Group Case Discussions 1 - Renal Cases Flashcards
(28 cards)
What is pyelonephritis? What does it lead to?
Inflammation of the kidney pelvis starting in the medulla and caused by UTIs => leads to destruction of all juxtomedullary nephrons and many outer-cortical nephrons (since their loops of Henle are in the medulla) => only functioning with a few outer cortical nephrons + no more gradient in the medulla so the collecting duct cannot reabsorb water => marked decrease in GFR and polyuria
Normal plasma [urea]?
20-40 mg/100 mL
What is specific gravity?
Density of substance/density of water
What is the specific gravity of isosmotic urine? Max and min?
1.003 <=> 1.010 <=> 1.055
How to calculate clearance if you are given excretion rate?
Simply divide by plasma concentration, since you already have Ux.V
What is urine specific gravity a measure of? Exception?
Measure of urine concentration, except during proteinurea (SG would increase more than concentration)
What is polyuria?
Frequent urination
What does it mean if Cx ««_space;Ccr
Net reabsorption in the kidney: E
What is a paradigm caused by pyelonephritis?
Very low GFR but very high urine flow rate
How do I know that a decreased GFR is not due to total obstruction of a kidney?
If the GFR decrease is by more than 50%, then it has to be something else
Effect of low protein diet on kidney function?
Low protein diet => low albumin production => low peritubular oncotic pressure => high urine volume
What effect would a low protein diet have on a patient with pyelonephritis?
It would simply decrease plasma and urine urea concentrations, but would have no effect on the clearance since the GFR is so low in these patients
Are plasma urea concentration or excretion rate alone a valuable index of the severity of a patient’s kidney function? Why?
NOPE - because it can change with diet
What is uremia? Symptoms?
High plasma urea
Symptoms: fatigue, loss of taste/metallic taste, anorexia, anemia
Treatment for pyelonephritis?
- Antibiotics to stop UTI
- Decrease protein intake to avoid uremia and to decrease GFR (more urea in blood means vasodilation to increase filtration to get rid of it)
What are the 5 types of diabetes insipidus (3 names for first one and 2 for second one)? Explain each.
- Central = neurogenic = hypothalamic: inability to synthesize or secrete active vasopressin
- Nephrogenic = renal: inability of kidney to detect vasopressin
- Gestational: placenta secretes vasopressinase that degrades vasopressin
- Dipsogenic: low thirst threshold
- Psychogenic: excessive drinking
What is diabetes insipidus characterized by?
Large dilute urine volume
How can you diagnose DI?
Patient has to be shown to excrete a hypotonic urine despite the presence of a hyperosmolar serum (aka when the patient is dehydrated)
+ administer AVP to determine if the DI is central
In what patients with polyuria do you see normal blood osmolarity and BP and why?
- Osmotic diuresis
- Central DI
- Nephrogenic DI
- Gestational DI
Because their thirst is intact and regulates blood osmolarity and BP
Treatments for DI? How do they work?
- Water
2. Antidiuretic agents (for central DI only) - AVP analogs (e.g. DDAVP)
What is diuresis?
Collecting duct is impermeable to water (normal state)
How else can we differentiate central DI from nephrogenic DI? When is this usually done?
Measure plasma AVP when blood is hyperosmolar (dehydrated)
Usually done after a formal water deprivation test
How come DDAVP can be administered orally or intranasally even though it’s a peptide?
It’s protected from degradation
When does a patient require dialysis?
When GFR falls to 15mL/min or less