Tubular N Renal Flashcards
1- TUBULOINTERSTITIAL
DISEASE (TID)
Have 2 types : - Infection : Pyelonephritis- Toxic TID / Ischemic TID
: Acute tubular necrosis (ATN)
PYELONEPHRITIS
• Definition:
1.Kidney inflammation mostly due to bacterial infection
2.Acute and Chronic pyelonephritis
3.More common in Female than in Male
• Etiology:
1.Urinary obstruction: congenital or acquired
2. Instrumentation of urinary tract
3.Vesicoureteral reflux
4.Pregnancy: 4-6% develops bacteriuria
5.Gender and age
6.Preexisting renal lesions : eg Kidney stones
7.Diabetes mellitus, immunosuppression & immunodeficiency
Vesicoureteral reflux
Definition:
1.BACKWARD FLOW of urine from
bladder to kidney
2.Lead to pyelonephritis and
hydronephrosis
• Etiology:
1. Due to failure of vesicoureteral valve
– Primary : Congenital
– Secondary : increase bladder
pressure such as in infection
causing obstruction of urinary
flow.
2. Early stage : asymptomatic
3. Symptomatic when patient start to
have UTI , fever, dysuria, frequent
urination but a small amount of
urine.
Pyelonephritis
1.Acute:
a) usually suppurative / presence of exudate (pus)
b) ascending infection through vesicoureteral reflux
c) Or hematogenous dissemination (rare)
2.Chronic:
a) inflammation with prominent scarring
b) recurrent infection
Clinical Features: fever, dysuria, white cell cast , bacteria in urine
culture
MAJOR COMPLICATION OF
PYELONEPHRITIS
1. Pyonephrosis (pus accumulation around the
kidney)
2. Urosepsis (a systemic inflammatory
response of the body to infection: sepsis due
to untreated UTI). Can lead to SHOCK
3. Kidney failure.
4. Death.
Acute tubular necrosis (ATN)
• Commonest causeofacute renal failure
• Tubular epithelial cells necrosis due to
reduced blood flow ornephrotoxic drug.
• Develops dueto :
1. direct poisoning of tubules (nephrotoxic
lesions) : TOXIC ATN
2. renal ischemia : ISCHEMIC ATN
Prolonged ischemia due to:
• Shock
• Septicemia
• Hemorrhage
• Other: severe burns, dehydration
Exposure to Nephrotoxic agents
• Direct effects of toxins (Nephrotoxic lesion).
• Therapeutic agents such as Antibiotics and
Chemotherapeutic agents.
• Heavy metals: mercury, lead.
Major complication
• Proteinuria = edema
• Hematuria = anemia
• Pyuria = neutrophilia
• Kidney Failure
• Presence of epithelial cells cast in urinalysis
• Fractional Excretion of Sodium (FENa) > 3%
2- Renal vascular disease
(nephrosclerosis)
NEPHROSCLEROSIS
1. BENIGN NEPHROSCLEROSIS
•associated with benign hypertension and hyaline arteriolosclerosis (protein
depositionat tunica media).
2.MALIGNANT NEPHROSCLEROSIS
•uncommon form of arteriolar nephrosclerosis
•affecting all the vessels of the body, especially the small arteries and
arterioles of the kidneys
•associated with malignant hypertension and hyperplastic arteriolosclerosis
(concentricproliferationof smooth muscle cells).
Nephrosclerosis
ETIOLOGIES:
• Atherosclerosis
• Fibromuscular Dysplasia
• Autoimmune
• Septicemia
• AND anything that can block / reduce blood
circulation to kidney!!
MAJOR COMPLICATIONS
• Clinical complication associated with renal failure
3- Renal tumors
Types :
1) Renal cell
carcinoma (most
common – adults)
2)Wilms tumor
(childhood)
Risk factors RCC
-Carcinogenic
compound
exposure
- Tobacco smoking
contributes to 24-
30% of RCC cases
- Tobacco results in
a 2-fold increased
risk
- Occupational
exposure to
cadmium, asbestos,
petroleum
Genetic Factors
•Von Hippel-Lindau disease
- Inherited mutation in one Von Hippel-Lindau
(VHL) allele
-Malignancy arises from inactivation of the
remaining VHL allele
•VHL gene mutation associated with 60% of
RCC
Pathogenesis of VHL
• Von Hippel-Lindau protein, product of
VHL gene, is a tumor suppressor
• VHL inhibits hypoxia-inducible genes
involved in angiogenesis such as VEGF,
TGF-α, GLUT-1
• Loss of VHL results in tumor
angiogenesis, tumor-cell proliferation
epithelial cell proliferation
Clinical presentation
Variety of
symptoms
Hematuria present
40% of patients
Flank pain, palpable abdominal mass
Tissue diagnosis:
• Tissue diagnosis obtained from nephrectomy or
biopsy of metastatic lesion
• Surgery indicated for solid renal masses >1.5cm
• Tumors <1.5cm require periodic follow-up
Wilma tumor
• Childhood tumor (peak age 2
years) and 98% < 10 years
• Most common abdominal solid
tumor in childhood
• Hereditary
• Associate with mutation of WT- 1
cancer suppressor gene
• Unilateral (90%)
• Bilateral more common in familial
cases (20%)
4- Urolithiasis kidney stones
• Urinary tract / kidney calculi
• May form in any part of UT
• Commonly – renal pelvis or bladder
• CF: Hematuria, urinary stasis, UTI
• Etiology :
• Calcium oxalate – small, hard + jagged edges – damage
ureteral mucosa
• Phosphate calculi – associate with urinary infections –
produce ammonia – urine alkaline – solitary + large + soft
– STAGHORN calculus.
• Uric acid calculi
