NRS 313 Study Guide - Final Guide: Glomerulonephritis, Biliverdin, Kidney Stone Disease
27 May 2018
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Detoxification and Filtration
• Deamination of amino acids
o Waste product + breakdown of protein molecules. Chains in peptide. DNA
replication makes codones -> ribosome w/ other peptide chains -> proteins.
▪ They need to be cleaned up-> if not we get a build up
o By product is Creatine
▪ From muscle activity.
▪ Needs to be cleared out
▪ Moves through ISF-> vascular space -> heart-> kidney
▪ Goes right through glomerular filter
▪ Creatine should all be in the urine
• Ammonia
o We can get ammonia build up from liver disease.
o Signs of confusion selling loss of motor control
o Can’t breakdown ammonia-> from urea
o Ammonia is made through the breakdown of AA
o Liver normally converts ammonia to urea
o Blood urea should be low
o If liver is damaged= Increase in ammonia which is neurotoxic
▪ Hepatic Encephalopathy= liquafactic necrosis
• Renal function tests
o Creatinine clearance: One indicator of GFR and renal health
▪ Creatinine produced at steady rate from muscle, cleared from vascular
system by glomeruli
▪ when renal function is normal serum creatinine levels will be LOW
• Measured with blood sample and 24-hour urine
• When GFR decreases (over weeks/months), serum creatine levels
will increase.
o Low MAP -> lower filtration rate -> more creatine
o LOW GFR
▪ Low blood pressure
▪ Serum creatine levels increase
o Blood Urea Nitrogen (BUN): measured with blood sample
▪ Urea formed in liver as by-product of protein metabolism and is
eliminated by kidneys along with nitrogen
▪ Looking at how well the liver is working converting ammonia to urea
▪ Variations in BUN levels may be caused by:
• Excess Dietary protein intake
o Too much protein in the liver means they can’t delaminate
quick enough
• Gastro-intestinal inflammation
o Look at excreationm of carbon + urea
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o The portal vein takes deoxygenated blood from the GI tract
o Excess breakdown of AA can be seen
o LKysis of RBCs
o Potassium: measured with blood sample
▪ Elimination regulated by GFR and Aldosterone levels
▪ Low GFR results in elevated serum K+ levels
▪ Low Aldosterone results in elevated serum K+ levels
• Kidneys need a strong GFR to excrete. Aldosterone helps with this
• Adrenal gland insufficiency
• Renal Hormones
o Erythropoietin released into blood from peri-tubular capillary endothelial cells in
response to hypoxia
▪ Stimulates erythrocyte proliferation
▪ Renal disease leads to chronic anemia r/t decreased erythropoietin
production
▪ Stimulates bone morrow to form new cells
▪ Pay attention to o2 levels from an Sp02 probe.
o Vitamin D converted to its active form (Calcitriol) in the kidney
▪ necessary for absorption of calcium from the small intestine.
▪ Renal disease impairs conversion of Vitamin D into active form – leads to
bone demineralization.
o Calcitonin: comes from thyroid. Promotes bone growth and releases osteoclasts
o Calcitrol: Kidney necessary for reabsorbing Ca++. Absorbed in microvilli of GI
tract
• Renal Injury
o Renal anemia
▪ Kidneys are sick. Chronic anemia due to decreased O2. Results in
tachycardia, tachypnea
• Glomerular Disorders
o Glomerulonephritis: multiple causes
▪ Toxins (Gentamycin is nephrotoxic)
▪ Hypertension (Chronic MAP greater than110)
▪ Diabetes - AGEs and ROS and endothelial cell damage
• Permanently bound glucose + protein molecules get embedded and
lead to ROS
• Glomerulus in endothelial cells -> neuropathy
▪ Increased glomerular capillary permeability and loss of negative ionic
charge barrier (podocytes) results in protein in urine.
o Proteinuria = Hypoproteinemia leads to edema
▪ Protein in the vascular space -> decrease in oncotic pressure
o Glomerulus: filtering Gentamycin is nephrotoxic wide spectrum antibiotic. If
they get too much we get damage to glomerulus. Inflammatory process and
dysfunction accompany
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