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186 Cards in this Set
- Front
- Back
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Major functions of the renal system (7):
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1. Excretion of metabolic waste products containing nitrogen (urea & creatinine)
2. Metabolism &/or excretin of other substances 3. Regulation of water & other electrolytes 4. Regulation of acid-base balance 5. Regulation of arterial BP 6. Regulation of erythropoiesis 7. Vitamin D metabolism |
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How does the renal system regulate arterial BP?
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Vasodilators: prostacyclin (PGI2), kinins
Vasoconstrictors: Prostaglandins (PGF2), thromboxane, Ang II |
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How does the renal system regulate erythropoiesis?
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The kidneys produce erythropoietin, the hormone tt stimulates production of RBCs. The amount of O2 in blood to kidneys stimulates release of erythropoietin.
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Negative result of renal regulation of erythropoiesis:
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Even if reduced O2 is from reduced blood flow rather than chronic hypoxemia, kidneys interpret as not enough RBCs. Can result in hypercythemia. People with chronic kidney disease almost always have hypercythemia
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What % of CO do the kidneys receive?
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20-25%
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The combined weight of the kidneys is what % of total body weight?
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<1%
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What body cavity do the kidneys lie in?
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Retroperitoneal cavity
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The indentation on the medial borders of the kidneys thru which the renal vessels, nerves & ureters exit
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Hilum
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Pathway of urine from the collecting ducts to exit
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Collecting duct
Apex of renal pyramid Minor calyx Major calyx Renal pelvis Ureter Bladder Urethra |
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Outer layer of the kidneys, stippled in appearance
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Cortex
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Inner layer of the kidneys
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Medulla
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Functional unit of the kidney
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Nephron
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How many nephrons in each kidney?
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1 million
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What are the 2 types of nephrons? Describe.
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Cortical nephrons: have glomeruli in outer cortex, have short Loops of Henle
Juxtamedullary nephrons: glomeruli next to the medulla, have long Loops of Henle |
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What % of nephrons can be lost before symptoms are seen?
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90%
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Renal corpuscle:
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Contains the glomerulus
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Glomerulus:
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The filtering component of the nephron
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Bowman's Capsule:
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Envelops the glomerular capillaries
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Capillaries derived from division of the afferent arteriole; reunite to form the efferent arteriole:
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Glomerular capillaries
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What are the two layers of Bowman's Capsule? What is in between them? Describe the layers.
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Parietal layer: single layer of squamous epithelial cells
Visceral layer: podocytes Bowman's spack: between parietal & visceral layers |
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Cells of the Bowman's Capsule tt form part of the filtration barrier:
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Podocytes
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What are the three layers of the filtration barrier? Describe.
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Fenestrated endothelium: capillary endothelial cells w/ very tiny pores
Basement membrane: glycoproteins & mucopolysaccharides Podocytes: have primary & 2ndary foot processes |
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Spaces between interdigitating foot processes:
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Filtration slits
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How wide are the filtration slits?
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~250 Angstroms
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Filtration slit membrane:
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Bridges the filtration slit, has very tiny openings tt allow molecules smaller than 15 Angstroms to pass through but molecules 35-40 Angstroms cannot (molecular sieving)
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Phagocytic cells tt clean the sieve from contaminants:
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Mesangial cells
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What do mesangial cells contain, and other than cleaning, what do they do?
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They contain myofilaments and lay down the mesangial matrix for structural support of the glomerular tuft
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What are the segments of the renal tubule?
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Proximal tubule
Loop of Henle Macula densa Distal tubule |
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Describe the proximal tubule
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Closest to glomerular corpuscle
2 parts: proximal convoluted tubule & pars recta |
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Describe the Loop of Henle
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2 parts: descending limb (penetrates into or toward medulla) & ascending limb (returns back to cortex)
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Describe the macula densa
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Part of the renal tubule tt passes between afferent & efferent arterioles of glomerulus. Acts as sentry apparatus & can monitor what the composition of the material flowing through tt part of the material is, can tell other cells to do things to change what's in the renal tubule
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Describe the distal tubule
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2 parts: distal convoluted tubule, connecting tubule
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Structure tt carries urine from the connecting segment of the nephron to a calyx of the renal pelvis:
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Collecting duct
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Specialized vascular cells in the afferent & efferent arterioles where renin is produced & stored in granules
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Juxtaglomerular cells, aka granular cells
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Three fns of the mesangial cells inside Bowman;s Capsule:
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Phagocytosis
Structural support Myofilaments |
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Associated with juxtaglomerular apparatus, sit on top of the macula densa:
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Extraglomerular mesangial cells; have same 3 functions as mesangial cells inside Bowman's Capsule
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Derived from division of efferent arterioles; intimately associated with the renal tubules:
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Peritubular capillaries
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What are the peritubular capillaries mainly associated with?
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Proximal convoluted tubule
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Long, straight vessels tt run parallel to & give rist to a capillary plexus tt is intimately associated with the both limbs of the Loops of Henle
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Vasa Recta
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What are the factors tt control GFR (where GFR = fluid flux, J)?
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J = k[Pc + pi-t) - (Pt + pi-c)]
k = filtration coefficient Pc = capillary hydraulic pressure pi-t = tissue oncotic pressure Pt = tissue hydraulic pressure pi-c = capillary oncotic pressure |
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What are the normal values for the Starling variables?
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k = 15 mL/min/mmHg
Pc = 45 mmHg Pt = 10 mmHg pi-c = 27 mmHg pi-t = 0 mmHg |
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What is the normal value for GFR?
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120 mL/min
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What are the factors affecting renal blood flow? (3)
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Myogenic mechanism
Neural control Tubuloglomerular feedback |
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How does the myogenic mechanism work?
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As perfusion pressure inceases, VSM is stretched, inducing VSM constriction, thereby increasing vascular resistance
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What is the arterial BP range tt the myogenic mechamism can autoregulate renal blood flow?
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90-180 mmHg.
Below 90, GFR decreases Above 180, GFR increases Between them, GFR is constant |
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How does neural control affect renal blood flow?
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Changing resistance in either afferent or efferent arterioles changes GFR. By balancing the two, GFR (& renal blood flow) can be regulated despite changes in body position, blood volume, etc.
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How does the tubuloglomerular feedback mechanism supposedly work?
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It is flow dependent. Some unknown variable (flow, NaCl, ?) is sensed by the macula densa & an effector substance (adenosine, ATP, NO, etc) is released tt regulates vascular resistance of afferent arterioles to change GFR
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Which cells produce renin?
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Juxtaglomerular cells
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Where is angiotensinogen produced?
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In the liver
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What factors affect renin release? (3)
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Low plasma Na+
Reduced renal BP Increased outflow from the renal sympathetic nerves |
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T/F: The kidneys are innervated by the sympathetic & parasympathetic systems
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False. Only the sympathetic system innervates the kidneys.
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What are the effects of Ang II and Ang III?
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Ang II & Ang III stimulate release of aldosterone;
Ang II is a potent vasoconstrictor, causes release of ADH, enhances neurotransmitter release from sympathetic nerve endings, & acts within brain to stimulate drinking |
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What are the 2 techniques to measure kidney function at different levels of the renal tubule:
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1. Micropuncture: used to measure pressures, withdraw samples, & infuse fluids of known composition
2. Stop-flow: flush tubules then clamp ureter so tubular cells work on stationary fluid. Clamp removed and fluid is collected as small samples, representing different segments of the tubule. |
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By what 2 pathways are materials reabsorbed?
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Transcellular (through cells) & paracellular (between cells) pathways
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What are the 5 ways tt substances cross membranes?
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Simple diffusion
Facilitated diffusion Cotransport Countertransport Primary active transport |
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What pathway is the most important for the reabsorption of water?
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Paracellular pathway
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What % of water, sodium, glucose, and urea are reabsorbed?
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99%
99.5% 100% 50% |
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What is the first way tt Na+ cross a membrane? Which membrane, and with what substances?
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Luminal membrane: cotransport with glucose, amino acids, phosphate, & lactate
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In what way is Na+ carried across the luminal membrane in the early segment of the proximal tubule only?
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Countertransport with H+
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How does Na+ move to the interstitium in the first half of the proximal tubule?
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It crosses the basolateral membrane by active transport via the Na-K-ATPase pump
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How does Na+ get reabsorbed in the second half of the proximal tubule?
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Cotransport with Cl-
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How does glucose cross the luminal surface?
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Cotransport with Na+. The downhill movement of Na carries glucose up its [c] gradient
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How does glucose cross the basolateral membrane?
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Simple facilitated diffusion
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What is the point at which the glucose transport proteins are pumping at their maximum ability? Name and number
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Maximal tubular transport capacity (Tm or Tmax)
160-180 mg/dl |
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What is a second pathway into the renal tubule other than glomerular filtration?
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Tubular secretion
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How does tubular secretion begin?
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Simple diffusion out of the peritubular capillaries
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What are 2 substances tt are secreted into the renal tubule lumen?
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Hydrogen & potassium ions
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What substance is given to reduce secretion of penicillin? By what mechanism does this work?
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PAH - para-aminohippuric acid. PAH is a competitive substrate for penicillin transporters. If transporters are saturated with PAH, it slows down the rate that penicillin is excreted
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What is the Standing Gradient Theory?
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The theory tt states tt the movement of water is coupled to Na+ transport, because solute & water reabsorption must be perfectly matched for the tubular fluid to remain isotonic with interstitial fluid
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How is water coupled to Na+ movement?
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As Na+ is pumped via Na-K-ATPase pumps into the intercellular space, the osmotic gradient freely pulls water from the tubular lumen
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What is the theory behind calculating clearance? What is the key assumption in the theoretical calculation of clearance?
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GFR is a key indicator of kidney fn. Assume there is compound tt is freely filterable at the glomeruli & is neither secreted nor reabsorbed in the tubules, so tt the amount filtered per unit time = the amount excreted per unit time
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How is the amount excreted per unit time measured?
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Urine [c] x volume per unit time
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How is the amount filtered measured?
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Plasma [c] times volume of filtrate (GFR)
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How is GFR measured?
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GFR = ([U]xV)/[P]
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What is the normal value for creatinine?
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0.6-1.2 mg/dL
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What is the unit for clearance?
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Volume of plasma per unit time
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Best definition of clearance:
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The volume of plasma tt supplies the amount excreted per unit time
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Why is inulin used to measure clearance?
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It is freely filterable, not reabsorbed, not secreted, not synthesized by the tubules, and not metabolized by the tubules. So what is filtered = what is excreted.
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How to determine if net secretion or reabsorption is taking place:
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Compare clearance of substance to clearance of inulin or creatinine, then compare clearance of substance to GFR. If amount excreted < inulin, some is being reabsorbed. If amount excreted > inulin, some is being secreted
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Clearance of substance / Clearance of inulin =
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Fraction excreted
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GFR / RPF (renal plasma flow) =
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Filtration fraction, the fraction of plasma entering the kidney in the renal artery tt is filtered at the glomerulus
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How can the renal plasma flow (RPF) be calculated?
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Renal blood flow x (1-hematocrit) = RPF
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How can the effective renal plasma flow (ERPF) be calculated?
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Know that all of PAH (p-aminohippuric acid) is filtered & secreted out of plasma, so if have known plasma [PAH], can calculate the amount of blood going into glomeruli with clearance of PAH.
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The minimum amount of water required to remove waste daily? Name and amount
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Obligatory water loss; 0.5L
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What is the max. urine [c] tt the kidneys can produce?
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1200-1400 mOsm/L
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What is the total amount of waste product excreted by the kidneys?
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600 mOsm/day
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What is the countercurrent multiplication system?
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The mechanism responsible for the production of concentrated urine.
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How is concentrated urine produced?
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The countercurrent multiplication system utilizes the existence of a concentrated fluid located within the medullary interstitium to pull water out of the renal tubules. The [c] must be built up in order to function.
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How is the [c] built up?
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From characteristics of the Loop of Henle:
1. Ascending limb reabsorbs Na out of tubular lumen by active transport, dilates fluid 2. The ascending limb is impermeable to water 3. Salt is transported out of the ascending limb and into medullary interstitium, raising its osmolality 4. The descending limb has high permeability to water 5. The Loop of Henle cells can sustain max. of 200 mOsm/L, so multiplication system reaches 1200-1400 mOsm/L. |
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What is the salt concentration at the tip of the Loop of Henle?
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600 mOsm/L
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The ability to concentrate urine depends on what property of the Loop of Henle?
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The relative length. Longer yields more concentrated urine.
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What are the 2 essential components of urine concentration?
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1. Active transport of Na+ in the ascending limb
2. Differences in the permeability between the ascending & descending limbs |
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The fluid that enters the collecting duct is very dilute. How is it concentrated?
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The collecting duct has valves that can change its permeability to water. To concentrate urine, valves open to let water flow out into the concentrated interstitial space.
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Diffusion of water out of the collecting duct would dilute the interstitium, affecting the countercurrent multiplication system. How is the concentration of the interstitial fluid maintained?
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The vasa recta equilibrates the concentration of its blood with the interstitial space, by either giving up some of the concentrated Na+ & urea tt it pulled into the plasma, and taking in excess water tt diffused out of the collecting duct.
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If dilute urine is produced, how is the interstitial concentration maintained, when there is no water diffusing out of the collecting duct but Na+ constantly being pumped out of the Loop?
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In equilibration, the vasa recta will take up excess Na+ out of the interstitium and will carry it away
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What are the properties of the vasa recta tt keep the intermedullary concentration?
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It equilibrates with the surrounding concentrations: As blood flows down the ascending limb of vasa, water diffuses out and salt in, to equilibrate with the interstitium. The tip of the vasa reaches concentration of 1200 mOsm/L. As blood flows up, the reverse occurs.
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What is the vasa maintenance system called and how does it work?
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Called the countercurrent exchanger; the NET salt and water entering the interstitium from the Loops and collecting ducts is carried away and the steady-state gradient is maintained
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What % of the medullary concentration is due to urea?
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50% - 600 mOsm/L urea and 600 mOsm/L salt to make 1200mOsm/L total
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Where is ADH synthesizes and stored, and what is its effect on the renal system?
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Synthesized in hypothalamus
Stored in posterior pituitary Increases water reabsorption by the collecting duct, has little effect on NaCl excretion |
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Where is ANP synthesized, when is it released, and what is its effect on the renal system?
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Synthesized in cardiac atrial cells
Released in response to increased BP Antagonizes effects of renin, Ang II, & aldosterone Decreases BP by decreasing TPR and enhancing urinary NaCl and water excretion |
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Where is urodilatin secreted, where does it act, and what is its effect on the renal system?
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Secreted hy distal tubule and collecting duct
Acts locally Inhibits NaCl & water reabsorption by the collecting duct |
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Which is more potent, atrial natriuretic peptide (ANP) or urodilatin?
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Urodilatin
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Where is aldosterone synthesized and what are its effects on the renal system?
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Synthesized by the glomerulosa cells of the adrenal cortex
Stimulates NaCl reabsorption by the thick ascending limb, distal tubule, & collecting duct Also stimulates K+ secretion by distal tubule & collecting duct |
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What effects do the catecholamines (NE and Epi) have on the renal system?
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Stimulate NaCl and water reabsorption by the proximal tubule, thick ascending limb, distal tubule, and collecting duct
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Where is the catecholamine Dopamine synthesized and what effect does it have on the renal system?
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Synthesized by dopaminergic nerves and possibly the proximal tubule
Inhibits NaCl and water reabsorption in the proximal tubule |
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By what 4 routes is the H+ ion balance regulated? Which is the major route?
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1. GI absorption of ingested acids or bases
2. Metabolic generation of H+ (major) 3. Sickness (vomiting, diarrhea) 4. Urine |
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What are the sources of H+ generated by the metabolic route?
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CO2 + H2O -> H2CO3 -> HCO3- + H+
Production of nonvolatile/fixed acids (phosphoric, sulfuric, lactic; ketone bodies, etc) |
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What is the normal amount of H+ produced per day via metabolism?
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40-80 mM
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Will a vegetarian diet result in net acidic or alkalytic production?
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Alkalytic
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Can hyperventilation lead to acidosis or alkalosis? Why?
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Alkalosis, because lose more CO2.
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How does sickness change the net H+ concentration?
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Vomitus is high in H+, causes net loss
Diarrhea is equivalent to a net gain in H+ because it's the equivalent of losing bicarb; intestinal contents are alkaline, large intestines pump in alkaline material to neutralize acid made by bacteria. |
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How does the urinary system regulate H+?
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Renal excretion of H+ is regulated to achieve a stable H+ balance in the body
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What system is used by intra & extracellular fluids to maintain H+ balance?
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Acid-base buffer systems, provide compounds tt combine with acid or base to prevent extreme changes in pH
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What are the major buffer systems used in the intracellular and extracellular fluids?
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Intracellular: phosphates and proteins
Extracellular: CO2-HCO3 system |
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Which H+-regulating system is the most powerful?
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The renal system; changes in H+ cause the kidneys to excrete either acidic or alkaline urine
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In what 2 ways do the kidneys control HCO3-?
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1. Variable reabsorption of HCO3- filtered at the glomerulus
2. Adding new HCO3- to the plasma flowing through the kidneys by the hydration of CO2 under the influence of carbonic anhydrase |
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The 2 mechanisms tt control HCO3- movement in the kidneys depend on what single mechanism?
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The tubular secretion of H+
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What is the max. [H+] that can be achieved by the countertransport of H+ with Na+?
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10e-4.5 M
(pH 4.5) |
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What happens to the H+ tt is secreted into the renal tubule?
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HCO3- is freely filterable at the glomerulus. The luminal membrane of th tubular cells is not very permeable to HCO3-. However, virtually all of the HCO3- is reabsorbed, beginning with a tubular reaction between HCO3- and H+ to form H2CO3, which dissociates into CO2 and water. CO2 diffuses readily into the peritubular capillaries and is carried to the lungs.
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What happens every time an H+ is formed?
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A HCO3- is also formed, and it diffuses into the extracellular fluid (this is the new bicarb), causing a net production of HCO3-, though it is a different HCO3- than the one that was filtered.
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What happens to most of the H+ secreted into the lumen?
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They are incorporated into water and reabsorbed
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Some H+ is excreted. How does this happen if it reacts with the HCO3- that is filtered?
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More H+ is secreted than HCO3- is filtered. The two ions titrate each other and some H+ is excreted.
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What is the ratio of HCO3- to CO2 when there is acidosis?
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<20
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How is acidosis corrected?
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When there are more H+ ions than HCO3-, the majority of the H+ ions combine with intratubular buffers (phosphate and ammonia)
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Why is phosphate buffer more potent in the urine than in the blood?
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It becomes more concentrated as water is reabsorbed;
The pK is 6.8, closer to that of urine; Excess H+ combines with filtered phosphate to form H2PO4- |
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What is the pH of fluid in the proximal tubule?
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6.0
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Which buffer system is more important, phosphate or ammonia?
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Ammonia
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How does the ammonia buffer system maintain H+ balance?
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Most tubular epithelial cells continually synthesize ammonia, which diffuses into the tubules where it combines with excess H+ to form ammonium ions, which are excreted in the urine
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What is the ratio of HCO3- to CO2 when there is alkalosis?
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>20
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How is alkalosis corrected?
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If there is more HCO3-, the amount filtered will increase. Then there is more HCO3- than H+; but since HCO3- cannot be reabsorbed unless first reacts with H+, the excess HCO3- stays in the fluid and is excreted with urine. This lowers the extracellular HCO3- levels and lowers pH of the blood. There is no buffering involved.
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Because PCO2 is known, and not blood [CO2], how is the ratio of [HCO3-] to [CO2], and subsequently pH, calculated?
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0.03 PCO2 = [CO2]
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Which cells of which segment of the renal tubule secrete K+?
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The Principle cells of the distal tubule & collecting duct
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Which cells of which segment of the renal tubule reabsorb K+?
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Intercalated cells of the distal tubule & collecting duct
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What are the 5 classes of diuretics?
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1. Osmotic diuretics
2. Carbonic Anhydrase Inhibitors 3. Loop diuretics 4. Thiazide diuretics 5. Potassium-sparing diuretics |
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What is the MoA of osmotic diuretics? What is an example of an osmotic diuretic?
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Mannatol - inhibits solute & water reabsorption by changing osmotic forces
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What is the MoA of carbonic anhydrase inhibitors? What is an example of a carbonic anhydrase inhibitor?
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Acetazolamide - inhibits reabsorption of HCO3- and Na+
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What is the MoA of loop diuretics? What are some examples of a loop diuretic?
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Furosemide, Bumetanide - organic anions tt block Na+ reabsorption in the thick ascending limb of the Loop; disrupt countercurrent multiplier
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What is the MoA of thiazide diuretics? What is an example of a thiazide diuretic?
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Chlorothiazide - inhibit Na+ reabsorption in the early distal tubule
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What are the two classes of potassium-sparing diuretics? What are their MoAs? What are examples of each?
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Both reduce K+ secretion and produce natriuresis/diuresis
Amiloride - blocks entry of Na+ thru aldosterone-controlled channels, can shut down the Na+ channels, resulting in diuresis Spironolactone - aldosterone inhibition at the transcriptional level; blocks production of aldosterone-induced Na+ channels, blocks production of protein tt binds to aldosterone. |
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Which class of diuretics is the most potent?
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Loop diuretics
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Which type of renal disease produces the majority of deaths?
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Chronic renal disease, usually develops over many years & is insidious
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What is functional reserve?
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As many as 90% of the nephrons may be destroyed before significant functional impairment is seen; 30-80% destroyed may produce signs, but not symptoms
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End Stage Kidney:
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Deterioration beyond the point of recognizing; etiology difficult to establish because disease is so far advanced
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Early signs & symptoms of renal disease:
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Proteinuria
Hematuria Polydipsia, polyuria, nocturia, oliguria, anuria Generalized edema Pain Palpably enlarged kidneys |
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How is proteinuria tested?
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Dipstick tt is mainly sensitive to albumin
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What is considered normal urin levels of albumin? What does abnormal indicate?
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Normal = up to 150 mg/day
Abnormal indicates disease of the glomerulus |
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How is occult blood measured? What does its presence indicate?
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Through dipstick or microscopic exam;
Indicates renal disease or lower urinary tract disease |
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What instrument measures specific gravity of urine, and what is the purpose?
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Urinometer used to estimate osmolality
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How is [H+] in the urine measured? What is normal? How does pH change with meals, sleep, and fever?
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Litmus paper dipstick;
Normal urine pH is 4.5-8.0; pH increases after meal because H+ ions pumped into stomach, leaving more HCO3- in plasma; pH decreases during sleep because breathing is repressed and less CO2 is exhaled; pH decreases with fever because core temp is elevated from increased metabolism, which puts more CO2 into the blood |
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What may persistent alkaline urine indicate?
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A chronic UTI
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What are abnormal findings upon microscopic exam of urine, for: RBC, WBC, & cast?
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RBC: >1 or 2 per field, indicates hematuria/filtration barrier damage
WBC: >3 or 4 per field, indicates infection Cast: presence of various types indicate different conditions |
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How are casts formed?
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The mucoprotein matrix traps cells and debris, forms cast of interior of renal tubule. Traps anything tt isn't liquid. Eventually breaks free and flows out in urine
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What are the types of casts? Describe them
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Hyaline - clear cylinders of protein, can exist in normal urine
RBC - indicate leaking glomeruli or trauma WBC - indicate infection Fatty - indicate nephrotic syndrome Broad, granular - indicates renal failure, contains dead cells. |
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How is tubular function tested? (3)
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1. A specific substance is given IV for excretion test
2. Concentration/dilution test 3. Urine acidification test |
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What are the 3 types of radiologic exam?
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1. Intravenous pyelogram
2. Retrograde pyelogram 3. Renal arteriogram |
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Describe an intravenous pyelogram.
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Contrast medium given, shows size, shape, and location of kidney, thickness of cortex & medulla, and presence of cysts, lesions, or obstructions
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Describe a retrograde pyelogram.
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Catheter advanced up the ureter, releases contrast medium into the renal pelvis
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Describe a renal arteriogram.
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Catheter advanced up the femoral artery to the aorta to the level of the renal artery. Determines arterial stenosis, presence of neoplasm, arrangement of arteries & veins for transplantation
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Describe nephrotic syndrome: what tissue is diseased, what is the result for that tissue, what are the general characteristics?
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Glomerular basement membrane is diseased, increases permeability to plasma protein. Characteristics: generalized edema, hypoalbuminemia, massive proteinuria, hyperlipidemia
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What disease is the most frequent cause of nephrotic syndrome?
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Minimal Change Disease
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Describe the nephritic syndrome: what causes it, what does it produce, what is the common result, what are the characteristics?
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Caused by inflammatory disorders. Produces proliferation of cells within the glomeruli in Bowman's space. Often results in neutrophil infiltration. Characteristics: acute onset, hematuria, RBC casts, hemoglobin casts, some oliguria, azotemia, HTN, ischemia to kidney, reduced GFR
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What is azotemia?
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Increase in nitrogenous waste.
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What disease that causes the nephritic syndrome is the most frequent of all glomerular lesions?
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Diffuse Proliferative Glomerulonephritis (Diffuse PGN)
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What is the prognosis of diffuse PGN?
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95% recover
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What is an exogenous form of diffuse PGN? What are its characteristics?
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Poststreptococcal diffuse PGN: develops in children 1-4 weeks after recovery of poststreptococcal infection, caused by nephritogenic strains of Beta-hemolytic streptococci, may advance to nephrotic syndrome. Can also follow mumps, measles, or varicella.
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What is an endogenous form of diffuse PGN?
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Endogenous form associated with systemic lupus erythematosus
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What disease is the #1 cause of renal failure?
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Chronic Glomerulonephritis
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What % of cases requiring chronic hemodialysis or kidney transplantation are from chronic glomerulonephritis?
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60%
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What is the end result of chronic glomerulonephritis? What is the prognosis?
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ESRD
Prognosis = poor, with relentless progression to uremia and death; better prognosis if caught early |
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What are two types of interstitial nephritis?
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1. Acute pyelonephritis
2. Chronic pyelonephritis |
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Describe acute pyelonephritis: what is it caused by, what is a predisposing factor, what are the characteristics and prognosis?
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Extremely common benign inflammatory disease usually caused by E. coli. May involve 1 or both kidneys. Predisposing factor: partial urinary obstruction. Characteristics: sudden onset, WBC casts, pain, chills, fever, malaise, pyuria, bacteriuria. Prognosis - usually benign & self-limiting, rarely recurrent or chronic
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Describe chronic pyelonephritis: associated with what condition, etiology, characteristics, and diagnostic test used?
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Common with urinary tract obstruction; etiology controversial, can be caused by use of LT high dose use of analgesics or reflux of urine; characterized by HTN, mild proteinuria, uneven interstitial fibrosis & fibrosis around Bowman's capsule, vascular changes similar to arteriolosclerosis; Dx by retrograde pyelogram
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What is the 2nd most common cause of renal failure death?
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Chronic pyelonephritis
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Describe hepatorenal syndrome: coupled with what other organ disease, characteristics, prognosis?
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Kidney normal but fails anyway; found only with liver disease. Pathogenesis unclear; characterized by sudden onset, marked oliguria, rapidly increasing BUN; extremely poor prognosis, die from ureic poisoning, but kidneys suitable for transplant
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Describe urolithiasis: occurrance, genetics, symptoms, result?
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Urolithiasis = calculus formation at any level. Occurs frequently where high [limestone] in water, has familial tendency. 80% unilateral, often with multiple stones. Often asymptomatic, may cause obstruction, trauma, bleeding, infection
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What device is used to treat kidney stones?
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Lithotripter: focuses high energy, high frequency sound waves on stone, causes it to shatter into smaller pieces, but those pieces may have jagged edges tt damage delicate tissue as they're passed
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Describe polycystic kidney disease: characteristics, genetics, complications, prognosis?
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Hereditary, swelling of tubules of nephrons into balloons. Both kidneys affected; may be full-blown at birth. Autosomal dominant gene. Produces enormous kidneys with cysts 3-4 cm in every nephron. Complications include HTN and UTIs, prognosis ultimately fatal without transplantation
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Describe hydronephrosis: cause, result, onset, treatment?
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Dilatation of renal pelvis due to obstruction of urinary flow, caused by genetics, foreign bodies, tumors, inflammation, neurogenic, normal pregnancy. Causes compression & atrophy of renal parenchyma, obstruction causes increased pressure within nephron, compression restricts vasculature causing ischemia. Produces massive kidneys with greatly distended pelvis. Onset sudden or insious at any level. If obstruction removed, normal function usually resumes in a few weeks
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How does the renal system contribute to HTN?
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The 10% of HTN cases tt are 2ndary are mostly 2ndary to renal disease or renovascular disease. May be benign or malignant: benign HTN produces benign nephrosclerosis, malignant HTN produces malignant nephrosclerosis. Malignant (DBP >120) can cause retinal hemorrhage, cerebrovascular accidents, & renal failure
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Describe benign nephrosclerosis: caused by, population affected, characteristics?
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Result of arteriolar narrowing caused by benign HTN. Common over age 60, more in males than females. Characteristics: severe kidney damage (rare), kidneys symmetrically atrophied & pale, loss of concentrating ability &/or reduced GFR, mild proteinuria
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Describe malignant nephrosclerosis: onset, symptoms, morphologic changes of kidneys, characteristics?
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Sudden onset. Symptoms include headache, nausea, vomiting, visual derangements, LOC, convulsions. Morphologic changes: intimal and medial thickening early on, ischemic damage, thrombi, and pronounced proteinuria later on. Causes transient episodes of gross hematuria. Usual cause of death is uremia, sometimes caused by CHF or CVA
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What is the most common type of kidney cancer?
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Renal cell carcinoma
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Describe renal cell carcinoma: prevalence, caused by, population, symptoms, metastasis, prognosis?
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80-90% of all malignant tumors of the kidney, arise from tubule epithelium. Most common in middle age, male 2x female, more common in smokers. Variable behavior. Symptoms vary, include hematuria, enlarged kidneys, fever of unknown origin. Often silent, metastasizes to lungs, bones, lymph nodes, liver, adrenals, or brain. 37% survival rate after 5 years.
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Describe Wilm's tumor: frequency, genetics, discovery, symptoms, treatment, prognosis?
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Infrequent in adults, usually children. 3rd most common cancer in children under 10. Usually inherited, usually very large when discovered (size is what is first noticed). Symptoms include fever, abdominal pain, hematuria, intestinal obstruction. Treatment is radioTx, nephrectomy, chemoTx. 90% survival after 2 years
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Describe tumors of the urinary collecting system (bladder): symptoms, prevalence, causes, prognosis?
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Symptoms: mainly painless hematuria, most common in men 50-70, males 4x females. Smoking & chronic cystitis are causes. Prognosis: 79% after 5 years, tends to return after tumor removal
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Which is the more frequent cause of death: tumors of the bladder or tumors of the kidney?
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Tumors of the bladder
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