Download Document

URINARY SYSTEM
REVIEW
DR. PRASANNA N KUMAR
OMC
DISEASES OF THE KIDNEY
 Glomerular - glomerulonephritis
 Tubular
tubulo interstitial nephritis,
pyelonephritis
 Interstitium
 Vascular diseases – nephrosclerosis,
benign and malignant
 All forms of chronic renal disease
ultimately to destroy all four components
of the kidney - CRF and end-stage kidneys
RENAL DISEASES
CLINICAL MANIFESTATIONS
 Oliguria (< 500ml of urine/day), anuria (< 50 ml/day)
 Proteinuria (normal protein (Tamm-Horsfall
proteins) excretion in urine - < 150 mg/day)
 Selective proteinuria – clearance of low molecular
weight proteins - albumin.
 Non-selective proteinuria - clearance of high MW
proteins – albumin, globulins, IgG, IgM
 Hematuria – macroscopic/microscopic
 Edema
OTHER RENAL DISEASES
CLINICAL MANIFESTATIONS
 Renal tubular diseases
polyuria, nocturia, electrolyte disorders
 Urinary tract infection – kidney (pyelonephritis),
bladder (cystitis)
symptomatic/asymptomatic bacteriuria,
pyuria
 Nephrolithiasis (renal stones)
renal colic, hematuria
NEPHROTIC SYNDROME
 Proteinuria? – disruption of glomerular basement
membrane
 Hypoalbuminemia – due to proteinuria
 Edema – due to decreased plasma oncotic pressure
due to ?
 Hyperlipidemia and lipiduria – due to increased
lipoprotein synthesis
NEPHRITIC SYNDROME
 Oliguria and azotemia – renal inflammation
 Hypertension – decreased clearance of
sodium and water
 Hematuria – leakage of blood into Bowman’s
capsule
GLOMERULAR DISEASES
CLINICAL MANIFESTATIONS
Nephritic syndrome
Nephrotic syndrome
Mild to moderate proteinuria
Heavy proteinuria
Visible hematuria
Microscopic hematuria ±
Edema
Severe edema
Oliguria
Hyperlipidemia, lipiduria,
hypoalbuminemia
Hypertension, azotemia
Thrombosis
RENAL FAILURE
 Acute renal failure – rapid deterioration of renal
function - oliguria/anuria + azotemia
 Chronic renal failure - end result of all chronic renal
diseases. GFR < 20-25% of normal
edema, hyperkalemia
prolonged uremia, ↑BUN
anemia (?), chronic bone disease (?)
GIT bleeding
 End stage renal disease - GFR < 5% of normal, terminal
stage of uremia
UREMIA
SOME CLINICAL FEATURES
 Hematologic – anemia, bleeding tendency
 Cardiac – hypertension, CCF, pericarditis
 Respiratory- pulmonary edema
 GIT – nausea, vomiting, gastritis
 Neuromuscular – myopathy, neuropathy
 Dermatologic – pruritus
 Bone – secondary hyperparathyroidism,
hypocalcemia, hyperphosphatemia
 Fluid & electrolytes – edema, hyperkalemia
GLOMERULAR DISEASES
Primary Glomerulonephritis
 Diffuse proliferative
glomerulonephritis√
 Crescentic GN
 Membranous GN√
 Lipoid nephrosis (minimal
change disease)√
 Focal segmental
glomerulosclerosis
 Membranoproliferative GN
 IgA nephropathy
 Chronic GN√
GLOMERULAR DISEASES
Secondary (Systemic) Diseases
 Systemic lupus erythematosus √
 Diabetes mellitus √
 Amyloidosis
 Goodpasture syndrome √
 Polyarteritis nodosa
 Wegener granulomatosis
 Henoch-Schönlein purpura
 Bacterial endocarditis
GLOMERULAR INJURY
IMMUNE PATHOGENESIS
ANTIBODY MEDIATED INJURY
1. circulating immune complex deposition – major
etiologic factor – granular deposits by IF
2. antibodies against fixed glomerular antigens – linear
deposits by IF
3. antibodies against planted glomerular antigens –
granular deposits by IF microscopy
IMMUNOLOGICAL MECHANISMS OF
GLOMERULONEPHRITIS
Goodpasture
antigen
Antibody to
Goodpasture
antigen
2
1
3
EXOGENOUS ANTIGENS
eg: streptococci,
Hepatitis B,C, Plasmodium
falciparum,
ENDOGENOUS
ANTIGENS
eg: SLE
1. IC MEDIATED
GLOMERULAR
INJURY
Passive
entrapment of
IC in GBM
Leukocyte infiltration on glomeruli,
proliferation of mesangial & endothelial
cells
GLOMERULAR
INJURY
NEPHROTIC SYNDROME
 If the history of massive proteinuria is in a child
(< 15 years) – minimal change disease, lipoid
nephrosis, foot process disease)
 If the history of massive proteinuria is in an adult, -
often associated with a systemic disease – DM,
SLE, amyloidosis, primary - membranous GN
MINIMAL CHANGE DISEASE
Light Microscopy – nearly normal
 Cells of proximal convoluted
tubules laden with lipids- Lipoid
Nephrosis.
Electron Microscopy
 Uniform diffuse loss of foot processes
Clinical course - Children, usually 2-3yrs –
nephrotic syndrome post URI
 No hypertension, normal renal
function.
 Prognosis- Good, >90% respond to a
short course of corticosteroids
MEMBRANOUS GN
Chronic immune complex nephritis
 Secondary membranous GN - circulating immune
complexes – SLE, hepatits B, syphilis, drugs,
malignancy
 Idiopathic membranous GN - immune complexes
in situ
LM – diffuse capillary and basement membrane
thickening
IF – diffuse granular pattern (Ig & C’ deposits)
EM – subepithelial deposits – “spike & dome” pattern
Poor response to steroids
DIABETIC NEPHROPATHY
Associated with long standing diabetes
Diabetic kidney –

Glomerular syndromes – nephrotic syndrome,
chronic renal failure

Recurrent & chronic pyelonephritis

Papillary necrosis

Arteriolosclerosis
Non-nephrotic proteinuria, nephrotic syndrome,
chronic renal failure in 4-5 years
Kimmelstiel – Wilson lesion –
nodular glomerulosclerosis –
nodular accumulation of
mesangial matrix material
Diabetic glomerulosclerosis – nodular
lesions + capillary basement membrane
thickening
DIABETIC NEPHROPATHY
 Hyaline arteriosclerosis of afferent and efferent
arteriole.
 Pyelonephritis – acute or chronic inflammation of
the interstitial tissues and tubules.
 Necrotizing papillitis – acute necrosis of renal
papillae due to acombination of ischemic injury
and infection
SYSTEMIC LUPUS ERYTHEMATOSUS
 SLE – kidney involvement in 70% of cases, renal
lesion severity and prognosis, most important cause
of death in SLE
 Immune complex disease - deposition of DNA-anti-
DNA complexes within glomeruli – C’ activation –
complement mediated damage (leukocytes, cytokines
etc.)
 Necrosis of glomeruli in severe cases
SLE – RENAL LESIONS
Focal, proliferative GN
Diffuse, proliferative GN
“wire-loop” lesions
ACUTE POSTSTREPTOCOCCAL
GLOMERULONEPHRITIS
 Acute diffuse glomerulonephritis, postinfectious GN
 Streptococci – group A β-hemolytic (most common)
– nephritogenic strain – infection of the pharynx or
skin – 1- 4 weeks later (?) - fever, oliguria, hematuria
(smoky urine) hypertension (nephritic syndrome)
 Recovery in 95% of children (with conservative
treatment), <1% - develop rapidly progressive GN or
chronic GN
CLINICAL COURSE
 Recovery in 95% of
children
 <1% - develop rapidly
progressive GN or
chronic GN
RBCs in
urine
RBC casts in urine
RAPIDLY PROGRESSIVE GN
(RPGN, CRESCENTIC GN)
 Manifestation of severe glomerular injury with
crescents that compress the glomeruli
 Etiology – Idiopathic (50%), post-streptococcal
(post infectious GN),SLE, Goodpasture syndrome
 Morphology – crescents
 Clinical – rapid deterioration,
with loss of renal function
Crescent-shaped mass of
proliferating parietal cells &
monocytes in the
Bowman’s space
CHRONIC GN
MORPHOLOGY
 GROSS – symmetrically contracted kidneys, finely
granular subcapsular surface
 MIC. – Glomeruli – hyalinized
Remainder of nephron - ischemic atrophy of
(lack of blood flow in glomerulus)
Interstitium - chronic inflammatory cells &
fibrosis, tubules - atrophy
Blood vessels - thickening of walls (chronic
ischemia - ↑ blood pressure)
 Patient with dysuria, WBCs (pus cells) in
urine and WBC casts – where is the
infection?
ACUTE PYELONEPHRITIS
Ascending infection
 During urethral instrumentation
catheterization and cystoscopy
 Urinary tract obstruction – stasis –
infection
 vesicouretral reflux in children
 prostatic hypertrophy
 uterine prolapse
Hematogenous - septicemia,
emboli from bacterial endocarditis
ACUTE PN
 One or both kidneys
involved.
 Gross - discrete yellow
raised abscesses on the
surface.
 Micro- suppurative
necrosis with abscess
formation, pus cell casts
in the urine.
 Necrotizing papillitis or
papillary necrosis in
diabetes
Neutrophils in tubules
& interstitium
ACUTE PN
CLINICAL/LAB FEATURES
 Fever, chills, costovertebral angle pain
 Urinalysis – pyuria, pus cells (may be present in upper
& lower UTI), pus cell casts (WBC casts, only in upper
UTI), bacteriuria
 Self-limiting infection, if recurrent - progress to chronic
PN
PUS CELL
CAST
PUS CELLS
ACUTE RENAL FAILURE CAUSES
 ATN – commonest cause of ARF – due to renal
ischemia – eg: due to hypotension, shock
 Patient presents with oliguria, azotemia,
hyperkalemia
 RPGN
 Acute papillary necrosis
 Drug induced interstitial nephritis – penicillin
derivatives, NSAIDs
CHRONIC PN
MICROSCOPY
 Interstitium – chronic
inflammation
 Tubules - atrophy,
dilatation and
“thyroidization”
 Blood vessels –
arteriosclerosis
 Glomeruli –
periglomerular fibrosis
Thyroidization
DISEASES OF THE BLOOD VESSELS
Benign nephrosclerosis

Renal changes in benign
hypertension.

Kidneys are atrophic with fine
granularity and
microscopically shows hyaline
arteriosclerosis
Malignant Nephrosclerosis

Malignant hypertension-

Fibrinoid necrosis of arterioles
hyperplastic arteriosclerosis.

Grossly- “flea bitten
kidney”
GRANULAR CONTRACTED
KIDNEYS
Chronic glomerulonephritis
Gross - small symmetrically atrophic
with fine granularity
Micro – Hyalinized glomeruli,
secondary tubulointerstitial and
vascular changes
Chronic pyelonephritis
Gross- asymmetric contraction with
coarse scarring
Mic.- interstitial chronic inflammation
fibrosis, secondary vascular and
glomerular involvement
Gross- small symmetrically atrophic
with fine granularity
Benign nephrosclerosis
Mic.- hyaline arteriolosclerosis,
secondary ischemic atrophy of
other structures
CYSTIC DISEASES OF THE KIDNEY
INHERITANCE
Adult polycystic
kidney disease
PATHOLOGICAL FEATURE
Autosomal
Large multicystic kidneys
dominant
liver cysts, berry aneurysms
CLINICAL FEATURE
AND OUTCOME
hematuria, pain,
CRF at 40-60
hypertension
Childhood
polycystic
kidney disease
Simple cysts
Autosomal
recessive
none
Enlarged cystic kidneys
at birth
single or multiple cysts
in normal sized kidneys
renal failure and death in infancy
hepatic fibrosis if child survives
usually asymptomatic
Autosomal dominant adult polycystic kidney Autosomal recessive
childhood polycystic kidney
Liver cysts in ADPKD
RENAL STONES
 Calcium oxalate stones
 Struvite stones – triple phosphate
stones (Mg, NH3 Ca PO4 ) staghorn
calculi - UTI
 Uric acid stones - gout, radiolucent
 Cystine stones
 Urine obstruction, colicky
pain, hematuria, infection,
squamous metaplasia in renal
pelvis – squamous cell ca.
Stag
horn
calculus
OBSTUCTIVE UROPATHY
HYDRONEPHOSIS –
atrophy of kidneys
RENAL CELL CARCINOMA
 Adenocarcinoma of the Kidney, Clear cell




carcinoma, hypernephroma
Tobacco - most significant risk factor –
cigarettes, pipes and cigars
70-80% of RCC – clear cell carcinoma
Grows into renal vein – IVC – right atrium
Mass, hematuria, weight loss, polycythemia,
Cushing syndrome, hypercalcemia
RENAL CELL CARCINOMA
Yellow C/S, hemorrhage, necrosis
Cells with clear or
granular cytoplasm with
glycogen or lipid
RENAL CELL CARCINOMA
CLINICAL
 Paraneoplastic syndromes - polycythemia,
hypercalcemia, hypertension, Cushing
syndrome, leukemoid reaction
METHODS OF SPREAD:
 Local, hematogenous, lymphatic
CYSTITIS
 ETIOLOGY – patient’s fecal flora, Proteus, Klebsiella,
candida (prolonged antibiotics),TB (secondary to
renal TB), Schistosomiasis (Egypt)
 PREDISPOSING FACTORS
instrumentation
bladder calculi
diabetes mellitus, immune deficiency
radiation (radiation cystitis)
cyclophosphamide (hemorrhagic cystitis)
TUMORS OF URINARY BLADDER
 Benign papillomas – 1-2 cm frond like structures
with fibrovascular cores covered by transitional
epithelium – usually solitary lesions which rarely
recur
 Transitional cell carcinoma
 Squamous cell ca – 5% of bladder carcinomas –
calculi, Schistosomiasis
 Adenocarcinoma – rare - urachul remnants
URINARY BLADDER CA
 Cigarette smoking, radiation






naphthylamines (industry),
analgesics, cyclophosphamide
S. hematobium – inflammation,
squamous metaplasia,
dysplasia, carcinoma (SCC)
Benign papillomas, TCC
Squamous cell ca – 5%
Adenocarcinomas – rare
TCC - M>F, 50-80 years
Painless hematuria, dysplastic
cells in urine