Flashcards in 10 Renal tuberculosis. Contrast-induced nephropathy Deck (20)
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?
Increased number of transplantation
PAATIENT WITH CKD AND ON HEMODIALYSIS - morbidity higher aswell
TB is caused by mainly which 2 bacteria?
TB is aerobic . The disease primary way of spreading is by air and secondary- hematogenic.
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.
Pain - dull to moderate NO IRRADTIAN UNLIKE RENAL COLIC
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?
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).
- 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)
а) radioisotope renography – asymetry;
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”
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
well balanced nutrition
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
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
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
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
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
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
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
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
PROPHYLATCI HEMODILAYSIS FOES NOT REDUCETHE RSK OF cin in chronic renal failure
elimination of contrast is available in 2 hours for normal kidney function
and 30 hours in css