10 Renal tuberculosis. Contrast-induced nephropathy Flashcards Preview

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what is Latent tuberculosis infection ?

viable Mycobacterium tuberculosis (MTB) bacilli are present in an individual but symptoms and signs of active disease are lacking, and the bacilli are relatively inactive metabolically

Latent period may vary from 10 to 40 years after initial Pulmonary TB


Predisposing factors for TB?


AIDS(Immunosuppressed patients)

Increased number of transplantation


drug addiction



TB is caused by mainly which 2 bacteria?

Mycobacterium tuberculosis
TB is aerobic . The disease primary way of spreading is by air and secondary- hematogenic.

Mycobacterium bovis


what are the stages in urogenital tuberculosis?

Begins with lesions around glomeruli (in cortex),
but yet without clinical manifestation.

Initial symptoms: when pyelocaliceal system is involved with development of caseous necrosis

lesions follow in direction of the urinary flow
Ureter involvement (10%); b) Urinary bladder; c) prostate; d) urethra – very rarel


clinical finding of renal tuberculosis ?

After widespread use of tuberculostatics the clinical findings have changed and course of the diseases has become significantly milder

fever, including and low grade and malaise. Patients with UG TB have healthy or normal appearance.

Usually caused by blood clots, devitalized tissue, secondary stones.


Hematuria (40%) – mostly intermittent and macroscopic
(dd with Nephrolithiasis and tumors of the urinary tract )


Hypertension (22%) – early symptom

Terminal Chronic Kidney Diseases and hemodalysis – very rarely if both kidneys are damaged


what is the diagnosis of renal tuberculosis?

Macroscopic :
urine analysis
pyuria - but sterile

Proteinuria(77%) low level below 1 gram per L


ESR (Erythrocyte Sedimentation Rate) (44%) – highly positive

Microbiologic diagnosis : only found in 30-60 percent
Guinea-pig inoculation for tuberculosis test with a blood of a patient

Urine sample (by Loevenstein)

X-ray of the abdomen: calcification of lymph nodes and skeleton changes

USD (ultrasound): hypo-echogenic zones (cavities and fibrosis) – differs from stone in the urinary bladder; thickened and firm urinary bladder wall.

Contrast imaging of the urinary tract:

Retrograde contrast imaging of the urinary tract (after cystoscopy).

antegrade urography

- shortened, narrow, amputated calices;

- rough and uneven renal papilla;

- single and merging caverns;

- ureter–narrowed, dilated, similar to a chaplet;

- rigid (firm) urinary bladder; microcystis.

• а) Mantoux Test – very rarely used nowadays (false negative = weak immune response)


Isotope diagnosis
а) radioisotope renography – asymetry;

Morphologic diagnosis:
Cystoscopy with consecutive forceps biopsy of urinary bladder

1) In cortex – yellow-whitish foci

2) Penetration towards medulla:
towards papilla, calices, pyelon, ureter strictures

3)Formation of caverns followed by consecutive fusion between them etc. “putty kidney”

microscopic picture

destruction or fibrosis of the caverns

renal parenchyma displaced by caseous tissue or fibrosis

Urinary bladder: multiple tubercula (nodules) around the 2 ureteral openings.


what is the treatment for urogenital tuberculosis

regular sanitation

well balanced nutrition

tuberculostatic therapy

Duration of therapy – 9 -12-24 months.

Streptomycin (SM) – 1gr per 24 hours
Rimicid – 10 mg per kg per 24 hours
Ethambutol – 15 gr per kg per 24 hours
• Side effects: hepatotoxic, nephrotoxic.


When fibrosis is more than 70% of parenchyma - hemodialysis
Surgical treatment

indications :
non-functioning kidney

partially functioning kidney with persisting pain and hematuria, marked hypertension, secondary uro- infection and persisting bacteriuria

The most frequent indication for urinary bladder surgery is tuberculotic shrinking of the bladder or microcystis (small urinary bladder

Operative procedures over urinary bladder:

Partial resection of urinary bladder.

Hydraulic enlarging of urinary bladder using the technique ”drop by drop”.

Intestinal plastics and creation of neocystis made of large bowel or most often small bowel

Follow up of TB patients

1 year of observation after a successful conservative treatment course.

All patient should have USD (ultrasound), radioisotope, contrast imaging and bacteriological test every 3 months for 1 year after successful conservative treatment

All memebers of the family should take Rimicid – 3х1 tabl. for 3 months.

Carsil, Essentialе, Legalon, Vitamin C u K


what is the definition of CIN?

sudden deterioration in renal function within 48 to 72 hours of contrast exposure
in these 72 hours

increase of the Serum Creatinine 44 mmol/l or with more than 25% above the starting value in lack of other etiological reasons.


major complication of CIN?

Significantly increased mortality in a development of CIN after previous angioplasty as a treatment of acute myocardial infarction


Risk factors for development of CIN

Presence of Kidney failure!! / renal insufficiency

 Diabetes mellitus(diabetic nephropathy)!!

 Congestive heart failure

 Dehydratation

 Arterial hypertension

 Age above 70 years

 Use of nephrotoxic medicine

HIGH osmolality of contrast media


what is the pathopshyiology of contrast induced nephropathy ?

1) the contrast media causes vasoconstriction - by increasing adenosine , endothelia and prostaglandin E2
and reducing nitrous oxides and prostaglandin e1

= this leads to medullary ischemia

2) the osmotic load of the contrast media
increase renal tubular viscosity ,

CSs are filtrated through the glomeruli and are not reabsorbed by the tubules

Hydrostatic pressure in the tubules is increased and the Ultrafiltration pressure in the glomeruli is decreased

RAAS is activated with vasoconstriction followed on vasa afferentia, which leads to low glomerular filtration


the osmotic loading distal tubules causes increased oxygen consumption

3) direct cellular toxicity - vacuolisation , necrosis and apoptosis in PCT = osmotic nephrosis

4) increase secretion of THP protein
tamm horsfall protein = tubular obstruction

5) increase in free radicals due to medullary ischemia causing endothelial dysfunction


what re the types of rdiocontrast agents ?

with high osmolality

low - ixoglate

iso osmolality
- iodixanol

decreased incidence of contrast nephropathy are with nonionic agents with low osmolality or iso osmolality


what are the symptoms of contrast induced nephropathy ?

non oliguria acute k i

feeling tired

sweelling in feet and ankles, puffiness around h eyes



what is the diagnosis of CIN ?

no standard criteria for it

diagnosis of AKI is made :
absolute serum creation is or above 0.3mg/dl

a percentage of increase of serum creatinin of or above 50 percent

urine output reduced to or below 0.5ml/kg/hr for atleast 6hrs


prevention of cin is one of the key managements how does this come about ?

hydration of the patient
- patents with gfr less than 30ml /min with high risk can do a renal guard system - isotonic saline +nac + limited furosemide

dopamine and fenoldopam

adenosine antagonist

n - acetyle cysteine = reduction in oxidative stress

diuretics/ acei stopped 24 hrs before and after
- furosemide and mannitol give a solid increase in risk of CIN

hemodilayisis and hemofiltration

choice of contrast

metformin - should be stopped

alternative to iodinated contrast = gadolinium for CAG


how do we do hydration in prevention of CIN ?

isotonic saline begins 4 hours before the procedure and continues for 24 hours after contrast application

dosage of 100ml/hr

this reduces raas
increase diuresis
dilute the contrast and decrease the vasoconstriction based on it


how does dopamine and fenoldopam prevent CIN ?

systemic renal vasodilation
= increase in renal blood flow to medulla and cortex

increase GFR

however dopamine increase the risk of sin in diabetic patients !

(they both faced to show renal protection in cin)


when is adenosine antagonist recommended in cin ?

lack of data for its prtetive role
but we give theophylline when hydration of patient is impossible such as heart failure


how is hemodialysisi and hemofiltration carted out for prevention of sin ?

hemofiltration 4-76 hours before and 18-24 hurts after contrast is introduced reduce the risk of CIN IN HEART DISEASE PATIENTS


elimination of contrast is available in 2 hours for normal kidney function
and 30 hours in css


how does choose of contrast act as prevention to cin ?

avoid high osmolarity contrast substances

important of the volume of it aswell