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CPR III > Proteinuria and Polyuria (Grin) > Flashcards

Proteinuria and Polyuria (Grin) Flashcards

1
Q

What are the 3 layers of the glomerular barrier?

A
  1. fenestrated capillary endothelium (keeps out cells)
  2. basement membrane (keeps out large proteins)
  3. podocytes (keeps out large proteins)
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2
Q

What gets through the glomerular filtration barrier?

A

low molecular weight proteins (beta 2 macroglobulin, light chains) but are REABSORBED in proximal tubules and small solutes and molecules (Na, K, glucose)

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3
Q

Normal daily protein excretion

A

low molecular weight proteins (ex. Tamm-Horsfall proteins)

Normal limits:
protein <150 mg/day
albumin <30 mg/day

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4
Q

Glomerular proteinuria

A

damaged glomerular filtration barrier (podocytes and basement membrane) leads to albuminuria

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5
Q

Overflow proteinuria

A

Filtered low-molecular-weight protein load>reabsorptive capacity of the kidney (multiple myeloma - lots of light chains)

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6
Q

Tubulointerstitial proteinuria

A

Tubular damage leads to impaired reabsorption of low molecular weight proteins (ex. Acute tubular necrosis)

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7
Q

Orthostatic proteinuria

A

increased urine protein excretion in the upright position but normal protein excretion in the supine position. typically seen in children. Urinalysis is positive when child is upright, then repeat and normal.

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8
Q

Pros and cons of a urinalysis

A

Pros: cheap and easy

Cons: only detects albumin when there is a lot present (>300 mg) low sensitivity.

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9
Q

Pros and cons of a spot urine albumin/creatinine ratio

A

Pros: can detect small amounts of albumin (unlike a urinalysis) - useful in early diabetic nephropathy

Cons: only detects albumin; not good for multiple myeloma

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10
Q

Pros and cons of a spot urine protein/creatinine ratio

A

Pros: detects all proteins (unlike a urinalysis and spot urine albumin/creatinine ratio) -good for multiple myeloma

Cons: not that good for diabetic nephropathy

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11
Q

What is the current gold standard for measuring proteinuria?

A

a 24 hour urine protein
pros: gold standard
cons: inconvenient

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12
Q

Pros and cons of a 24 hour urine protein test

A

pros: gold standard
cons: inconvenient

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13
Q

What test is needed in the case of suspected multiple myeloma?

A

Need spot urine protein/creatinine ratio to detect light chain proteinuria

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14
Q

Nephrotic syndrome pathophysiology

A

damaged glomerular filtration barrier allows plasma proteins to pass into the nephron tubule. proteinuria >3.5 g/day (albumin and antithrombin III)

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15
Q

What are the two main proteins being excreted in nephrotic syndrome?

A
  1. albumin (hypoalbuminemia- low oncotic pressure-edema)
  2. anti-thrombin III (anticoagulant - thrombotic and thromboembolic complications)
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16
Q

How does nephrotic syndrome lead to edema

A
  1. (underfill theory) proteinuria leads to hypoalbuminemia, leads to decreased oncotic pressure; edema
  2. (overfill theory) decreased renal blood flow leads to RAAS activation, leads to increased Na retention then water retention; edema
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17
Q

What are the 5 major features of nephrotic syndrome?

A
  1. Proteinuria >3.5 g/day
  2. Edema
  3. Hyperlipidemia (fatty casts, xanthelasmas)
  4. Hypoalbuminemia
  5. Hypercoagulability (DVT/PE and renal vein thrombosis)
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18
Q

What are the 5 main causes of nephrotic syndrome?

A
  1. Diabetes (most common)
  2. Minimal change (children)
  3. Focal Segmental Glomerulosclerosis (FSGS) - HIV/heroin use
  4. Membranous (idiopathic primary or secondary with Hep.B/C, syphilis, solid tumors, SLE
  5. Amyloid
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19
Q

Early pathophysiology of diabetic nephropathy

A

Lots of glucose in the blood causes non-enzymatic glycation. Increases the pressure in the afferent arterioles, increases the GFR, and causes hyperfiltration. Increase pressure in the bowman capsule and tubules and causes damage of the glomerulus.

Note: early stages creatinine and eGFR will be NORMAL

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20
Q

Late pathophysiology of diabetic nephropathy

A
  1. adaptive changes will cause a thickened basement membrane
  2. mesangial expansion
  3. Kimmelstiel-Wilson nodules
  4. Disruption of podocytes
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21
Q

Workup for nephrotic syndrome

A

basic metabolic panel
urinalysis with microscopy
urine albumin/creatinine ratio and urine protein/creatinine ratio
addition labs (HIV, Hep B/C, lipid panel, A1c)
Renal biopsy

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22
Q

What is the most common cause of end-stage renal disease in the US?

A

Diabetic glomerulonephropathy

23
Q

What are the levels of creatinine and eGFR in early diabetic nephropathy?

A

early stages creatinine and eGFR will be NORMAL

24
Q

The use of ACEis/ARBs in Nephrotic Syndrome

A

Stop ACEis/ARBs in patient with AKI b/c we want angiotension to do the job of vasodilation of afferent and constriction of efferent to increase GFR pressure. In AKI the GFR is decreased.

Start ACEis/ARBS in patient with CKD because leads to inhibition of angiotensin which will lead to decreased GFR to prevent further damage.

25
Q

Nephritic Syndrome

A

Inflammation affecting the glomerular filtration barrier (specifically capillary endothelium) and allows passage of cells and proteins into the renal tubule.

26
Q

Features of Nephritic Syndrome

A

Hematuria (RBCs are able to leak through barrier)
Proteinuria <3.5 g/day (not many proteins get through)
New onset hypertension (Na/H2O retention)
AKI/oliguria (rapidly progressive glomerulonephritis RPGN) which can progress to renal failure over days/weeks

27
Q

Causes of Nephritic Syndrome

A
  1. Immune complex (low complement - post strep/SLE; norm complement - IgA nephropathy)
  2. Anti-GBM
  3. ANCA- associated (GPA, eGPA, and MPA)
28
Q

Post-strep glomerulonephritis

A

Low complement immune complex disorder that can cause nephritic syndrome. Patient will present with recent strep throat infection or strep skin infection and then will have glomerulonephritis

NOTE: contrast with IgA when a patient presents with URI at the SAME time as hematuria.

29
Q

SLE nephritis

A

Low complement immune complex disorder that can cause nephritic syndrome. Patient will present with other systemic findings (malar rash/butterfly rash, polyarticular arthritis).

Can present with rapidly progressive glomerulonephritis (RPGN) which is a medical emergency.

30
Q

Which disorder can rapidly progress to glomerulonephritis?

A

SLE and pulmonary-renal syndromes (ANCA associated and anti-GBM/Good Pastures)

31
Q

IgA nephropathy

A

Normal complement immune complex disorder can cause nephritic syndrome. Typically presents with gross episodic hematuria (kidney) at the SAME time as a URI (synpharyngitic) or GI infection. When associated with systemic symptoms then called IgA vasculitis.

NOTE: contrast with post-infectious GN when a patient presents with URI and THEN glomerulonephritis.

32
Q

Anti-GBM/Good Pastures

A

Pulmonary-renal syndrome can cause nephritic syndrome. Presents with hemoptysis (alveolar hemorrhage- lung), hematuria and severe AKI.

90% of cases progress to rapidly progressive glomerulonephritis (fatal if untreated)

33
Q

What are the three ANCA-associated disorders associated with Nephritic Syndrome?

A
  1. Granulomatosis with polyangiitis (GPA): c-ANCA
  2. Microscopic polyangiitis (MPA): p-ANCA
  3. Eosinophilic granulomatosis with polyangiitis (eGPA)
34
Q

Granulomatosis with polyangiitis (GPA)

A

ANCA-associated (c-ANCA) disorder that can cause nephritic syndrome. Pt can present with a saddle nose deformity, chronic sinusitis, hemoptysis, and hematuria with severe AKI

35
Q

Microscopic polyangiitis (MPA)

A

ANCA-associated (p-ANCA) disorder that can cause nephritic syndrome. Think GPA WITHOUT upper respiratory symptoms.

36
Q

Eosinophilic granulomatosis with polyangiitis (eGPA)

A

ANCA-associated disorder that can cause nephritic syndrome. Look for adult-onset asthma, eosinophilia, palpable purpura, hematuria and AKI

37
Q

What is the workup for nephritic syndrome?

A

Basic metabolic panel
Urinalysis with microscopy
Urine albumin/creatinine ratio and urine protein/creatinine ratio
Additional labs (ANCA, Anti-GBM, complements)

38
Q

Proteinuria (<3.5 g/day), hematuria, dysmorphic RBC and RBC casts

A

Nephritic Syndrome

39
Q

Heavy proteinuria (>3.5 g/day), fatty casts, oval fat bodies, minimal hematuria

A

Nephrotic Syndrome

40
Q

Management of Rapidly Progressive Glomerulonephritis (RPGN)

A

Urgent renal consult
High dose steroids
Plasma exchange

41
Q

Polyuria

A

production of >3L urine in 24 hours

42
Q

Urinary frequency

A

increase in frequency of urination, regardless of volume voided

43
Q

Nocturia

A

increase in frequency of urination at night

44
Q

Role of ADH

A

produced by the hypothalamus and released from the posterior pituitary, acts on the distal convoluted tubules in the kidneys to insert aquaporins to retain water and increase blood volume and dilute blood to normal osmolality levels.

45
Q

What is the maximally concentrated urine ADH can produce?

A

ADH at its max effect can maximally concentrate urine to 1200 mosm/kg

46
Q

What are the 4 main causes of polyuria?

A
  1. Osmotic diuresis
  2. Central diabetes insipidus
  3. Nephrogenic diabetes insipidus
  4. Primary polydipsia
47
Q

Osmotic diuresis

A

Glucosuria (diabetes mellitus)

Uncontrolled diabetes mellitus leads to too much glucose to be reabsorbed by the kidneys. The excess solute pulls the water into the filtrate and prevents the reabsorption of water (polyuria)

Dipstick will be positive for glucose. Uosm >300 mOsm/L

48
Q

Central diabetes insipidus causes?

A

Head trauma
Brain tumor
Congenital malformation
Idiopathic

49
Q

Central diabetes insipidus key features?

A

Serum Na normal or high
Uosm <300 mOsm/L
Urine osmolality does NOT increase with water deprivation
Urine osmolality INCREASES with admin of desmopressin (corrected underlying prob)

50
Q

Nephrogenic diabetes insipidus key features?

A

Kidney does not respond to ADH - can be caused by lithium (bipolar medication)

Serum Na normal or high
Uosm <300 mOsm/L
Urine osmolality does NOT increase with water deprivation
Urine osmolality does NOT increase with admin of desmopressin (more ADH I’m not responding to)

51
Q

Does diabetes insipidus lead to hypernatremia?

A

If thirst mechanism is intact, often not. Yes we are retaining more Na, but patients compensate by drinking more water!

If thirst mechanism is NOT intact or there is no access to water we can see hypernatremia. Think hospitalized patient with altered mental status

52
Q

Primary polydipsia

A

Patient inappropriately drinking excessive amounts of water. Commonly seen in psychiatric disorders (OCD)

Serum Na will be low
Uosm <300 mOsm/L
Urine osmolality INCREASES with overnight deprivation (think now the body is appropriately concentrating the urine)

53
Q

Polyuria treatment

A

Glucosuria- get diabetes mellitus under control
Central diabetes insipidus- desmopressin
Nephrogenic diabetes insipidus- thiazide diuretic
Primary polydipsia- behavioral modification

CPR III (20 decks)

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