitial
disease, usually in the third to fourth
decades of life.

Hypertension is almost always present


o
in the absence of appropriate testing or careful
exposure history, lead nephropathy is often
misdiagnosed as so-called hypertensive kidney disease.

Patients with lead nephropathy tend to have disproportionately


worse hyperuricemia compared to patients with other kidney
diseases because of the unique effects of lead on urate
metabolism

(EDTA) lead mobilization test


o
many patients presumed to have either gouty
nephropathy or hypertensive nephrosclerosis are
discovered to have lead nephropathy. Identification of
the lead etiology in patients presumed to have gout
nephropathy has cast doubt on the existence of this
entity.
Obstructive uropathy

A variety of causes contribute to obstructive uropathy which can


cause retroperitoneal fibrosis and obstruction
o
prostate disease in elderly males

TUBULOINTERSTITIAL DISEASES

Dr. PINLAC

pelvic or colonic tumors involving both ureters in both


sexes
o
nephrolithiasis, with or without urinary tract infection
o
radiation to the pelvic area
o
drugs, such as methysergide
Recurrent urinary tract infection
o
can cause ammonium magnesium phosphate stones,
further aggravating tubulointerstitial disease and
perpetuating infection.
Papillary necrosis and infection
o
may complicate the course and may lead to acute
pyelonephritis with fever, flank pain, hematuria, and,
especially in elderly patients, urosepsis.

Sjgren syndrome

chronic tubulointerstitial nephritis is the most frequent cause of


renal impairment found through kidney biopsy.

A systemic autoimmune disorder primarily targets the exocrine


gland esp. lacrimal and salivary glands

Presents with dry eyes and mouth sicca syndrome associated


with Distal RTA , Nephrogenic DI and moderate renal failure
DX- (+) serologictesting for anti-Ro (SS-A) and anti-La(SS-B)
antibodies Have polyclonal hypergammaglobulinemia

Treatment
o
Steroids with maintenance therapy with azaor
mycophenolate mofetil to prevent relapse
Balkan endemic nephropathy

Epidemiology and natural history clearly implicate environmental


factors in the pathophysiology of Balkan endemic nephropathy
o
Lead contamination of food has been considered but
ruled out as a cause of this disease.
o
Some studies have implicated a fungal toxin, called
"ochratoxin," which can grow in moist grains in storage
and which has been shown to cause a similar kidney
disease in pigs in several central European countries.

However, most experts agree that the evidence for its role in this
endemic nephropathy is weak.

More recent studies have linked aristolochic acid, the underlying


factor in chinese herb nephropathy , as a causative agent.
Chinese herb/aristolochic acid nephropathy

In the early 1990s, aristolochic acid was recognized as a potent


nephrotoxin that can cause rapidly progressive interstitial fibrosis
and end-stage renal disease (ESRD) in young women using a
Chinese herb as part of a slimming regimen in Belgium. Since
then, many other cases of so-called Chinese herb (CH)
nephropathy

Associated with uroepithelial cancers reminiscent of Balkan


nephropathy.
o
Aristolochic acid not only can trigger severe renal
fibrosis, but it also can cause oncogene mutations that
can explain the high incidence of renal cancer with this
type of interstitial nephritis. Patients have also been
found to have abnormal function of TP53, a known
tumor suppressor gene.

A recently recognized cause of interstitial kidney disease is


immunoglobulin G (IgG)-4related disease.
o
characterized by high serum levels of IgG and IgG4
o
associated with a tubulointerstitial nephritis with an
abundant IgG4-positive plasma cell interstitial
infiltration and has a good response to steroid
Metabolic disorders and nephropathy

Can lead to Chronic tubulointerstitial nephritis due to:


o
Hypercalcemia
o
Chronic potassium depletion
o
Cystinosis

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

A complete set of chemistries, including blood urea nitrogen


(BUN) and serum creatinine
o
provides information on whether renal insufficiency
exists.

A low bicarbonate level (total carbon dioxide < 24-23 mEq/L)


o
may indicate acidosis.

Low serum potassium levels


o
may indicate a proximal tubular disorder

Elevated serum potassium levels with a low bicarbonate level


o
may indicate type 4 renal tubular acidosis

observed with lead nephropathy and

nonsteroidal anti-inflammatory drug


(NSAID)induced analgesic nephropathy,
among other conditions.
Urinalysis

proteinuria, hematuria, and the presence of white blood cells


(WBCs), with or without bacteria.

A microscopic analysis of urine sediment may reveal casts, WBCs,


eosinophils, and crystals.

If allergic interstitial nephritis is suspected


o
send a cytospin specimen to determine if eosinophils
are in the urine.

the absence of eosinophiluria does not rule


out the diagnosis

it can be observed in other diseases,


including cholesterol microembolism,
urinary tract infections, parasitic disorders,
and glomerulonephritis.

In NSAIDinduced acute tubulointerstitial nephritis


o
eosinophiluria is usually absent.

Quantitative determination of urine protein may also be helpful.

Low-molecular weight proteins are increased in chronic


tubulointersitital nephritides
o
beta-2 microglobulin
o
retinol binding protein (RBP)
o
alpha-1 microglobulin
o
and immunoglobulin light chains

Beta-2 microglobulinuria

TUBULOINTERSTITIAL DISEASES
o

has been found helpful in the diagnosis of Balkan


endemic nephropathy and cadmium nephropathy

Ultrasonography and Radiography


Ultrasonography

is a noninvasive imaging technique that is extremely helpful in


identifying hydronephrosis in obstructive disease as well as calculi
in stone disease. Both radiolucent and radiopaque stones can be
visualized with this modality.
o
A combination of ultrasonography and flat plate
kidney, ureter, and bladder (KUB) radiography is
helpful in the workup and identification of radiopaque
versus radiolucent stones.

Normal kidney size by ultrasonographic examination generally


favors but does not prove a diagnosis of acute (thus potentially
reversible) kidney disease.
o
In contrast, small (shrunken) kidneys with increased
echogenicity indicate chronic and irreversible kidney
disease.

Once widely used, intravenous pyelography seldom plays a role in


the workup of kidney diseases in modern medicine. In many
instances, similar information can be obtained by ultrasonography
without exposing the patient to potentially nephrotoxic contrast

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

The renal cortex shows a diffuse interstitial, predominantly


mononuclear, inflammatory infiltrate with no changes to the
glomerulus. Tubules in the center of the field are separated by
inflammation and edema, as compared with the more normal
architecture in the right lower area (periodic acid-Schiff, 40 X).

The diagnosis is based on the active inflammatory infiltrate on


the right with unaffected glomeruli. Interstitial edema and
fibrosis are present on the left side of the field, where some
tubules show thickened basement membrane (hematoxylin and
eosin, 20 X).

The interstitium is expanded by mononuclear inflammatory


infiltrate and edema. Acute tubular damage is present; some
tubules are distended and contain granular casts (hematoxylin
and eosin, 40 X).

Computed tomography (CT) scanning

provides information similar to ultrasonographic scanning in the


workup of kidney disease, generally with greater resolution.
o
However, an ultrasonographic examination is sufficient
in most kidney diseases.

A high-resolution scan showing microcalcifications in renal


papillary tips can be very helpful in diagnosis of analgesic
nephropathy.

The kidneys may be very small in Balkan endemic nephropathy


and aristolochic acid nephropathy.
EDTA Lead Mobilization Test

Consider the possibility of lead nephropathy in patients


presenting with chronic renal insufficiency, hypertension, and
gout.
o
In the absence of documented episodes of acute
symptomatic lead poisoning
o
the medical history is not reliable in ascertaining the
lead etiology in patients presenting with chronic
tubulointerstitial nephritis.

Diagnosis of lead nephropathy requires an estimation of the


cumulative body stores of lead by either
o
EDTA lead mobilization test or
o
by determination of bone lead content by radiographic
fluorescence.

The EDTA lead mobilization test is performed by


o
measuring 24-hour urine lead excretion after
intravenous or intramuscular administration of 2 g
EDTA (calcium disodium versenate).
o
Excretion of more than 0.6 g of lead per 24 hours is
considered an abnormal finding.

Blood lead levels, although elevated during acute or recent


exposure, are not very helpful in the evaluation of chronic lead
poisoning.
o
During acute exposure, lead is concentrated in the red
blood cells (RBCs) and later extracted to tissues and
bone as the RBCs senesce.
Kidney Biopsy and Histologic Features

Kidney biopsy is the definitive test for diagnosing acute allergic


interstitial nephritis, particularly in cases in which the clinical
diagnosis is difficult. Because the differential diagnosis of acute
tubulointerstitial nephritis encompasses multiple etiologies,
consider kidney biopsy when the diagnosis is not obvious.

shows mononuclear and often eosinophilic cellular infiltration of


the renal parenchyma with sparing of the glomeruli (see the
following images). Sometimes, interstitial changes such as fibrosis

TUBULOINTERSTITIAL DISEASES

Dr. PINLAC

CHOLESTEROL MICROEMBOLISM

The mononuclear inflammatory infiltrate contains abundant


eosinophils, suggesting an allergic etiology. Severe tubular
damage is observed

The inflammatory infiltrate forms an ill-defined granuloma,


suggesting allergic or infectious etiologies. A partially destroyed
tubule is present (periodic acid-Schiff, 40 X).

The 2 arterioles in the center are occluded by elongated crystals


(hematoxylin and eosin, 20 X).

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).

ACUTE CRESENTERIC GLOMERULONEPHRITIS

Acute crescentic glomerulonephritis. The glomerular tuft is


compressed by the proliferation of epithelial cells, forming a
crescent. The interstitium shows mononuclear inflammatory
infiltrate and edema (periodic acid-Schiff, 40 X).

CHRONIC TUBULOINTERSTITIAL NEPHRITIS

MANAGEMENT
Management of Acute Tubulointerstitial Nephritis

In cases due to hypersensitivity reactions (allergic interstitial


nephritis)
o
early recognition and prompt discontinuation of the
offending drug are helpful
o
cessation of the offending agent usually, but not
always, results in complete recovery in patients.
o
However, the rate of recovery is variable, and, in some
patients, renal failure persists for many weeks before
renal function improves. Some patients may progress
to chronic renal insufficiency.

Obtain a thorough history of previously documented drug


allergies before prescribing a new drug.

If no sign of improvement is observed within a few days of


discontinuation of the offending agent
o
consider therapy with steroids.
o
Although controlled trials are lacking, many authors
suggest using prednisone at relatively high doses (eg,
1 mg/kg for 4-6 wks with rapid tapering of the dose).
This intervention may improve the outcome, speeding
renal recovery and reducing the requirement for
dialysis.
Management of Chronic Tubulointerstitial Disease

Treatment of chronic tubulointerstitial nephritis


o
depends on the etiology
o
generally consists of supportive measures, such as
adequate blood pressure control and management of
anemia.

The interstitium is expanded by fibrosis, with distortion of tubules


and periglomerular fibrosis. Glomeruli do not show pathologic
changes

Analgesic nephropathy

Treatment of analgesic nephropathy is supportive and also


includes discontinuation of analgesic use.
o
Long-term follow-up studies have shown progression
to end-stage renal disease (ESRD) requiring dialysis,

TUBULOINTERSTITIAL DISEASES
and increased incidence of uroepithelial cancers is also
observed in patients with analgesic nephropathy.
Cyclosporine/tacrolimusinduced renal failure

Reduce the cyclosporine/tacrolimus doses and target trough


levels. Discontinuing these medications and/or switching to other
immunosuppressives (eg, rapamycin), especially in those with
more advanced renal failure, should also be considered
Lead nephropathy

Body burden of lead and bone lead concentration can be reduced


by extended chelation treatment using EDTA (versenate).

Chelation therapy is of proven value and must be implemented in


acute lead poisoning.
o
Although the oral chelating agent succimer (Chemet)
has proved highly successful in treating children, it has
not been widely used in adults. Nevertheless, it
appears effective in reducing body lead stores.

Chelation therapy with EDTA may slow progressive renal


insufficiency in patients with mild lead intoxication.
o
Several studies from Taiwan have shown that chelation
therapy in patients with modest increases in body lead
burden (ie, 80-600 g of lead) significantly slowed
and/or reversed the rate of decline in the glomerular
filtration rate (GFR) compared with placebo

Because no effective therapy reverses the long-term


consequences of lead poisoning,
o
the best therapy is prevention and awareness of
potential environmental and occupational sources for
lead exposure.

Therefore, implement environmental measures, such as


o
removal of lead from indoor paint and gasoline, and
o
eliminate other sources of exposure.
o
Use caution with imported ceramics, particularly if
glazed.

In patients with established lead nephropathy


o
treatment consists of management of hypertension,
gout, and chronic renal insufficiency.

Many patients with lead nephropathy progress to end-stage


kidney failure and require dialysis.
These agents promote the excretion of lead.
Succimer (Chemet)

a metal chelator, an analogue of dimercaprol that is used in lead


poisoning.

This agent is particularly useful in children with lead blood levels


> 45 mcg/dL.

is approved for chelation therapy in children for lead poisoning.

However, its value in chronic lead nephropathy is not established


Edetate calcium disodium (Calcium Disodium Versenate)

is used for lead chelation; only the calcium disodium preparation


should be used.

is confined to testing (ie, to EDTA lead mobilization test for


diagnosing lead as the etiology of chronic tubulointerstitial
nephritis).

Extended therapy with this agent to reduce body lead stores may
be of possible benefit.
Atherosclerotic kidney disease and cholesterol microembolic disease

No specific therapy is available for atherosclerotic kidney disease,


but
1. good control of hypertension
2. cessation of smoking
3. vigorous control of dyslipidemia with diet
4. with hepatic 3-methylglutaryl coenzyme A (HMG-CoA),
reductase inhibitors are expected to result in improved
outcomes.

There is also no effective treatment available for cholesterol


microembolic disease.

Dr. PINLAC

For acute allergic interstitial nephritis,

if no spontaneous recovery in renal function is observed after


cessation of the offending agent,
o
implementing a short course of steroid therapy is
generally recommended.

No controlled studies exist on the effect of corticosteroids;


o
therefore, no well-defined dosage and duration exist.

Most practitioners recommend a relatively high dose (eg, 1 mg/kg


prednisone) with a rapidly tapering regimen within several
weeks.
Glucocorticoid agents have immunosuppressant effects and are used for
treatment of autoimmune disorders
Prednisone (Sterapred)

has anti-inflammatory properties and causes profound and


varied metabolic effects by modifying the body's immune
response to diverse stimuli.

This agent may decrease inflammation by


o
reversing increased capillary permeability and
o
suppressing polymorphonuclear lymphocyte (PMN)
activity.

Prednisone also stabilizes lysosomal membranes and suppresses


lymphocytes and antibody production.
NOTETAKER:

RALPH COSUE

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