Kidney/Urology-Exam 3 Flashcards
Describe the components of the nephron
- glomerulus. mechanically filters blood.
- proximal convoluted tubule. reabsorbs 75% of the water, salts, glucose, and amino acids.
- loop of henle. countercurrent exchange, which maintains the concentration gradient.
- distal convoluted tubule: regulating extracellular fluid volume and electrolyte homeostasis.
Urine is formed as a result of:
- glomerular filtration
- reabsorption of substances into the blood
- excretion of substances from the blood into the renal tubules
What are the structures of the glomerular membrane?
- fenestrated endothelial cell
- glomerular basement membrane
- Podocyte
Glomerular Membrane: fenestrated endothelial cell
Structure:
Network of capillaries in the
renal cortex that is covered by epithelium called Bowman’s capsule
Function:
Blood is filtered and fluid is
collected in Bowman’s capsule
Glomerular Membrane: glomerular basement membrane (GBM)
Structure:
is a ribbon-like extracellular matrix that lies between the endothelium and the podocyte foot processes (FPs)
Function:
glomerular filtration barrier. It provides a scaffold that supports the physiological function of the glomerular endothelium and podocytes.
Glomerular Membrane: podocyte
Structure:
have long foot processes called pedicles,
Function:
play an important role in glomerular function. Together with endothelial cells of the glomerular capillary loop and the glomerular basement membrane they form a filtration barrier.
4 ways of increasing GFR
- Increase glomerular capillary hydrostatic pressure
- Hormones
- nitric oxide, prostaglandin, bradykinin
- autacoids
Increase GFR by:
Increase glomerular capillary hydrostatic pressure
works by:
- increasing intravascular volume or MAP
- dilation of afferent arterioles=more blood flow
- constrict efferent arterioles=slower flow and greater blood volume
Increase GFR by:
Hormones and autacoids
works by:
-Local angiotensin II: constricts efferent arterioles>>increasing blood flow>>inc GFR
Increase GFR by:
nitric oxide, prostaglandin, bradykinin
works by:
dilate afferent arterioles >> increasing blood flow >> increasing GFR
Increase GFR by: autacoids
works by:
-Local angiotensin II: constricts efferent arterioles>>increasing blood flow>>inc GFR
4 ways of decreasing GFR
- Increased Bowman’s capsule by hydrostatic pressure
- Increase glomerular capillary colloid osmotic pressure
- Sympathetic nervous system
- Hormones
Decrease GFR by:
Increased Bowman’s capsule by hydrostatic pressure
works by:
obstruction of urinary tract (kidney stones)
Decrease GFR by:
Increase glomerular capillary colloid osmotic pressure
works by:
high protein intake and hyperglycemia
Decrease GFR by:
Sympathetic nervous system
works by:
- norepinephrine: increases sympathetic action>> constricts afferent arterioles >> dec blood flow >> dec GFR
- epinephrine (from adrenal medulla): constricts afferent arterioles >> dec blood flow >> dec GFR
Decrease GFR by:
Hormones
works by:
Denothelin (from vascular endothelium): constricts afferent arterioles >> dec blood flow >> dec GFR
Acute Kidney Inury
Definition: sudden decline in GFR, UOP and clearance of waste products and electrolytes
Onset: within a few hours or a few days
Common Etiologies: ischemia, hypoxia or nephrotoxicity.
Chronic Kidney Disease
Definition:
also known as chronic kidney failure, means a gradual loss of kidney function over time
Onset: 3 months
Common Etiologies: HTN, DM, high cholesterol, kidney infections, glomerulonephritis, polycystic kidney disease, blockage of urine (kidney stones or enlarged prostate), or long term use of NSAIDS
Pre-renal
Risk factors:
hypovolemia, hemorrhagic blood loss, loss of plasma volume, water and electrolyte losses, septic shock, cardiac failure, massive PE, stenosis or clamping of renal artery, increased intraabdominal pressure
Etiology:
•Lack of perfusion
•Hypotension, hypovolemia
•Renal blood flow
*cause of decrease blood flow into kid.
* kid injury is before the kidneys
Patho:
Decreased renal blood flow >> hypoperfusion >> decreased GFR >> increased proximal tubule Na and H2O reabsorption >> increased aldsosterone and ADH secretion >> increase distal tubule Na and H2O reabsorption >> oliguria
Intra-renal
Risk factors:
acute tubular necrosis, glomerulopathies, acute interstitial necrosis (tumors or toxins), vascular damage, malignant hypertension, vasculitis, coagulation defects, renal artery/vein occlusion, bilateral acute pyelonephritis
Etiology: a tubular, glomerularnephritis, or interstitial area issue. Cant filter blood properly and cells are damanaged that reabsorption and secretion is effected
- Acute tubular necrosis (nephrotoxins) caused by ischemia most common cause of intrarenal AKI; happens a lot after surgery and severe sepsis
- glomerulonephritis
- Acute insterstial nephritis ( can be d/t medications)
Patho: reanal tubular injury >> cast formation >> intratubular obstruction >> increased intratubular pressure >> tubular back leack >> decreased GFR >> oliguria
Post-renal
Risk factors:
Obstructive uropathies (usually bilateral), ureteral destruction (edema, tumors, stones, clots), bladder neck obstruction (enlarged prostate), neurogenic bladder
Etiology:
Urinary obstruction
Urine is unable to drain and system
“backs up”
Patho:
bilateral obstruction to urine flow >> increase intraluminal pressure >> release of inflammatory mediators and vasscular endothelial cell injury >> renal vasoconstriction >> cellular/interstitial edema >> decreased GFR >> oliguria
CKD stage I
Severity: mild kidney damage
GFR: 90% ore more
Progression:
Symptoms: no specific symptoms, but kidney function can slowly decline; high bp, swelling in legs, UTIs, abnormal urine test
CKD stage II
Severity: mild loss of kidney function
GFR: 60-89%
Progression:
Symptoms: no specific symptoms, but kidney function can slowly decline; high bp, swelling in legs, UTIs, abnormal urine test
CKD stage III
Severity: mild to severe loss of kidney function
GFR: 30-59%
Progression:
Symptoms: changes in urinations, swelling hands and feet, weakness/fatigue, dry/itchy skin, back pain, muscle cramping
CKD stage IV
Severity: severe loss of kidney function
GFR: 15-29%
Progression:
Symptoms: anemia, decreased appetite, bone disease, abnormal levels of phosphorus, calcium, vitamin D
CKD stage V
Severity: kidneys can no longer keep up with removing waste products and extra water. This is called kidney failure. No cure, but treatment options-HD
GFR: <15%
Progression:
Symptoms: Uremia, fatigue, SOB, N/V, abnormal thyroid levels, swelling in hands/legs/eyes/lower back, lower back pain
Polycystic Kidney Disease
Etiology: Autosomal dominant kidney disorder
Patho:Production of polycystins >> change epithelium growth creating cysts >> obstruct and destroy renal parenchyma
*Cysts may occur in other organs
Manifestations: High BP, back or side pain, blood in urine, fullness in abd, increase size of abd due ENLARGED KIDNEYS, headaches, kidney stones, kidney failure
Hemolytic Uremic Syndrome
Etiology: most common cause of community acquired AKI in CHILDREN; caused by E. COLI (shiga toxin)
Patho: results in the destruction of blood platelets (cells involved in clotting), a low red blood cell count (anemia) and kidney failure due to damage to the very small blood vessels of the kidneys.
Manifestations: Abdominal pain, BLOODY DIARRHEA a, fever,
Macroangiopathic hemolytic anemia (schistocytes), thrombocytopenia, and systemic microvascular clots that can clog the glomeruli >> AKI
Prostate Hypertrophy
Etiology: Obstructive process overdistension of bladder hydronephrosis
Patho:May be “benign” or cancer
“Benign” r/t imbalance between androgens and estrogens with increased age
Cancer linked to males with family history of BRCA1 and BRCA2 breast cancer
Manifestations: Overflow incontinence, frequency, UTI
Functions of Kindeys
- excrete metabolic waste products (urea, creatinine, drugs, and hormone metabolites)
- regulate water and electrolyte balance
- regulate arterial blood pressure (renin-angiotensin-aldosterone system – RAAS)
- regulate acid base balance
- erythrocyte production (erythropoietin)
- I,25-dihydroxy vitamin production (calitriol)
- glucogenesis
Cortex
outer portion of kidney
Medulla
inner portion of kidney
Renal pyramids
organized tissue in the medulla that communicates with the renal pelvis
Minor and major calyx
collect urine made by the kidneys and lead to the renal pelvis >> ureters >> bladder
Nephrons
- functional unit of the kidney located in the cortex and medullar
- cannot be regenerated
Glomerulus
tuft of gomerular capillaries
- site where fluid is filtered from the blood which creates a filtrate which enters the tubule
- network of capillaries in renal cortex
- blood is filtered and fluid is collected in Bowmans’ capsule
Tubule
tube in which filtrate is processed into urine
what controls the rate of filtration in the glomerulus?
vascular tone of afferent and efferent arterioles
Tubule system
Bowman’s capsule >> proximal
tubule >> loop of Henle
[descending (thin) and ascending
(thick) limbs] >> macula densa >>
distal tubule >> collecting tubules
>> 8-10 collecting tubules
combine to medullary collecting
tubule >> collecting duct >> renal
pelvis
Formation of Urine
- glomerular filtration
- reabsorption of substances from the renal tubules into the blood
- excretion of substances from the blood into the renal tubules
What is the glomerular filtration rate
sum of hydrostatic and colloid osmotic pressures across the glomerular membrane (net filtration pressure)
What is the glomerular filtration membrane made of
- endothelium (fenestrae)
- basement membranes (collagen and proteoglycan)
- podocyte (filtration slits/slit membranes)
Cells that should not be in urine and if they are present, what do they mean?
- RBCs: glomerulonephritis, trauma, kidney stones,
- WBCs: infection
- Casts – coagulated proteins
• Cellular debris = acute kidney injury
• RBC = tubular or glomeruli injury
• WBC = inflammation
• Epithelial = tubular injury
• Broad waxy = stasis and tubular injury; poor sign
Types of nephrons
- Cortical nephron: glomerulus in the outer cortex and tubules that only go a short way into the medulla
- Juxtaglomerular nephron: glomerulus deep in the cortex with tubules that go a long distance into the medulla. These nephrons have specialized vasculature surrounding their peritubular capillaries called vasa recta which absorb fluid into systemic concentration determining the urine concentration
Lab monitoring and kidnsey
- Creatinine clearance
- cystatin C
Proteinuria
Protein is not usually filtered by kidney (molecules are too big)
Proteinuria (albumin) in urine
Normal ≤ 150mg/d
Significant 300-500mg/d
Nephrotic > 3grams/day
grams/d glomerular disease
grams/day tubular disease
Albumin:creatineratio can substitute for 24-hour urine (“n” <30mg alb: g Cr)
Nephrotic Syndrome
- Presents with significant proteinuria
- Associated with chronic glomerulonephritis, drugs and infections
- Manifestations: swelling around the eyes and in the feet and ankles, foamy urine, and weight gain due to excess fluid retention.
Nephritic syndrome
- Presents as hematuria and RBC casts
- Proteinuria but less significant
- Associated with infection related and rapidly progressive glomerulonephritis
- Manifestations:
Blood in the urine (urine appears dark, tea-colored, or cloudy)
Decreased urine output (little or no urine may be produced)
Swelling of the face, eye socket, legs, arms, hands, feet, abdomen, or other areas.
High blood pressure.
AKI
Sudden decline in GFR, UOP and clearance of waste products and electrolytes
-3 stages
Pre renal
- inadequate perfusion: hypotension/hypovolemia, renal blood flow-renal stenosis, abd compartment syndrome
- most common cause of AKI
Renal/intrinsic
- cellular damage; injury to the cells that make filtering possible
- inflammatory conditions: acute tubular necrosis (ATN), nephrotoxins-most common cause ATN from ischemia
Post renal
obstruction
-urine is unable to drain and the system backs up
Manifestations of AKI
Essential manifestations: Elevated Cr and oliguria –important feature of AKI
Electrolyte abnormalities: K, Phos, BUN
Metabolic acidosis
Edema, dyspnea (Fluid overload)
Fatigue, altered mental status
Muddy brown urine?
CKD
Progressive and irreversible
Causes of CKD
Diabetes
HPTN
Glomerulonephritis
Polycystic kidney disease
Obstructive processes
Manifestations of CKD
AKI manifestations + chronic affects
*Hyperparathyroidism
*Osteodystrophy
*Anemia
*HPTN, dyslipidemia CVD
*Impaired platelet function, hypercoagulable
*Insulin resistance
*Peripheral neuropathy
What happens in the proximal tubule?
Reabsorbed:
•Sodium, chloride, potassium, phosphorous, bicarbonate, glucose, amino acids
•Very permeable to water
Secreted:
•Hydrogen ions, organic acids, organic bases (metabolic byproducts, bile salts, uric acid,
catecholamines)
What controls it:
•Angiotensin II (increase Na and water absorption)
•Parathyroid hormone (decreased phosphorous reabsorption)
What happens in the thin descending loop of Henle
Reabsorbed:
•Small amounts of Na
•Highly permeable to water
•Creates highly concentrated filtrate
Secreted:
None
What controls it: NA
What happens in the thin ascending loop of Henle?
Reabsorbed:
•Sodium, chloride, potassium, calcium, magnesium, bicarbonate
•Impermeable to water
•Dilutes filtrate
Secreted:
Hydrogen ions
What controls it:
•Angiotensin II (NaCl reabsorption and H secretion)
•Parathyroid hormone (Calcium reabsorption)
What contributes to the glomerular filtration rate?
sum of hydrostatic and colloid osmotic pressures
across the glomerular membrane (net filtration pressure)
What happens in the thick ascending loop of Henle?
Reabsorbed:
*sodium, chloride, potassium, calcium, magnesium, bicarbonate
*impermeable to water-dilutes filtrate
Secreted:
*hydrogen ions
What controls it:
*angiotensin II (NaCL reabsorption and H secretion)
*parathyroid hormone (calcium reabsorption)
What happens in the medullary collecting ducts?
Reabsorbed:
*sodium, chloride, calcium, bicarbonate
*permeable to water-antidiuretic hormone required
Secreted:
*potassium, hydrogen ions, urea
What controls it:
*aldosterone (increases NaCl and K secretion)
*vasopressin/ADH (increase water reabsorption)
*ANP (decreases Na reabsorption)
What happens in the medullary collecting tubules?
Reabsorbed:
*urea
*water if vasopressin/ADH
Secreted:
*sodium, potassium, hydrogen ions, bicarbonate
What controls it:
*vasopressin/ADH (increase water reasborption)
What labs can assist in monitoring kidney function
Creatinine clearance: reflects GFR, estimate that overestimates function
• Blood x1 and 24 hour urine
• Normal level varies by age and gender
• Useful if kidney function is stable
• Picks up small, significant early changes in serum creatine
• Cystatin C: marker of kidney function, measure of serum protein filtered by
glomerulus and metabolized by tubules
• Elevated level correlates with decreased GFR
• Not affected by infection, diet, inflammation, gender, age, race
What changes occur in the kidney with aging?
Renal cells may hypertrophy as compensatory adaptation
• Donate a kidney, renal trauma or disease
• The number of nephrons decrease with age
• That decreases renal blood flow and GFR
• Tubular atrophy also occurs
• Decreases glucose, bicarb and sodium reabsorption
• Decrease production of Vitamin D changes intestinal Ca absorption
• Bladder symptoms are more common
• Neurogenic changes and other external causes: hormone changes, prostate
hypertrophy, CV disease
Causes of CKD
Chronic injury to nephron / glomeruli
• Diabetes
• HPTN
• Glomerulonephritis
• Polycystic kidney disease
• Obstructive processes
Manifestation of CKD
- AKI manifestations + chronic affects
- Hyperparathyroidism
- Osteodystrophy
- Anemia
- HPTN, dyslipidemia CVD
- Impaired platelet function, hypercoagulable
- Insulin resistance
- Peripheral neuropathy
Function of kidneys
- excrete metabolic waste
- regulate water and electrolyte balance
- Regulate arterial bp
- regulate acid-base
- erythrocyte production
- 1, 25-Dihydroxy vitamin production (calitriol)
- Gluconeogenesis
Creatine clearance
reflects GFR
normal levels means kidneys stable
What is cystatin C
marker of kidney function measure of serum protein filtered by glomerulus and metabolized by tubules
*elevated level correlates with decreased GFR
*not affected by infection, diet, inflammation gender, age, race
What does i mean if you have RBC in urine
glomerulonephritis, trauma, kidney stones
What happens if WBC are in urine
infection
What if cast - coagulated proteins are in urine?
- Cellular debris = acute kidney injury
- RBC = tubular or glomeruli injury
- WBC = inflammation
- Epithelial = tubular injury
- Broad waxy = stasis and tubular injury; poor sign
What is proteinuria
Protein is not usually filtered by kidney (molecules are too big)
- Normal ≤ 150mg/d
- Significant 300-500mg/d
- Nephrotic > 3grams/day
>3.5 grams/d is glomerular disease
>1-2 grams/d is tubular disease
What is prostate hypertrophy and manifestations?
•Obstructive process overdistension of bladder
hydronephrosis
- Manifestations
- Overflow incontinence, frequency, UTI
Etiology Nephrolithiasis and Urolithiasis
Etiology: Masses of crystals, protein or substances that cause obstruction in of urinary tract
• Located in the kidneys, ureters or bladder – typically unilateral
Pathology of Nephrolithiasis and Urolithiasis
Patho: salts in urine precipitate and form crystals that
grow (aggregate)
Classified according to primary salt that makes up the stone
• Calcium oxalate or phosphate
• Uric acid
• Struvite: magnesium, ammonium, phosphate
• pH of urine can promote stones
• Alkaline, pH >7.0 calcium, phosphate and struvite
• Acidic, pH <5.0 uric acid
Manifestations of Nephrolithiasis and Urolithiasis
- severe pain on either side of lower back
- n/v
- fever and chills
- urine that smells bad or looks cloudy
- blood in urine
- vague pain or stomach ache that doesn’t go away
Etiology of Nephrotic syndrome
Etiology: Presents with significant proteinuria; too much fat or cholesterol in blood caused by damage to tiny vessels aka glomeruli of your kidneys
Patho of Nephrotic syndrome
Patho: caused by increased permeability through the damaged basement membrane in the renal glomerulus especially infectious or thrombo-embolic. It is the result of an abnormality of glomerular permeability that may be primary with a disease-specific to the kidneys or secondary to congenital infections, diabetes, systemic lupus erythematosus, neoplasia, or certain drug use.
Manifestations of Nephrotic syndrome
Manifestations: :
hypoalbuminemia
edema/weight gain
hyperlipidemia
lipiduria
foamy or bubbly urine
Path of Acute Glomerular Nephritis
Patho:
-Rapidly progressive glomerulonephritis: accumulation of macrophages and proliferation of epithelial cells in Bowman space, forms crescents and occludes glomerular capillary blood flow
-IgA Nephropathy: deposits of IgA
48 hours post URI and viral GI infection
Related to lupus nephritis or early diabetic nephropathy
Etiology of Acute Glomerular Nephritis
Etiologies: Post-infectious: deposits of IgG and complement complexes
Kids: post group A-beta hemolytic strep, Adults: post staphylococcus
Manifestations of Acute Glomerular Nephritis
Manifestations:
Pink or cola-colored urine from red blood cells in your urine (hematuria)
Foamy urine due to excess protein (proteinuria)
High blood pressure (hypertension)
Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen.
Etiology of Chronic Glomerular Nephritis
Etiologies:
Typically associated with chronic inflammatory processes (infections/autoimmune disease like lupus)
-can be caused by HTN, DM
Path of Chronic Glomerular Nephritis
Patho:
•Slow developing
•varying degrees of glomerular scarring that is always accompanied by cortical tubular atrophy, interstitial fibrosis, interstitial infiltration by chronic inflammatory cells, and arteriosclerosis.
*condition is characterized by irreversible and progressive glomerular and tubulointerstitial fibrosis, ultimately leading to a reduction in the glomerular filtration rate (GFR) and retention of uremic toxins. If disease progression is not halted with therapy, the net results are chronic kidney disease (CKD), end-stage renal disease (ESRD),
Manifestations of Chronic Glomerular Nephritis
Manifestations:
Pink or cola-colored urine from red blood cells in your urine (hematuria)
Foamy urine due to excess protein (proteinuria)
High blood pressure (hypertension)
Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen
Cortical nephron
glomerulus in the outer cortex and tubules that only go a short way into the medulla
Juxtaglomerular nephron
glomerulus deep in the cortex with tubules that go a
long distance into the medulla
2 types of nephrons
- cortical
- juxtagglomerular
what happens in the afferent arterioles
where filtration occurs
what happens in the efferent arterioles
where water, electrolytes an substances exchange between blood and filtrate making urine
Cause of glomerular disease
injury to endothelium, basement membrane, podocytes
manifestations of glomerular diseases
proteinuria, hematuria, urinary sediment
oliguria, edema, hypertension, azotemia
What happens with inflammatory glomerular disease?
Glomerulonephritis can damage your kidneys so that they lose their filtering ability. As a result, dangerous levels of fluid, electrolytes and waste build up in your body.
Can lead to: AKI, CKD, HTN, NEPHROTIC SYNDROME
What is most common cause of intrarenal AKI?
Avascular tubular necrosis (ATN)
What is acute interstitial nephritis?
Inflammation of Interstitium
can last days to weeks
Often due to NSAIDs, PCN, rifampin, proton pump inhibitors, or diuretics
Causes of acute glomerulonephritis
- rapidly progressive glomerulonephritis (decrease in kidney funtion days to weeks)
- hmolytic-uremic synrome
