Kidney + Urinary Tract Flashcards
Kidney Functions
Elimination - kidney is a giant filter from blood
Metabolic waste removal
Drugs & toxins removal
Homeostasis - maintaining balance in the body
Electrolytes, water, pH, blood pressure (renin) balance
Regulate ion balance to maintain blood pressure
Bone metabolism
Vit. D activation
Ca2+ and PO4- balance
Bone marrow RBC production (hormone erythropoietin)
Kidney problems → anemia
Kidney Gross Anatomy
Two kidneys are located in the posterior wall of the abdomen at the level of the 11th and 12th ribs and are wrapped by a protective layer of fat.
The kidney can be divided into the renal cortex (outer region) and the medulla (inner region).
Renal cortex - filtration occurs
Renal pyramids - concentration of urine occurs
The renal columns are connective tissue extensions that radiate downward from the cortex through the medulla to separate the most characteristic features of the medulla, the renal pyramids and renal papillae.
The papillae are bundles of collecting ducts that transport urine made by nephrons to the calyces of the kidney for excretion.
The pyramids and renal columns taken together constitute the kidney lobes.
Renal pelvis → after blood is filtered, fluid enters collecting system (renal pelvis) → ureter → bladder
Glomeruli
Nephrons are the “functional units” of the kidney; they cleanse the blood and balance the constituents of the circulation.
Afferent arterioles form high-pressure capillaries called the glomeruli.
The rest of the nephron consists of a tubule whose proximal end surrounds the glomerulus—this is Bowman’s capsule.
The glomerulus and Bowman’s capsule together form the renal corpuscle.
These glomerular capillaries filter the blood based on particle size.
After passing through the renal corpuscle, the capillaries form a second arteriole, the efferent arteriole.
Filtration of the Bowman’s Capsule
One layer of the Bowman’s capsule is composed of uniquely shaped cells (podocytes) with extending finger-like arms to cover the glomerular capillaries.
These projections interdigitate to form filtration slits, leaving small gaps between the digits to form a sieve.
As blood passes through the glomerulus the plasma filters between these sieve-like fingers to be captured by Bowman’s capsule.
Overall, filtration is regulated by fenestrations in capillary endothelial cells, podocytes with filtration slits, and the basement membrane between capillary cells.
Vascular side
Filter consists of endothelial lining with holes, protein meshwork (physical barrier, negative charge so charge barrier)
Slits between podocytes too
Structure of the Nephron
After leaving the renal corpuscle, the filtrate passes through the renal tubule in the following order:
Proximal convoluted tubule (found in the renal cortex)
Epithelium has a lot of surface area (microvilli present)
Involved with resorption of water/ions, and organic nutrients
Loop of Henle (mostly in the medulla)
Reabsorption of water (descending)
Reabsorption of sodium chloride ions (ascending)
Distal convoluted tubule (found in the renal cortex)
Reabsorption of calcium, sodium ions under hormonal control
Secretion of ions, acids, drugs, toxins
Collecting tubule (in the medulla)
Collecting duct (in the medulla)
Urine delivery
Acute Kidney Injury
- Pre-Renal - rapid decrease in blood flow (decrease blood pressure)
Shock, dehydration, hemorrhage
Often related to the heart and the low cardiac output. - Renal - directly affect tissues
Inflammation, infection, ischemia
Drugs and toxins - Post-Renal - insults happening in collecting system
Acute urinary tract obstruction
Acute kidney failure
Acute onset of symptoms, if treated early enough the damage is not permanent
Chronic Kidney Injury (systemic things that affect the kidneys)
- Pre-Renal
Hypertension, diabetes - Renal
Primary glomerulopathies
Chronic tubulointerstitial diseases - Post-Renal
Chronic urinary tract obstruction
Acute vs. Chronic Kidney Injury
Acute Injury
Acute onset of symptoms
Potentially reversible
Chronic injury
Loss of glomeruli, chronic inflammation, scarring
Often asymptomatic at first
Slow progressive and irreversible damage
Consequences of Kidney Injury
Loss of water regulation - Edema, often exacerbated by protein loss in the urine.
Electrolyte disturbances - minerals lost Na+, K+ , Ca2+, PO4
Lower Blood pH - Acidosis (kidneys not regulating blood pH)
Increased Waste products
Anemia - due to loss of vitamin D.
Lower bone density- due to loss of vitamin D.
Management of Chronic Renal Failure
- Medication
a. Treat underlying conditions - Dialysis
a. Chronic renal failure - Transplant
a. Chronic renal failure - Diet management
Primary glomerulopathy
Affect kidney primarily or exclusively (glomerulus)
Secondary glomerulopathy:
Systemic diseases that affect multiple organs (and kidney)
E.g. diabetes, systemic lupus, vasculitis
What underlies most types of primary glomerular diseases and many of the secondary glomerular diseases?
Immune Mechanisms
Most damage the glomerular filter in some way
The deposition of circulating immune complexes in the glomerulus initiates complement and/or Fc receptor-mediated leukocyte activation resulting in glomerular injury.
CLINICAL EXAMPLE
27 year old male
2 day history of sore throat/cold
Mildly swollen ankles
Brown discoloration of urine
INVESTIGATIONS FOR RENAL DISEASE
1. Urinalysis:
a. Hematuria (blood in urine)
b. Proteinuria (protein in urine)
2. Blood:
a. Increased Creatinine and urea (impaired waste elimination)
3. Kidney biopsy:
a. Needed for definitive diagnosis → pathologist
b. Use light microscopy, immunofluorescence and electron microscopy.
i. Light microscopy: inflamed (many cells), thickened matrix, obscured capillaries
ii. Immunofluorescence: immune complex deposition (IgA)
iii. Electron Microscopy: abnormal proteinaceous deposits (dark areas) in the glomerulus
EXAMPLE: IGA NEPHROPATHY
Presents in childhood
Microscopic or gross hematuria (spill blood into urine)
Develops during infection of mucosal lining
Infection → IgA1 production (abnormal) → forms immune complexes of antibodies → deposits in glomerular mesangium → inflammation
Presentation
Nephritic Syndrome
Inflammation of glomeruli
Dark urine, oliguria, hypertension
Nephrotic Syndrome
Hypoalbuminemia (decreased blood protein)
Massive proteinuria
Hyperlipidemia (increased lipid production)
Peripheral edema
Acute Tubular Necrosis (ATN)
Clinicopathologic entity characterized by damage to tubular epithelial cells and an acute decline in renal function.
Ischemic injury - decreased blood flow
Low cardiac output (heart failure)
Low blood volume (hemorrhage)
Vasodilation (sepsis, anaphylaxis)
Nephrotoxic injury - direct injury
Exogenous (drugs, toxins)
Endogenous (muscle injury, transfusion reaction)
*ATN is potentially reversible (it is acute)
Consequences
Soughing of dead cells
Oliguria - decreased urine flow
Increased backpressure (waste products not being removed)
Hyperkalemia (potassium; electrolyte imbalance)
Metabolic acidosis (accumulation of acid)
Azotemia (nitrogen in blood)
Kidney Cyst
Cystic diseases of the kidney are a heterogeneous group comprising hereditary, developmental, and acquired disorders.
ACQUIRED
Simple
End-stage failure
GENETIC
Polycystic kidney diseases
NEOPLASTIC
Renal carcinoma variant
DEVELOPMENTAL
Congenital syndromes
Kidney Cyst
Cystic diseases of the kidney are a heterogeneous group comprising hereditary, developmental, and acquired disorders.
ACQUIRED
Simple
End-stage failure
GENETIC
Polycystic kidney diseases
NEOPLASTIC
Renal carcinoma variant
DEVELOPMENTAL
Congenital syndromes
PATHOGENESIS OF KIDNEY CYSTS
Altered growth and differentiation of tubular epithelium.
ACQUIRED SIMPLE CYST
Simple cysts are generally innocuous lesions that occur as multiple or single cystic spaces of variable size.
Simple cysts are a common postmortem finding that has no clinical significance
ADULT POLYCYSTIC KIDNEY DISEASE
Acquired cystic kidney disease: occurs in patients with end-stage renal disease who have undergone dialysis for many years.
Multiple cysts may be present in both the cortex and the medulla and may bleed, causing hematuria.
Dialysis is ultimately required
Families must be screened (familial)
ATHEROSCLEROSIS of the kidney
Embolic infarcts
Artery narrowing (low perfusion, atrophy) in the kidney
HYPERTENSION of the kidney
Thickening of small vessel walls in the kdney
