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CPR Test II > approach to proteinuria, oliguria, and polyuria > Flashcards

approach to proteinuria, oliguria, and polyuria Flashcards

1
Q 
definitions:
Anuria?
Oliguria?
Polyuria?
Azotemia?
Uremia?
A

Anuria: UOP < 50-100 mL/aday

Oliguria: UOP < 400-500 ml/day

Polyuria: UOP > 3000 ml/day

Azotemia: elevated blood urea nitrogen (BUN) without symptoms

Uremia: Elevated BUN with symptoms (N/V, confusion, pruritus, metallic taste in mouth, fatigue, anorexia)
-symptoms of uremia are non-specific with multiple etiologies causing them

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2
Q

what is the definition of CKD

A

markers of kidney damage: albuminuria

  • urine sediment abnormalities
  • electrolyte and other abnormalities due to tubular disorders
  • abnormalities detected by histology
  • strctural abnormalities detected by imaging
  • history of kidney transplant

or

GFR< 60 ml/min

has to be present for > 3 months
-if not it is an AKI

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3
Q

which is worse stage 1 or 5 CKD

A

Stage 5 < 15 GFR

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4
Q

what are major risk for CKD

A

DM
HTN
Cardiovascular disease
Acute Kidney Injury

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5
Q

what are some signs and symptoms of CKD

A

some patients are asymptomatic and find out when coming in for routine lab testing

  • Edema
  • HTN
  • Decreased urine output
  • Foamy urine
  • Uremia
  • Pericardial friction rub
  • Asterixis
  • Uremic frost
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6
Q

what are 3 simple tests to identify most CKD patients

A
  • eGFR
  • Urine albumin to creatinine ratio or urine protein to creatinine ratio
  • urinalysis with microscopy
  • renal biopsy
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7
Q

what is the limitations to eGFR?

A
  • not reliable when GFR > 60 ml/min
  • not reliable in AKI
  • Not reliable in low muscle mass
  • Patient is < 18
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8
Q

what are the renal U/S findings for CKD

A
  • Atrophic or small kidneys
  • Cortical thinning
  • Increased echogenicity
  • Elevated resistive indices
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9
Q

CKD treatments for proteinuria

A

low salt diet
BP control
ACEi ARB aldosterone antagonist, renin inhibitor, non dihydropyridine CCB

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10
Q

CKD treatment for HTN

A

SBP < 120 mmHg

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11
Q

CKD treatment for hyperlipidemia

A

Statin

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12
Q

CKD treatment for anemia

A

Oral or IV iron

EPO stimulating agents

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13
Q

CKD treatment for Metabolic acidosis

A

Bicarbonate supplementation if HCO3

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14
Q

CKD treatment for CKD BMD

A

previously known as renal osteodystrophy

  • secondary hyperparathyroidism
  • renal failure diet (low salt, potassium and phosphorus
  • Vitamin D supplementation
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15
Q

CKD treatment for VOlume overload

A

Diuretics, fluid restriction, or dialysis

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16
Q

what are the renal replacement therapies

A

Hemodialysis
Peritoneal dialysis
Renal transplantation

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17
Q

What are the indications for dialysis

A

A: severe acidosis
E: Electrolyte disturbance (usually hyperkalemia
I: Ingestion (ex: ethylene glycols, methanol, etc)
O: Volume overload
U: Uremia

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18
Q

what are the two ways that AKI are defined

A

Serum creatinine increase or Urine output decrease

which ever one is the worse is how it is staged

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19
Q

What are the causes of Prerenal AKI

A 
Hypotension
Hypovolemia
Reduced cardiac output
-HF, Cardiac tamponade, massive PE
Systemic vasodilation
-sepsis, SIRS, Hepatorenal syndrome
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20
Q

what are the causes of Intrinsic AKI

A

Acute tubular necrosis

  • ischemia
  • toxins

Interstitial Nephritis

Glomerulonephritis

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21
Q

What is the clinical presentation of AKI

A

similar to CKD

  • Edema
  • HTN
  • Decreased urine output
  • Foamy urine
  • SOB
  • Uremia (N/V, confusion, pruritus, metallic taste in mouth)
  • Pericardial friction rub
  • asterixis
  • uremic frost
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22
Q

what are the common diagnostic test of AKI

A

UA with urine microscopy
Urine albumin/cr ratio or protein/cr ratio
Renal U/S

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23
Q

what is a >20:1 BUN: Creatinine ratio suggestive of

A

Prerenal azotemia

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24
Q

what is a fractional excretion of Na indicative of

A

FeNa < 1% = prerenal azotemia

FeNa> 2% = ATN

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25
Q

what is a fractional excretion of Urea indicative of

A

FeUrea < 35% = prerenal azotemia

FeUrea > 50 % = ATN

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26
Q

Urinary pattern: Renal tubular epithelial celss, transitional epithelial cells, granular cells, or waxy casts

A

Acute tubular necrosis

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27
Q

urinary pattern: WBC, WBC cast or urine eosinophils

A

Acute interstitial nephritis (AIN) or pylonephritis

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28
Q

urinary pattern: Dysmorphic RBCs, RBC casts

A

Vasculitis or Glomerulonephritis

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29
Q

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

A

Nephritic syndrome

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30
Q

urinary pattern: Heavy proteinuria (>3.5g/day), lipiduria, minimal hematuria

A

Nephrotic syndrome

31
Q

urinary pattern: Hyaline cast

A

Non-specific, prerenal azotemia

32
Q

urinary pattern: WBC, RBC, bacteria

A

urinary tract infection

33
Q

what are complications of AKI

A

Hypervolemia

  • PE
  • HF

Electrolyte abnormalities

  • hyperkalemia
  • hyperphosphatemia
  • hypocalcemia
  • hypermagnesemia
hyperuricemia
uremia
pericafrditis
Metabolic acidosis
Bleeding
-platelet dysfunction
Need for dialysis
34
Q

Treatment for AKI

A

Mostly supportive

  • avoid hypotension
  • discontinue Nephrotoxins
  • renal replacement

Prerenal patients need IV fluid

ATN need supportive

GLomerulonephritis need immunosuppression or plasmapheresis

Acute interstitial nephritis needs discontinuation of offending agent or steriods

35
Q

what is the Nephrotic syndrome definition

A 
Proteinuria
->3-3.5 g/day
Hypoalbuminemia
Peripheral edema
Hyperlipidemia
Lipiduria
36
Q

what does it mean if serum albumin is normal in the setting of nephrotic range proteinuria?

A

then the patient does not have nephrotic syndrome but instead has nephrotic range proteinuria

37
Q

what are some Nehrotic syndrome complications

A

Edema

  • low serum albumin
  • increased TBW and Na+

Hyperlipidemia

Infection

  • urinary loss of IgG
  • occasionally have to supplement with IVIG

Thrombosis

  • urinary loss of antithrombotic factors
  • increased levels of procoagulant factors
  • potentially renal vein thrombosis

Vitamin D deficiency
-loss of Vitamin D binding protein

Anemia
-urinary loss of transferrin and Erythropoietin

38
Q

what are the pathogenesis of edema in Nephrotic syndrome

A

low intravascular oncotic pressure

Renal sodium retention

39
Q

what is the classical presentation of Nephrotic syndrome

A

New onset hypertension
new onset edema
-severe anasarca
-SOB from pulmonary edema or pleural effusion

proteinuria

  • typically>3.5 g/day
  • foamy urine

Lipiduria
Hyperlipidemia
Minimal hematuria

My have renal failure

40
Q

what is a common nephrotic syndrome in children

A

Minimal change disease

41
Q

what Nephrotic syndrome is common with HIV infection

A

Focal Segmental glomerular sclerosis

42
Q

what are 3 examples of Monoclonal disease causing nephrotic syndrome

A

Multiple myeloma
amyloidosis
Monoclonal immunoglobulin deposition disease
-can be light, heavy, or light and heavy chain

43
Q

what nephrotic syndrome is associated with underlying malignancy and or renal vein thrombosis

A

Membranous Nephropathy

44
Q

what is the main diagnostic of Nephrotic syndrome

A

Renal Biopsy

45
Q

how to treat the edema of the nephrotic syndrome

A

Dietary sodium restriction

diuretics

46
Q

how to treat the proteinuria of the nephrotic syndrome

A

Lower blood pressure
ACE or ARB
alternative anti proteinuric medications
-nondihydropyridine CCB, Aldosterone antagonist, renin inhibitors

47
Q

what is the nephritic syndrome definition and what is one key point in its characteristics

A

Proteinuria <3.5g/day
Hematuria
HTN
Renal failure common

Key point

  • usually have active urinary sediment
  • nephrotic has bland urinary sediment
48
Q

Clinical presentation of Nephritic syndrome

A 
New onset HTN
New onset hematuria
-microscopic or gross hematuria
Acute kidney injury
-can progress to RPGN
Proteinuria
-typically <3.5 g/day
-foamy urine

can have edema but not severe compared to nephrotic syndrome

49
Q

what are some DDx for Nephritic syndrome

A
  • IgA nephropathy
  • THin basement membrane nephropathy
  • alports nephropathy
  • Membranoproliferative glomerulonephritis
  • Lupus Nephritis
  • Anti-GBM antibody disease
  • ANCA associated Vasculitis
  • cryoglobulinemia
  • Thrombotic microangiopathy
  • Post infectious glomerulonephritis
  • Endocarditis
50
Q

how is the diagnosis of Nephritic syndrome made

A

Renal biopsy is the best

can do glomerulonephritis serologic evaluation

51
Q

what is the DDx of Glomerulonephritis with low complement levels

A
  • Lupus Nephritis
  • Post-infectious GLomerulonephritis (PIGN)
  • Membranoproliferative Glomerulonephritis (MPGN)
  • Cyroglobulinemia
  • atypical hemolytic uremic syndrome
  • endocarditis
  • cholesterol embolus
  • HIV associated immune complex disease
52
Q

what is polyuria

A

urine output > 3 L/day

53
Q

what are the two different types of diuresis that can lead to diuresis

A

Solute diuresis

Water diuresis

54
Q

what are the types of solute diuresis that can lead to polyuria

A

Glucosuria

  • Hyperglycemia
  • SGLT-2 inhibitor use

Urea:

  • resolution of azotemia
  • exogenous urea administration
  • tissue catabolism

Sodium
-IV fluids

Mannitol

55
Q

what are the types of water diuresis causes that lead to polyuria

A

Primary polydipsia
Central diabetes insipidus
Nephrogenic Diabetes insipidus

56
Q

what are the two requirements for forming Concentrated urine

A

Hypertonic Medullary interstitium
-generates osmotic gradient necessary for water reabsorption

High levels of Antidiuretic Hormone (ADH)
-increase water permeability of distal convoluted tubule and collecting duct

57
Q

what are the 2 main systems that regulate serum osmolality

A

Osmoreceptor-ADH system
-ADH has short half life that allows for rapid means to alter water excretion by the kidney

Thirst mechanism

58
Q

where is ADH produced and what are the 2 ways these detections occur to generate more ADH

A

prehormone of ADH is produced in the Supraoptic Nuclei (majority) and Paraventricular nuclei (PVN)
-then transported down to the posterior pituitary in secretory granules

2 ways detections are increase in serum osmolality via the osmoreceptors in the anterior hypothalamus

other is decrease in blood pressure or increase in blood volume
-detected by arterial baroreceptors and atrial stretch receptors

59
Q

what are the effects of ADH on the collecting duct and why in dehydration is the urea levels increase

A

binds V2 receptors to increase cAMP levels which lead to insertion of AQP-2 and urea transporters

that is why in dehydration the urea levels go up

60
Q

what are the two types of Diabetes insipidus

A

Central Diabetes Insipidus

Nephrogenic diabetes insipidus

61
Q

what is the cause of Central diabetes inspidus

A

Caused by decrease release of antiduretic hormone (ADH)

  • idiopathic
  • hereditary
  • primary or secondary tumors
  • infiltrative diseases
  • Neurosurgery
  • Trauma
  • Meningitis/encephalitis
62
Q

what are the cause of Nephrogenic diabetes insipidus

A

Caused by decrease response to antidiuretic hormone (ADH)

  • Hereditary (seen in children)
  • lithium toxicity
  • hypercalcemia
  • hypokalemia
63
Q

what is the net result of hypercalcemia induced polyuria

A

Basolateral calcium sensor in TAL leads to inactivation of luminal K+ channel ultimately leading to inactivation of Na-K-2Cl cotransporter

Net result is similar to giving loop diuretic

also CaSr induces degradation of AQP-2 leading to nephrogenic DI

64
Q

what are the clinical manifestations of Diabetes Insipidus

A
  • Polyuria
  • Nocturia
  • Polydipsia
  • Nypernatremia
  • Orthostasis

also have manifestations from underlying causes, trauma, lithium toxicity, hypercalcemia, hypokalemia, etc

65
Q

how is the diagnosis of Diabetes insipidus made

A

24 hour urine volume collection
Urine osmolality < 300 mOsm/kg
Water deprivation test

66
Q

Urine osmolality with water deprivation >800, serum vasopressin after dehydration >2 and little or no increase in urine osmolality with desmopressin

67
Q

Urine osmolality with water deprivation <300, serum vasopressin after dehydration undetectable and substantial increase in urine osmolality with desmopressin

A

Complete central diabetes insipidus

68
Q

Urine osmolality with water deprivation 300-800, serum vasopressin after dehydration <1.5 and increase of >10% of urinary osmolality after water deprivation in urine osmolality with desmopressin

A

Partial Central diabetes insipidus

69
Q

Urine osmolality with water deprivation <300-500, serum vasopressin after dehydration >5 and little or no increase in urine osmolality with desmopressin

A

Nephrogenic vasopressin after dehydration

70
Q

Urine osmolality with water deprivation >500, serum vasopressin after dehydration <5 and little or no increase in urine osmolality with desmopressin

A

Primary polydipsia

71
Q

what is the treatment for central diabetes insipidus

A

Vasopressin

72
Q

what is the treatment for Nephrogenic diabetes insipidus

A

Decreased solute intake

Thiazide diuretics
-induces mid volume depletion, increases proximal tubular sodium and water reabsorption

NSAIDs

  • decreased medullary prostaglandin production
  • medullary prostaglandins antagonize action of ADH

Vasopressins
-most patients nephrogenic DI have a partial rather than complete resistance to ADH

73
Q

what is the treatment for Hypernatreima

A

replace free water deficit

-patient drinks water to give IV D5W

CPR Test II (6 decks)

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