Urinary System and Male Genital

Fajar L. Gultom
Departemen Patologi Anatomik FK UKI
December 2017
“What is a human but an ingenious
machine designed to turn, with finite
artfulness, the red wine of Shiraz into
urine?”
Isak Dinesen
• Convert >1700 L blood per day  1 L
concentrated fluid  ….?
• Excretes waste products of metabolism (H20,
Na, Ca, PO4, anion, cation, acid balance)
• Endocrine organ: erythropoietin, renin,
prostaglandin, regulating vit D
Afferent arteriole – vascular pole, distal convoluted tubule
 Kidney
Four (4) basic morphologic:
1. Glomeruli
2. Tubules
3. Interstitium
4. Blood vessels
 Clinical Manifestation Renal Disease
• Azotemia  BUN and creatinine ↑
Acute and chronic kidney injury
PreRenal - PostRenal
• Nephritic syndrome
Hematuria (gross/ microscopic), GFR ,
proteinuria, hypertension.
Acute poststreptococcal GN.
• Nephrotic syndrome
Proteinuria ↑↑, hypoalbuminemia, severe
edema, hyperlipidemia, lipiduria
 Clinical Manifestation Renal Disease
• Asymptomatic hematuria/ proteinuria
• Acute kidney injury
Rapid decline GFR  oliguria – anuria
• Chronic kidney disease (previously CRF)
GFR , < 60 mL/minute/1,73 m2 for 3 months
• End Stage Renal Disease (ESRD)
GFR < 5%  terminal stage
 Clinical Manifestation Renal Disease
• Renal tubular defects
Polyuria, nocturia, electrolyte disorder
• Urinary tract obstruction – renal tumor
UTI – bacteriuria/ pyuria
Pyelonephritis, Cystitis
• Nephrolithiasis
Renal colic, hematuria
Glomeruli
 Glomeruli
• Anastomosing network of capillaries lined by
fenestrated endothelium invested by two layers
of epithelial cells.
• Fenestra Ø 70-100 nm.
• Glomerular basement membrane (GBM).
• Visceral epithel cell (podocytes).
• Mesangial cells.
• Normal: highly permeable to water and small
solutes, impermeable protein size of albumin
 Glomerulonephritis
• Nefritis dengan peradangan lengkung kapiler
dalam glomerulus ginjal (Dorland ed 29,
2015).
• Inflammation of the glomeruli/ of the small
blood vessels (Wikipedia).
 Glomerulonephritis
• Acute: bentuk akut yang ditandai proteinuria,
edema, hematuria, gagal ginjal dan hipertensi,
terkadang didahului oleh tonsillitis dan
faringitis.
• Chronic: GN yang berkembang dengan lambat
umumnya menyebabkan gagal ginjal
ireversibel.
 Pathologic Manifestations
• Cellular proliferation (hypercellularity)
– Mesangial
– Endothelial
• Leucocyte infiltration (neutrophil, lymphocyte)
• Crescents (RAPIDLY progressive): glomerular
epithelial cell
• Basement membrane thickening
• Hyalinization and sclerosis
 Acute glomerulonephritis
• Hematuria, Azotemia, Oliguria, in children
following a strep infection
• Hypercellular glomeruli
• Increased endothel and mesangial
• IgG, IgM, (not IgA), C3 along GMB focally
• 95% full recovery
 Rapidly Progressive
Glomerulonephritis
• Clinical definition, NOT a
specific pathologic one

•“Crescentic”
• Anti-GBM Ab
 Nephrotic Syndrome
• Podocyte injury  Massive
proteinuria
• Hypoalbuminemia
• Edema
• Lipidemia/Lipiduria
• Numerous causes:
– Membranous, Minimal change, Focal Segmental
– Diabetes, Amyloid, SLE, Drugs
 MINIMAL CHANGE GLOM.
• Most common cause of Nephrotic Syndrome
in children
• Effacement of foot processes
• Dramatic response to corticosteroid
 Chronic Glomerulonephritis
• Result from ANY of the previously
described
–THIN CORTEX
–HYALINIZED (fibrotic) GLOMERULI
–OFTEN SEEN IN DIALYSIS PATIENTS
Chronic Glomerulonephritis
 Tubular Diseases
• Acute Tubular Injury/ Necrosis (ATI/ ATN)
• Tubulointerstitial Nephritis
– Pyelonephritis
• Acute
• Chronic
– Drugs
– Toxins
• Urate nephropathy
• Hypercalcemia/nephrocalcinosis
• Multiple myeloma
 Acute Tubular Injury/ Necrosis
(ATI/ ATN)
• Destruction of renal TUBULAR epithelium
• Loss of renal function
• 50% of ACUTE renal failure – reversible
process
• Two types: Ischemic, Nephrotoxic
-AMINOGLYCOSIDES
-AMPHOTERICIN B
-CONTRAST AGENTS
NORMAL
ATN
ATI Pathogenesis
 Pyelonephritis - UTI
• Inflammation: tubulus, interstitium and pelvis
• Acute-chronic pyelonephritis  bacterial
infection
• Ascending or hematogenous route
• 85% gram negative bacil normal intestinal tr
Pathogenesis
Pathogenesis
Acute VS Chronic
Acute VS Chronic
 Pyelonephritis - UTI
• Obstruction: Congenital or Acquired
• Instrumentation
• Vesicoureteral Reflux
• Pregnancy
• Age, Sex, why sex? F>>>M
• Previous lesions
• Immunosuppresion or Immunodeficiency
 Obstructions
• Urolitihiasis
• Congenital
• Prostate enlargement
• Tumors
• Inflammation
• Sloughed clots, papillae
• Pregnancy
• Neurogenic
 Urolithiasis
• Calcium (70%)
Hypercalcemia - hypercalciuria
• Magnesium (15%)
• Uric acid (5-10%)
• cystine
 Tumors
• Benign
Renal papillary adenoma, oncocytoma,
angiomyolipoma
• Malignant
RCC (clear cell)
 Renal Cell Carcinoma (RCC)
• Tobacco related, STRONGLY
• Some hereditary/familial – sporadic
• Most are “CLEAR CELL” - few PAPILLARY
• YELLOW gross - “CLEAR” cells microscopic
Macros – Micros
 Male Genital
• Phimosis – paraphimosis
• Torsio testis
• Rupture urethra
 BPH
• Men > 50 yrs (50%)
• Urinary obstruction – LUTS
• Hesitancy, intermitten interruption, urgency,
frequency, nocturia - UTI
• Central zone diff with Prostate Ca
 BPH
• Androgen dependent growth – castrated before
puberty ≠ BPH
• Testosterone  DHT – proliferation stromal n
epithelial
• Proliferation epithelial and stromal – compress
urethra
• Th/ - inhibit DHT formation (≠ enzyme 5 R1, 2)
-  blocker
BPH

Robbins basic pathology 9th ed, 2013

Netter’s Illustrated human pathology. 2014
 BPH

BPH VS normal ??
 BPH

Prostate normal – gland – fibromuscular stroma – Prostate hyperplasia

corpora amylacea
PCa

Robbins basic pathology 9th ed, 2013