approach to proteinuria, oliguria, and polyuria Flashcards
(73 cards)
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
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
3
Q
which is worse stage 1 or 5 CKD
A
Stage 5 < 15 GFR
4
Q
what are major risk for CKD
A
DM
HTN
Cardiovascular disease
Acute Kidney Injury
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
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
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
8
Q
what are the renal U/S findings for CKD
A
- Atrophic or small kidneys
- Cortical thinning
- Increased echogenicity
- Elevated resistive indices
9
Q
CKD treatments for proteinuria
A
low salt diet
BP control
ACEi ARB aldosterone antagonist, renin inhibitor, non dihydropyridine CCB
10
Q
CKD treatment for HTN
A
SBP < 120 mmHg
11
Q
CKD treatment for hyperlipidemia
A
Statin
12
Q
CKD treatment for anemia
A
Oral or IV iron
EPO stimulating agents
13
Q
CKD treatment for Metabolic acidosis
A
Bicarbonate supplementation if HCO3
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
15
Q
CKD treatment for VOlume overload
A
Diuretics, fluid restriction, or dialysis
16
Q
what are the renal replacement therapies
A
Hemodialysis
Peritoneal dialysis
Renal transplantation
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
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
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
20
Q
what are the causes of Intrinsic AKI
A
Acute tubular necrosis
- ischemia
- toxins
Interstitial Nephritis
Glomerulonephritis
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
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
23
Q
what is a >20:1 BUN: Creatinine ratio suggestive of
A
Prerenal azotemia
24
Q
what is a fractional excretion of Na indicative of
A
FeNa < 1% = prerenal azotemia
FeNa> 2% = ATN
25
what is a fractional excretion of Urea indicative of
FeUrea < 35% = prerenal azotemia
FeUrea > 50 % = ATN
26
Urinary pattern: Renal tubular epithelial celss, transitional epithelial cells, granular cells, or waxy casts
Acute tubular necrosis
27
urinary pattern: WBC, WBC cast or urine eosinophils
Acute interstitial nephritis (AIN) or pylonephritis
28
urinary pattern: Dysmorphic RBCs, RBC casts
Vasculitis or Glomerulonephritis
29
urinary pattern: Proteinuria (<3.5g/day), hematuria, dysmorphic RBC and RBC casts
Nephritic syndrome
30
urinary pattern: Heavy proteinuria (>3.5g/day), lipiduria, minimal hematuria
Nephrotic syndrome
31
urinary pattern: Hyaline cast
Non-specific, prerenal azotemia
32
urinary pattern: WBC, RBC, bacteria
urinary tract infection
33
what are complications of AKI
Hypervolemia
- PE
- HF
Electrolyte abnormalities
- hyperkalemia
- hyperphosphatemia
- hypocalcemia
- hypermagnesemia
```
hyperuricemia
uremia
pericafrditis
Metabolic acidosis
Bleeding
-platelet dysfunction
Need for dialysis
```
34
Treatment for AKI
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
what is the Nephrotic syndrome definition
```
Proteinuria
->3-3.5 g/day
Hypoalbuminemia
Peripheral edema
Hyperlipidemia
Lipiduria
```
36
what does it mean if serum albumin is normal in the setting of nephrotic range proteinuria?
then the patient does not have nephrotic syndrome but instead has nephrotic range proteinuria
37
what are some Nehrotic syndrome complications
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
what are the pathogenesis of edema in Nephrotic syndrome
low intravascular oncotic pressure
Renal sodium retention
39
what is the classical presentation of Nephrotic syndrome
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
what is a common nephrotic syndrome in children
Minimal change disease
41
what Nephrotic syndrome is common with HIV infection
Focal Segmental glomerular sclerosis
42
what are 3 examples of Monoclonal disease causing nephrotic syndrome
Multiple myeloma
amyloidosis
Monoclonal immunoglobulin deposition disease
-can be light, heavy, or light and heavy chain
43
what nephrotic syndrome is associated with underlying malignancy and or renal vein thrombosis
Membranous Nephropathy
44
what is the main diagnostic of Nephrotic syndrome
Renal Biopsy
45
how to treat the edema of the nephrotic syndrome
Dietary sodium restriction
| diuretics
46
how to treat the proteinuria of the nephrotic syndrome
Lower blood pressure
ACE or ARB
alternative anti proteinuric medications
-nondihydropyridine CCB, Aldosterone antagonist, renin inhibitors
47
what is the nephritic syndrome definition and what is one key point in its characteristics
Proteinuria <3.5g/day
Hematuria
HTN
Renal failure common
Key point
- usually have active urinary sediment
- nephrotic has bland urinary sediment
48
Clinical presentation of Nephritic syndrome
```
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
what are some DDx for Nephritic syndrome
- 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
how is the diagnosis of Nephritic syndrome made
Renal biopsy is the best
can do glomerulonephritis serologic evaluation
51
what is the DDx of Glomerulonephritis with low complement levels
- Lupus Nephritis
- Post-infectious GLomerulonephritis (PIGN)
- Membranoproliferative Glomerulonephritis (MPGN)
- Cyroglobulinemia
- atypical hemolytic uremic syndrome
- endocarditis
- cholesterol embolus
- HIV associated immune complex disease
52
what is polyuria
urine output > 3 L/day
53
what are the two different types of diuresis that can lead to diuresis
Solute diuresis
| Water diuresis
54
what are the types of solute diuresis that can lead to polyuria
Glucosuria
- Hyperglycemia
- SGLT-2 inhibitor use
Urea:
- resolution of azotemia
- exogenous urea administration
- tissue catabolism
Sodium
-IV fluids
Mannitol
55
what are the types of water diuresis causes that lead to polyuria
Primary polydipsia
Central diabetes insipidus
Nephrogenic Diabetes insipidus
56
what are the two requirements for forming Concentrated urine
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
what are the 2 main systems that regulate serum osmolality
Osmoreceptor-ADH system
-ADH has short half life that allows for rapid means to alter water excretion by the kidney
Thirst mechanism
58
where is ADH produced and what are the 2 ways these detections occur to generate more ADH
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
what are the effects of ADH on the collecting duct and why in dehydration is the urea levels increase
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
what are the two types of Diabetes insipidus
Central Diabetes Insipidus
| Nephrogenic diabetes insipidus
61
what is the cause of Central diabetes inspidus
Caused by decrease release of antiduretic hormone (ADH)
- idiopathic
- hereditary
- primary or secondary tumors
- infiltrative diseases
- Neurosurgery
- Trauma
- Meningitis/encephalitis
62
what are the cause of Nephrogenic diabetes insipidus
Caused by decrease response to antidiuretic hormone (ADH)
- Hereditary (seen in children)
- lithium toxicity
- hypercalcemia
- hypokalemia
63
what is the net result of hypercalcemia induced polyuria
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
what are the clinical manifestations of Diabetes Insipidus
- Polyuria
- Nocturia
- Polydipsia
- Nypernatremia
- Orthostasis
also have manifestations from underlying causes, trauma, lithium toxicity, hypercalcemia, hypokalemia, etc
65
how is the diagnosis of Diabetes insipidus made
24 hour urine volume collection
Urine osmolality < 300 mOsm/kg
Water deprivation test
66
Urine osmolality with water deprivation >800, serum vasopressin after dehydration >2 and little or no increase in urine osmolality with desmopressin
Normal
67
Urine osmolality with water deprivation <300, serum vasopressin after dehydration undetectable and substantial increase in urine osmolality with desmopressin
Complete central diabetes insipidus
68
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
Partial Central diabetes insipidus
69
Urine osmolality with water deprivation <300-500, serum vasopressin after dehydration >5 and little or no increase in urine osmolality with desmopressin
Nephrogenic vasopressin after dehydration
70
Urine osmolality with water deprivation >500, serum vasopressin after dehydration <5 and little or no increase in urine osmolality with desmopressin
Primary polydipsia
71
what is the treatment for central diabetes insipidus
Vasopressin
72
what is the treatment for Nephrogenic diabetes insipidus
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
what is the treatment for Hypernatreima
replace free water deficit
| -patient drinks water to give IV D5W
