GU Block I Flashcards
1
Q
What is a nephrologist
A
Nephrology is a subspecialty of internal medicine that focuses on the diagnosis and treatment of diseases of the kidney.
2
Q
What is a urologist
A
Urology is a surgical specialty that deals with diseases of the male and female urinary tract and male reproductive organs.
3
Q
What is a independent signifigant risk factor for cancer and ESRD
A
Persistent, isolated, asymptomatic, microscopic hematuria is an independently significant risk factor
4
Q
A postive dipstick for UA leads to what
A
Microscopy
5
Q
When is microscopy best
A
Clean catch,
midstream sample preferred
-1st morning void best for microscopy
-Test within an hour or refrigerate
6
Q
Large numbers of Transitional Epithelial Cells in a UA
Think..
A
Neoplasm
Confirm with Urinary cytology
7
Q
Renal tubular cells are ALWAYS….
A
Clinically relevant
8
Q
What is the threshold for RBCs in the urine
A
Presence of > 3 RBCs per HPF is considered significant & warrants further investigation
R/O menstruation in female patients
9
Q
What shape of RBCs indicates nephritic syndrome
A
Dysmorphic shape
10
Q
What is the threshold for WBCs in the urine
A
Presence of > 5 leukocytes per HPF is considered pyuria
Neutrophils → consider bacterial infection
Eosinophils → consider allergic interstitial nephritis
11
Q
Where are Casts formed
A
Formed in distal convoluted tubules (DCTs) & collecting ducts
Precipitation of Tamm-Horsfall mucoprotein forming an ‘organic matrix”
12
Q
What is the hallmark of Glomerulonephritis
A
Red Blood Cell Casts
13
Q
What is the cast seen in acute tubular necrosis
A
Renal Tubular Epithelial Cell Casts
14
Q
What Dz is associated with White cell Casts
A
Characteristic of acute pyelonephritis & useful in distinguishing this disorder from lower tract infections.
May also be seen in acute interstitial nephritis (eosinophils).
15
Q
When would you see granular casts (MUDDY)
A
Nonspecific, but usually pathologic (correlate clinically) for acute tubular necrosis (ATN).
16
Q
When would you see Waxy Casts
A
Represents end stage disintegration of cellular casts
Indicates severe urine stasis in renal tubules
Frequently found in cases of chronic renal failure
Seen in CKD!
17
Q
When would you see Broad Casts
A
Formed in tubules that have become dilated & atrophic due to chronic parenchymal disease
Indicative of severe urinary stasis in renal tubules
Suggestive of end-stage renal failure
18
Q
What do fatty casts tell you
A
Found in numerous renal diseases & are particularly associated w/ nephrotic syndrome
19
Q
What is the most common yeast found in urine
A
Candida
20
Q
When should you order a Urine Culture
A
Order in cases of suspected UTI or Pyelonephritis
100,000 Colony Forming Units (CFUs) is considered “positive”
21
Q
Slide 34, cast in summary Lecture 1
A
22
Q
Increased BUN indicates
A
Dehydration Reduced renal perfusion (congestive heart failure, hypovolemia) ↑ Dietary protein Accelerated catabolism (fever, trauma, GI bleeding) Steroids Tetracycline
23
Q
Decreased BUN indicates
A
Over-hydration
↑ Renal perfusion (
pregnancy, SIADH)
Restriction of dietary protein/malnutrition
Liver disease
(impaired metabolism of ammonia to urea)
24
Q
An increased BUN:Cr of 20:1
Look for
A
prerenal & postrenal azotemia
AKI
25
What would a BUN:Cr be in dehydration
increase to 20:1 or higher
26
How will the BUN:Cr be in intrinsic renal dz
Decreased
27
What are the two regulators of GFR
2 main regulation mechanisms
Control of blood flow in & out of glomerulus:
-By changing diameter of afferent & efferent arterioles.
-Control of glomerular surface area:
Via contraction or relaxation of mesangial cells.
28
How do you do a timed urine collection for creatinine
One way to measure creatinine clearance is to perform a timed urine collection and determine the plasma creatinine level midway through the collection.
29
What is Cystatin C
Prominent non-traditional renal biomarker for GFR estimation and is less influenced by muscle mass, age, and sex.
More strongly associated with adverse non-renal outcomes (e.g., Death) compared to serum creatinine.
30
What Fractional excretion of sodium used for
Used when suspecting an acute kidney injury (AKI)
31
If the FE-NA is less than 1%
From decreased kidney profusion
Kidneys retain Na &
water to ↑ intravascular volume, so urine Na is low
32
If FE-NA is greater than 1%
Intrinsic renal disease
Kidney loses Na inappropriately, so urine Na is high
33
When should you do a Kidney Biopsy
To confirm the extent of renal involvement and to guide management.
Unexplained AKI or CKD, proteinuria, and hematuria
Systemic diseases associated with kidney dysfunction:
- Systemic lupus erythematosus (SLE), anti-GBM disease (Goodpasture syndrome), and granulomatosis with polyangiitis.
- Kidney transplant dysfunction and evaluation for transplant rejection.
34
Define osmolality
the concentration of a solution expressed as the total number of solute particles per kilogram.
35
Define osmolarity
the concentration of a solution expressed as the total number of solute particles per liter.
36
Define tonicity
the ability of an extracellular solution to make water move into or out of a cell by osmosis.
A solution's tonicity is related to its osmolarity, which is the total concentration of all solutes in the solution.
37
What is the gold standard for renal electrolyte excretion
Fraction (24 hour urine collection)
38
What is a osmolol gap
An osmolal gap suggests the presence of unmeasured osmoles such as ethanol, methanol, ethylene glycol, mannitol, propylene glycol, and isopropanol.
39
What stimulates osmo- receptors
Osmoreceptors are stimulated by a rise in tonicity.
40
WHat is the primary stimulus for ADH secretion
Hypertonicity
41
Define Severe Hyponatremia
Severe (below 125 mEq/L)
42
Define isotonic Hyponatremia
Isotonic hyponatremia (pseudohyponatremia): is a laboratory error underestimating sodium concentration in an abnormally elevated percentage of serum that is solid rather than liquid (hyperlipidemia or hyperproteinemia). Mostly older analyzers.
43
What are the two classic types of hypertonic Hyponatremia
Hypergl and Mannitol
44
How can you determine if Hypovolemic hypotonic Hyponatremia is renal or extra renal
Renal (U/Na greater than 20mEq/L)
| Extrarenal (U/Na below 10mEq/L)
45
What is the DDX for Euvolemic Hypotonic Hyponatremia
- Syndrome of inappropriate antidiuretic hormone
- Hormonal abnormalities
- Psychogenic Polydipsia/Low Solute Diet
- Reset Osmostat
- Exercise induced Hyponatremia
46
Can you tell the difference between Hormonal abnormalities and SIADH
No
Severe hypothyroidism and glucocorticoid insufficiency can cause hyponatremia that cannot be differentiated from SIADH by urine or serum electrolytes alone.
47
What does psychogenic polydipsia lead to
This leads to the kidney’s retaining water, as they cannot excrete pure water.
48
How does the body respond to Hypervolemic Hypotonic Hyponatremia
Body sacrifices osmolality in an attempt to restore effective arterial blood volume.
49
A pt presents with hypotonic Hyponatremia with an absence of cardiovascular, kidney, or liver dz
Has normal thyroid and adrenal function
And a turbine sodium greater than 20
With a low BUN and hypourecemia
Think
SAIDH
Look at ADH levels if need be
50
How do you sodium correct chronic hypotonic Hyponatremia
For chronic hypotonic hyponatremia, generally recommend 4-6 mEq/L/24 h and no more than 6-8 mEq/L/24 h.
Avoid rapid shifts that may lead to osmotic demyelination syndrome.
This is a neurologic disorder characterized by flaccid paralysis, dysarthria, and dysphagia.
51
How do we treat Hypovolemic Hypotonic Hyponatremia
Address the underlying etiology
Fluid resuscitation, usually with isotonic fluid, to suppress the hypovolemic stimulus for ADH release.
Give fluids
52
What is the tx approach to Hypervolemic Hypotonic Hyponatremia
Goal is to remove salt and water…but more water.
Tolvaptan (AVP V2 receptor antagonist) is just as effective as 3% saline for correcting hyponatremia at 48hrs.
Consider diuretics
Patients with severe acute/chronic kidney generally require dialysis.
53
What medication can be used to Tx SIADH
Tolvaptan
54
What is the tx option for acute SZR Hyponatremia
Acute (Seizures) 100 mL of 3% hypertonic saline infused over 10 minutes – Goal is symptom reversal.
24-hour correction goal rate
(4-6 mEq/L) is still recommended after symptoms reversal.
Avoid demyelination from rapid correction
Chronic –100 mL of 3% hypertonic saline given at an initial rate of 0.5-2 mL/kg/Hr
55
What are the S.s of hyper Na
Lethargy, irritability, and weakness are early signs.
Hyperthermia, delirium, seizures and coma are seen in severe hypernatremia.
Symptoms may be delayed as water shifts from the cells to intravascular space to protect volume status.
Symptoms in older adults may be nonspecific.
56
What is the treatment for hypernatremia with euvolemia
Water ingestion or intravenous 5% dextrose in water will result in the excretion of excess sodium in urine.
57
What is the tx for hypernatremia with Hypervolemia
Hypernatremia with hypervolemia
- Treatment includes 5% dextrose solution to reduce hyperosmolality.
- Loop diuretics may be necessary to promote natriuresis and lower total body sodium.
- May require hemodialysis.
58
What is the most common cause of Hypokalemia
Most common cause is gastrointestinal loss from infectious diarrhea.
Hypokalemia in the presence of acidosis suggests profound potassium depletion.
Loop diuretics can cause substantial renal potassium and magnesium losses.
59
A pt presents with Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis.
think what electrolyte
Severe Hypokalemia
60
What is the tx for Hypokalemia
Oral potassium supplementation is the safest and easiest treatment for a mild to moderate deficiency.
Intravenous potassium is indicated for patients with severe hypokalemia or cannot tolerate oral intake.
Concentrations up to 40 mEq/L
61
What is the most common cause of hypocalcemia
The most common cause of hypocalcemia is advanced CKD, in which decreased production of active vitamin D3 and hyperphosphatemia both play a role.
62
What is the most common cause of low total serum calcium
Hypoalbunemia
63
What is the relationship to calcemia and vitamin d
True hypocalcemia implies insufficient action of PTH or active vitamin D.
64
What are the two major causes of hypercalcemia
Cancer and Hyperparathyroidism
65
At what level do calcium S/s usually manifest
Higher than 12 mg/dl
66
What is the tx approach to hypercalcemia
Aggressive hydration and calciuresis
Bisphosphates are the Tx of choice for hypercalcemia of malignancy
Calcitonin may be helpful in the short-term until bisphosphates reach therapeutic effect.
67
What is winters formula
PCO2 = 1.5 [HCO3]+8 ± 2.
68
Increased Anion Gap means
DKA
Uremia
Láctic acidosis
69
Define lactic acidosis
In lactic acidosis, lactate levels are at least 4–5 mEq/L but commonly 10–30 mEq/L.
70
What are the two major causes of normal gap acidosis
Gastrointestinal HCO3– loss
Defects in renal acidification (renal tubular acidosis)
71
define type 2 RTA
PROXIMAL!
Decreased threshold for bicarbonate reabsorption.
HCO3- wasting and urinary K losses occur until low level serum HCO3- causes reabsorption of HCO3-.
Urine becomes acidic until net acid production = acid secretion with low serum HCO3-
72
Define type 1 RTA
DISTAL!!
Failure to produce ammonia leads to inability excrete adequate net acid.
Serve Acidosis (<7.2)
Alkaline urine (pH >5.3)
Leads to stones
73
Define type 4 RTA
Type IV is the most common RTA in clinical practice.
The defect is aldosterone deficiency or antagonism, which impairs distal nephron Na+ reabsorption and K+ and H+ excretion.
Renal salt wasting and hyperkalemia are frequently present.
Common causes are diabetic nephropathy, tubulointerstitial renal diseases, hypertensive nephrosclerosis, and AIDS.
74
What is the treatment for high anion gap acidosis
Treatment is aimed at the underlying disorder, such as insulin and fluid therapy for diabetes and appropriate volume resuscitation to restore tissue perfusion.
75
Saline responsive alkalosis is a sign of…
extracellular volume contraction.
76
Saline unresponsive alkalosis implies
implies excessive total body bicarbonate with either euvolemia or hypervolemia.
77
How many red blood cells is required for hematuria
Greater than 3 per HPF
78
Define proteinuria
Urinary excretion of ≥150 mg/24hrs of protein
79
Define microalbuminuria
30-300 mg/day
80
Define macro albuminuria
Greater than 300 mg/day
| Dip stick positive at this level
81
Define nephrotic proteinuria
Greater than 3.5 grams a day
82
Define overload proteinuria
Overload proteinuria: from overproduction of plasma proteins such as Bence Jones proteins
( plasma cell myeloma);
myoglobinuria
(rhabdomyolysis and hemoglobinuria).
83
What is the hallmark of DM nephropathy
Microalbuminuria
84
if a postive dipstick for protein occurs.. what is the next step
Repeat test w/ 1st morning void
—NOT after exercise
Scored from NEGATIVE to 4+
Consider up to 3 separate samples w/ urine microscopy
Dipstick primarily detects albumin
85
What is the gold standard protein urine assay
24-hour urine collection is the gold standard to quantify the level of protein excretion.
Normal value: <150 mg/day
86
What is the recommended screening for DM protienuria
Morning Spot Test
| Albumin:Cr ratio
87
What is the role of the UPCR test
protein:creatinine ratio (UPCR)
Detects at higher level proteinuria
Better for monitoring of established proteinuria
88
What should you rule out in protineuria
Rule out Ortho proteinuria
Check a serum chemistry panel
Conduct a renal ultrasound
COnduct Urinary Electrophoresis
+/- renal biopsy
89
If a pt has established prtoineuria
| What is the best test to monitory the progresssion
UPCR
Protein:creating level urine test (SPOT)
90
What is the Tx approach to proteinuria
Lowering proteinuria is more important than lowering BP w/ respect to CKD progression.
Goal: Lower proteinuria to <0.5 g/day
Use an ACEI or ARB (RAAS inhibitors)
91
Wt loss of 5% can decreases proteinuria by up to…
20-30%
Dietary protein restriction may be of some benefit In selected patients
In consultation w/ dietician
92
How many samples do you need to confirm hematuria
3 samples at least 1 week apart to confirm
93
Gross Hematuria in adults over age 40 is a sign of..
malignancy until proven otherwise!!
94
DDX of presence of blood throughout the urination stream
bladder or upper tract source
stone, tumor, tuberculosis, nephritic syndrome
95
What does PP on this stand for
```
Period (menses)
Prostate, papillary necrosis
Obstructive uropathy
Nephritic syndrome (Inflammation)
Trauma, tumor, tuberculosis, thrombosis (renal vein)
Hematologic (blood disorder, sickle cell)
Infection/inflammation
Stones
```
96
What is the hematuria W/u
1st morning void is best
Dipstick can detect as few as 2 RBC/HPF
If positive → get 3 samples at least 1 week apart for confirmation
False positive dipstick results:
Myoglobinuria, hemoglobinuria, bacteria, concentrated urine, menses, vigorous exercise, beets/rhubarb
False negative dipstick results:
High vitamin C/ascorbic acid levels
97
If you have a positive dipstick UA for urine microscopy what is the next step
Confirm with microscopy
Repeat UA in 4-6 weeks
98
If a pt has persistent unexplained hematuria what is the assay of choice
Urinary Cytology
Highly sensitive and specific for detection of high-grade urothelial carcinoma.
99
When should you refer hematuria to nephrology
Persistent hematuria referral:
| Nephrology if findings support renal parenchymal etiology.
100
When should you refer hematuria to urology
Calculi
| Ureteral, cystic, or urethral origin
101
Define psuedo hematuria
Dipstick positive, microscopy negative
102
If the dipstick is positive for hematuria but the microscopy is negative
What is the DDX
Hemoglobinuria (Black urine)
Myoglobinuria ( Rhabdo, electric burns)
Beets, berries, food coloring
Drugs: pyrdium, sulfa, Nitrofurantoin, rifampin, Ibuprofen, phenytoin, levodopa
103
What is pyridium
Numbing medication for UTI that turns the urine orange
104
What is the best test to evaluate for bladder cancer
Cycsocopy
105
If you find a solid renal mass think
CA UPO
106
What is the C/I to US of the kidney
Unable to lay down
107
What type of ultrasound can look at the prostate
Transrectal US
108
What is the role of Doppler US
Useful for the evaluation renal vessels, and vascularity of renal masses
Acute testicular pain work-up
(i.e., torsion vs epididymitis)
109
What is the role of intravenous pyelographhy
Use to be the preferred imaging modality, but has largely been replaced by CT, US, and MRI.
Still useful in diagnosing certain disorders such as medullary sponge kidney and papillary necrosis.
110
Any time you want to give Contrast what must you check
kidney Function
CrCl less than 2 mg/dL
111
What is the role or CT
Renal CT is most commonly used in the evaluation of acute flank pain, hematuria, trauma, renal infections, and staging of renal neoplasm.
Evaluation of renal anatomy and pathology generally requires intravenous injection of iodinated contrast media.
112
What is the study of choice for a renal stone
Non con helical CT
113
What is the perferred radiograph for uppper GU tract eval
CTU
114
What is the rads study for acute pyelonephritis
CTU
115
What is the imaging study for renal artery stenosis
MRI
116
describe nephro genie systemic fibrosis
The use of gadolinium contrast in MRI is contraindicated in patients with CKD stage 4 or 5, AKI, or a kidney transplant due to the risk of nephrogenic systemic fibrosis (NSF).
117
What is renal arteriography
Renal Arteriography: involves taking X-rays following an injection of contrast medium directly into the renal artery.
Indicated in the evaluation of atherosclerotic or fibrodysplastic stenotic lesions, aneurysms, vasculitis, and renal mass lesions.
Gold standard but not typically used
118
What is the role of renal venography
Renal Venography: indicated as best test for diagnosis of renal vein thrombosis, though CT scanning and MRI are less invasive for this purpose.
119
What is the best test for renal artery stenosis
CT Angiogram
120
What is the imaging for a pt with allergy to iodinated contrast
MR- uro
121
What is the role of retrograde urethrogram
Minimally invasive procedure that requires cystoscopy and the placement of catheters in the ureters.
Suspected urethral trauma:
- Inability to void
- Blood at urethral meatus
- Perineal ecchymosis
- “High-riding” prostate
- Inject contrast into urethra toward bladder
122
Define Cystography
Contrast study specifically for bladder evaluation
Procedure:
- Bladder is catheterized
- Urine is drained
- Inject contrast into bladder
(~400 cc of contrast to completely fill)
Images are obtained
Oblique view is also needed to see entire length of urethra
123
What is the role of voiding cystourethrogram
Method for:
- Detecting urinary vesicoureteral reflux
- Bladder function
- Urethral Anatomy
Radiographs of the bladder and urethra obtained during micturition.
Also indicated in neonates and infants with congenital grade 3 or 4 hydronephrosis and in any child with ureteral dilation
124
Define AKI
clinical syndrome defined as an absolute increase in serum creatinine by 0.3 mg/dL
or
more within 48hrs or a relative increase ≥1.5 times baseline
or
presumed to have occurred with 7 days;
or
a urine volume less than 0.5mL/kg/hour for 6 hours.
125
What is the number one reason for hospital nephrology consult
AKI
Think multi organ failure
126
What is the most common cause of AKI
Prerenal causes
127
What are the stage 1 of AKI
Stage 1 is a 1.0 to 1.5-fold increase in serum creatinine
Or urine out decline of 0.5 mL/kg/h over 6-12hrs
128
Stage 2 AKI
Stage 2 is a 2.0 to 2.9-fold increase in serum creatinine
Or urine out decline of 0.5 mL/kg/h over 12hrs
129
Stage 3 AKI
Stage 3 is a 3-fold or greater increase in serum creatinine
Or urine out decline of 0.3 mL/kg/h over 24hrs
Or anuria for 12hrs
Or initiation of renal replacement therapy
130
What is the BUN clue to a Prerenal AKI cause
In prerenal AKI, the BUN: creatinine ratio often exceeds 20:1
due to increased urea reabsorption.
131
What are the RSk Fx for AKI
Dehydration / volume depletion
Hypoalbumenia
Advanced age (65-75 years)
Female gender (Maybe)
Black race (Maybe)
Previous AKI
132
A pt presents with Nausea, vomiting, malaise, anorexia, fatigue, pruritis, and altered sensorium and Coca Cola colored urine
Think
AKI maybe uremia
133
What is the W/u findings for AKI.
Elevated serum creatinine (and often BUN)
—Metabolic acidosis
Hyperkalemia as a result of metabolic acidosis
Hypocalcemia
Hyperphosphatemia
Anemia due to decreased erythropoietin production
Platelet dysfunction is typical but occurs a little later
134
What are the microscopy findings of Prerenal azotemia
bland urine sediments, hyaline casts
135
What are the microscopy findings of acute tubular necrosis
Renal tubular epithelial cells or muddy brown (granular) casts
136
What are the benchmarks of AKI Tx
Treatment of prerenal AKI depends entirely on the underlying cause, but achievement of euvolemia, attention to serum electrolytes, and avoidance of nephrotoxic drugs are the benchmarks of therapy.
137
What is the most common cause of POST renal failure in men
BPH (obstruction)
138
What is the Tx approach to Post renal AKI
Admit
—Nephrology and/or Urology Consult.
Bladder catheterization
Identify the obstruction:
Bladder and/or renal US
—CT, MRI (if needed)
Correct obstruction
—Catheters, stents, or other surgical procedures
After reversal of underlying process → post-obstructive diuresis occurs ,
AVOID volume depletion
139
What are the 3 major types of intrinsic AKI
```
Acute tubular necrosis (ATN)
Acute glomerulonephritis (AGN)
Acute interstitial nephritis (AIN)
```
140
What two disorder present with WBC casts
Acute interstitial nephritis
And
Plyeolnephritis
141
What is the Tx approach to Intrinsic AKI
Treatment
Early Nephrology consult!
Offending medications must be determined and discontinued.
Two-week course of tapering glucocorticoids.
General supportive care
142
When do you refer AKI
If a patient has signs of AKI that have not reversed over 1–2 weeks without uremia, the patient can usually be referred to an outpatient Nephrologist rather than admitted.
If a patient has signs of persistent urinary tract obstruction, the patient should be referred to a Urologist.
143
When should we admit AKI
The patient should be admitted if there is sudden loss of kidney function and outpatient setting cannot handle: -hyperkalemia
- volume overload
- uremia
- requires emergent procedures.
144
What are the two major causes of Acute tubular necrosis
The two major causes of ATN are ischemia and nephrotoxin exposure.
Accounts for 85 % of intrinsic AKI
145
A pt presents with general edema, N/V, oliguria, HOTN, AMS, and muscle weakness
With muddy brown casts in the urine
And renal tubular epithelial cells/ tubular cell casts
What type of AKI should be suspected
Intrinsic Kidney Injury possible ATN
| BUN:Cr ratio <20:1
FE-Na is elevated
primary kidney problem
+/- Hyper K
146
What is the Tx for ATN
```
Admit
Fluids (but avoid volume overload)
Diuretics as necessary,
(Furosemide, thiazide)
Diet restriction
```
147
A pt presents with fever , transient maculopapular rash, and arthralgias and hematuria
With WBC casts
Look for
Eosinophilia for Acute interstitial Nephritis
148
What is the most common cause of acute intestinal nephritis
DRUGS!
2*: infections and immunological
149
What are the lab findings in the AIN
BUN: creatinine ratio: <20:1
UNa: variable
FENa: variable, usually >1%
Urinalysis: RBCs, WBCs, & WBC casts
Eosinophiluria
Proteinuria (<2 g/day)
Peripheral blood smear:
Eosinophilia (Wright or Hansel stain, non-specific)
150
```
BUN: creatinine ratio: <20:1
UNa: variable
FENa: variable, usually >1%
Urinalysis: RBCs, WBCs, & WBC casts
Eosinophiluria
Proteinuria (<2 g/day)
Peripheral blood smear:
Eosinophilia (Wright or Hansel stain, non-specific)
```
With NO bacteria!
What is the AKI
Acute intrinsic nephritis
151
What is the Tx for AIN
nephrology consult and supportive care
If renal failure persists → short course of steroids
—High dose methylprednisolone (0.5-1 g/day IV for 1-4 days) followed oral taper (60mg/day orally for 1-2 weeks)
152
A pt presents with periorbital and scrotal edema, with an abnormal urinary sediment
Look for
Red blood cell casts
For acute Glomerulonephritis
153
Slide 46 of AKI lecture
154
What is type 1 cardiorenal syndrome
Type 1 consists of AKI stemming from acute cardiac disease.
155
What is type 2 Cardiorenal syndrome
Type 2 is CKD due to chronic cardiac disease.
156
What is type 3 cardiorenal syndrome
Type 3 is acute cardiac disease as a result of AKI.
157
What Is type 4 Cardiorenal syndrome
Type 4 is chronic cardiac decompensation from CKD.
158
What is type 5 cardiorenal syndrome
Type 5 consists of heart and kidney dysfunction due to other acute or chronic systemic disorders (such as sepsis).
159
Define CKD
Evidence of:
```
Abnormal urinalysis
(proteinuria, albuminuria, hematuria)
or
Structural abnormality (i.e., by US)
or
GFR <60 mL/min/1.73m2
```
For > 3 months
160
What defines Kidney Damage in CKD
Kidney Damage:
- Albuminuria ≥30mg/24hr
- Abnormal urine sediment
- Electrolyte abnormality
- Structural abnormality on imaging
- History of renal transplant
161
What type of casts are seen in CKD
Waxy casts
162
What GFR is stage 1 CKD
Greater than 90
163
GFR for StageII CKD
60-89
164
Stage 3a and B GFR for CKD
30-59
165
Stage 4 GFR for CKD
15-29
166
A GFR less than 15 is what stage CKD
Less than 15
Pt needs dialysis at this point
167
What are the most common causes of CKD
DM
HTN
Vasc Dz
168
A pt presents with HTN, urinary abnormalities, edema, excercise intolerance, fatigue, and anorexia
These are all clues to what underlying pathology
CKD
169
What is the most common physical exam finding of CKD
HTN
| +/- fluid overload
170
Persistent protienuria is a sign of…
suggestive of CKD, regardless of GFR
171
A pt presents with an elevated BUN/Cr and Decreased GFR over the past 3 months
Think
CKD
Also look for
```
Anemia
CMP
A1C
Metabolic acidosis
Hyperphosphatemia
Hyperkalemia
Hypocalcemia
```
172
What is the progression of findings for CKD
```
HTN to increased PTH
To Anemia
To increased phosphorus
To Acidosis and HyperK
And lastly Uremic syndrome
```
173
How does CKD effect atherosclerosis
Accelerates it
Increases vessel stiffness
2/2 increased mineral metabolism
174
What is the most common bone dz in CKD
Osteitis fibrosa cystica:
— most common bone disease
- Bone reabsorption
- Subperiosteal lesions
- Bone pain
- Proximal muscle weakness.
175
What is the 1st step in the Tx of metabolic bone Dz in CKD
control of hyperphosphatemia.
176
How does CKD cause Anemia of Chronic Dz
Due to decreased erythropoietin production
(manifests around stage 3 CKD).
CKD also impairs GI iron absorption and mobilization of iron from body stores resulting in functional iron deficiency—the so-called “anemia of chronic disease.”
177
How does CKD effect Clotting
```
Mainly due to platelet dysfunction
Presentation:
-Petechiae
-Purpura
-↑ Bleeding during surgery
```
-Dialysis → improves bleeding time but doesn’t normalize it
178
When does uremic encephalopathy occur in CKD
Uremic encephalopathy does not occur until GFR <5-10 mL/min/1.73 m2
Symptoms: Difficulty concentrating initially → can progress to lethargy, confusion, seizure & coma
Improvement w/ dialysis
179
A thiazides effective below a GFR of 30
Thiazide diuretics may be less effective at GFR <30
180
What is the most common complication of peritoneal dialysis
peritonitis (most common)
```
Presentation:
Nausea/vomiting
Abdominal pain
Diarrhea or constipation
Fever
Cloudy dialysate
```
Peritoneal fluid: >100 WBCs/mcL
S. aureus (most common pathogen)
181
What is the survival rate of kidney transplants
However, living donor is better option:
-1-year survival rate → ~95% (living donor) & 89% (deceased donor)
-5-year survival rate → ~80% (living donor) & 66% (deceased donor)
182
When do we admit pts with CKD
Admission should be considered for patients with decompensation of problems related to CKD, such as worsening of
- acid-base status
- electrolyte abnormalities
- volume overload, that cannot be appropriately treated in the outpatient setting.
Admission is appropriate when a patient needs to start dialysis and is not stable for its outpatient initiation
183
Stable creatinine in the face of significant weight loss suggests
Progression of Kidney Dz
184
What is the definitive Dx for Glomerular Dz
Definitive Diagnosis → visualization of specific histologic patterns on renal biopsy.
185
Are there casts in Nephrotic spectrum
NO CASTS!
186
Describe Nephritic Specturm
Hematuria
—Dysmorphic red blood cells
With or without proteinuria (<1 g/day)
```
Nephritic Syndrome
-Hematuria
-Subnephrotic proteinuria
(<3g day)
-Edema (periorbital/scrotal)
-Elevated creatinine
-RBC Casts
```
187
Describe Nephrotic Spectrum
Proteinuria of at least 0.5-1g/day and bland urine sediment
—No casts!
```
Nephrotic Syndrome
Proteinuria
>3g/day
Hypoalbuminemia
Edema
Hyperlipidemia
Urinary Oval Bodies!!
```
188
What are the two main pathogens of Glomerulonephritis
Staph and strep Viridans
189
A pt presents with cola colored urine
With RBC casts and erythrocytes in the urine
With edema and azotemia
Think
Nephritic Syndrome
190
What is the tx approach to Nephritic syndrome
Admit in most cases
Early consult
Aggressive HTN and Fluid overload reduction
-diuretics ect
REDUCE GLOMERULAR INFLAMMATION
191
What is the cause of post infectious Glomerulonephritis
infection with a nephritogenic group A beta-hemolytic streptococcal infection (pharyngitis or impetigo).
192
What titers are high in Post infectious GN
(Strep A) anti-streptolysin O (ASO) titers may be high.
193
What is the Tx for post infectious GN
```
Underlying cause
And supportive
-Anti-HTN
-Salt restriction
-diuretics
```
194
What is the most common primary glomerular disease worldwide
IgA Nephropathy
195
A pt presents with hematuria after a recent URI
Think
IgA Nephropathy
196
What is the difference between IgA Nephropathy and Post Infectious GN
It occurs quickly in conjunction with a URI versus post-infectious GN which may take weeks.
197
Describe IgA Vasculitis
Form of vasculitis marked by IgA disposition within the small blood vessels of affected tissues.
Commonly affects the skin, joints, intestines, and kidneys.
More common in men
198
A pt presents with palpable purpura, with arthralgias, nausea, cramps, melena, and bloody diarrhea, with hematuria
Think ?
IgA Vasculitis
199
What is the other name of Henoch-Schonlein Purpura
IgA Vasculitis
200
What is the Tx for IgA Vasculitis
Conservative:
Control HTN
Bed Rest, hydration, analgesics
+/- steroids
201
When should you admit a pt with IgA Vasculitis
Inability to maintain adequate hydration w/ oral intake
Severe abdominal pain
Significant gastrointestinal bleeding
Mental status changes
Severe joint involvement limiting ambulation and/or self-care
Renal insufficiency (elevated creatinine), hypertension, and/or nephrotic syndrome
202
Describe Pauci-Immune GN
Pauci-immune necrotizing glomerulonephritis caused by systemic ANCA-associated vasculitides:
-Granulomatosis with polyangiitis
—Formerly —-Wegener's granulomatosis.
Eosinophilic granulomatosis with polyangiitis
—Formerly —-
Chugg-Strauss disease
Microscopic polyangitis
Circulating ANCA Ag
203
What is the treatment approach to Pauci-Immune GN
Treatment: REDUCE Inflammation!
High dose steroids and cytotoxic agents
Poor prognosis without treatment!
204
Describe Antio-GBM
Anti-GBM–associated glomerulonephritis accounts for 10–20% of patients with acute RPGN.
Greatest in young adult males and older patients
Caused by circulating antibodies directed at glomerular basement membrane.
May cross-react with pulmonary capillaries.
205
Describe Good Pasture Syndrome
Goodpasture Syndrome: If kidneys and lungs
(pulmonary hemorrhage) are involved (combination of GN and alveolar hemorrhage in the presence of anti-GBM antibodies).
Goodpasture syndrome has been associated with pulmonary infection, tobacco use, and exposure to hydrocarbon solvents or alemtuzumab; HLA antigens may predispose as well.
206
What are the clinical manifestations of Anti-GBM/ Goodpastures
Hemoptysis, dyspnea, possible respiratory failure, malaise, anorexia, & headache w/ possible preceding URI.
Other findings are consistent with an RPGN (edema, previous flu-like illness within 4 weeks, severe oliguria, rare HTN, hematuria, proteinuria)
Rapidly progressive & fatal in many cases
207
Kidney Bx shows crescent formation with light microscopy
Think
Anti-GBM/Goodpasture Syndrome
208
What are the tx options for Anti-GBM/ Goodpastures
Treatment options are limited:
—Admit
Plasmapheresis → remove circulating anti-GBM antibodies
Corticosteroids (i.e., Prednisone)
Cyclophosphamide
Medications → inhibit formation of new antibodies
Treatment duration is typically 3 months.
209
Describe Cryoglobuliun- Assoc GN
Most common from HCV infection
Patients exhibit purpuric and necrotizing skin lesions in dependent areas, arthralgias, fever, and hepatosplenomegaly.
Serum complement levels are low and rheumatoid factor is often elevated.
210
What is the tx approach to Cryoglobulin- Assoc with GN
Treatment consists of aggressively targeting the causative infection.
± Corticosteroids, plasma exchange, rituximab, and cytotoxic agents.
211
Describe Membranoproliferative GN
rare pattern of glomerular injury presenting along the nephritic spectrum.
The presentation is usually slowly progressive disease with hematuria and non-nephrotic proteinuria, but nephrotic syndrome and more severe presentations occur.
Chronic infection
most commonly HCV
212
You see Tram track on light microscopy
Think
Membranoproliferative - GN
213
What are the lab findings in Membranoproliferative GN
Hematuria, Nephritic spectrum proteinuria
Light microscopy: “tram track”
I
mmunofluorescence and electron microscopy:
—IgG, IgM and C3 staining.
214
What is the Tx approach to Membranoproliferative GN
Find and treat underlying cause.
Mild disease:
—ACE inhibitors and ARBs.
—Steroids and cytotoxic agents.
215
Describe Hepatitis C associ Kidney Dz
Often a nephritic condition that progresses to nephrotic
—Membranoproliferative glomerulonephritis
—Cryoglobulinemic glomerulonephritis
—Membranous nephropathy
Typically have hematuria, proteinuria, HTN, & anemia
216
What is the Tx approach to Hepatitis C Kidney Dz
Treatment for HCV associated kidney disease:
| Viral suppression or eradication is the cornerstone of treatment of HCV–associated kidney disease.
217
What should All pts with Lupus get in the W/u
All patients with SLE should have routine urinalyses to monitor for the appearance of hematuria or proteinuria.
If urinary abnormalities are detected, kidney biopsy is often performed.
More than 3g of protien in the urine is protein uria in nephrotic dz
218
What is the tx approach to Lupus renal dz
In mild disease = no treatment necessary
Moderate SLE renal disease:
Corticosteroids or calcineurin inhibitors with nephrotic-range proteinuria.
Patients with severe SLE nephropathy should receive aggressive immunosuppressive therapy!
219
Study slide 38 of Glomerulus Dz slides
220
Describe Nephrotic Syndrome
Characterized by:
-Heavy proteinuria >3.0g/24h
- Hypoalbuminemia
- Edema: Rapid, severe edema presents as anasarca
- Hyperlipidemia
- Oval fat bodies in urine
- HTN & hematuria are uncommon
221
What is the most common cause for nephrotic syndrome in the US
DM
222
A child pt presents with facial edema, pulm edema, with serum albumin is <3g/dl with positive protienuria
Think what syndrome
Nephrotic Syndrome
223
If a kid comes in with an unexaplined DVT think
Nephrotic Syndrome cause
224
What is the Tx approach to Nephrotic Syndrome
Goal is the slow progression
For protein (albumin) loss:
- ACEI or ARB → ↓ glomerular capillary pressure, ↓ protein loss
- Dietary protein restriction.
Consider nutrition consultation
For edema:
-Dietary sodium restriction
-Diuretic therapy (i.e., loop diuretics)
For hyperlipidemia:
- Diet & exercise
- Anti-hyperlipidemics (i.e., statins)
225
When should we admit a kid with nephrotic syndrome
ADMIT for:
- Evidence of renal failure
- Edema refractory to outpatient therapy
- Increasing edema w/ respiratory distress
- Tense scrotal or labial edema
Complications: sepsis, peritonitis, pneumonia, thromboembolic problem, or failure to thrive
226
What is the tx approach to Nephrotic Syndrome
Nephrotic syndrome → Nephrology consultation
Adults more urgently than kids (typically)
Patient education on ↑ infection risk (i.e., pneumonia, peritonitis)
Serum albumin <2 g/dL:
- May require IV albumin
- Require long-term anticoagulation therapy (at least 3-6 months)
227
What is the most common cause of primary nephrotic syndrome in children
Minimal Change Dz
228
A kid presents with sudden wt gain, periorbital edema, proteinuria, HTN, hematuria with NO RBC casts
What is the most common primary cause of this condition
Minimal Change Dz
229
You see effacement of podocyte foot processes
Think
Minimal Change Dz
230
What is the tx approach to Minimal change Dz
Treatment:
—Prednisone
(~90% response rate)
4-8 weeks in children
(“steroid responsive MCD”)
Up to 16 weeks in adults
Continued for several weeks after complete remission of proteinuria → taper off
Adults may need longer courses of therapy than children (up to 16 weeks).
231
describe focal segmental glomerulosclerosis
Common renal pattern of injury resulting from damage to podocytes.
Primary/renal-limited disorder:
Heritable abnormalities in podocyte proteins (African Decent)
Typically present with:
Asymptomatic proteinuria or edema.
Hypertension is common
Light microscopy shows sclerosis of segments of some glomeruli
232
What is the Tx approach to Focal Segmental Glomerulosclerosis
Dieuretics for edema
ACE/ ARB
Statins as needed
Oral prednisone (only if primary)
233
What is the most common causes of primary nephrotic syndrome in adults
Membranous Nephropathy
Circulating antibodies combine with antigens to form immune complexes on the epithelial side of the basement membrane leading to proteinuria.
234
An older pt presents with frothy urine and S/s of DVT
| Think
Membranous Nephropathy
235
If you find PLA2R abs think
Membranous Nephropathy
236
Kidney biopsy indicated for all glomerular diseases except for classical presentations of….
diabetic nephropathy and minimal change disease.
237
You see a spike and dome pattern on biopsy think
Membranous Nephropathy
238
What is the Tx approach to membranous Nephropathy
Largely based on level of proteinuria and risk of disease progression
—Corticosteroids + Cytotoxic therapy
R/O secondary causes
(i.e., cancer, infection, autoimmune disease)
Roughly 30% of patients presenting with subnephrotic proteinuria (less than 3 g/day) have a good prognosis with conservative management:
—Antiproteinuric therapy with ACE inhibitor or ARB if blood pressure is greater than 125/75 mm Hg.
239
What is the most common cause of ESRD in the US
DM Nephropathy
240
What is the most common lesion in DM nephropathy
Nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) is pathognomonic.
241
If there is a sudden onset of proteinuria, or greater than 10g/day
Or urinary celllurla casts
What should you do
Bx
242
Look at the stages of Tx for DM nephropathy on slide 64 of glomeluar dz
243
What is the clinical manifestation of Fibromuscular dysplasia
No cardiovascular risk factors
New onset hypertension
Young women
Headache and pulsatile tinnitus
244
What is the gold standard for renal artery stenosis
Renal Artireograph
245
What is the C/I for Renal Arteriogrpahy
eGFR <30 mL/min → NO gadolinium contrast → gadolinium-associated nephrogenic systemic fibrosis
246
What are the go to imaging for Renal Artery Stenosis
CTA or MRA
247
What is the tx approach to renal Art Stenosis
Tobacco cessation
Blood pressure control
—ACE or ARB – Monitor for abrupt decrease in eGFR
Lipid lowering agent such as statin
Low dose aspirin
To date revascularization surgery shows no significant benefit compared medical management.
In patients with fibromuscular dysplasia balloon angioplasty is the treatment of chose of choice. !!
248
What is the most common cause of renal infarction
A fib
249
A pt presents with acute onset of flank pain, Nausea and fever with HTN
Think
Renal Infarction
250
What is the definitive DX for renal infarct
CT w and W/o con
251
What is the tx approach to Renal Infarction
Anti coag Unfrac heparin or LMWH
Aggressive blood pressure control (ACEI or ARB)
Goal between 110/70 and 135/88 mmHg
If traumatic renal artery thrombosis= surgery
252
You see enlarged kidney, stretching of the calyces and notching of the uterus
Think
Renal vein Thrombosis
Bottom Line – Consider renal vein thrombosis in patient with nephrotic syndrome and acute flank pain; and don’t forget to consider cancer.
253
What is the common cause of acute tubuklointerstitial Dz
Acute disease is most commonly associated with medications, infectious agents, and systemic rheumatologic disorders.
254
What is the common cause of chronic tubulointerstitial dz
Chronic disease may result from acute factor or progressive “trauma” without any obvious acute cause.
255
What is the most common cause of chronic tubuklointerstitial dz
Obstructive Uropathy
Prostate Dz
Stones
256
Describe Vesicourectal reflux
The second most common cause of chronic tubulointerstitial disease is reflux nephropathy from vesicoureteral reflux.
Urine can extravasate into the interstitium, triggering an inflammatory response that leads to fibrosis over time
257
What effect does NSAIDs have on glutathione
Decrease production which means less glutathione detoxifiacation
258
How does tubularinterstial dz manifest
Un concentrated urine
With salt wasting defect
Serum hyperkalemia
WBC with a negative culture
Broad waxy casts
Sloughed papillae from papillary necrosis
“Ring shadow sign”
259
What is the general manifestation of obstructive uropathy
Azotemia and HTN
Poly or oliguria
+Hematuria, Pyruvate, and bacteriuira
260
How can vesicoureteral reflux be detected in utero
Can be detected before birth via screening fetal ultrasonography or after birth via voiding cystourethrography.
261
What is the tx of Mesoamérican nephropathy
Stay hydrated
Minimize heat exposure
Avoid NSAIDs
262
What stage of CKD needs referal
Patients with stage 3–5 CKD should be referred to a nephrologist when tubulointerstitial diseases are suspected.
Other select cases of stage
1–2 CKD should also be referred.
Patients with urologic abnormalities should be referred to a urologist.
263
What effect do bence-jones proteins have on the kidney
Bence Jones protein in the urine cause renal toxicity and tubular obstruction by precipitating in the distal tubules.
Found in Myeloma Kidnay (CA)
264
What is the treatment to plasma cell myeloma (Bence Jones Proteins)
Correction of hypercalcemia, volume repletion, and chemotherapy for the underlying malignancy.
265
What med should be used early in sickle cell
ACEI/ARB
266
What is the classic renal manifestation of TB kidney
Steroids pyuria
| Microscopic hematuria
267
What is the gold standard for TB kidney
Urine cultures are the gold standard for diagnosis.
268
What is the tx for gout kidney
Avoid hyperuricemic foods
Allopurinol/febuxstat
Increase fluid intake
269
What is the most common renal fusion anomaly
Horse shoe kidney
270
Where are Wilms tumors found?
In horseshoe kidney
271
If you are specifically looking for uro bleeding what study/>
CY urogram
