Tuberculosis Of Urinary Tract

9% of extrapulmonary TB is caused by glanderourinary TB.
Not just kidney involvement, but also signs of epididymitis, prostatitis, segmental vesiculitis, and orchitis will be present in 70 to 80 percent of males.  There will also be genital involvement.

Pathogenesis

First, there will be a primary complex, or Ghon focus, formation.
Observed with a first infection. It may be inactive or active. Following activation, it spreads hematogenously and enters the kidney. Following that, it becomes lodged in the capillaries and glomerulus. The main infection is this one. In this case, it starts out latent and can activate at any time. The capillaries' cortical granuloma becomes active. Following that, it multiplies, bursts, and overflows into the tubules. It slowly makes its way into the medulla after entering the proximal tubule first.  It finds the right habitat to multiply in the medulla. 

This means that medullary osmolality, decreased blood flow, increased ammonia, and decreased immunity must all be maintained. Because of all these factors, it is a very likely environment for germs to grow.
It bursts in the collecting system. It multiplies in the medulla. Leads to bacilluria. Ulcers may also develop from it.
It also enters the bloodstream and travels to the kidneys via the thoracic duct. The medulla has elevated ammonia, poor blood flow, and hypertonicity. As a result of all of these, the medulla has a high TB bacteria proliferation. The most often involved region is the medial lemna. It is typically unilateral.

• Mesenchymal granulomas experience caseous necrosis.
• Ruptures that result in ulcers and cavities.
• Have necrosis of the papillaries
• Fibrosis and scarring are possible outcomes of chronic inflammation.
• Creates scars and structures.
• Dystrophic calcification: conceals bacterial slumber.
• Putty kidney or cement kidney are terms used to describe dystrophic calcification of the kidney.
• Bladder: Anemia close to the opening.
• Results in granulomatous alterations in all layers and superficial ulcers.
• Pan Cystitis.
• Fibrosis-induced healing at the ureteral orifice
• The golf hole ureter refluxing.
• The wall of the bladder fibrosis
• Small-capacity, thick bladder
• Belly button bladder

Also Read: Alport Syndrome and Familial Glomerular Disorders

Clinical Features

 Visible in the 20–40 age range,  2:1 male to female, 5–15 years since the initial infection, seldom in young people.

Proteinuria And Nephrotic Syndrome

Prolonged tubular proteinuria. Presents with glomerular involvement; May exhibit secondary amyloid or mesangio growth.

Low GFR

Diffuse interstitial nephritis, Granulomatous interstitial nephritis

Pain

Obstruction- Colicky pain. It may be a stone, blood clot, sloughed papilla

Cystitis- Dysuria, suprapubic pain, Involvement of bladder.

Stone Formation

Found in 7–18%.  Stone formation is frequent as a result of blockage; E. coli is the cause of secondary infection.  Urinary stasis, hydronephritis, and hydroureter will all occur.

Genital Involvement

Most prevalent in men, or 75%  Just 5% of females experience it; epididymitis is the most prevalent; a cold abscess can burst; and it can result in a posterior scrotal sinus that never heals. Vascular thickening; Beaded texture; Prostate appears firm and slick; Possibility of sexual transmission. Women: 5%  Causes infertility and subsequent amenorrhea.

Other Manifestations

Renin release;  Hypertension;  Anemia;  Segmental ischemia; Nephrogenic diabetic insipidus or renal tubular acidosis.

Pathology

Based on the fundamental circumstance  TB distribution in the miliary or ulcer cavernous cavity; miliary form; cortex dotted with firm, yellowish-white, pinhead-sized nodules. Cavernous ulcers; Surface yellow nodules;  Granulomas or ulcers in the medulla or renal pyramid.
Thimble bladder; contracted; low capacity; enlarged kidneys; indicates amyloidosis. Hydronephrosis and pyonephrosis.

Diagnosis And Differential Diagnosis

50% sterile pyuria. Cultures of urine for common bacteria are -ve
The presence of pus cells suggests a urinary infection.  rine culture-based M tuberculosis isolation Similar to how we collect sputum samples in the morning, we collect fully voided pee samples in the morning to increase the likelihood of catching the organism. 

 In a span of three to five days. Insert Standard Culture 1 into Middlebrook and LJ medium. 

 AFB stain of urine is non-specific; Growth occurs within 6–12 weeks; Caused by M. smegmatis;  Appears regularly as a commensal in the urine.

Diagnosis

Renal calcification; thick, wavy, puffy, cloud-like; X-ray of the abdomen; ELISPOT/IGRA test; LAM assay in urine. The symptoms include an excretory urogram, erosion of the calyces' tip, incomplete filling, distortion, infundibular stenosis, hydroropterephrosis, hydroureter, hiked-up pelvis/Kerr kink sign, and obliteration and distortion of the renal pelvis, which was initially hiked up.

The most sensitive way to detect parenchymal thinning and scarring is CT. Global or focal cortical thinning can be seen with ultrasonography. The ureter located in the golf hole can be identified. Pus, a white substance that resembles toothpaste, is ejected.

Treatment

• ATT reaches the kidney and urinary tract (amenable to treatment)
• Irritative bladder symptoms - Streptomycin
• When the fibrosis starts, the bladder capacity will decrease, leading to worsening irritative symptoms.
• Treatment- Healing by fibrosis, Obstruction of ureter, Causes Hydronephrosis
• Allergic interstitial nephritis- Rifampicin, Intermittent administration

Renal modification is required for ethambutol. Bile is the excretory organ during rest.  Usually, 75% dose modification is carried out if GFR is less than 50. 

Modifications are also necessary for streptomycin.
• Because it has the potential to become autotoxic when its level is raised.
• Not a medicine taken frequently.
• Peripheral neuropathy may result with isoniazid.
• Supplementation with pyridoxine is provided.
• Pyrazinamide dosages for dialysis patients might be lowered by 50%.
• Ethambutol is administered on different days.

Surgical Treatment

• Ureteral stricture
  • Stent
• Reconstructive surgery
  • Excessive fibrosis of pelvis, ureter, and bladder.
  • Pyeloplasty, ureterostomy, bladder augmentation
• Ablative surgery
  • Removal of the kidney.
  • Uncontrollable pain
  • Bleeding
  • Hypotension
  • Putty Kidney

Special Situations

Pregnancy

Because of the fetus's ototoxicity, streptomycin is prohibited; ethambutol can be administered; medication can be continued during nursing; the baby should receive isoniazid and BCG as prophylaxis; and rifampicin is administered if the women are placed on oral contraceptives.
Because it is an enzyme inducer, it can lessen the effects of rifampicin and should not be taken.

Patients with Liver Disease

Because of the fetus's ototoxicity, streptomycin is prohibited; ethambutol can be administered; medication can be continued during nursing; the baby should receive isoniazid and BCG as prophylaxis; and rifampicin is administered if the women are placed on oral contraceptives.
Because it is an enzyme inducer, it can lessen the effects of rifampicin and should not be taken.

Patient with Chronic Kidney Disease

H, R, Z - Biliary route, Normal range

Streptomycin and ethambutol- Dose modification. Streptomycin

Every 48 to 72 hours. Ethambutol- 36 to 48 hours, Has to undergo renal modification.

Renal Transplantation

HE - 18 months + pyrazinamide for 3 months + ofloxacin 200 mg daily for first 9 months . Rifampicin is an enzyme inducer; it causes cytochrome, which breaks down tacrolimus or cyclosporine.  There is severe rejection.  Avoid using rifampicin—CNI  We start a HZE regimen with ofloxacin for three months, followed by HE+ O for nine months, then HE for eighteen months.  Patients who are not CNIs: Double the prednisolone maintenance dose.

Monitoring

Treatment of completion; two months of chemotherapy; urine culture; and three successive monitoring samples. If scanning; Calculation; Urinary culture every year. In cases of dystrophic calcification, the organism may not actively grow.

The kidney's medulla contains the tubercle bacilli. The most prevalent side effect is caused by decreased blood flow, hyperammonia, and high osmolality. Thimble bladder, low-capacity bladder, golf-hole ureter, fibrosis of all bladder layers, and refluxing ureter seen following ureteral opening hyperemia in tuberculosis. Pulling up, destroyed, dysmorphic; elevated pelvis/Kerr kink sign. Cement or putty kidneys; dystrophic calcification. Males only. MC symptoms of genital TB. Epididymitis. Significance of urine AFB staining. Non-specific. Possibility of Mycobacterium smegmatis. False positive reaction.

Hope you found this blog helpful for your NEET SS Nephrology Preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.