Interstitial Nephritis

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 Objectives
Ø Definition
Ø Classification.
Ø Causes.
Ø Clinical presentation.
Ø Management

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ØA group of inflammatory, inherited and
other diseases affect renal tubules and the
surrounding interstitium.
ØThe clinical presentation is often simply
with renal impairment. Proteinuria is
generally low.
ØInterstitial Nephritis classified into Acute
and Chronic

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Acute Interstitial
Nephritis

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Ø In acute interstitial nephritis, the tubular
damage leads to renal tubular
dysfunction, with or without renal failure.
Ø Regardless of the severity of the damage
to the tubular epithelium, the renal
dysfunction is generally reversible,
possibly reflecting the regenerative
capacity of tubules with preserved
basement membrane.
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in

ØUrine may contain red and white blood cells.

ØAcute inflammation within the tubulo-
interstitium is most commonly allergic,
particularly to drugs, but other causes include
toxins and a variety of systemic diseases and.
ØDeterioration of renal function in drug-induced
AIN may be dramatic and resemble rapidly
progressive glomerulonephritis.

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 Prognosis
ØTubulointerstitial disease may progress to end-
stage renal disease.
ØAnalgesic nephropathy is 5-6 times more

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common in women. This is generally
attributed to women taking more analgesics
than men.
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CAUSES OF ACUTE INTERSTITIAL NEPHRITIS
Penicillins, Rifampin PPI
NSAIDs, Diuretics
Allergic Allopurinol
Many other drugs

Immune Autoimmune nephritis ± uveitis

Acute bacterial pyelonephritis
Infections Leptospirosis
Tuberculosis
Hantavirus

Toxic Myeloma light chains

Mushrooms (Cortinarius)

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Ø Only a minority (perhaps 30%) of patients with drug-
induced AIN have a generalised drug hypersensitivity
reaction (e.g. fever, rash, eosinophilia) and dipstick
testing of the urine is usually unimpressive. However,
leucocyturia is common, and eosinophils are found in
the urine in up to 67% of patients.
Ø Proteinuria is usually absent or modest. < 1
glory
Ø Urinalysis may show microscopic hematuria and/or
sterile pyuria (with or without eosinophils).
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ØU/S is normal in size and slightly enlarged
ØRenal biopsy is usually required to confirm the
diagnosis
diagnosis. only way to confirm the

ØMany patients are not oliguric despite

moderately severe ARF, and AIN should
always be considered in patients with non-
oliguric ARF.

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 Management
ØRemoval of inciting agent.
ØBut corticosteroids (e.g. prednisolone 1
mg/kg/day) accelerate recovery and may
prevent long-term scarring.
Ø Dialysis is sometimes necessary, but is usually
only short-term. Other specific causes should be
treated where possible.
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just treat

the &
cause Complications

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Cystic kidney
diseases
 Autosomal Dominant
Polycystic kidney disease
Ø ADPKD is a common condition that is inherited
as an autosomal dominant trait.
Ø Small cysts develop from infancy or childhood
and enlarge slowly and irregularly. -

Ø Renal failure is associated with grossly enlarged

kidneys.
the patient do not present in a
so
later aye
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Ø Mutations in the PKD1 gene account for 85%
of cases and PKD2 for about 15%.

Ø ESRD occurs in approximately 50% of

patients with PKD1 mutations with a mean age

of onset of 52 years, but in a minority of
patients with PKD2 mutations with a mean age
of onset of 69 years.
 Adult Polycystic kidney disease: Common
Clinical Features
Vague discomfort in loin or abdomen due to increasing mass of
renal tissue
Acute loin pain or renal colic due to haemorrhage into a cyst

C.Hypertension (Is one of the most common early manifestations of ADPKD)

Haematuria (with little or no proteinuria) usually is self-limited
Urinary tract infection
Renal failure usually in the fourth to sixth decade of life
Ø Affected subjects are usually asymptomatic

until later life.

Ø After the age of 20 there is often insidious

onset of hypertension.

Ø One or both kidneys may be palpable and the

surface may feel nodular. There is then a

gradual reduction in renal function.
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Ø About 30% of patients with PKD have
hepatic cysts, but disturbance of liver
function is rare. Sometimes (almost
always in women) this causes massive
and symptomatic hepatomegaly, usually
concurrent with renal enlargement, but
occasionally with only minor renal
involvement.

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Ø Berry aneurysms of cerebral vessels are an associated
feature, and about 8% of patients have a subarachnoid
haemorrhage. This feature appears to be largely
restricted to certain families (and presumably specific
mutations).
Ø Mitral and aortic regurgitation are frequent (25%)but
rarely severe.
Ø Colonic diverticula and abdominal wall hernias may
occur.
Ø ADPKD is not a pre-malignant condition. The rate of renal
malignancy is no different from that of other patients
with renal failure (but is higher than the general
population). there are some other

cyst that can progress

to co .
 Investigations and screening
Ø The diagnosis is usually based on family
history, clinical findings and ultrasound.
Ultrasound demonstrates cysts in ∼95% of
affected patients over the age of 20, but may
not detect small developing cysts in younger
patients.
Ø Computed tomography (CT) scan more
sensitive than ultrasonography.
 Investigations and screening
Ø Specific genetic diagnosis.
Ø Screening for intracranial aneurysms is not
generally indicated. Where non-invasive MR
angiography is available, some centres screen
patients in families with a history of
subarachnoid haemorrhage.→
only

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Ultrasonographic diagnostic criteria for ADPKD1
are as follows:
ØAt equal or more than 3 cysts unilateral or
bilateral younger than 40 years.
ØAt least 2 cysts in each kidney in an at-risk
patient aged 40-59 years
ØAt least 4 cysts in each kidney for an at-risk
patient aged 60 years or older
in admission to + we f- Hae

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 mainly
Treatment treat the
Cemlicnhwns

Ø High water intake exert protective effect. delay progression

Ø Hypertension control with a target blood pressure of
130/80 mmHg or less is recommended.
Ø Lipid-soluble antimicrobials such as trimethoprim-
sulfamethoxazole and fluoroquinolones that have
good cyst penetration are the preferred therapy for
infected kidney.
Ø Tolvaptan is selective vasopressin V-2 receptor
antagonist was approved in united state to slow the
kidney function deterioration. aw € per day

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n Surgical drainage for renal or hepatic cyst
indicated when cyst does not respond to
conventional therapy and usually done under
ultrasound guide.
n Those undergoing kidney transplantation
may require bilateral nephrectomy if the
kidneys are massively enlarged or have been
the site of infected cysts

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normal kidney
< wog

fuss kidney is 4.7

kg
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 OTHER CYSTIC DISEASES
Ø Medullary cystic diseases: Medullary sponge kidney
is characterised by cysts confined to papillary collecting
ducts. The disease is not inherited and its cause is
unknown.
Ø Patients usually present as adults with renal stones.
These are often recurrent, and preventive measures
need to be implemented if so, but the prognosis is
generally good. The diagnosis is made by ultrasound
or IVU. Contrast medium is seen to fill dilated or cystic
tubules, which are sometimes calcified.
Ø The childhood variants are characterised by
thirst and polyuria due to nephrogenic diabetes
insipidus, often with a family history of similar
disease. Sometimes affected patients are 'salt-
losing', which aggravates the degree of renal
failure. Even when they are treated
appropriately, serious renal failure is usual.
 Acquired cystic disease years
>

~
Ø Patients with a very long history of renal failure
(usually on long-term dialysis) often develop
multiple renal cysts in their shrunken kidneys.
Ø Kidneys are enlarged but not to the size of
kidneys in PKD. Acquired cystic disease is
associated with increased erythropoietin
production, and sometimes with the
development of renal cell carcinoma.
menignant
Acquired
.

are pre
cysts
-
Thanks
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