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CPR 3 Renal Exam > Grin Proteinuria and Polyruia > Flashcards

Grin Proteinuria and Polyruia Flashcards

1
Q

What makes up the glomoerular filtration barrier?

A
  1. Fenestrated Capillary endothelium keeps cells out
  2. GBM keeps out plasma proteins
  3. Podocytes, keeps out plamsa proteins
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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
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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
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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
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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
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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
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7
Q

Spot urine Protein/creatine ratio pros and cons?

A

Pro

  • detects all proteins

Con

  • not as well validated in diabetic nephropathy
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8
Q

24 hour urine protein pros and cons

A
  • Gold standard but inconvienent
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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

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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
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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
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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
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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

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14
Q

What diseases cause nephrotic syndrome?

A
  • Diabetic nephropathy
  • Minimal change disorder
    • most common cause in kids
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Amyloidosis
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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
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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
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
Q

What two mechanisms regulate serum osmolality?

A

ADH release and thirst

26
Q

Where does ADH come from and how does it work?

A
  • 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
Q

What are the causes of polyruia?

A
  • osmotic diuresis
  • central diabetes insipidus
  • nephrogenic diabetes insipidus
  • Primary polydipsia
28
Q

What occurs with osmotic diuresis

A
  • 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
Q

Central diabetes insipidus causes and features?

A
  • 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
Q

What are features of nephrogenic diabetes insipidus and causes?

A
  • 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
Q

Does diabetes insipidus lead to hypernatremia?

A
  • 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
Q

What is primary polydipsia? What are the features?

A
  • Patient drinks excess water
  • commonly seen with psychiatric disorders including psychosis and OCD
  • low osmolality
  • urine osmolality increases with overnight water deprivation
33
Q

How do you treat polydipsia due to glucosuria, central diabetes insipidus, nephrogenic diabetes inspidus, and primary polydypsia?

A
  • control diabetes
  • drink more water and give desmopressin for central
  • drink more water and take thiazide diuretics for nephrogenic
  • behavioral modification

CPR 3 Renal Exam (14 decks)

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