Renal Flashcards
kidney function
-excrete excess/harmful substances
-maintain constant volume and composition of fluid
-endocrine function- secrete renin, erythropoietin (stimulate RBC production), and 1,25-dihydroxycholescalciferol (vitamin D for calcium homeostasis)
medulla
-outer medulla- has outer and inner stripe
-inner medulla
-papilla- innermost tip of inner medulla -> minor and major calyces
nephron
-afferent arterioles -> filter blood in glomerulus -> ultrafiltration -> efferent arterioles -> peritubular capillaries
-function unit of the kidney
-efferent arteriole then loops down along the loop of henle (becomes the vasa recta) -> allows for reabsorption from loop to vasa recta -> goes into venous system
-afferent and efferent arteriole before and after allow for regulation
filtration
-we dont filter out proteins, RBC, glucose
-any glucose that does filter gets reabsorbed in a healthy individual
diabetes
-transporters are saturated
-excrete glucose
-with glucose comes water
-diabetics c/o thirst and frequent urination
parts of nephron
-glomerulus- filters out plasma
-proximal convoluted tubule- reabsorption
-loop on henle- filtrate/concentrated urine
-distal convoluted tubule- acid base regulation and water reabsorption
-collecting duct- absorbs water, concentrates urine
-ureter
-each part has different epithelial cell based on its function -> each part has different transport membranes and permeability
juxtamedullary nephron
-peritubular capillaries have specialization -> VASA RECTA -> follow same course as loop of henle
-vasa recta reabsorbs from loop of henle -> goes into venous
-vasa recta serve as osmotic exchanges for production of concentrated urine
-longer loop on henle
-filters a lot more blood
-greater concentrating ability
-removes water to concentrate urine
-higher GFR
superficial nephrons
-peritubular capillaries branch off efferent arterioles and deliver nutrients to epithelial cells
-peritubular capillaries also serve as blood supply for reabsorption and secretion
-reabsorption and secretion
total body water
-total body water is inversely proportional to body fat
-60% total body water/weight -> ICF (40%) and ECF (20%)
-1/3- ECF -> Na, Cl, HCO3-
-2/3- ICF -> K, Mg, anions (Proteins and organic phosphates)
-ECF is made up of interstitial fluid (around cells 3/4) and plasma (blood 1/4)
-plasma and interstitial fluid is separated by capillary wall
gibbs-donnan effect
-small differences in concentrations of small cation and anions between interstitial fluid and plasma
-plasma contains slightly negative plasma proteins -> slight retention of Na and slight repellant of Cl -> goes into interstitial fluid
dilution method
-use substance that will only stay in
transcellular compartment
-small
-CSF, pleural, peritoneal, digestive fluids
plasma
-aqueous blood
-55% of blood
-hematocrit- % of blood volume occupied by RBCs
-plasma protein- 7%
-93%- plasma water
osmolarity
-from ICF to ECF (vice versa) based on osmolarity
-disturbances- diarrhea, dehydration, adrenal insufficiency, infusion of isotonic saline, NaCl intake, syndrome of inappropriate antidiuretic hormone (SIADH)
-hyperosmolic - water shifts in
-osmotically active solutes- depends on Na, Cl, and HCO3-
-plasma osmolarity determined by Na, glucose, BUN
-plasma osmolarity is the one we can alter - give fluids
-steady state- all osmolarity is equal
volume contraction and volume expansion
-volume contraction- decrease in ECF volume
-volume expansion- increase in ECF volume
-influenced by hypo, hyper, iso osmotic state
isosmotic disturbance
-diarrhea
-isosmotic change
-losing water, Na, Cl
-volume we are losing is isosmotic to plasma
-osmolarity between ECF and ICF stay the same
-losing NaCl and water from ECF at the same proportion of ICF*
-ECF volume decreases*
-ICF volume remains the same
-tx- infusion isotonic fluid into plasma -> increase ECF volume without changing osmolarity
hyperosmotic volume contraction
-dehydration
-not drinking water, sweating
-1. losing pure water from ECF
-2. ECF higher in osmolarity (hyperosmotic) -> sucks fluid out of ICF
-3. reduction of volume is both ICF and ECF in order to maintain a equal osmolarity between each
-each reduce volume and increase osmolarity
-hyperosmotic volume contraction!!
hypoosmotic volume contraction
-adrenal insufficiency
-not enough aldosterone (holds onto sodium)
-1. loss of Na in ECF
-2. ECF becomes hypoosmotic
-3. water sucked into ICF from ECF (bc ICF is hyperosmotic to ECF)
-overall- ECF decreases volume and ICF increases volume AND both reduce osmolarity
isotonic volume expansion
-infusion of isotonic NaCl
-adding into ECF straight into plasma
-increases ECF volume
-no water shift bc substance added is the same osmolarity
hyperosmolar volume expansion
-high salt diet- increase NaCl intake
-1. increases the osmolarity of ECF (hyperosmotic)
-2. ECF sucks fluid from ICF
-overall both compartments increase osmolarity and ECF increases volume and ICF loses volume
hypoosmotic volume expansion
-increased ADH (holds onto pure water)
-1. increased water in ECF
-2. decrease osmolarity in ECF
-3. ICF is hyperosmotic to ECF
-4. ICF sucks fluid from ECF
-increased volume and decrease osmolarity in ICF and ECF
renal clearance
-volume of plasma cleared of substances by the kidney per unit of time
-urine concentration x urine flow (how fast its being produced) / plasma concentration of substance
clearance of proteins
-kidneys do not filter proteins
-albumin renal clearance is zero
-albumin shouldnt even enter the urine in a normal healthy pt
renal clearance: glucose
-zero
-kidneys can filter glucose but gets completely reabsorbed into blood at the proximal convoluted tubule after its been filtered
-no glucose should be in the urine
-glucose is reabsorbed with Na via Na glucose cotransporter (SGLT) across lumen of proximal tubule against glucoses concentration gradient
-Na is able to flow down its concentration gradient due to gradient created by Na K pump in peritubular membrane (blood side) -> pumps Na out of proximal tubule and K in
-secondary active transport
-once glucose is in the proximal tubule -> glucose concentration in blood is lower so it is able to undergo facilitated diffusion (GLUT1/2) across and enter into the blood stream
-if transports become saturated with glucose -> glucose is excreted in urine
glucose trends
-as glucose increases glucose filtration increases
-as glucose increase reabsorption increases to a point…plateous due to saturation of transporters
-as glucose increases past maximal reabsorption -> increases excretion of glucose
-glucosuria
-water follows glucose -> dehydration -> thirst -> frequent urination
inulin renal clearance
-high
-freely filtered across glomerular capillaries
-not reabsorbed or secreted
-all inulin that is filtered is excreted
-amount filtered = amount excreted = clearance of inulin = GFR
-glomerular marker*
-if substance isnt cleared well -> inulin is high relative to it
-if substance is over excreted/cleared -> filtered and secreted into the nephron -> it will be higher than inulin
glomerular marker
-must be freely filtered across membrane
-cannot be reabsorbed or secreted into nephron
-when infused/injected into blood it should not change GFR
-inulin must be injected
-creatinine is used as endogenous molecule- mostly fits the criteria
clearance ratio
-substance clearance / inulin clearance = clearance ratio
-Clearance ratio = 1 -> same as inulin -> filtered but not reabsorbed or secreted
-clearance ratio < 1 -> substance is being reabsorbed or not being filtered (ex. albumin, glucose)
-clearance ratio > 1 -> substance is being filtered and secreted into nephron (ex. K, and organic acid and bases)
atrial natriuretic peptide (ANP)
-also brain natriuretic peptide (BNP)
-cause dilation of afferent arterioles and constriction of efferent arterioles
-greater affect on afferent arterioles -> overall decrease in renal resistance -> increase RBF -> increase GFR
prostaglandins
-vasodilation of afferent and efferent arterioles
-same stimuli that increase sympathetic tone and angiotensin 2 during hemorrhage -> activate prostaglandin production
-protective measure for RBF -> opposes excessive sympathetic and angiotensin 2 effects
-NSAIDs inhibit prostaglandins -> interfere with protective property of prostaglandins during hemorrhage
dopamine
-low dopamine- dilates cerebral, cardiac, splanchnic, and renal arteries -> constricts skeletal muscle and cutaneous arterioles
-low dose dopamine administered during hemorrhage bc its protective (vasodilatory) effect on blood flow in several organs (including kidney)
renal blood flow*
-tells us how much blood is going to kidneys
- = pressure gradient / resistance
-25% of CO
-between 80-200 MAP renal blood flow remains the same
-below 80 -> RBF also decreases -> shock
-this is done by constriction/dilation of renal arterioles
-renal autoregulation is thought be controlled by afferent rather than efferent
-increase renal arterial pressure -> increase RBF -> increase GFR
too much diuretic
-decrease BP too much (below 80) -> no filtration
-too much dehydration -> not enough blood to kidney -> no filtration -> renal failure
renal blood restriction in relation to GFR
-if you constrict either afferent or efferent renal artery you increase resistance -> renal blood flow decreases
-if you constrict the efferent arteriole independently -> you increase hydrostatic pressure of glomerulus -> increase GFR
-if you constrict afferent arteriole -> restricts blood flow -> decrease GFR
-high sympathetic flow (activation of alpha 1 receptors) and/or high angiotensin 2 increases constriction of both afferent and efferent arterioles but mainly afferent (normally during hypovolemic shock)
-low angiotensin 2 increases constriction of efferent arteriole -> reduce renal blood flow -> increase GFR
-both afferent and efferent have sympathetic vasoconstriction and angiotensin 2 effects but afferent has more alpha 1 receptors and efferent are more sensitive to angiotensin 2
myogenic hypothesis
-increase in arterial pressure -> Stretches artery -> increase in constriction -> increase resistance -> maintains normal BP to kidneys
-this is thought to happen due to activation of stretch activated Ca channels -> stimulates contraction of smooth muscle
tubuloglomerular feedback / juxtaglomerular apparatus
-macula densa in the early distal convoluted distal tubule senses whats getting filtered
-by sensing this we determine if we need to increase or decrease renal blood flow
-increase renal BP -> increase RBF -> increase GFR -> macula densa senses too much filtrate in nephron -> releases vasoactive substances -> constricts afferent arterioles via paracrine mechanism -> increase resistance of afferent arteriole -> reduces RBF and GFR
high protein diet
-high protein -> high BUN
-BUN must be reabsorbed with Na within proximal convoluted tubule
-more BUN and Na being reabsorbed into blood -> macula dense senses less filtrate -> increases GFR
fick principle*
-measure renal blood flow by measuring renal plasma flow
-substance entering must equal substance exiting
-concentration in renal artery = concentration in urine + concentration in renal vein
glomerular filtration
-amount leaving renal capillary system into nephron = GFR
-ultrafiltrate- substance leaving to nephron -> no blood cells or protein
-20% of RBF enters
-filtered in bowmans capsule
glomerular filtration barrier*
-does let proteins and blood cells past
-endothelium- pores, stops blood cells
-basement membrane- strong, prevents filtration of plasma proteins
-epithelium- podocytes also prevent filtration of plasma proteins -> podocytes only big enough for solutes and water
-negative charged glycoproteins on basement membrane-> prevent movement of neg charge proteins across
-glomerular disease- negative charge removed -> allows for proteinuria
-24 hour urine- detect protein in urine -> measure renal function
starling forces
-no proteins leave capillaries
-only influenced by how much protein is in the capillaries
-oncotic pressure of bowmans space is considered 0 bc filtration of protein is negligible
-suction effect of plasma proteins in the glomerulus
-GFR depends on net ultrafiltration pressure -> depends on sum of starling pressures across glomerular capillary wall
-K filtration coefficient is extremely high to promote filtration bc of high SA and water permeability
-hydrostatic pressure in glomerular capillaries is high across the whole capillary
-hydrostatic pressure within the nephron- opposes filtration
3 starling forces
-hydrostatic pressure in bowmans space
-hydrostatic pressure in glomerular capillary
-oncotic pressure in glomerular capillary
oncotic pressure
-changes across the glomerular capillary
-oncotic pressure increases as we go along the glomerular capillary
-as we filtrate more and more substances the amount of plasma proteins relative to plasma increases
-increases due to reduction of plasma in the capillary and increase in proteins relatively (bc so much was filtrated at the start of capillary)
-increase protein concentration -> increase oncotic pressure -> decrease GFR
-decrease protein concentration -> decrease oncotic pressure -> increase GFR
bowmans capsule pressure
-increase pressure in the capsule -> reduce GFR
-can be caused by obstruction in urethra/ureter
creatinine and BUN
-decrease GFR -> increases creatinine and BUN blood concetration bc its not filtered out into urine
-volume contraction (hypovolemia) -> decrease RBF -> decrease GFR (prerenal azotemia) -> BUN and creatinine increase bc its not being filtered in the urine
-prerenal azotemia secondary to hypovolemia - BUN is reabsorbed but creatinine is not -> BUN increases more than creatinine -> BUN/creatinine ratio > 20
-bc volume contraction (Hypovolemia) causes increase reabsorption of all solutes -> causes higher BUN level
-renal failure- increase in both BUN and creatinine -> doesnt increase BUN/creatinine ratio
filtration fraction
-how much is getting filtered relative to blood flow
-20%
-20% of plasma that goes through renal artery gets filtered
-80% unfiltered leaves and becomes peritubular capillary blood flow
-constriction of afferent arteriole -> decrease GFR -> no change in filtration fraction
-everything else has filtration fraction direct relationship with GFR
reabsorption and secretion
-factors of reabsorption and secretion determines how much of filtered load is going to excreted
-substances are secreted from peritubular capillary into nephron or excreted from nephron into peritubular capillary
-how much is filtered, how how is reabsorbed, how much is excreted = excretion
-net reabsorption/secretion rate = filter load - excretion rate
-you excrete less Na that you filter -> must be reabsorbing
-you excrete more PAH than you filter -> must be secreting
urea** study more
-transported in almost all parts of nephron
-reabsorbed and secreted based on diffusion
-moves down concentration gradient when membrane is permeable to it
-follows water basically
-if water is reabsorbed -> concentration of urea increases in nephron -> moves down concentration gradient into blood
-40% excreted -> broken down into ammonia -> pee smell
weak acids and bases
-can be charged or uncharged
-only non-charged state can diffuse across cell
-amount of each depends on pH of urine
-secreted by proximal tubule
-weak acids- PAH, salicylic acid
-weak bases- quinine, morphine
apical vs basal side
vasoconstrictors
-sympathetic nerves (catecholamines)
-angiotensin 2 (renin)
-endothelin
vasodilation
-PGE 2 (prostaglandins)
-PGI 2 (prostaglandins)
-nitric oxide
-bardykinin
-dopamine
-atrial natriuretic peptide
