Kidney and Male Tract Flashcards
Main functions of the kidney
blood filtration and urea excretion
Additional role of kidneys
regulating blood pressure through angiotensin-aldosterone system
Na concentration sensed by
macula densa cells
Renin secreted by
juxtaglomerular cells
Glomerulus attached to
tubule
Blood is filtered in the
glomerulus
Kidneys convert _____into 1L of urine
1700L blood/day
3 hormones released by kidneys
Erythropoietin (EPO)
Renin
Active form of vitamin D biosynthesis
____ regulates blood pressre through the Renin-Angiotensin system
Renin
____ stimulates the bone marrow to make red blood cells
EPO
_____ helps maintain calcium for bones and for normal chemical balance in the body
Vitamin D
2 most common causes of kidney disease
diabetes
high blood pressure
Clinical manifestations of renal diseases
azotemia
parenchymal disease of the glomeruli
uremia
Elevation of blood urea nitrogen (BUN) and creatinine, generally reflects decreased GFR
azotemia
Characterized not only by failure of renal excretory function but also by a host of metabolic and endocrine alterations resulting from renal damage
uremia
- GFR less than 60 mL/minute/1.73m2 for at least 3 months
- and/or persistent albuminuria
- GFR about 30% to 50% of normal
chronic kidney disease
Renal agenesis
Ectopic Kidney
Horseshoe kidney
Renal dysplasia
congenital anomalies
Congenital Cystic kidney disease.
Acquired cystic kidney Disease
Cystic Kidney diseases
Minimal change Glomerulopathy (nephrotic)
Focal segmental glomerulosclerosis (FSGS) (nephrotic)
Membranous glomerulopathy (nephrotic)
Type I membranoproliferative Glomerulonephritis (MPGN type I)
Type II membranoproliferative Glomerulonephritis (MPGN type II)
IgA nephropathy (Berger disease) (nephritic)
Anti-Glomerular basement membrane Glomerulonephritis (nephritic)
Acute post infectious glomerulonephritis (nephritic)
ANCA Glomerulonephritis
Immune mediated glomerular inflammation
Lupus glomerulonephritis (2ry) Diabetic Glomerulosclerosis (2ry)
Secondary to systemic diseases glomerular inflammation
Hereditary nephritis (Alport Syndrome) (mutation of IV collage) Thin Glomerular Basement membrane Nephropathy
Isolated glomerular abnormalities glomerular inflammation
Renal vasculitis Hypertensive nephrosclerosis (benign nephrosclerosis) Malignant hypertensive nephropathy Renovascular hypertension Thrombotic microangiopathy Cortical necrosis
vascular diseases
Acute tubular necrosis (ATN) Pyelonephritis Analgesic nephropathy Drug-induced (hypersensitivity) tubulointerstitial nephritis Light-chain cast nephropathy Urate nephropathy
Tubulointerstitial diseases
Allograft nephropathy
Drug toxicity
Recurrent diseases
Transplant glomerulopathy
diseases in the transplant
Wilms’ Tumor (nephroblastoma)
Renal Cell Carcinoma (RCC)
Transitional Cell Carcinoma
Malignant Tumors of the Kindey
Complete bilateral agenesis (still born)
Unilateral agenesis: compensated by the contralateral kidney (hypertrophy), not a serious matter if there is no associated anomalies.
Renal agenesis
Misplaced in the pelvis
ectopic kidney
Single large midline organ
Infant born with fused kidneys
May increase risk of obstruction and pyelonephritis; ureters cross over the junction between the two kidneys and are fused at the lower pole.
Horseshoe Kindey
Undifferentiated tubular structures, primitive mesenchyme, heterotopic
tissue such as cartilage. Cysts form from the abnormal tubules.
Familial, genetic and somatic causes.
Palpable flank mass
Unilateral Dysplasia (removal of the involved kidney)
Bilateral aplastic dysplasia (Potter sequence
renal dysplasia
typical physical appearance and associated pulmonary hypoplasia of a neonate as a direct result of oligohydramnios and compression while in utero.
Potter syndrome
Numerous cysts in the renal parenchyma
The most common congenital disease with renal cysts
1:400-1:1000 individuals in the USA
50% develop end-stage renal failure
Mutation in PKD1 (85%)
The primary cilia of the renal tubular epithelium (tubule growth and sensing urine)
1/3 of ADPKD: have hepatic cysts
1/5 of ADPKD: have cerebral aneurysm and intracranial hemorrhage (cause of death in 15% of ADPKD).
Autosomal Dominant Polycystic Kindey
Rare, infants
In the collecting ducts
1:6000-1:40000
25% succumb to the disease in perinatal period (potter sequence)
Those who survive, progress to renal insufficiency.
Mutation of PKHD1 (fibrocystin protein)
Pancreatic cysts, hepatic biliary dysgenesis, fibrosis, and Cystic transformation of the renal collecting ducts
Smooth external surface of kidney.
Bilateral
Autosomal Recessive Polycystic Kidney Disease
Rarely clinically symptomatic, unless very large.
Usually in the outer cortex, simple ones in medulla.
In 50% of people over 50 years of age
simple renal cyst
Often develop multiple cortical and medullary cysts (hyperplastic and neoplastic proliferation may develop)
long term dialysis
These cells are phagocytic and secrete the amorphous basement membrane-like material known as the mesangial matrix. They are typically separated from the lumen of the capillaries by endothelial cells.
It is in the middle (meso) between the capillaries (angis). It is contained by the basement membrane, which surrounds both the capillaries and the mesangium
intraglomerular mesangial cells
The most common cause of Glomerulonephritis in the world.
nephritic syndrome
IgA nephropathy (Berger disease) (Nephritic)
First two major diagnostic considerations for patients with asymptomatic glomerular hematuria (Nephritic):
Thin Glomerular Basement membrane
IgA Nephropathy
HEMATURIA (visible or microscopic)
Variable degrees of proteinuria
Decreased glomerular filtration rate. Elevated BUN, serum creatinine
Oliguria, salt and water retention, edema, and hypertension
Inflammatory damage: endocapillary, extracapillary hypercellularity, leukocyte infiltration and necrosis, hyperplasia of the glomerular cells.
Nephritic syndrome
characteristic of classic anti-GBM disease
Linear
Increased glomerular capillary permeability
Severe PROTEINURIA (>3.5g protein/24hrs)
Hypoalbuminemia (<3gm/dl)
Generalized edema
Hyperlipidemia, & lipiduria ( increase lipoprotein synthesis in liver)
All glomerular diseases occasionally produce mixed nephritic and nephrotic manifestations (confound clinical diagnosis), except for Minimal-change glomerulopathy ( only Nephrotic Syndrome)
Nephrotic Syndrome
Minimal-change glomerulopathy causes ____ in 75% of children, focal segmental glomerulosclerosis in 35% of adults, and membranous glomerulopathy in 30% of adults
Nephrotic sydrome
arecellsin theBowman’s capsulein thekidneysthat wrap around the capillaries of theglomerulus.
podocytes
is most frequently mediated by immune mechanisms
Glomerular inflammation
common, highly variable manifestations of lupus nephritis (variable immune complexes)
can have many morphologic manifestations on renal biopsy.
In general, the more immune complex deposition and the more cellular proliferation, the worse the disease.
In this case, there is extensive immune complex deposition in the thickened glomerular capillary loops, giving a so-calledwire loopappearance.
Autoantibodies against nuclear and nonnuclear antigens (DNA,RNA, nucleoproteins, and phospholipids)
Lupus glomerulonephritis
Leading cause of end-stage renal disease in the US
The most common cause of secondary nephrotic syndrome
diabetic glomeruloscelerosis
Most frequent abdominal solid tumor in children (1:10,000)
WT1
Malignant Tumors of the kidney
most common Primary cancer of the kidney.
80% of Renal Cancers
VHL, Von Hippel Lindau
renal cell carcinoma
obstructive symptoms ofurinary tract infection, obstruction, acute urinary retention, bladder hypertrophy
NODULAR HYPERPLASIA OF THE PROSTATE (BENIGN PROSTATE HYPERPLASIA
230,000 new cases annually in the US.
27,000 die annually
INSITU AND INVASIVE ADENOCARCINOMA OF THE PROSTATE
