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150 Cards in this Set

  • Front
  • Back
Excretory Functions of the Kidney (3)
1 - Remove waste products that came from the body's metabolism
2 - Regulate the composition of blood by controlling the amount of water, acid-base balance, and quantity and concentration of ions
3 - Excrete foreign substances
-bean shaped organ in the back of abdomen
-one on each side
-level of the lower ribs
-each weighs about 1/4 pound
Approx. 4 inches long by 2.5 inches wide by 1.5 inches thick
Kidney
-Blood returns to the heart through the inferior vena cava
Renal Vein
-major branch from aorta
-receives = 20% of blood from heart
-blood flows through kidneys at about 1.2 liters/min
Renal Artery
-enters at hilus
-conncets kidney to bladder
-urine collection duct
Ureter
-contains light colored cone shaped masses known as the pyramids
-towards the middle of the kidney
-where active transport and inactive transport occur along with filtration
Medulla
-part of the medulla
-made up of all tubules
Pyramids
-falt funnel shaped cavity that collects the urine into the ureters
-near hilus
-pool to collect urine
Pelvis
-outer 1/3 of kidney
-contains most of filtration units
-very active blood filtration area
Cortex
-found in cortex and medulla
-perpendicular to surface of kidney
-1 million in each kidney
-each one produces urine
-main function is to clean the blood
-ball of capillaries at end of artery
-long thin tube with a hair-pin loop
-closed at one end
-surrounded by peribulbar capillaries
Nephron
Main Parts of Nephron (6)
1 - Glomerulus
2 - Proximal convoluted tubule
3 - Descending Loop of Henle
4 - Ascending Loop of Henle
5 - Distal Tubule
6 - Collecting Duct
-part of nephron
-about the size of pinhead
-contain Bowman's capsule and Juxtaglomerular cells
-ball of capillaries
-like having your hand in a closed balloon
Glomerulus
-part of glomerulus
-located in cortex
-the tissue that surrounds the glomerular capillaries
Bowman's capsule
-closed end at the beginning of the nephron
Vascular Pole
-open end of nephron
Urine Pole
-artery bringing blood into glomerulus
Afferent arteriole
-vessel that takes blood out/away from glomerulus
Eferent arteriole
-part of glomerulus
-baroreceptors
-enlarged smoothe muscle cells of afferent arteriole
-produce, store, and excrete renin, which results in vasoconstriction
Juxtaglomerular cells
-has fenestrated endothelium and incomplete basement membrane supported by podocytes
-held together by mesangial cells that have a phagocytic function and contractile capabilities to control blood flow
Glomerular Capillaries
-part of glomerular capillaries
-epithelial cells
-allow the filtration to occur easily
-similar structure to choriocapillaris and RPE cells
-have space between them and spaces contain nephrin which forms slit diaphragm
Podocytes
-helps control the blood flow of nephron
-causes the constriction of afferent arteriole and release of renin from juxtaglomerular cells
-constriction causes slower blood flow and less filtration pressure
Sympathetic system
-helps control the blood flow of nephron
-renin-->angiotensin II, which causes constriction of efferent arteriole
-helps achieve a constant rate of filtration in glomerulus
Renin system
-helps control the blood flow of the nephron
-influence renal blood vessels
-PGs, NO, Endothelin
Chemical mediators
-cause dilation of blood vessels
PGs
-cause constriction of vessels
NO and Endothelin
-part of nephron
-first twisted region after Bowman's capsule
-in cortex
-almost all of glucose, bicarbonate, aa, and other metabolites are actively reabsorbed here
-approx 2/3rds of Na is actively reabsorbed from the tubules here - depends on angiotensin
-Cl and water reabsorbed passively by following the sodium
-K actively reabsorbed
-some meds actively excreted at this point
-filtrate is isotonic here
Proximal convoluted tubule
-part of nephron
-at entrance the filtrate is isotonic
-osmolarity increases becase the only thing that can be reabsorbed here is water
-"water falls out" passively
-this water will be reabsorbed by peritubular capillaries
Descending Loop of Henle
-part of nephron
-long hairpin loop after proximal tubule
-extend from cortex into medulla and back out to cortex
-at entrance filtration is hypertonic
-"water can't flow up stream"
-cells lining this tube are impermeable to water
-active reabsorption of sodium, potassium, and chloride occur here
-another major site for salt reabsorption
-this reabsorption of salt makes the medulla very hypertonic
-at exit filtrate is hypotonic
Ascending Loop of Henle
-part of the nephron
-second twisted part of nephron in cortex
-cells of early one also impermeable to water
-reabsorption of chloride
-calcium excretion regulated here by PTH
-active K excretion also occurs partly in exchange for Na
-filtrate remains hypotonic
Distal Tubule
-at the junction between ALH and distal tubule
-chemoreceptors that respond to decreased concentration of sodium and chloride in filtrate to encourage release of renine from juxtaglomerular cells
-respond to too little Na and too little Cl by telling the body to release renin
Macula densa cells
-part of nephron
-sodium reabsorbed by active processes
-potassium excreted by exchange with Na - aldosterone increases this activity
-urea passively reabsorbed here
-presence of ADH allows water to pass through walls of collecting ducts and be reabsorbed
-makes urine hypertonic in the end
-long straight portion after the distal tubule that is the open end of nephron
-extends from cortex to medulla
-collects fluid from several nephrons
Collecting Duct
Processes of Kidney (3)
1 - Filtration
2 - Reabsorption
3 - Excretion
-process of kidney
-occurs as blood passes through glomerulus
--> pressure in glomeruli is 2-3 times higher than other capillary beds of the body
-glomerulus shows selective permeability influenced by the size, charge, and configuration of the substance
-higher concentration of substance in capillaries increases concentration in filtrate
-filtrate in water, ions, glc, aa, bicarbonate
Filtration
-process of kidney
-ions, glc, aa get reabsorbed from lumen of nephron
-specialized transporters on membranes of epithelial cells of nephrons
-different transporter types located in different parts of nephrons
-some transporters are active and some passive process
-reabsorption of most substances related to Na reabsorption- by exchange, via share transporters or via solvent drug
-also occurs along tubules
-usually passive
-this is huge!
-only 1% of total filtrate volume becomes urine
Reabsorption
Two Major Modifiers of Absorption
1 - Concentration of molecules
2 - Rate of flow of filtrate
-addition of substance to filtrate
-unwanted components such as ammonia
-can be a function of transporter cells or passive process
-these processes try to maintain a balance in your blood stream
Excretion
Follow the Filtrate!
Glomerulus --> Proximal Tubule --> Descending LoH --> Ascending LoH --> Distal Tubule --> Collecting ducts
-controlled by two main mechanisms
--> structure and transport properties of the nephron
-->ADH secreted by the pituitary
Water balance maintainance
-major stimulus for secretion is decreased blood volume
--> baroreceptors in many places
--> decreased bp causes release of ADH
- next is increased osmolarity of blood
--> osmoreceptors located in ant hypothalamus
--> most responsive to Na and mannitol
-> Glc also has some effect
-more of this increases water reabsorption
ADH
-increase the blood flow to kidney
--> prevent vasoconstriction
-impair water reabsorption by several mechanisms
--> block ADH in collecting duct
--> prevents water and sodium reabsorption
--> prevents K excretion
-can be countered by NSAIDs and steroids and cause decreased initial filtration which results in edema
Renal PGs
-type of kidney endocrine function
-manufactured by kidney
-released in response to hypoxia
-stimulates bone marrow to produce RBCs
Erythropoietin
-type of kidney endocrine function
-conversion of Vit D to active metabolic form
-impt for absorbing Ca from intestine
Calcitrol
-type of kidney endocrine function
-combines with angiotensin --> angiotensin I --> angiotensin II
-produced and released by juxtaglomerular cells
-also causes the release of aldosterone from adrenal cortex
-increases release of ADH from neurohypophysis
-also stimuates thirst
-helps regulate blood pressure
Renin
-increases Na reabsorption at distal tubules and collecting ducts which increase water reabsorption
Aldosterone
-kidney function
-remember that body keeps blood at a relative pH of 7.4
-excess hydrogen ions combine with bicarbonate
-kidney helps control this
--> regeneration of bicarbonate
--> excretion of hydrogen ions when blood is too acidic
--> excretion of bicarbonate ions when blood is too alkaline
Acid-base balance
-type of kidney function test
-amt of filtrate formed in all nephrons
-about 20% of renal plasma flow is filtered
-normal rate is 125ml per min
-used to assess renal functions
-measured clinically by collecting timed blood and urine samples
Glomerular filtration rate
-type of kidney function test
- a product of creatine metabolism of muscle
-filtered by kidney but not reabsorbed out of tubules
-urine is collected for 24 hours with blood draw at end
-normal is about 100ml per min
- less than 60 is significant indicator of kidney disease
Creatinine clearance rate
-type of kidney function test
-normal = 1.0mg/100mL
-depends on gender and size of individual
-if value doubles consider GFR and kidney function to have fallen to half of normal state
-if value triples it suggests 25% of normal kidney function
Serum creatinine level
-type of kidney function
-an end product of protein metabolism
-filtered and controlled by kidney function
- about 50% is excreted and 50% is reabsorbed
-if glomerular filtration rate is slow the excretion of urea goes way down because more is reabsorbed the longer the tubular fluid stays in the kidney
-normal value is 7-20 mg/dL
-increases with decreasing kidney function
Urea
-kidney function test
-expect no protein, blood or glc
-if found, suggest kidney disease
-a gross test
Urinalysis
-type of serum lab test
-tend to increase with kidney failure
Potassium and phosphate
-type of serum lab test
-tend to decrease with kidney failure
Calcium, pH, bicarbonate
-future test
-has advantage because it is good at showing when someone has had acute trauma to the kidney
-used to look for acute problems as can be caused by sx - some forms of acute renal failure can be reversed if found quickly and doing right things
Neutrophil gelatinase assoc lipcalin
-type of imaging
-visualize the urethra, bladder, and ureteral orifices
-allows for biopsy
Cystoscopy
-type of imaging
-for evaluation of structure, tumors, abnormalities
Ultrasound
-type of imaging
-CAT scan detect tumors
-radiopaque iodine contrast medium allows visualization of urinary structures
-IV pyelogram allos xray visualization of renal tissues as injected dye is cleared by kidneys
Radiologic exams
-4-16% of US adults has some kind of chronic of this
-84,000 deaths per year due to renal problems
-more than 335,000 americans suffer fom failure and need dialysis or transplantation to live
-more than 74,000 pts are waiting for transplants but only 17000 receive them each year because of shortage of donors
-increasing in the US
Kidney Disease
-these underlie the most causes of primary kidney disease
Immune Mechanisms
-most common cause of kidney failure - 40% of cases
Diabetes
-commonly results from kidney problems
-always damages the kidneys to some extent
-second most common cause of chronic kidney failure in the US
Hypertension
Common First Symptoms of Kidney Disease (10)
1 - HTN
2 - Swelling of legs
3 - Pulmonary edema
4 - Fatigue
5 - Headaches
6 - Weight loss
7 - N and V
8 - Itching
9 - Increased tendency to bleed
10 - Cognitive Impairment
Diseases that cause ocular and renal effects (6)
1 - Diabetes
2 - HTN
3 - TINU
4 - MPGN
5 - Von Hippel-Lindau
6 - Wilms'
Ocular symptoms that renal disease can present with first (7)
1 - Eyelid edema
2 - Ca deposits on lids or conj
3 - Aniridia
4 - Uveitis
5 - ONH edema
6 - Drusen around macula
7 - Retinal changes
-leads to increased risk of cardiovascular death and increased risk of stroke
Impaired renal function
-an abrupt decrease in renal function that leads to retention of nitrogenous waste products in body over a few days
-multiple causes
-signs and symptoms reflect loss of regulatory, excretatory, and endocrine functions of kidney
-if pt survives this, 90% change of full recovery of kidney function
--> intial survival depends on cause and severity
Acute Renal Failure
-part of ARF
-decreased blood flow from volume loss or occlusion
-kidney would still function if had enough fluid
-hemorrhage, heart failure, shock, burns, diarrhea and vomiting, and thromboemboli
Pre-Renal
Diseases that Involve Kidney structures (3)
1 - Vessels
--> malignant HTN
--> Vasculitis
2 - Glomerulus
--> Infectious
--> Immune mediated
3 - Tubular
--> Toxicity
-most common instrinsic cause of ARF
-abrupt decline in GFR
-occurs within min to days
-response to acute ischemic or neprotoxic insult
-destruction of tubular epithelial cells decreases ion transport
-damages vasculature --> increases endothelin, decreases nitric oxide and decreases PG --> vasoconstriction
-causes reduced volume of urine and increased waste products in blood
-due to medical illness: 30% mortality rate
-due to prego: 10-15% mortality rate
-if pt survives original cause there is a 90% chance of recovery
-later death most likely due to infection
Acute Tubular Necrosis
-uncommon form of HTN
-diastolic BP
-> 120mm Hg
-ON head edema
-encephalopathy
-CV abnormalities
-renal failure
-True medical emergency
-immediate and aggressive anti-HTN therapy
-vascular damage to kidney
-increased permeability of small vessels
-leads to fibrosis which causes narrowing of vessl lumen
-results in ischemia to kidney
-causes release of renin which causes further vasoconstriction
-develops vicous cycle
Malignant Hypertension
Specific Agents that cause ARF (4)
1 - Radiographic contrast agents
2 - Aminoglycosides
3 - NSAIDS
4 - Ethylene Glycol
-specific agent that causes ARF
-reported rates in literature vary from 0-76%
-especially at risk are patients with pre-existing renal insufficiency
-dehydration also a risk
Radiographic contrast agents
-specific agent that causes ARF
-nephrotoxicity occurs in about 10% of pts taking these meds
-avoiding overdoes is impt
-typically comes within 1 week of treatment
-prognosis for recovery is very good
Aminoglycosides
-specific agent that causes ARF
-inhibit PG synthesis
-discontinuation often allows resolution
NSAIDs
-specific agent that causes ARF
-anti-freeze
-maifests after 48-72 hours
-pts are disoriented
-develop stupor, coma, cardiovascular collapse
-often fatal
Ethylene Glycol
-clinical manifestations are variable
-tend to manifest when GFR is less than 10mL/min
-related to toxic effects of:
--> retained products normally excreted by kidneys
--> normal products such as hormones that are now present at higher than normal levels
--> loss of normal products of kidneys ( loss of erythropoietin)
Chronic Renal Failure
-when the pt has clinical signs and symptoms of azotemia
-affects every organ system
--> likely due to multiple factors being out of balance not just excess urea
-includes fatigue, N,V,D, headache, and azotemia
Uremia
GI signs of Uremia (4)
1 - Metallic taste
2 - anorexia
3 - NVD
4 - GI bleeding
-tend to be freq and occur early
-start with subtle changes in cognitive ability
-poor memory and sleep disturbance also common
-progresses to lethargy, irritability, confusion, seizures
-can have loss of peripheral sensation in glove and stocking distribution
-decreased deep tendon reflexes
-can improve with dialysis
Neurological Manifestations of Uremia
Musculoskeletal Manifestations of Uremia (2)
1 - Late in disease
2 - Osteoporosis
Hematologic Problems with Uremia (2)
1 - Anemia
2 - Bleeding disorders
Endocrine Abnormalities (3)
1 - thyroid disease
2 - Enlarged thyroid is found in as many as 1/3 of uremic pts
3 - Decreased libido
Immunological function in Uremia (2)
1 - Immunosuppressed
2 - Increased risk of infections of all kids
-diabetics show decreased insulin requirements as kidney function decreases
-decreased sensitivity to insulin in peripheral tissues - due to electrolyte dysfunction
Metabolic disorders and Uremia
Dermatologic Manifestations and Uremia (4)
1 - Ca Sulfate and PO4 precipitate in the sweat
2 - Itching
3 - Yellow discoloration of skin
4 - Odor
Types of Glomerular Disease (2)
1 - Nephritic syndrome
2 - Nephrotic syndrome - membranoproliferative glomerulonephritis
Types of tubule and interstitial disease (3)
1 - TIN
2 - Pyelonephritis
3 - Interstitial nephritis
-constitutes some of the major problems in nephrology
-characterized by altered glomerular function - could be faster or slower but usu slower
-changes in filtration rate
-changes in permeability of glomerular capillaries partly due to nephron that makes small slits in capillaries
-can be caused by immunologic mechanisms
-can be caused by injury often secondary to metabolic imbalances such as in DM
Gomerular Disease
Initial nonspecific Manifestions of Glomerular Disease (5)
1 - HTN
2 - Edema
3 - Malaise
4 - Proteinuria
5 - Hematuria
-type of glomerular disease
-acute inflammation of glomeruli
-abrupt onset of hematuria and proteinuria with impaired renal function that results in small amts of urine
-one of first manifestations may be oliguria
-retention of salt causes fluid retention and HTN
-mild edema usually of the eyelids and face first
-less urine volume, less glom filtration, and blood in urine
Nephritic Syndrome
-prior stretococcal infection
--> 10-14 days after acute strep infection
--> inflammation from Ag-Ab reaction
-more common in children
-more common in summer and fall
- post strep throat infection in northern US
--> <5% of individuals
-post strep pyoderma in southern US
--> As many as 50% develop this
-SLE
--> consider if no prior strep infection
- subacute bacterial endocarditis
- can be idiopathic
Common causes of nephritic syndrome
-cause of nephritic syndrome
- an infection of heart tissue
-usually valvular and end up where pooling of blood occurs with bacteria that grow in it and is caused by blood isn't getting pushed out like it should
Subacute bacterial endocarditis
-salt restriction
-diuretics and other anti-hypertensives
-complete recovery in 90-95%
-can take 1-2 years in some individuals
-rarely progresses to chronic renal failure
Treatments of Nephritic syndrome
-type of glomerular disease
-derangement of capillary walls of glomerulus
-massive PROTEINURIA - seen as bubbly and frothy urine by patients
- generalized EDEMA - eyelids first and very extensive
- HYPOALBUMINEMIA triggers the production of all plasma proteins including lipoproteins
- HYPERLIPIDEMIA and HYPERLIPIDURIA - peripheral breakdown of lipoproteins also impaired that causes an increase risk of thromboembolism
-not inflammation of glomerulus
-get huge amt of protein
-can develop into pitting edema
Nephrotic syndrome
-beleived to be immune mediated
-diabetes, SLE, NSAID induced, Membranoproliferative glomerulonephritis, and idiopathic
Common causes of Nephrotic syndrome
-ACE inhibitors or ARB decrease protein by decreasing glomerular filtration rate, improve charge and size selectivity of glomerular BM
- more than 90% of pts respond to corticosteroids
- proteinuria recurs in more than 66% of initial responders
- use is controversial as may become steroid dependent
-other immune suppressive meds can be used
-thrombro-prophylaxis during first 6 months
-place pt on meds to alter renin-angiotensin because who renin cascade will end up causing vasoconstriction of efferent arteriole which increases the pressure and makes the glom leaky
Treatment for Nephrotic syndrome
- a very specific form of nephrotic syndrome
-immune system damages capillaris and supporting mesangium
- at least two subtypes often of unknown cause
- can cause HTN and signs of nephrotic syndrome
- Type II assoc with bilateral central clustered DRUSEN
-often found in teens
-initially VA of VF unchanged
- long term = poor night vision, SRNVM, Macular detachment, central serous retinopathy, and retinal atrophy
Membranoproliferative glomerulonephritis - dense deposit disease
- a group of inflammatory kidney diseases that primarily involve the interstitium and tubules
- spares the glomeruli and renal vessels
- can be acute or chronic
TIN
-type of TIN
-often caused by bacterial infection of the renal pelvis
- due to infection
Pyelonephritis
-type of TIN
-if noninfection in origin
-drugs and metabolic disorders
-physical injury
Interstitial nephritis
- type of TIN
- in young adults between 10 and 33
- occurs in females more than males
- bilaterial uveitis in majority
- conjunctival injection, fine KP, iridocyclitis
- ocular symptoms occur first in about 35%
- often recurrent
- fever, weight loss, fatigue that is very nonspecific
- oral corticosteroids
Acute idiopathic tubulointerstitial nephritis and uveitis
-inflammation of kidney and renal pelvis
- almost always bacteria getting to kidney retrograde via the bladder and ureters
- almost exclusively in women due to length and location of urethra
- esp common in pregos
- clinically there is fever, dysuria, flank/back pain, and pyuria
-usually very responsive to abxs
Acute pyelonephritis
- slowly progressing and insidious disease which slowly destroys the kidney due to retrograde flow of urine
- often the only signs and symptoms are "fatigue, dont feel well" and other vague symptoms so ususally diagnosed late
-there is usually some pus in urine
-primary underlying disorder is frequent UTI from obstruction, vesicoureteric reflux, or diabetic nephropathy, many of these pts wind up on renal dialysis
- pts with diabetes have reduced immune system and glc in urine allows bacteria to grow easily
- something causes urine to go back into kidneys
Chronic pyelonephritis
-common cause of acute renal failure
- kidney based hypersensitivity reaction - type 4
- primarily includes tissue surround glom and tubules
Acute interstitial nephritis
-med that can cause acute interstitial nephritis
- body breaks these meds and is carried through glom they combine with proteins of kidney and get stuck within the kidney and we get haptun form - byproduct of something that attaches itself to protein and sets up immune response of the body
(3)
1 - Abx
--> PCN, sulfonamides, ciprofloxacin
2 - NSAIDs
--> Ibuprofen, indomethacin
3 - Diuretics
--> Thiazides, furosemide
-classic presentation of acute renal failure, fever, rash, arthralgias, and eosinophilia
- mild to no proteinuria
- no edema
- no HTN
- treat by removing causative agent
Acute interstitial nephritis
- causes include drugs such as analgesics, and cytotoxic/immunosuppressive agents
- gout
- lead exposure
- immune disorders
Chronic interstitial nephritis
- single most impt cause of ERSD in US
- direct result of metabolic changes in DM
- good glood sugar control is protective against this disease
- ACE inhibitors and angiotensin II receptor blockers are protective
- microalbuminuria and proteinuria even early on in diagnosis
- nephrotic syndrome and azotemia develop 3-5 years after proteinuria
- end stage renal disease 1-5 years after that
- accelerated decline with HTN, infection, nephrotoxins
- glomerulus capillary basement membrane thickening
- renal athersclerosis
--> affects both afferent and efferent arterioles
--> changes blood flow to kidneys
- pyelonephritis
--> increased susceptibility to infection due to warm env, poor wbcs, and sugar in urine that allows bacteria to grow
Diabetic neuropathy
-epithelium lined cavities filled with fluid or semisolid debri
Cystic diseases of the kidney
-present in up to 505 of pts over 50 and are often asymptomatic
- can be confused with tumors
- ultrasound and CT scan help differentiate
- part of cystic diseases of the kidney
Simple Cysts
-type of cysitc diseases of the kidney
- multple cysts throughout the kidneys with enlargement of kidneys
- can be inherited
- can result in chronic renal failure
PKD
-type of PKD
- autosomal dominant PKD
- most common heriditary disease in US
- M=F
- progresses slowly
- accts for about 10% of pts on dialysis
- HTN = most common cardiovascular manifestation
Adult PKD
-type of PKD
- autosomal recessive
- universally fatal by third decade
- often fatal within first year as it occurs with congenital hepatic fibrosis
-much more concerning but much less common
- involves liver and other internal organs, not just kidney
- very often causes death
Childhood PKD
- type of urinary outflow obstruction
- formation of a calculus in the collecting system
- travels down stream until too large for duct
- usually occurs in the ureters
- blockage of flow of urine
- due to coalition of ions and or minerals - get pushed down until it gets to a tube that is too smale and stops the urine flow
-occur with symptoms in 1 out of 20 people at some time in their life
- a frequent disorder found in about 1% of all autopsies
- peak incidence is between 20 and 45 years of age
- symptomatic urolithiasis is more common in males
Nephrolithiasis
-usually occurs when pt becomes dehydrated
- meds and gout
Polygenic Nephrolithiasis
Composition of Nephrolithiasis (3)
1 - Calcium - 75%
2 - Magnesium - 15%
3 - Uric acid or cystine - 10%
- hematuria
- pain is common because stone is impinging on ureter
-sudden onset, very severe
- diagnosed with CAT scan
Signs and Symptoms of Nephrolithiasis
- 90% of stones pass spontaneously
- pain relief
- meds to allow spontaneous passage
--> alpha adrenergic blockers, calcium channel blockers
- dietary modifications
- antibiotics given after they are passed
- shockwave lithotripsy - extremely strong sound wave applied to kidney area to break up large stones into smaller ones and tend to develop HTN
- very large stones may require surgery if shockwave doesnt work
Treatment of Nephrolithiasis
- causes kidney stones and we use it for ONH edema and angle closure glaucoma
- remain well hydrated to decrease the effect of kidney stones
- if pt has angle closure glaucoma you dont want them to drink alot so you can decrease IOP
Acetazolamide
- accounts for 80-90% of all malignant tumors of the kidney
- 2/1 male dominated
- accts for 2% of all cancers in adults
--> greater freq in cig smokers
- assoc with Von-Hippel Lindau disease
- long standing fever
- elevated sedimentation rate
- systemic signs of cancer like weight loss and fatigue
- develops from proximal tubules
- highly vascular
- usually treated by surgical removal of kidney
- percutaneous cryoablation and VEGF being explored
- 5 year survival rate about 70% if no metastasis
--> metastasize via bloodstream
--> the metastases may remit when primary tumor is removed
- will occasionaly spontaneously remit and nobody knows why
Renal cell carcinoma
- causes vascular tumors in many places
- has to do with renal cell carcinoma
Von Hippel Lindau disease
- most common presenting manifestation of Renal Cell Carcinoma
Painless hematuria
Classic Triad of Renal Cell Carcinoma
1 - Hematuria
2 - Dull flank pain
3 - Palpable flank mass
- second most common kidney malignancy
- third most common organ cancer in children less than 10
- can grow to an incredible size and result in abdominal distention
- high incidence of this in kids with aniridia
- treated with radiotherapy, nephrectomy, and chemotherapy
- good prognosis
--> 90% survival for 2 years
Wilms' tumor
-part of Wilm's tumor
- loss of iris or failure of iris to develop properly
- can be absent or just part of it is missing
- 20% of children with this have Wilms'
Aniridia
-remove or treat cause if known
-treatment of HTN - decreases the progression of renal failure
-treatment of secondary manifestations - heart disease, HTN, edema, anemia
-restriction of dietary protein
-avoid toxic meds
-short or long term dialysis
-renal transplantation
-has to be both the dr and pt decision
Treatments for chronic renal failure
-diuretics
-beta blockers
-ACE inhibitors
-angiotensin II antagonists
-Calcium channel blockers
-Renin inhibitors
-some of the most common and impt meds taken by pts in your practice
Antihypertensive drugs
-shown to be renal protective in diabetics beyond level expected from blood pressure drop
-and some say in all with kidney disease
-three anti hypertensive drugs
1 - ACE inhibitors
2 - Angiotensin II antagonists
3 - Renin inhibitors
-type of antihypertensive
-decrease the re-absorption of Na in kidneys
-therefore increased urine output
-initially reduce blood volume
-but blood volume may return to normal with time
--> especially if kidney function is normal
-very useful in pts with HTN due to chronic renal disease
Diuretics
Types of diuretics that are typically used for kidney, heart, and bp treatment (3)
1 - Thiazide
2 - Loop
3 - Potassium sparing
-types of Thiazide diurectics (2)
1 - Hydrochlorothiazide
2 - Chlorthalidone
-Types of Loop Diuretics
1 - Bumetanide
2 - Furosemide
Types of K sparing diuretics
1 - Spironolactone
2 - Triamterene
-type of diuretic that is commonly used in eye care for glaucoma or disc edema
-acetazolamide
CAI
-type of diuretic that is used for glaucoma
-includes mannitol, urea, and isosorbide
Osmotic diuretics
-current criteria for initiation for dialysis
-glomerular filtration rate
--> 15ml/min for diabetics
--> <10ml/min for nondiabetics
-uremia
-edema not responsive to diuretics
-acidosis
-persistent hyperkalemia
-heart failure
-encephalopathy
-two choices
-any combo of these things can cause you to do this
-decision is based on lifestyle, what symptoms pt has, and how close they live to a hospital
-want to decrease the load on kidneys in diabetics
Renal Replacement therapy
-Types of Replacement Therapies (4)
1 - Hemodialysis
2 - Peritoneal dialysis
3 - Renal treansplantation
4 - Choice depends on many factors: age, underlying disease, pt preference and motivation, donor availability, and accessibility of dialysis sites
-type of renal replacement therapy
->100,000 pts with ERSD are maintained on this
-most common tx in US
-blood circulates out of body into artificial kidney machine
-another fluid called dialysate is pumped through machine in opposite direction of blood
-semi-permeable membrane separates these two fluids
-allows diffusion of ions and low mw substances from blood into dialysate
-blood circulated back into the body
-requires 3.5 hours of dialysis three times a week
-yields minimal creatinine clearance
-strict dietary modification also needed espeically dealing with protein and phosphorous and calcium
-studies have shown that more visual impairment in pts on dialysis than expected for age - includes VA, contrast sensitivity, and depth perception
-pts don't feel the greatest
-use about 20-25% of kidney function
-risks are anemia, ionic dysfunction, heart dysfunction, pulmonary edema, and infection
Hemodialysis
-type of renal replacement therapy
-pt has indwelling catheter in peritoneal cavity
-installation of 1-3ml of dialysate into peritoneal cavity
-stays in peritoneal cavity for specific period of time
-peritoneum acts as semipermeable membrane to remove solute
-dialysate removed and more added
-in continuous ambulatory PD, fluid is constantly in peritoneum
-treated differently when prescribing meds
-
Peritoneal Dialysis
Adv of Peritoneal dialysis over Hemodialysis (4)
1 - Less time spent in dialysis activities per se
2 - Less dietary restrictions
3 - Generally more consistent filtration
4 - Residual kidney function retained longer
Risks of Peritoneal Dialysis (2)
1 - Peritonitis: not easy infection to tx
2 - Death: two times more common than with hemodialysis esp if cardiovascular disease is present and unsure why
-most satisfactory treatment for ESRD
-kidney recipients have improved health related quality of life
-preferred method of renal replacement therapy
-kidney is from a living related donor or cadaver
--> donor and recipient method for HLA type, blood type, gender
--> living donation has a better chance of graft and pt survival
-most pts take immunosuppressive durg therapy as prophylaxis for life
Renal Transplantation
-types of immunosuppressants taken with renal transplantation (3)
1 - Corticosteroids
2 - Cyclosporine
3 - Rapamune sirolimus - acute rejection
-type of immunosuppressant
-previously discussed by dr. smith
-some centers are moving away from using them due to side effects but more than 50% still use them
-ocular side effects include cats, increased risk of glaucoma, and papilledema due to increase in intracranial pressure
Corticosteroids
-type of immunosuppressant
-comes from soil fungus
-introduced in early 1980s
-increased graft survival rate by 20% for the first year
-works by suppressing cell mediated immune reactions
-prevents cytokines from activating T lymphocytes
-ususally administered concurrently with glucocorticoids
Cyclosporine
-nephrotoxicity
-hepatotoxicity
-HTN
-increased risk of infections
-increased risk of lymphoma
-interacts with many meds - increased levels of cyclosporine to toxic levels
Adverse effects of cyclosporine
-immunosuppressive disorders
-secondary HTN due to prednisone and native kidney renin production
-infections such as UTI, hepatitis, and pneumonia
-malignancy
--> 100 times greater than general population
--> skin cancer
--> kaposi's sarcoma
--> ocular sq cell carcinoma
-graft rejections are known to occur
Transplantation Complications
-a transplantation complication
-very common to show up in conj and looks like a sub-conjunctival hemorrhage
-wont change colors if it is this
-decreased with Rapamune
Kaposi's sarcoma
-try to avoid meds toxic to kidney such as aminoglycosides and tetracyclines except docycycline
-adjust amt of meds gived based on the creatinine clearance result
-can be decreased dose or increased interval
Prescribing meds for Renal Transplanation pts
Two possible formulas for dosing meds on kidney pts
Dose = (pts CrCl/ normal CrCl) x normal dose

Dosing interval = (normal CrCl/pts CrCl) x normal interval
-drug used for infection
-excretion: bile primarily
-epocrates indicates no renal adjustment but caution advised if severe impairment
Azithromycin