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74 Cards in this Set
- Front
- Back
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Body water distribution and measurement
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TBW - 60% weight - tritiated water, D20
ICF - 40% weight (2/3 TBW) - Indirect via TBW - ECF ECF - 20% weight (1/3 TBW) - mannitol, inulin Plasma - 1/4 ECF - radioactive albumin, evans blue Interstitial - 3/4 ECF - indirect via ECF - plasma Volume = amount (injected-excreted) / plasma concentration |
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Water shifts: Infusion of isotonic fluid
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i.e. NS infusion
Increase in ECF volume (and arterial BP) No change in osmolarity Reduced hematocrit and protein concentration in serum |
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Water shifts: Loss of isotonic fluid
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ie. diarrhea
ECF volume decreases (BP down) No change in osmolarity Increased hematocrit and protein concentration |
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Water shifts: Hyperosmotic volume expansion
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ie. increased NaCl intake
Increased ECF osmolarity ICF water shifts to ECF to match ECF osmolarity (less ICF volume, more ECF) Reduced hematocrit, protein concentration |
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Water shifts: Hyperosmotic volume contraction
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ie. sweating
Loss of ECF volume, osmolarity rises ICF water shifts to ECF to match (both compartments lower water) Hematocrit and protein unchanged (cells shrink) [JUST WATER LOST] |
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Water shifts: hyposmotic volume expansion
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ie. SIADH, gain of pure water
ECF volume increases, osmolarity decreases Fluid moves into ICF to match (ECF and ICF have higher volume and lowered osmolarity) Hematocrit and protein unchanged (cells grow) [JUST WATER GAINED] |
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Water shifts: Hyposmotic volume contraction
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ie. adrenocortical insufficiency (NaCl loss)
ECF osmolarity decreases Fluid moves into ICF to match (ECF low volume, ICF high volume) Hematocrit and protein increased, BP decreases |
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Clearance equation
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C = urine flow rate x urine concentration / plasma concentration
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RBF controls
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SNS and high Ag II decreases RBF
Low dose Ag II preferentially decreases efferents to increase GFR but not affect RBF Macula densa senses increased fluid and causes afferent arteriole vasoconstriction too |
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ACEi preventing diabetic nephropathy
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Reduce Ag II effect on efferent arterioles, they dilate and have lowered GFR so reduce hyperfiltration
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PAH, use, RPF vs RBF
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Filtered and secreted in renal tubules; used to measure RPF; underestimates by 10%
Clearance PAH = RPF RBF = clearance PAH / (1-hematocrit) |
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Measuring GFR
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Inulin clearance
Estimate with BUN and creatinine. Both increase if GFR decreases; in disease though this is not useful (ie prerenal azotemia has BUN: creatinine > 20 due to BUN increase more); GFR also drops with age. Underestimates because creatinine is secreted a little |
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Why are proteins not filtered
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Size (capillaries are fenestrated)
Negative charge on filtration barrier (lost in glomerular disease so get proteinuria, generalized edema and hyperlipidemia) |
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Filtered load vs excretion rate
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Filtered load = GFR x [plasma]
Excretion rate = Urine flow x [urine] Reabsorption rate = Filtered load - excretion rate Secretion rate = excretion rate - filtered load |
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Relative clearances
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PAH > K+ (high K diet) > inulin > urea > Na+ > glucose, amino acids, HCO3-
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Removing acids (i.e. salicylic acid poisoning) from body
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Alkalinize urine, A- acid form predominates so can't be reabsorbed as easily and excreted in urine
Reverse for removing bases |
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TF/Px ratio, TF/P inulin
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Ratio of concentration in tubular fluid to plasma
TF/Px > 1 if it is not being reabsorbed or is less so than water =1 for anything filtred freely in Bowman's space TF/P inulin - Tells fraction of water reabsorbed Fraction reabsorbed = 1 - (1 / (TF/P inulin) Ratio of TF/Px / TF/P inulin tells fraction reabsorbed at any point on nephron |
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Why does reabsorption increase with GFR increase, volume contraction
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Oncotic pressure at end of capillary blood increases b/c more filtred so there is greater pull back in
In volume contraction, reduced hydrostatic pressure so so favors reabsorption |
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Sodium reabsorption across nephron
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2/3 PCT, early via cotransport (glucose, a.a., bicarb, Phosphate, lactae), or antiport with H+, Late via Na/Cl cotransport
TAL - some via Na/K/2Cl- cotransporter, impermeable to water here so dilutes urine Early DCT - little, early due to Na/Cl cotransport, impermeable to water so dilutes; Late DCT and CCT - Principle cells absorb Na+ and water; secrete K+. Aldosterone increases. ADH brings water in. Alpha-intercalated secrete H+ and reabsorb K+ |
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Aldosterone stimulation
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Increases Principal cell Na+ and water reabsorption and K+ secretion
Increases H+ secretion at alpha intercalated cells, acidifies urine as binds to titratable acids like phosphate Increases Na/K pump in principal cells to raise intracellular K+ |
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K+ regulation, distal secretion
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Varies based on diet, aldosterone and acid-base
PCT absorbs most with Na+ and water, TAL does some with cotransport Low K diet - alpha-intercalated cells H+/K+ ATPase reabsorb. High K diet - principal cells pump out Distal secretion - Increased - High K+, Hyperaldosterone, Alkalosis (more in the cell); Thiazide and Loop diuretics (higher flow rate), Luminal anions (bind up) Decreased - Low K+, hypoaldosteronism, Acidosis (less in cell via H/K exchange), K+ sparing diuretics (block excretion) |
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K+ shifts between ICF and ECF
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Hyperkalemia - caused by Insulin def, Beta antagonists, Acidosis (H+/K+ exchange), Hyperosmolarity (water out pulls K with), Na/K Pump inhibition, Exercise, cell lysis
Hypokalemia - caused by insulin, B-agonists, Alkalosis (H+/K+ exchange), hyperosmolarity (water flow in) |
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Phosphate, Calcium and Magnesium balance
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Most for all reabsorbed in PCT
PTH - increases Ca++ reabsorbed in DCT (cAMP) and decreases phosphate reabsorbed in PCT (HIGH URINE cAMP) Hypercalcemia - inhibits Mg reabsorption and Hypermagnesia inhibits Ca reabsorption in TAL due to competition for same Thiazide diuretics - increase DCT Ca++ reabsorption |
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Intermedullary gradients, countercurrent exchange and urea recycling
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Built up via urea reabsorption in CCT (ADH mediated) and sodium reabsorption. Water impermeable TAL and early DCT help prevent washout; vasa recta also equilibrate as go down (very permeable)
Loop diuretics cause washout |
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Free water clearance
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Water balance
Negative - hyperosmotic urine in ADH presence Positive - hypoosmotic urine in ADH absence (or diabetes insipidus) Zero - due to loop diuretic because removes corticopapillary osmotic gradient so cannot dilute or concentrate urine |
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Contraction alkalosis
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ECF volume contraction leads to AgII production
Na+/H+ exchange stimulated, more HCO3- reabsorbed Can be superimposed on metabolic alkalosis (vomiting) or metabolic acidosis (diarrhea) |
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Serum anion gap
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Anion gap = [Na+] - ([Cl-] + [HCO3-])
Elevated when there is another acid or something present with reduced bicarb (ie. sialcylic acid, keto acids, methanol to formaldahyde, renal failure with ammonium, lactic acids) Not elevated if acidosis has chloride increased to compensate Anion Gap Acidosis - MUDPILES Methanol, uremia, Diabetic ketoacidosis, Propylene glycole, Iron or INH, Lactic acid, Ethylene glycol (oxalic acid), Salicylates (late) Non-AG acidosis - HARD-ASS Hyperalimentation, Addison's disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion |
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Aceetazolamide MOA, Effect, tox
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Carbonic anhydrase inhibitor
Used for altitude sickness (metabolic alkalosis), glaucoma, urinary alkalinization, pseudotumor cerebri Act on PCT to inhibit carbonic anhydrase. Increases HCO3- excretion Tox - hyperchloremic metabolic acidosis, sulfa allergy, NH3 tox |
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Furosemide, Ethacrynic acid, Bumetanide, MOA, effect, tox
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Loop diuretics, Act on Na+/K+/2Cl- cotransport
Increase excretion of Na, Cl, K (also due to high flow) Also increase Ca++ excretion (treat hypercalcemia) Reduce ability to concentrate urine (loss of gradient) Reduce ability to dilute urine (inhibits diluting segement) Use - Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema, HTN, HYPERCALCIURIA) Tox - OH DANG - ototoxicity, Hypokalemia, dehydration, allergy (sulfa drugs), Nephritis (interstitial), Gout (NEVER use for gout Ethacrynic acid if have sulfa allergy |
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Chlorothiazide, hydrochlorothiazide, MOA, Effect, Tox
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Act on Early DCT to inhibit Na/Cl cotransport
Na/Cl wasting, K+ excretion due to high flow (less reabsorbed) Ca++ LESS excrete (treat hypercalciuria) Reduces ability to dilute urine (early DCT is a diluting segment b/c impermeable to H20) No effect on concentrating urine (doesnt affect gradient) Use - HTN, CHF, idopathic hypercalciuria, nephrogenic diabetes insipidus Tox - HyperGLUC, (glycemia, lipidemia, uricemia and calcemia) also causes hypokalemic metabolic alkalosis |
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Spironolactone, triamterene, amiloride, MOA, Effect, Tox
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Late DCT and CCT, usually oppose aldosterone effects
Inhibits Na+ reabsorption Inhibits K+ secretion - used to prevent Loop and thiazide K wasting Inhibits H+ secretion Spironalactone antagonizes aldosterone, others block ENaC channel. Spironalactone also reduces LV remodeling due to CHF Use - Hyperaldosteronism, K+ depletion, CHF Tox - Hyperkalemia (arrhythmia) endocrine effects with spironalactone (gynecomastia, antiandrogen) |
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Renal Embryology
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Pronephros - degenerates
Mesonephros - interim kidney for 1st trimester, later male system. Uteric bud from caudal end becomes ureter, pelvises, calyces, collecting ducts Metanephros - permanent, 5th week starts, when interacts with ureteric bud becomes glomerulus to DCTs Uteropelvic jxn is last to canalize and most common obstruction site leading to hydronephrosis |
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Potter's Syndrome
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Oligohydramnios leading to compression of fetus, limb and face deformation.
Death by pulmonary hypoplasia Due to ARPKD, posterior urethral valves, bilateral renal agenesis |
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Multicystic dysplastic kidney
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Abnormal ureteric bud and metanephric mesenchyme interaction; nonfunctional kidney with cysts and CT. OK if unilateral
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Modulation of filtration
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Prostaglandins (PGE) dilate afferent arteriole to increase RPF and GFR (constant FF) - blocked by NSAIDs
AgII - constricts efferent arteriole preferentially at low dose to raise GFR more and get higher FF |
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Hartnup's disease
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Deficiency of neutral amino acid transporter (tryptophan) so rises in urine
Results in pellagra |
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RAAS regulation
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JG cells in afferent arteriole (smooth muscle origin) sense low blood flow, macula densa cells in DCT sense low sodium, and B1 receptor activation all cause JG cell renin release
Renin converted to AgII then AgII. Ag II acts on: a) AT1 receptors on smooth muscle to vasoconstrict and raise BP b) Efferent arteriole constriction - raise FF to preserve renal function in low volume c) Aldosterone production to enhance Na+ reabsorption and K+ and H+ excretion. Favors water reabsorption d) ADH release from posterior pituitary to reabsorb water e) PCT Na+/H+ activity to reabsorb Na+, HCO3-, H20 and can lead to contraction alkalsosis f) Hypothalamus thirst reflex stimulation |
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ADH main regulator
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Primarily osmolarity but low blood volume takes precedence
Aldosterone does volume but both work in concert for low volumes |
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Electrolyte Disturbances High/Low: Na+
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High - Irritability, stupor, coma
Low - Nausea, malaise, stupor, coma |
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Electrolyte Disturbances High/Low: K+
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High - Arrhythmias, muscle weakness, Wide QRS and peaked T waves on ECG
Low - Arrhythmias, muscle weakness, U waves and flat T waves on ECG |
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Electrolyte Disturbances High/Low: Ca++
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High - Stones, groans, bones and psych overtones, not necessarily calciuria
Low - Tetany, seizures |
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Electrolyte Disturbances High/Low: Mg++
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High - DTRs less, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
Low - Tetany, arrhythmias |
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Electrolyte Disturbances High/Low: Phosphate
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High - renal stones, metastatic calcifications, hypocalcemia
Low - bone loss, osteomalacia |
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RTA type 1
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Distal type
Defect in CCT H+ secretion, urine pH >5.5 Hypokalemia and risk for calcium phosphate stones due to high pH and bone resorption |
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RTA type 2
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Proximal type
Defect in PCT HCO3- reabsorption, associated with Fanconi's syndrome, urine pH < 5.5 Hypokalemia and risk for hypophosphatemic rickets |
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RTA type 4
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Hyperkalemic type
Hypoaldosteronism or lack of CCT response to aldosterone Hyperkalemia impairs ammoniagenesis in PCT, reduced buffering capacity and low urine pH |
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Urine casts
a) RBC casts b) WBC casts c) Fatty casts ("oval body casts") d) Granular ("muddy brown") casts e) Waxy casts f) Hyaline casts |
Casts = renal origin vs hematuria/pyuria of bladder w/o
a) RBC casts - glomerulonephritis, ischemia, malignant HTN b) WBC casts - Tubuloinsterstitial inflammation, acute pyelonephritis, transplant rejection c) Fatty casts ("oval body casts") - Nephrotic syndrome d) Granular ("muddy brown") casts - Acute tubular necrosis e) Waxy casts - Advanced renal disease/chronic renal failure f) Hyaline casts - nonspecific, may be normal |
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Nephrotic syndromes
Nephritic syndromes Overlap |
Pure nephrotic - Focal segmental glomerulosclerosis, Membranous nephropathy, Minimal change disease, amyloidosis, diabetic glomerulonephropathy
Proteinuria > 3.5g/day, frothy urine, hyperlipidemia, fatty casts, edema. Risk of thromboembolism due to AT III loss and infection due to Ig loss Pure nephritic - Acute poststreptococcal glomerulonephritis, Rapidly progressive glomerulonephritis (crescent), Berger's IgA glomerulonephropathy, Alport syndrome Inflammation, hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria <3.5g/day Both - Diffuse proliferative glomerulonephritis, membranoproliferative glomerulonephritis |
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Focal Segmental Glomerulosclerosis, Cause
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Nephrotic syndrome - Proteinuria > 3.5g/day, frothy urine, hyperlipidemia, fatty casts, edema. Risk of thromboembolism due to AT III loss and infection due to Ig loss. MOST COMMON ADULT CAUSE
Cause: HIV, heroin abuse, obesity, IFN treatments, chronic kidney disease due to congenital absence or surgical removal Segmental sclerosis and hyalinosis, effacement of foot processes similar to minimal change; |
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Membranous nephropathy, Cause
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Nephrotic syndrome - Proteinuria > 3.5g/day, frothy urine, hyperlipidemia, fatty casts, edema. Risk of thromboembolism due to AT III loss and infection due to Ig loss.
Cause: SLE nephrotic syndrome, or drugs, infection, solid tumor Diffuse capillary and GBM thickening, "spike and dome" appearance with subendothelial deposits, granular immunoglobulin complexes on IF NOT mesangium involvement (membranoproliferative glomerulonephritis) |
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Minimal change disease, Cause
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Lipoid nephrosis
Nephrotic syndrome - Proteinuria > 3.5g/day, frothy urine, hyperlipidemia, fatty casts, edema. Risk of thromboembolism due to AT III loss and infection due to Ig loss. Normal glomeruli, just FOOT PROCESS EFFACEMENT Loss of albumin (not globulins), caused by polyanion loss on basement membrane Cause: recent infections or immune stimuli, usually in children. STEROIDS |
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Amyloidosis Nephrotic syndrome, Cause
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Nephrotic syndrome with congo red stain showing apple green birefringence
Cause: chronic conditions like multiple myeloma, TB, RA |
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Membranoproliferative glomreulonephritis, Types, Cause
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Combination nephrotic and nephritic syndrome
Type I - subendothelial immune complex deposits with granular IF "train-track", MESANGIAL ingrowth (distinct from membranous nephropathy Associated with HBV, HCV Type II - Intramembranous immune complex deposits "dense deposits" Associated with type 3 nephritic factor |
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Diabetic glomerulonephropathy
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Nephrotic syndrome - Proteinuria > 3.5g/day, frothy urine, hyperlipidemia, fatty casts, edema. Risk of thromboembolism due to AT III loss and infection due to Ig loss.
Nonenzymatic glycosylation of GBM leads to thickening; also in efferent arterioles leads to increased GFR and mesangial expansion. Eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) |
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Acute poststreptotoccal glomerulonephritis
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Nephritic syndrome - Inflammation, hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria <3.5g/day
Glomeruli enlarged, hypercellular, neutrophils, "lumpy-bumpy", subEPITHELIAL immune complexes, Granular due to IgG, IgM and C3 deposits. Children with periorbital edema, dark urine and hypertension. Spontaneous resolution After streptococcal infection (impetigo, pharyngitis, etc) Age most impt factor for full recovery |
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Rapidly progressive glomerulonephritis
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Crescentic glomerulonephritis
Nephritic - Inflammation, hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria <3.5g/day Crescent moon shape of fibrin and plasma proteins, monocytes, macrophages and parietal cells. POOR PROGNOSIS and RAPID DETERIORATION. FIBRIN DEPOSITS Cause a) Goodpasture's - Type II HSN, LINEAR IF b) Granulomatosis with polyangiitis (Wegener's), -cANCA; immune complexes c) Microscopic polyangiitis; p-ANCA |
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Diffuse proliferative glomulonephritis
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Both nephrotic and nephritic
MOST COMMON SLE death "wire looping" of capillaries, subendothelial and intramembranous IgG based immune complexes with C3 deposition. Granular IF |
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Berger's disease
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IgA nephropathy, Nephritic syndrome
Presents as flares with a URI or gastroenteritis Mesangial proliferation, immune complex deposits with IgA. Related to Henoch-Schonlein purpura |
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Alport syndrome
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Type IV collagen mutatoin leads to split BM
Glomerulonephritis, deafness, and rarely eye problems |
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Kidney stone types
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a) Calcium, MOST, radiopaque, high pH calcium phos, low pH calcium oxalate. Caused by hypercalcemia (cancer, PTH) or ethylene glycol (oxalate), Vit C abuse. THIAZIDES and citrate treat. Usually have normocalcemia
b) Ammonium magnesium phosphate - radiopaque, due to urease positive infection (Proteus, Staphylococcus, Klebsiella); urien converted to ammonia (alkalinization) - STAGHORN calliculi c) Uric acid - radiolucent, visible on CT and US though. Gout association or high turnover (leukemia); alkalinize urine to treat d) Cysteine - radiopaque, secondary to cystinuria, hexagonal crystals, alkalinize urine to treat |
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Renal Cell carcinoma
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polygonal clear cells (carbs and lipid), from PCT cells
Most common in elderly males who smoke and obese. Hematuria, palpable mass, secondary polycythemia, flank pain, fever, weight loss Invades hematogenously. C3 deletion or von Hippel-Landau Resists chemo |
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Wilms tumor associations
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WAGR - Wilms tumor (early childhood), Aniridia, GU malformation, Mental retardation
WT1 gene deletion Beckwith-Wiedemann syndrome |
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Causes of transitional cell carcinoma
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Anywhere in urinary tract
Pee SAC Phenacetin, Smoking, Aniline dyes, Cyclophosphamide |
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Acute vs chronic pyelonephritis
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Acute - mostly cortex, sparing glomeruli/vessels. Fever, costovertebral angle tenderness, nausea and vomiting. WHITE CELL CASTS
Chronic - recurrent episodes (vesicoureteral reflex or stones); Coarse, asymmetric scarring. Eosinophilic casts sometimes |
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Drug induced interstitial nephritis causes
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Acute renal interstitium infiltration. Pyuria (often with eosinophils) and azotemia after drugs. 1-2 weeks post
Diuretics, penicillins, sulfonamides, rifampin |
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Diffuse cortical necrosis
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Acute cortical infarction both kidneys due to vasospasm and DIC
Often an obstetric catastrophe like abrupto placentae or septic shock |
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Acute tubular necrosis and stages
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Most common intrinsic renal failure, can be reversed. Renal ischemia (shock, sepis, injury, drugs, myoglobin) causes
1) Inciting event 2) Maintenance phase - oliguric, hyperkalemia risk over 1-3 weeks 3) Recover phase - polyuric, BUN and creatinine fall, risk of hypokalemia |
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Renal papillary necrosis, causes
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Sloughing of papillae with gross hematuria and proteinuria.
Associations: DM, Acute pyelonephritis, chronic phenacetin use (tylenol derivative), sickle cell anemia and trait |
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Prerenal azotemia, intrinsic renal failure and postrenal azotemia
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Normally BUN reabsorbed for countercurrent multiplication; creatinine not.
ALL are acute renal failure signaled by rise in both Prerenal azotemia - Reduced flow (hypotension) leads to low GFR, Retention of sodium, water, urea for volume. 20: 1 BUN to creatinine ratio with HIGH urine osmolality (>500) and low sodium Intrinsic renal failure - ATN or ischemia/toxins, rarely crescentic glomerulonephritis. Patchy obstruction of tubule, fluid backflow, reduced GFR. Granular/epithelial casts. BUN reabsorption impaired so reduced BUN/Creatinine ratio (<15), low urine osmolarity (can't concentrate), high sodium Postrenal azotemia - similar, outflow obstruction reduces GFR and BUN reabsorption (stones, BPH, neoplasia) ONLY if BIL will occur. Low urine osmolarity, high sodium and low ratio |
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Renal failure consequences
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Can't make urine or excrete nitrogens
Salt/water retention (CHF and edema) Hyperkalemia, acidosis uremia - nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction Anemia - no EPO Renal osteodystrophy - no Vit D so SUBperiosteal thinning of bone due to hyper PTH Dyslipidemia Growth retardation and delay |
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PKD types, associations
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ADPKD - adult form, multiple large BIL cysts, flank pain, hematuria, HTN, UTIs and progressive renal failure. Increased renin production due to PKD1 or 2 mutation.
Associations: Berry aneurysm, MVP, benign hepatic cysts ARPKD - infantile form, congenital hepatic fibrosis link, renal failure in utero (Potter's syndrome) possible, HTN, portal HTN and progressive renal insufficiency |
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Medullary cystic disease
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Inherited disease causing tubulointerstitial fibrosis and renal insufficiency with inability to concentrate urine, Shrunken kidneys with poor prognosis
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Mannitol, MOA, Tox
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Osmotic diuretic, increases urine flow on PCT and descending loop (water permeable)
Used to reduce intracranial or intraocular pressure Tox - pulm. edema and dehydration. DO NOT GIVE IN CHF or anuria |
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Lisinopril, Catopril, Enalapril, MOA, use, tox
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ACEi
MOA - inhibit ACE in lung, no Ag II, reduced GFR renin increases due to feedback loss Also prevents inactivatoin of bradykinin (vasodilator) Use - HTN, CHF, proteinuria, diabetic renal disease, prevent heart remodeling Tox - Catopril's CATCHH; Cough, Angioedema (ARBs best for these two), Teratogen, Creatinine increase, Hyperkalemia and hypotension AVOID in BIL renal artery stenosis because can cause renal failure |
