Grin Proteinuria and Polyruia Flashcards
(33 cards)
1
Q
What makes up the glomoerular filtration barrier?
A
- Fenestrated Capillary endothelium keeps cells out
- GBM keeps out plasma proteins
- Podocytes, keeps out plamsa proteins
2
Q
What gets through the glomerular filtration barrier?
A
- Low molecular weight proteins such as beta 2 macroglobulin and light chains they get reabsorbed in the proximal tubules
- soolutes and small molecules like Na K and glucose
3
Q
When is proteinuria not pathologic? What are the numbers?
A
- Small amounts can be normal as low molecular weight proteins pass through filtration barrier and not all get reabsorbed
- Also includes amounts of Tamm Horsfall protein produced by renal tubules
- Protein <150 mg/day
- albumin <30 mg/day
4
Q
what are the three types of proteinuria?
A
- glomerular occurs with a damaged glomerular filtartion barrier allowing for albuminuria to occur
- Overflow occurs when filtered low molecular weight protein load is greater than the reabsorptive capacity, this is seen in multiple myeloma with light chains
- Tubulointerstitial occurs with tubular damage which imparis reabsorption of low molecular weight proteins, this is seen in ATN
5
Q
Urinalysis pros and cons?
A
- cheap and easy and cant detect other urine abnormalities
- Con is it only detects albumin and has low sensitivity for low quantities of protein
6
Q
Spot urine albumin/creatine ratio pros and cons?
A
Pro:
- can detect small amounts of albumin (good for recognzing early diabetic nephropathy)
Con:
- only detects albumin
7
Q
Spot urine Protein/creatine ratio pros and cons?
A
Pro
- detects all proteins
Con
- not as well validated in diabetic nephropathy
8
Q
24 hour urine protein pros and cons
A
- Gold standard but inconvienent
9
Q
With light chain nephropathy due to multiple myeloma what needs to be done?
A
Urinalysys and spot urine albumin/creatinine ration may show a false negative meaning no protein, so you need to do a spot urine protein/creatine ratio to detect light chain proteinuria
10
Q
Nephrotic syndrome?
A
- Inflammation and damage to podocytes allowing albumib to pass into tubules
- main problem is albuminuria (>3.5 grams), urine looks frothy
- mild or no hematuria
- can lead to edema
11
Q
In Nephrotic syndrome what other protein is lost besides albumin?
A
- Antithrombin III an anti coagulant protein creating a hypercoagulable state leading to risk of clot formation
- liver also increases lipoprotein production leading tohyperlipidemia
12
Q
What contributes to nephrotic syndrome edema?
A
- low intravascular oncotic pressure due to loss of albumin in the blood
- Due to decreased intravascuoalr volume you get decreaased return to heart and then decrease blood through kidney leading to activation of RAAS
- renal sodium retention
13
Q
Nephritic vs nephrotic syndrome?
A
Nephritic:
- Htn
- RBC casts
- AKI/Oliguria
- Proteinuria
- Immune complex, Anti GBM or ANCA associated
Nephrotic:
- Edema
- Hyperlipidemia
- Hypoalbuminuria
- Proteinuria >3.5
- Hypercoagulability
- Diabetes
- Minimal change disease
- FSGS
- Amyloid
- Membranous
MPGN is in both
14
Q
What diseases cause nephrotic syndrome?
A
- Diabetic nephropathy
- Minimal change disorder
- most common cause in kids
- Focal segmental glomerulosclerosis
- Membranous nephropathy
- Amyloidosis
15
Q
What labs do you order with suspected nephrotic syndrome?
A
- Serum creatinie with eGFR
- UA with microscopy
- Urine albumin to creatinine ratio and urine protein to creatinine ratio
- Additional labs such as HIV Hepatitis serologies, SPEP, lipid panel, A1c
- Renal biopsy
16
Q
How do you manage nephrotic syndrome?
A
- manage underlying condition
- diuretics and sodium restriction
- Proteinuria
17
Q
Nephritic syndrome?
A
- Inflammation affecting capillary endothelium allowing passage of cells and proteins into renal tubule
18
Q
Features of nephritic syndrome?
A
- Hematuria
- Proteinuria less than 3.5 g/day
- New onset htn
- AKI/oliguria
19
Q
Break down nephritic syndroms into the causes?
A
- Immune complex related
- low complement, seen in post strep SLE
- normal complement levels, IgA nephropathy
- Pulmonary renal syndromes:
- Anti GBM
- ANCA associated
20
Q
Describe the two immune complex diseases associated with low complement that result in nephritic syndrome
A
- post infectious GN
- hx of recept strep infection
- SLE nephritis
- can present with systemic findings in lypus
- can present with rapidly progressive glomerulonephritis emergency
21
Q
Describe the immune complex diseases associated with normal complement that result in nephritic syndrome
A
- IgA nephropathy
- most common nephritic syndrome
- gross hematuria at time of URI (synpharyngitic)
- May present with isolated gross or microscopic hematuria
- benign course
22
Q
What nephritic syndromes fall under pulmonary renal syndromes?
A
- Anti GBM presenting with rapidly progressive GN
- hemoptysis due to alveolar hemorrhage, hematuria, severe AKI
- ANCA associated
- GPA
- respirartory sx including chronic sinusitis and saddle nose and hemoptysis
- renal sx hematuria with severe AKI
- Miceroscopic polyangitis
- GPA without upper respiratory sx
- Eosinophilic granulomatosis with polyangiitis (Churg Strauss)
- adult onset asthma eosinohpihlia palpable purpura hematuria and AKI
- GPA
23
Q
How do you work up nephritic syndrome?
A
- Seerum creatinine with GFR
- UA with microscopy
- Urine albumin to creatine
- Urine protein to creatine
- ANCA Anti GBM ANA complement
- Renal bx
24
Q
Plolyruia vs urinary frequency
A
- production of >3L of urine in 24 hrs is polyuria while an increase in frequency of urination regardless of volume is frequency
25
What two mechanisms regulate serum osmolality?
ADH release and thirst
26
Where does ADH come from and how does it work?
* released from posterior pituitary where it binds vasopressin receptor 2 causing aquaporins to move to apical surface allowing water to move from lumen to blood decreasing osmolality
27
What are the causes of polyruia?
* osmotic diuresis
* central diabetes insipidus
* nephrogenic diabetes insipidus
* Primary polydipsia
28
What occurs with osmotic diuresis
* excess solutes in urine filtrate draws water into the filtrate causing polyuria
* glucosuria is an example
* uncontrolled DM leads to excess glucose in the urine and this excess solute prevents the reabsorption of water
29
Central diabetes insipidus causes and features?
* head trauma
* brain tumor
* congenital malformation
* idiopathic
ADH isn't being released or produced
* urine osmolality is low and doesn't increase with water deprivation
* Urine osmolality increases with administration of desmopression (synthetic ADH)
30
What are features of nephrogenic diabetes insipidus and causes?
* Kidneys are unresponsive to ADH
* Lithium is most common cause used to tx bipolar disorder
* urine osmolality is low
* doesn't increase with water deprivation
* doesn't increase with administration of desmopression (synthetic ADH)
31
Does diabetes insipidus lead to hypernatremia?
* If thirst mechanism is intact it does not, it will be a high normal, they compensate for ADH inactivity by drinking more water
* If thirst mechanism is not intact or the patient can't get water you see hypernatremia
32
What is primary polydipsia? What are the features?
* Patient drinks excess water
* commonly seen with psychiatric disorders including psychosis and OCD
* low osmolality
* urine osmolality increases with overnight water deprivation
33
How do you treat polydipsia due to glucosuria, central diabetes insipidus, nephrogenic diabetes inspidus, and primary polydypsia?
* control diabetes
* drink more water and give desmopressin for central
* drink more water and take thiazide diuretics for nephrogenic
* behavioral modification
