Renal Flashcards
Proximal convoluted Tubule
brush border reabsorbs ALL glucose and AA
reabsorbs most bicarb, sodium, chloride, potassium, water, uric acid, and PO4^3-
(PTH inhibits sodium/phosphorus cotransport)
Thick Ascending Loop of Henle
reabsorb Na (20%), K, Cl, Mg/Ca
Na/K ATPase, Cl/K pump
impermeable to water
urine less concentrated
Distal Convoluted tubule
reabsorb Na (5-10), Cl
can’t reabsorb water
Na/K ATPase
PTH: Na/Ca antiporter; inc ca reabsorption via Ca/Na exhange
makes urine fully dilute (hypotonic)
Collecting Tubule
reabsorbs Na (3-5) in exchange for K/H aldosterone regulates impacting exchanger of Na/H20
ADH increases aquaporin on apical side of membrane (urine side) > inc urea reabsorption
Where is angiotensinogen made
liver
Where is renin secreted from
Juxtaglomerular cells in kidney
What stimulates renin
decrease in renal perfusion, b1 adrenergic effect
Where is angiotensin converting enzyme (ACE) made
lung and kidney
located in multiple tissues; conversino occurs most in the lung, provided by vascular endothelial cells in lung
What does angiotensin II do
increase sympathetic activity
increase aldosterone
tubular Na, Cl reabsorption and K excretion, H20 retention
arteriolar vasoconstriction, increase BP
increase ADH to increase H20 reabsorption
limit reflex bradycardia
renin function
decrease NaCl reabsorption
Inhibition of RAAS
normal renal profusion, ANP/BNP
ANP/BNP (atrial/brain natriuretic peptide)
released from…
due to..
functions
released from atria and ventricles d/t inc volume to inhibit RAA system
inhibit RAAS; relaxes vascular smooth muscle via cGMP leading to increased GFR and decreased renin, dilates afferent arteriole
ADH (vasopression)
functions
regulates serum osmolality
responds to low blood volume states
stimulates reabsorption of water and urea in collecting ducts
Respiratory acidosis
low pH, high CO, high bicarb
hypoventilation (obstruction, lung dz, opiods, sedatives, weak respiratory muscles) > hypoxia
respiratory acidosis clinical
rapid, shallow respirations, hypotension, dyspnea, headache, hyperkalemia, dysrhythmias, drowsiness, dizziness, disorientation, muscle weakness, hyperreflexia
metabolic acidosis w/ high anion gap
low ph, low bicarb, elevated anion gap
GOLDMARK
glycols, oxoproline, l-lactate, methanol, aspirin, renal failure, ketones
Anion gap
sodium- cl+bicarb
metabolic acidosis w/ normal gap cause
HARDASS
hyperchloremia, Addison dz, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion
Respiratory alkalosis
low CO2, high pH
Respiratory alkalosis clinical/cause
hyperventilation (anxiety, hypoxemia, salicylates, tumor, PE, pregnancy)
tachycardia, hypo or N BP, hypokalemia, numbness and tingling of extremities, hyper reflexes & muscle cramping, seizures, irritability
Saline-resistant metabolic alkalosis
high chloride
hyperaldosteronism
Bartter syndrome
Gitelman syndrome
saline-responsive metabolic alkalosis
low chloride
vomiting
recent loop/thiazide diuretics
antacids
respiratory acidosis causes
airway obstruction acute lung disease chronic lung disease opioids, sedatives weakening of respiratory muscles
metabolic acidosis w/ high anion gap causes
diabetic ketoacidosis
hypoxia
carbonic anhydrase inhibitor
renal tubular acidosis
metabolic acidosis clinical
headache, hypotension, hyperkalemia, muscle twitching, warm flushed skin, N/V, dec muscle tone. dec reflexes, kussmaul respirations,
respiratory alkalosis cause
anxiety, hypoxemia, salicylates, tumor, PE, pregnancy
metabolic alkalosis clinical
restlessness followed by lethargy dysrhythmias compensatory hypoventilation confusion N/V diarrhea tremors muscle cramps hypokalemia paresthesia
Nephritic syndrome path
glomerular inflammation leads to basement membrane damage > loss of RBC in urine > hematuria
Nephritic syndrome clinical
hematuria, RBC cats, oliguria, azotemia, HTN, proteinuria (mild), increased renin release
thin descending loop of henle
passive reabsorption of water
impermeable to sodium
makes urine hyeprtonic (concentrated)
ACE function
catalyzes conversion of angiotensin I to II
aldosterone function and mechanism
regulates extracellular volume and sodium content by targeting kidneys in response to hypovolemic and hyperkalemic (inc potassium excretion) states
low bicarb =
metabolic acidosis
high bicarb =
metabolic alkalosis (check urine chloride)
with low bicarb you suspect ___ and should check ___
metabolic acidosis, anion gap
with high bicarb you suspect ___ and should check ___
metabolic alkalosis, urine chloride
nephritic syndrome ex
infxn-associated glomerulonephritis goodpasture syndrome igA nephropathy (berger dz) alport syndrome membranoproliferative glomeulonephritis
infxn associated glomerulonephritis etiology
type II hypersensitivity rxn
kids: group A strep
Adults: straph or strep
IgA nephropathy (berger disease)
episodic hematuria occuring concurrently with respi or GI infxn
igA secreted by mucosal linings
alport syndrome
mutation of type IV collagen
irregular thinning and thickening and splitting of glomerular basement membrane
x-linked dominant condition
cant see, cant pee, cant hear a bee
nephrotic syndrome etiology
podocyte damage > impaired charge barrier > MASSIVE proteinuria
associated with hypercoagulable state d/t antithrombin III loss in urine
nephrotic syndrome clinical characteristics
edema, hypoalbuminemia, HLD, frothy urine with fatty casts
nephrotic syndrome ex
primary
secondary - amyloidosis, diabetic glomerulonephropathy, lupus nephritis, fabry dz
both - focal segmental glomerulosclerosis, minimal change dz, membranous glomerulopathy, membranoproliferatie glomerulonephritis
glomerulosclerosis etiology
idiopathic, or due to other conditions:
HIV, sickle cell, heroin use, obesity, congenital malformations, drug induced
glomerulosclerosis complication
CKD
erythryopoietin:
released from where
in response to what
function
released from interstitial cells in peritubular capillary bed in response to hypoxia
stimulate RBC proliferation in BM
calciferol (VitD) conversion process, and stimulation
PCT converts OH > OH calcitrol active form via 1a hydroxylase
^ by PTH
prostaglandins are secreted from where to do what
secreted by paracrine to vasodilate afferent arterioles to increase RBF
dopamine is secreted by what cells to do what
secreted by PCT cells to promote natriuresis
low doses: dilate interlobar arterise, aff arterioles, and eff arterioles to inc RBF
with little to no change in GFR
high doses: acts as a vasoconstrictor
PTH:
secreted from where
in response to what
function
secreted by hypothalamus/pituitary in response to dec Ca, inc phosphate or dec vit D
causes increase of Ca RA in DCT, dec phos RA in PCT, inc active D production
increases both Ca and phos absorption from gut
what is the primary fuel source for the kidneys
glutamine
nitrogen is used to help with acid-base balance, but not a fuel source
clinical characteristics of low Na
N, malaise, stupor, coma, serizures
clinical characteristics of high Na
irritability, stupor, coma
causes of hyponatremia
hypovolemic: renal loss/GI loss
euvolemic: SIADH, hypothyroid, adrenal insufficiency, primary polydipsia
hypervolemic: HF, cirrhosis, nephrotic syndrome
clinical characteristics of low K
U waves and flat T waves on ECG, arrhythmias, cramps, spasm, weakness
clinical characteristics of high K
wide QRS, peaked T wave, arrthmyias, muscle weakness
clinical characteristics of low Ca2+
tetany, seizures, QT prolongation, twitching chovsteks and spasm trousseau
clinical characteristics of high Ca2+
stones, bones, groans, thrones, psychiatric overtones
clinical characteristics of low Mg
tetany torsades de pointes, hypokalemia, hypocalcmia
clinical characteristics of high Mg
hyporeflexia, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa
what electrolyte is used to treat vasospasm
Mg
clinical characteristics of low phosphate
bone loss, osteomalacia, rickets
clinical characteristics of high phosphate
renal stones, metastatic calcification, hypoCA
defining/differentiating clinical characteristics for acute cystitis
pyuria, no casts
defining/differentiating clinical characteristics for bladder CA and kidney stones
hematuria, no casts
what do urine casts indicate when present with hematuria or pyuria
hematuria and pyuria is from glomerulus or renal tubules
what dx do RBC casts suggest
GN, malignant HTN
what dx do WBC casts suggest
acute PN, tubulointerstitial inflammation, transplant rejection
what dx do fatty casts suggest
nephrotic syndrome
what dx do granular casts suggest
ATN
what dx do waxy casts suggest
ESRD, CRF
what dx do hyaline casts suggest
nonspecific, often seen in concentrated urine
membranous glomerulopathy etiology
damage due to immune complexes activating complement which causes damage to podocytes and mesangial cells
primary (idiopathic) 75%
secondary: hodgkins, lupus, drugs (NSAIDs, gold, mercury, captopril, penicillamine), infxn (hep B/C, syphilis), solid tumors (colorectal carcinoma)
what cells are damaged in membranous glomerulopathy
podocytes an mesangial cells
RF membranous glomerulopathy
white
membranous glomerulopathy complications
RVT (renal vein thrombosis)
membranous glomerulopathy clinical characteristics
HTN
nephrotic sx
what are general sx of all nephrotic syndromes
HIGH proteinuria edema (pitting, periorbital) hypoalbuminemia hyperlipidemia lipiduria proteinuria frothy urine
focal segmental glomerulosclerosis etiology
primary: idiotpathic, podocyte foot processes damaged
secondary: heroin drug use, HIV, sickle cell, interferon tx, congenital malformations
focal segmental glomerulosclerosis RF
african american pts
young adults
what nephrotic syndrome makes up 1/6 of all
focal segmental glomerulosclerosis
focal segmental glomerulosclerosis prognosis
poor
minimal change disease etiology
primary: unclear; can occur afer URI or immunization
secondary: drugs (NSAIDS, antibiotics, lithium), hodgkins, syphilis, TB, allergy
minimal change disease clinical characteristics
none to mild
nephrotic sx
LM: mild mesangial prolif and few deposits
EM: epithelial foot process flattened
membranoproliferative glomerulonephritis (MPGN) etiology
immune complexes and complement
primary: idiopathic
secondary: RA, HCV, HBC
variant: C3 GN-C3 deposits: hematuria after URI
membranoproliferative glomerulonephritis (MPGN) complication
RPGN
membranoproliferative glomerulonephritis (MPGN) clinical characteristics
nephrotic sx
insidious
histology: difuse thickening (hypercellularity) of glomerular capillary wall with Ig deposits
diabetic glomerulonephropathy etiology
occurs several years after onset of DM (I and II)
excess glucose causes BSM of efferent arteriole to thicken, creating obstruction and inc pressure > expansion of mesangial cells
diabetic glomerulonephropathy complication
renal failure
diabetic glomerulonephropathy clinical
no overt sx
histology:
glomerulosclerosis - nodular (kimmelsteil wilson disease), diffuse, or nodular diffuse
microalbuminuria
macroalbuminuria
dec GFR
lupus nephritis etiology
anti DNA and anti dsDNA immune complexes deposit on glomerular mesangium
lupus nephritis RF
african amerians (APO1 gene variants common)
lupus nephritis clincal
renal involvement + skin, joint sx, anemia, photosensitivty, pericardial or pleural effusion
hematuria
proteinuria
casts
low C3, C4
wire loop lesions on biopsy
fabry disease etiology
x linked deficiency of alpha galactosidase A leading to an accumulation of glycolipids
fabry disease clinical characteristics
proteinuria, renal failure
lipids in: joints skin eyes heart GI
pre-renal acute renal failure pathophys
dec renal flow inc Na + H2O retention, baroceeptors activate > inc sympathetioc > afferert vasoconstriction > dec GFR renin/aldosterone > inc Na + H2O water resroption
pre-renal acute renal failure causes
dec intravascular volume (hemorrhage, dehydration, pancreatitis, burns, trauma)
changes in vascualr resistance (sepsis, anaphylaxis, drugs [ACEi, NSAIDs], renal artery stenosis)
low CO (CHF, PE, pericardial tamponade)
pre-renal acute renal failure RF
DM, hypertensives, geriatrics
pre-renal acute renal failure complications
death
fluid accumulation
acute renal failure general sx for all types
N/V malaise ecchymosis pallor arrhythmias edema fasiculation seizure blood volume abnormalities dehydration
3 types of acute renal failure differentiating clinical characteristics
pre-renal:
osmol >500, FeNa <1, BUN/Cr >20
dehydration sx, orthostatic hypo, tachycardic
intrinsic:
osmol <350, FeNa >1, BUN/Cr N (10-15:1)
WBC casts (PN, AIN), RBC casts (PSGN)
hearing loss, ischemic toe, uveitis, scleroderma, bruit
post-renal:
osmol >500, BUN/Cr 10-20:1
renal pain, lower ab pain, post surgery urine leak, overhydration, abd disten
Na <20 early, >40 late
intrinsic acute renal failure etiology
damage to tubules, interstitium, vasculature, glomeruli > loss of function
ATN: cannot resorb Na, water, electrolytes, urea
AIN: loss of concentation ability
intrinsic acute renal failure causes
ATN, AIN
PSGN, RPGN, acute pyelonephritis, vasculitis, nephrotic syndromes
intrinsic acute renal failure RF
DM, hypertensives, geriatrics, IV drugs, URI
post-renal acute renal failure etiology
abrupt obstruction of urine from both kidneys > inc nephron intraluminal back pressure > inc bowmans capsule hydrostatic pressure > dec GFR
post-renal acute renal failure causes
prostatic enlargement, tumors, urolithiasis, renal vein stenosis, neurogenic bladder, meds, trauma, post-surgical
post-renal acute renal failure RF
DM, hypertensives, geriatrics
chronic renal failure etiology
loss of functioning nephron leads to buildup of urea, cant regulate fluids and electrolytes
chronic renal failure causes
diabetes, HTN, PCKD, focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferatie GN, IgA nephropathy, PIGN, RPGN, nephrolithiasis, tumor, prostate conditions, drugs/toxins, sickle cell, amyloidosis, SLE, renal artery stenosis
chronic renal failure sx
HTN edema fatigue weakness SOB N/V numbness low SG low osmol broad waxy casts dec GFR anemia azotemia low Bun:Cr microalbuminemia hyperkalemia, hyperphosphatemia hypocalcemia
what is the most common cause of ARF
acute tubular necrosis (ATN)
acute tubular necrosis (ATN) etiology/pathophys
patchy focal nerosis of tubule, lumens fill with casts, cellular debris; due to drugs, contrast, lithium
ATN - contrast induced nephropathy etiology
iodinated radiocontrast agent
48 hrs causing renal hypoxia and tubular obstruction
ATN - contrast induced nephropathy RF
elderly, DM, CHF, liver dz
ATN general sx
Bun:Cr <15 dec GFR brown granular casts, hyaline casts dilute urnie inc K FeNa >2 RTE + RTE casts osmol <400 inc creatinine hematuria mild proteinuria
ATN - cisplatin induced nephropathy etiology
chemotherapeutic agent causes both vascular damage and tubular inflammation
ATN - lithium induced nephropathy etiology
one month onset of lithium
ATN - lithium induced nephropathy differentiating sx
cardiotoxicity polydipsa obtundation polyuria ortho hypo
ischemia/hypotension ATN causes
shock, trauma, surgery, DIC, vasoconstrictive drugs (ACE, ARBs)
ischemic ATN etiology
partchy PCT and DCT due to hypovolemia, shock, renal artery stenosis, embolism in renal artery, etc. causes skin lesions through tubules
ischemia/hypotension ATN clinical characteristics
pericardial friction rub uremic pruritis HTN edema oliguria
hydronephrosis etiology
congenital or acquired
dilation of renal pelvis and calyces from obstruction/retained urine
back pressure causes renal atrophy, compresses renal vasculature > dec ability to conc urine, damage to gloomeruli
retained urine diffuses into interstitium and perineal spaces, returns to lympathic and venous system
leads to scarring and atrophy of papillae > inability to conc urine, salt wasting, HTN
if complete: anuria (>death)
hydronephrosis clinical characteristics
flank, lower abd, testes/labia pain pain in flank during urination abdominal mass N/V urgency, frequency polyuria/nocturia HTN anuria
BUN/Cr inc
hypernatremia, hyperkalemia
what are two main inflammatory urinary tract diseases?
AIN, chronic pyelonephritis
acute interstitial nephritis (AIN)
inflammation of renal interstitium from cell mediated immune response binding to interstitial proteins, leading to dec in renal function
1-2 weeks after taking NSAIDS/ibuprofen, acetaminophen, penicillins, thiazides, sulfa, PDE5 in, acyclovir
infxn: strep, s aureus, corynebacterium, brucella, pneumococcus, TB, HIV, EBV, lepto
SLE, sarcoidosis, sjogrens
AIN sx
fever wt loss flank pain fatigue hadache polyuria rash hematuria oliguria N/V malaise
inc eosinnophils, WBC, neutrophils WBC casts proteinuria, hematuria, no bacteria inc BUn and cr FeNa >1 dec urine conc, dec GFR
chronic pyelonephritis etiology/path
often bilateral pyogenic kidney infxn or congenital reflux nephropathy > renal parenchymal scarring and atrophy of calyces
chronic pyelonephritis RF
elderly, DM, chronic urolithiasis, low water intake, infrequent urination, urine reflux, sedentary lifestyle, BPH with obstruction, chornic analgesic use, recurrent bacterial UTI
chronic pyelonephritis sx
asx
HTN
olioguria late stage
bactururia, pyuria if active infxn
dec SG and osmol
late: granular, waxy, broad casts
small atophic kidney, irregular outline, poor exception of contrast
what are some common congenital urinary diseases?
alport syndrome
ADPKD
renal agenesis
vesicouretal reflux (VUR)
alport syndrome etiology
hereditary or familial nephritis
inherited collagen synthesis defect leading to GBM thinness and dysfunction
alport syndrome RF
males
alport syndrome complication
progression > ESKD
alport syndrome sx
sensorineural hearing loss ocular lesions HTN edema hematuria aftre URI proteinuria oliguria
autosomal dominant polycystic kidney disease (ADPKD) etiology
mutation in PKD 1 or PKD 2
mutation in renal tubule cell causes cellular divison until cysts develop
major cause of CKD
autosomal dominant polycystic kidney disease (ADPKD) complications
CKD, ESRD, rupture, UTI, nephrolithiasis, HTN, ESRF, cerebral aneurysm, MVP, aortic aneurysm, colonic diverticula, cyst in liver, pancreas, spleen, CNS
autosomal dominant polycystic kidney disease (ADPKD) sx
hematuria flank pain HTN kidney stones pain over both kidneys nocturia HA N/V wt loss progressive uremia bacteruria pyuria proteinuria anemia
autosomal dominant polycystic kidney disease (ADPKD) diagnostic criteria
15-39 - 3 cysts in both k
40-59 - 2 cysts in both k
pos fam hx
CT diagnostic
vesicouretal reflux (VUR) etiology
malposition or incompetent closure of UVJ allows for urine to reflux from bladder
congenital or acquired (scarring, obstruction)
vesicouretal reflux (VUR) sx
asym
present as recurrent UTI (esp pyelonephritis)
HTN
common urinary vascular diseases
hemolytic uremic syndrome (HUS) hyperensive nephrosclerosis renal artery stenosis renal infarction sickle cell nephropathy
hypertensive nephrosclerosis etiology
chronic HTN (>10 yrs) damages microvascualture, glomeruli, tubules, interstitial tissues > nephrosclerosis
may progress to ESRD
injuries include ischemic glomerular tuft collapse, glomerulosclerosis, interstitial fibrosis and tubular atophy
hypertensive nephrosclerosis RF
aging, poorly controlled HTN, DM, black individuals, genetics (APOL1)
hypertensive nephrosclerosis complications
second most common cause of ESRD
hypertensive nephrosclerosis clinical
inc BUN, cr
hyperuricemia
kidneys may look small from scarring
no sediments/proteinuria
renal artery stenosis etiology
from atherosclerotic plaque or fibromuscular dysplasia (intractable HTN from renin release)
renal artery stenosis causes
HTN
renal artery stenosis RF
older males, atherosclerotic plaques, HTN
in younger pts, from fibromuscular dysplasia of renal arteries (more in F)
renal artery stenosis clinical
bruit
inc BP
hypokalemia
stenotic kidney inc renin
contralateral kidney responds to HTN by dec renin
renal infarction etiology/causes
reduction of blood flow to one or both kidneys
caused by thromboemboli (from heart or aorta) and in situ thrombosis
renal cell carcinoma (RCC) etiology
malignant
originates from PCT cells, polygonal clear cells filled with accumulated lipids and carbs
most common primary renal malignancy
renal cell carcinoma (RCC) RF
smoking, analgesics, toxin exposure, high coffee consumption, chemo, hysterectomy, obesity, cystic kidney dz, contrast, HTN, dialysis, von hippel landau dz
males 50-70
renal cell carcinoma (RCC) complications
invades the renal vein and may develop a variocele if L sided
can go into IVC and spread hematogeously, mets to bone and lung
renal cell carcinoma (RCC) sx
hematuria palpable mass polycythemia flank pain fever wt loss
nephroblastoma (wilms tumor) etiology
malignant
most from defects on chromosome 11
most comnmon primary renal tumor of childhood
nephroblastoma (wilms tumor) RF
black pts
fhx
children 2-5
nephroblastoma (wilms tumor) complications
mets to lungs
nephroblastoma (wilms tumor) sx
abdominal enlargment flank mass abd pain N/V constipation loss of appetite SOB hematuria HTN anemia
acute pyelonephritis etiology
common
inflammation affecting the tubules, interstitium, and renal pelvis
ascending infxn most common
85-90% from gram neg bacilli (usually e coli)
acute pyelonephritis causes
urinary tract obstruction/stasis (organisms multiply)
vesicouretal reflux
intrarenal reflux
acute pyelonephritis complications
renal abcess
recurrent infxns
papillary necrosis (worse prognosis)
acute pyelonephritis sx
fever N/V chills unilateral flank pain abd pain myalgia fatigue weakness CVA tenderness
WBC in urine WBC cats leukocytosis pyuria bacteruria hematuria
bacterial cystitis etiology
e coli, proteus, klebsiella, enterbacteria
cystitis RF
females
cystitis sx
urgency, frequency, dysuria, nocturia hematuria pain with filling/emptying suprapubic pain burning pressure chronic pelvic pain
interstitial cystisis sx
cystitis sx pain with bladder fullness severe frequency hunners ulcers bladder distention
sx > 6 weeks, absences of other sx
gonoccocal urethritis etiology
STI
common
men
neisseria gonorrhoeae
gonoccocal urethritis complications
epididymitis, prostatic involvement, infertility, prostatitis, recurrent infxns
gonoccocal urethritis sx
copious, purulent urethral discharge (yellow, brown)
dysuria urethral itching meatal edema urethral tenderness pyuria bacteriuria hematuria
gram neg diplococci
non-gonoccocal urethritis etiology
chlamydia
incubation 2-35 days (less acute onset)
non-gonoccocal urethritis complications
epididymitis, prostatitis, proctitis, reactive arthritis, lymphogranuloma venereum
non-gonoccocal urethritis sx
scant, white to clear watery urethral discharge
dysuria
urethral itching
meatal edema and erythema
cant culture chlamydia
acute urethritis in women etiology
gonorrheal or chlamydial
acute urethritis in women sx
asx frequency urgnecy lower abdominal pain cervicitis
maple syrup urine disease (AR) etiology
blocked degradation of branch chain amino acids (isoleucine, leucine, valine)
dec branched chain a ketoacid dehydrogenase
inc a keto acids in blood
maple syrup urine disease (AR) sx
vomiting poor feeding urine smells like syrup severe CNS defects intellectual disability death
embryologic origin of bladder
endoderm: epithelial lining
embryologic origin of kidneys
mesoderm
bladder circulatory supply
internal iliac arteries
ureters plug into bladder at the
bottom
Ureters pass where in relation to the uterine artery or vas deferens
under (retroperitoneal)
renal artery and vein enter and exit at the
hilium
the glomerulus is surrounded by the
bowmans capsule
the nephron includes
afferent + efferent arterioles glomerulus/bowmans capsule PCT loop of henle DCT collecting duct
two types of nephrons
cortical (only have asc and desc loops)
juxtamedullary (thin loop of henle)
afferent arteriole brings blood
into glomerulus
efferent arteriole brings blood
out of glomerulus
where does the peritubular capillary system/vasa recta come off of?
afferent or efferent
efferent arteriole
peritubular capillary sys keeps you from reabsorping bad stuff, keeps good stuff going back into blood.
glomerulus is made up of
type 2 capillaries; mildly leaky, can filter
afferent arterioles are sensitive to
epinephrine (constriction/dec GFR)
efferent arterioles are sensitive to
angiotensin-2 (constriction/inc GFR)
epinephrine effect on GFR
decreases
angiotensin 2 effect on GFR
increases
glomerulus filtration type + components
pure filtration;
pressure, fluid, pore size
> urinary filtrate
peritubular capillaries function
resorb good stuff
secrete bad stuff
macula dense function and location
sensory apparatus at end of tubular system and wound up near afferent/efferent arterioles
renal blood flow (RBF) values compared to renal plasma flow (RPF) values
RBF is about double RPF
why is normal filtration fraction high?
FF = GFR / RPF
type II glomerular capillaries ONLY filter plasma, and RPF is half of RBF
interpretation of clearance > GFR
filtration + net secretion
interpretation of clearance = GFR
filtration only (or secretion = resorption)
interpretation of clearance < GFR
filtration and net resorption
most common cause of hyperosmolality
dehydration
hyperosmolality results in:
thirst
ADH release
trying to thin blood out
where are receptors for osmoregulation located
hypothalamus
what are the receptors for volume regulation
baroreceptors
macula densa
blood volume loss results in:
sympathetic activation
renin release from JGA
proximal tubule reabsorption/activity
67% Na reabsorption via Cotransporter + countertransporter in Na/H exhange
67% K reabsorption along with Na + H2O
all glucose, PCO3, and amino acids
thick asc loop of henle reabsorption/activity
25% Na resorption
20% K resorption
Na-K-2Cl transporter
distal tubule/collecting duct reabsorption/activity
8% Na resorption via Na-Cl cotransporter
site of thiazide diuretic action
either reabsorbs (low blood potassium) or secretes K+ into urine (high blood potassium) based on dietary intake
carbonic anhydrase inhibitiors site of action
proximal tubule
loop diuretic site of action
henle loop
thiazide diuretics site of action
distal tubule
where is H+ secreted and as what
proximal and distal tubule
NH4, phosphate, uric acid, H+
recovery of bicarbonate takes place mostly where
proximal tubule
juxtoglomerular apparatus function
low Na/Cl at macula densa > low GFR > JGA releases renin in response to low GFR > forms ANG-II > constricts EFF art > inc GFR
low GFR =
ion levels
= inc Na/Cl reabsorption in loop of henle
= low Na/Cl at macula densa
angiotensinogen produced by the
liver
activation of aldosterone-renin-angiotensin system
dec GFR (low blood vol/high blodo osmolarity) > juxtoglomerular cells release renin which converts angiotensin to angiotensin I
conversion of angiotensin I-angiontensin II
conversion by ACE enzyme from lungs
activities of angiotensin II
- GFR inc by efferent arteriole constriction
2. zona glomerulosa (adrenal cortex) activation of aldosterone
aldosterone action
> distal tubule, causes Na reabsorption, K excretion
inc H2O resorption, inc blood vol, dec osmolarity
renin produced by the
kidney (JGA)
ANP produced by the
heart
aldosterone-renin-angiotensin system function
regulation of blood volume
activated by dec in renal blood flow
less ADH effect on osmolarity and urine volume
inc urine vol
dec urine osmolarity
inc plasma osmolarity
more ADH effect on osmolarity and urine volume
dec urine volume
inc urine osmolarity
dec plasma osmolarity
ADH response to dehydration
increases
transamination and amine transfer occur in the
liver (most)
kidneys
oxidative deamination
taking amine off of amino acid > alpha keto acid
reductive amination
taking alpha keto acid > amino acid
transamination rxns consist of
oxidative deamination
reductive amination
transamination rxns purpose
removing nitrogen
transaminases require
vit B6
where does urea cycle occur
liver cell
main purpose of urea cycle
the way the liver takes two very dangerous metabolites (CO2 + NH4/ammonia) > combines them > converts them to urea > excrete into blood > filtered out via tubular system
why is urea safer to excrete than CO2 and ammonia?
because CO2 and NH4 (ammonia( are directly toxic to every cell, urea is mildly inert unless it builds up a LOT
what part of the urea cycle happens in the mitochondria?
CO2 + NH4 > carbamyl phosphate (CP) via CP synthase
CP + ornithine > citrulline via ornithine transcarbamoylase
what part of the urea cycle happens in the cytosol?
citrulline > arginosuccinate > arginine
argninase cleaves urea molecule off of arginine to leave to liver + kidney
residue ortnithine goes back into mitochondria
backup for N excretion
glutamate shuttle (glutamate is multi-N carrier)
glutamate shuttle
glutamate > deaminated > NH3 to urine
NH3 meet H+ > NH4 > excreted into urine
NH4 excreted DIRECTLY into urine
acute post-strep glomerulonephritis clinical characteristics
RBC casts, 1-2 wks after sore throat
kids 6-10, mod proteinuria
IgA nephropathy/bergers dz patho
inc IgA in response to viruses, bacteria, food proteins
antibodies injure glomerulus
IgA nephropathy/Bergers dz clinical characteristics
hematuria comes and goes, chronic GN
goodpastures syndrome patho/etiology
rapid GN with type II autoantibodies to basement membrane
goodpastures RF
young men who smoke
goodpastures complications
death due to renal failure or lung hemorrhage
henoch schonlein purpura patho/etiology
purpuric skin lesions on extensor surface of extremities and buttock
igA precipitation after respiratory infxn, kids 3-8
hematuria recurres for years
pyelo- indicates
renal pelvis
most common cause of nephrotic syndrome in kids
primary kidney dz
most common causes of nephrotic syndrome in adults
membranous GN, SLE, DM, amyloidosis
pyelonephritis affects which locations
tubules and interstitium
common causes of pyelonephritis
ascending fecal flora, females, pregnancy, BPH (secondary to stasis of urine)
what is hydronephrosis
dialtion of renal pelvis and calyces asso. with progressive atophy of kidney due to obstruction of urine outflow
ways pyelonephritis can kill you
kidney failure
bacteria > blood > sepsis
most common kidney stone substance
Ca Oxalate
intrinsic causes of obstruction
renal calculi, strictures, blood clots, tumors
extrinsic causes of obstruction
pregnancy, periureteral inflammation/salpingitis/peritonitis, tumors of rectum/bladder/prostate/ovaries
uric acid calculi are secondary to
gout
causes of obstruction of bladder neck
prostate enlargement
chronic cystitis
tumors, foreign body, calculi
what is the number one RF for renal cancer
smoking
what is a common sx of renal cancer
painless hematuria
most common bladder tumor
transitional cell carcinoma
wilms tumor (nephroblastoma) occurs in what age group
2-5
what would you suspect in a child 2-5 with abdominal mass
nephroblastoma (renal)
neuroblastoma (adrenal medulla)
kidneys role in maintaning acid-base balance of the blood
reabsorb bicarbonate HCO3- from urine > blood
secrete H+ ions > urine
which kidney has a longer renal vein
left
describe renal blood flow
renal a > segmental a > interlobar a > arcuate a > interlobular a > afferent art > glomerulus > efferent art > vasa recta/peritubular cap > venous outflow
what part of the kidney is more susceptible to ischemia and hypoxia? why?
renal medulla (less blood flow than cortex)
the visceral layer of bowmans capsule is made up of
podocytes
3 common points of uretal obstruction
uretopelvic junction
pelvic inlet
ureterovesical junction
