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GOUTY NEPHROPATHY Incidence GOUTY NEPHROPATHY Incidence

GOUTY NEPHROPATHY Incidence - PowerPoint Presentation

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Uploaded On 2022-08-03

GOUTY NEPHROPATHY Incidence - PPT Presentation

Pathology Of Gouty Nephropathy Uric acid crystals and urates are deposited in the kidney This leads to irritation and acute inflammationmore time more deposition This deposits act as ID: 933749

gouty nephropathy acid uric nephropathy gouty uric acid acute chronic renal hyperuricemia treatment drugs kidney cell reaction failure gout

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Presentation Transcript

Slide1

GOUTY NEPHROPATHY

Slide2

Incidence

Slide3

Slide4

Pathology Of Gouty Nephropathy

Uric acid crystals and

urates

are deposited in the kidney.

This leads to irritation and acute

inflammation,more

time, more deposition.

This deposits act as

forgein

body granulomatous reaction ( macrophages,

lymphocytes,fibrpblasts

) forming white chalky nodules which is the ‘

TOPHUS’

Slide5

Slide6

Slide7

Signs and symptoms

The chief sign is : Decrease production of the urine.

In a blood test : Rise in the creatinine level.

In a urine sample : Uric acid/creatinine Ratio > 1

Slide8

TYPES OF GOUTY NEPHROPATHY

Slide9

Acute gouty nephropathy

Overproduction of uric acid occurs primarily when tissue breakdown is accelerated.

Acute uric acid nephropathy is the term applied to the development of acute

oligoanuric

renal failure caused by renal tubular obstruction by

urate

and uric acid crystals. This is observed almost exclusively in the setting of malignancy, especially leukemia and lymphoma, in which rapid cell turnover or cell

lysis

occurs from chemotherapeutic agents or radiation therapy

Slide10

Chronic Gouty Nephropathy

A widely accepted belief is that the overproduction of uric acid and the presence of

hyperuricemia

can cause acute kidney failure; however, whether chronic

hyperuricemia

independently results in chronic interstitial nephritis and progressive kidney failure is less clear.

In patients with chronic

hyperuricemia

and gout, early studies revealed

microtophi

formation in the renal medullary

interstitium

. These deposits were found to contain monosodium

urate

monohydrate and to be surrounded by a giant cell reaction. Thus, the theory was that

urate

deposition triggers a foreign body reaction and leads to chronic inflammation and fibrosis

.

Slide11

Cases associated With gout

During

treatement

for

leukaemia

or lymphoma.

Other malignancies, such as metastatic breast cancer, lung cancer, or disseminated adenocarcinoma.

Seizures and pregnancy-related pre-

eclampsia

or

eclampsia

may also have an association with gouty nephropathy.

Moreover renal transplantation or longstanding use of a medication by the name of cyclosporine may also lead to gouty nephropathy.

Slide12

General measures

Serum uric acid concentrations may be reduced with non-pharmacologic therapy :

Useful dietary and lifestyle changes include:

Weight reduction

Decrease alcohol ingestion

Decrease consumption of foods with a high purine content

Control of hyperlipidemia and hypertension.

However, these measures will probably not reduce serum uric acid levels to normal, which is the treatment goal for the prevention of acute gout attacks.

Symptomatic

hyperuricemia

usually requires medication.

Slide13

Treatment of acute gouty nephropathy

Cholchicine

and

demicholine

( specific anti-inflammatory drugs)

NSAIDS as

indomethacine

(in patients who cannot tolerate colchicine )

Glucocorticoids and ACTH (If NSAIDS are ineffective)

Slide14

Slide15

Slide16

Slide17

Treatment of chronic gouty nephropathy (prophylactic treatment)

Uricosuric

drugs

:

probenicid

,

sulphinpyrazone,benzbromarone

, aspirin

Uricostatic

drugs

:

allopurinol,Fuboxostat

Slide18

Thank YoU