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Senoir 21-2 > GU Block I > Flashcards

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.

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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.

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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

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4
Q

A postive dipstick for UA leads to what

A

Microscopy

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5
Q

When is microscopy best

A

Clean catch,
midstream sample preferred
-1st morning void best for microscopy
-Test within an hour or refrigerate

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6
Q

Large numbers of Transitional Epithelial Cells in a UA

Think..

A

Neoplasm

Confirm with Urinary cytology

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7
Q

Renal tubular cells are ALWAYS….

A

Clinically relevant

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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

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9
Q

What shape of RBCs indicates nephritic syndrome

A

Dysmorphic shape

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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

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11
Q

Where are Casts formed

A

Formed in distal convoluted tubules (DCTs) & collecting ducts

Precipitation of Tamm-Horsfall mucoprotein forming an ‘organic matrix”

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12
Q

What is the hallmark of Glomerulonephritis

A

Red Blood Cell Casts

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13
Q

What is the cast seen in acute tubular necrosis

A

Renal Tubular Epithelial Cell Casts

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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).

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15
Q

When would you see granular casts (MUDDY)

A

Nonspecific, but usually pathologic (correlate clinically) for acute tubular necrosis (ATN).

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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!

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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

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18
Q

What do fatty casts tell you

A

Found in numerous renal diseases & are particularly associated w/ nephrotic syndrome

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19
Q

What is the most common yeast found in urine

A

Candida

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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”

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21
Q

Slide 34, cast in summary Lecture 1

A
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22
Q

Increased BUN indicates

A 
Dehydration
Reduced renal perfusion 
(congestive heart failure, hypovolemia)
↑ Dietary protein
Accelerated catabolism
 (fever, trauma, GI bleeding)
Steroids
Tetracycline
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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)

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24
Q

An increased BUN:Cr of 20:1

Look for

A

prerenal & postrenal azotemia

AKI

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25
Q

What would a BUN:Cr be in dehydration

A

increase to 20:1 or higher

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26
Q

How will the BUN:Cr be in intrinsic renal dz

A

Decreased

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27
Q

What are the two regulators of GFR

A

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.

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28
Q

How do you do a timed urine collection for creatinine

A

One way to measure creatinine clearance is to perform a timed urine collection and determine the plasma creatinine level midway through the collection.

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29
Q

What is Cystatin C

A

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.

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30
Q

What Fractional excretion of sodium used for

A

Used when suspecting an acute kidney injury (AKI)

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31
Q

If the FE-NA is less than 1%

A

From decreased kidney profusion

Kidneys retain Na &
water to ↑ intravascular volume, so urine Na is low

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32
Q

If FE-NA is greater than 1%

A

Intrinsic renal disease

Kidney loses Na inappropriately, so urine Na is high

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33
Q

When should you do a Kidney Biopsy

A

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.
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34
Q

Define osmolality

A

the concentration of a solution expressed as the total number of solute particles per kilogram.

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35
Q

Define osmolarity

A

the concentration of a solution expressed as the total number of solute particles per liter.

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36
Q

Define tonicity

A

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 itsosmolarity, which is the total concentration of all solutes in the solution.

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37
Q

What is the gold standard for renal electrolyte excretion

A

Fraction (24 hour urine collection)

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38
Q

What is a osmolol gap

A

An osmolal gap suggests the presence of unmeasured osmoles such as ethanol, methanol, ethylene glycol, mannitol, propylene glycol, and isopropanol.

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39
Q

What stimulates osmo- receptors

A

Osmoreceptors are stimulated by a rise in tonicity.

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40
Q

WHat is the primary stimulus for ADH secretion

A

Hypertonicity

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41
Q

Define Severe Hyponatremia

A

Severe (below 125 mEq/L)

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42
Q

Define isotonic Hyponatremia

A

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.

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43
Q

What are the two classic types of hypertonic Hyponatremia

A

Hypergl and Mannitol

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44
Q

How can you determine if Hypovolemic hypotonic Hyponatremia is renal or extra renal

A

Renal (U/Na greater than 20mEq/L)

Extrarenal (U/Na below 10mEq/L)

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45
Q

What is the DDX for Euvolemic Hypotonic Hyponatremia

A
  • Syndrome of inappropriate antidiuretic hormone
  • Hormonal abnormalities
  • Psychogenic Polydipsia/Low Solute Diet
  • Reset Osmostat
  • Exercise induced Hyponatremia
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46
Q

Can you tell the difference between Hormonal abnormalities and SIADH

A

No

Severe hypothyroidism and glucocorticoid insufficiency can cause hyponatremia that cannot be differentiated from SIADH by urine or serum electrolytes alone.

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47
Q

What does psychogenic polydipsia lead to

A

This leads to the kidney’s retaining water, as they cannot excrete pure water.

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48
Q

How does the body respond to Hypervolemic Hypotonic Hyponatremia

A

Body sacrifices osmolality in an attempt to restore effective arterial blood volume.

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49
Q

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

A

SAIDH

Look at ADH levels if need be

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50
Q

How do you sodium correct chronic hypotonic Hyponatremia

A

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.

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51
Q

How do we treat Hypovolemic Hypotonic Hyponatremia

A

Address the underlying etiology
Fluid resuscitation, usually with isotonic fluid, to suppress the hypovolemic stimulus for ADH release.

Give fluids

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52
Q

What is the tx approach to Hypervolemic Hypotonic Hyponatremia

A

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.

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53
Q

What medication can be used to Tx SIADH

A

Tolvaptan

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54
Q

What is the tx option for acute SZR Hyponatremia

A

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

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55
Q

What are the S.s of hyper Na

A

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.

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56
Q

What is the treatment for hypernatremia with euvolemia

A

Water ingestion or intravenous 5% dextrose in water will result in the excretion of excess sodium in urine.

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57
Q

What is the tx for hypernatremia with Hypervolemia

A

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.
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58
Q

What is the most common cause of Hypokalemia

A

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.

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59
Q

A pt presents with Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis.

think what electrolyte

A

Severe Hypokalemia

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60
Q

What is the tx for Hypokalemia

A

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

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61
Q

What is the most common cause of hypocalcemia

A

The most common cause of hypocalcemia is advanced CKD, in which decreased production of active vitamin D3 and hyperphosphatemia both play a role.

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62
Q

What is the most common cause of low total serum calcium

A

Hypoalbunemia

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63
Q

What is the relationship to calcemia and vitamin d

A

True hypocalcemia implies insufficient action of PTH or active vitamin D.

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64
Q

What are the two major causes of hypercalcemia

A

Cancer and Hyperparathyroidism

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65
Q

At what level do calcium S/s usually manifest

A

Higher than 12 mg/dl

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66
Q

What is the tx approach to hypercalcemia

A

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.

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67
Q

What is winters formula

A

PCO2 = 1.5 [HCO3]+8 ± 2.

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68
Q

Increased Anion Gap means

A

DKA
Uremia
Láctic acidosis

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69
Q

Define lactic acidosis

A

In lactic acidosis, lactate levels are at least 4–5 mEq/L but commonly 10–30 mEq/L.

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70
Q

What are the two major causes of normal gap acidosis

A

Gastrointestinal HCO3– loss

Defects in renal acidification (renal tubular acidosis)

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71
Q

define type 2 RTA

A

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-

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72
Q

Define type 1 RTA

A

DISTAL!!

Failure to produce ammonia leads to inability excrete adequate net acid.
Serve Acidosis (<7.2)
Alkaline urine (pH >5.3)
Leads to stones

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73
Q

Define type 4 RTA

A

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.

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74
Q

What is the treatment for high anion gap acidosis

A

Treatment is aimed at the underlying disorder, such as insulin and fluid therapy for diabetes and appropriate volume resuscitation to restore tissue perfusion.

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75
Q

Saline responsive alkalosis is a sign of…

A

extracellular volume contraction.

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76
Q

Saline unresponsive alkalosis implies

A

implies excessive total body bicarbonate with either euvolemia or hypervolemia.

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77
Q

How many red blood cells is required for hematuria

A

Greater than 3 per HPF

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78
Q

Define proteinuria

A

Urinary excretion of ≥150 mg/24hrs of protein

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79
Q

Define microalbuminuria

A

30-300 mg/day

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80
Q

Define macro albuminuria

A

Greater than 300 mg/day

Dip stick positive at this level

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81
Q

Define nephrotic proteinuria

A

Greater than 3.5 grams a day

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82
Q

Define overload proteinuria

A

Overload proteinuria: from overproduction of plasma proteins such as Bence Jones proteins
( plasma cell myeloma);
myoglobinuria
(rhabdomyolysis and hemoglobinuria).

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83
Q

What is the hallmark of DM nephropathy

A

Microalbuminuria

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84
Q

if a postive dipstick for protein occurs.. what is the next step

A

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

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85
Q

What is the gold standard protein urine assay

A

24-hour urine collection is the gold standard to quantify the level of protein excretion.

Normal value: <150 mg/day

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86
Q

What is the recommended screening for DM protienuria

A

Morning Spot Test

Albumin:Cr ratio

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87
Q

What is the role of the UPCR test

A

protein:creatinine ratio (UPCR)

Detects at higher level proteinuria

Better for monitoring of established proteinuria

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88
Q

What should you rule out in protineuria

A

Rule out Ortho proteinuria

Check a serum chemistry panel

Conduct a renal ultrasound

COnduct Urinary Electrophoresis

+/- renal biopsy

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89
Q

If a pt has established prtoineuria

What is the best test to monitory the progresssion

A

UPCR

Protein:creating level urine test (SPOT)

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90
Q

What is the Tx approach to proteinuria

A

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)

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91
Q

Wt loss of 5% can decreases proteinuria by up to…

A

20-30%

Dietary protein restriction may be of some benefit In selected patients
In consultation w/ dietician

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92
Q

How many samples do you need to confirm hematuria

A

3 samples at least 1 week apart to confirm

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93
Q

Gross Hematuria in adults over age 40 is a sign of..

A

malignancy until proven otherwise!!

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94
Q

DDX of presence of blood throughout the urination stream

A

bladder or upper tract source

stone, tumor, tuberculosis, nephritic syndrome

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95
Q

What does PP on this stand for

A 
Period (menses)
Prostate, papillary necrosis
Obstructive uropathy
Nephritic syndrome (Inflammation) 
Trauma, tumor, tuberculosis, thrombosis (renal vein) 
Hematologic (blood disorder, sickle cell)
Infection/inflammation
Stones
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96
Q

What is the hematuria W/u

A

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

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97
Q

If you have a positive dipstick UA for urine microscopy what is the next step

A

Confirm with microscopy

Repeat UA in 4-6 weeks

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98
Q

If a pt has persistent unexplained hematuria what is the assay of choice

A

Urinary Cytology

Highly sensitive and specific for detection of high-grade urothelial carcinoma.

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99
Q

When should you refer hematuria to nephrology

A

Persistent hematuria referral:

Nephrology if findings support renal parenchymal etiology.

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100
Q

When should you refer hematuria to urology

A

Calculi

Ureteral, cystic, or urethral origin

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101
Q

Define psuedo hematuria

A

Dipstick positive, microscopy negative

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102
Q

If the dipstick is positive for hematuria but the microscopy is negative

What is the DDX

A

Hemoglobinuria (Black urine)

Myoglobinuria ( Rhabdo, electric burns)

Beets, berries, food coloring

Drugs: pyrdium, sulfa, Nitrofurantoin, rifampin, Ibuprofen, phenytoin, levodopa

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103
Q

What is pyridium

A

Numbing medication for UTI that turns the urine orange

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104
Q

What is the best test to evaluate for bladder cancer

A

Cycsocopy

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105
Q

If you find a solid renal mass think

A

CA UPO

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106
Q

What is the C/I to US of the kidney

A

Unable to lay down

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107
Q

What type of ultrasound can look at the prostate

A

Transrectal US

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108
Q

What is the role of Doppler US

A

Useful for the evaluation renal vessels, and vascularity of renal masses

Acute testicular pain work-up
(i.e., torsion vs epididymitis)

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109
Q

What is the role of intravenous pyelographhy

A

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
Q

Any time you want to give Contrast what must you check

A

kidney Function

CrCl less than 2 mg/dL

111
Q

What is the role or CT

A

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
Q

What is the study of choice for a renal stone

A

Non con helical CT

113
Q

What is the perferred radiograph for uppper GU tract eval

114
Q

What is the rads study for acute pyelonephritis

115
Q

What is the imaging study for renal artery stenosis

116
Q

describe nephro genie systemic fibrosis

A

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
Q

What is renal arteriography

A

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
Q

What is the role of renal venography

A

Renal Venography: indicated as best test for diagnosis of renal vein thrombosis, though CT scanning and MRI are less invasive for this purpose.

119
Q

What is the best test for renal artery stenosis

A

CT Angiogram

120
Q

What is the imaging for a pt with allergy to iodinated contrast

121
Q

What is the role of retrograde urethrogram

A

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
Q

Define Cystography

A

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
Q

What is the role of voiding cystourethrogram

A

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
Q

Define AKI

A

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
Q

What is the number one reason for hospital nephrology consult

A

AKI

Think multi organ failure

126
Q

What is the most common cause of AKI

A

Prerenal causes

127
Q

What are the stage 1 of AKI

A

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
Q

Stage 2 AKI

A

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
Q

Stage 3 AKI

A

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
Q

What is the BUN clue to a Prerenal AKI cause

A

In prerenal AKI, the BUN: creatinine ratio often exceeds 20:1

due to increased urea reabsorption.

131
Q

What are the RSk Fx for AKI

A

Dehydration / volume depletion

Hypoalbumenia

Advanced age (65-75 years)

Female gender (Maybe)

Black race (Maybe)

Previous AKI

132
Q

A pt presents with Nausea, vomiting, malaise, anorexia, fatigue, pruritis, and altered sensorium and Coca Cola colored urine

Think

A

AKI maybe uremia

133
Q

What is the W/u findings for AKI.

A

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
Q

What are the microscopy findings of Prerenal azotemia

A

bland urine sediments, hyaline casts

135
Q

What are the microscopy findings of acute tubular necrosis

A

Renal tubular epithelial cells or muddy brown (granular) casts

136
Q

What are the benchmarks of AKI Tx

A

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
Q

What is the most common cause of POST renal failure in men

A

BPH (obstruction)

138
Q

What is the Tx approach to Post renal AKI

A

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
Q

What are the 3 major types of intrinsic AKI

A 
Acute tubular necrosis (ATN)
Acute glomerulonephritis (AGN)
Acute interstitial nephritis (AIN)
140
Q

What two disorder present with WBC casts

A

Acute interstitial nephritis

And

Plyeolnephritis

141
Q

What is the Tx approach to Intrinsic AKI

A

Treatment
Early Nephrology consult!

Offending medications must be determined and discontinued.

Two-week course of tapering glucocorticoids.

General supportive care

142
Q

When do you refer AKI

A

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
Q

When should we admit AKI

A

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
Q

What are the two major causes of Acute tubular necrosis

A

The two major causes of ATN are ischemia and nephrotoxin exposure.

Accounts for 85 % of intrinsic AKI

145
Q

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

A

Intrinsic Kidney Injury possible ATN

BUN:Cr ratio <20:1
FE-Na is elevated
primary kidney problem
+/- Hyper K

146
Q

What is the Tx for ATN

A 
Admit 
Fluids (but avoid volume overload) 
Diuretics as necessary, 
(Furosemide, thiazide) 
Diet restriction
147
Q

A pt presents with fever , transient maculopapular rash, and arthralgias and hematuria

With WBC casts

Look for

A

Eosinophilia for Acute interstitial Nephritis

148
Q

What is the most common cause of acute intestinal nephritis

A

DRUGS!

2*: infections and immunological

149
Q

What are the lab findings in the AIN

A

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
Q 
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

A

Acute intrinsic nephritis

151
Q

What is the Tx for AIN

A

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
Q

A pt presents with periorbital and scrotal edema, with an abnormal urinary sediment

Look for

A

Red blood cell casts

For acute Glomerulonephritis

153
Q

Slide 46 of AKI lecture

154
Q

What is type 1 cardiorenal syndrome

A

Type 1 consists of AKI stemming from acute cardiac disease.

155
Q

What is type 2 Cardiorenal syndrome

A

Type 2 is CKD due to chronic cardiac disease.

156
Q

What is type 3 cardiorenal syndrome

A

Type 3 is acute cardiac disease as a result of AKI.

157
Q

What Is type 4 Cardiorenal syndrome

A

Type 4 is chronic cardiac decompensation from CKD.

158
Q

What is type 5 cardiorenal syndrome

A

Type 5 consists of heart and kidney dysfunction due to other acute or chronic systemic disorders (such as sepsis).

159
Q

Define CKD

A

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
Q

What defines Kidney Damage in CKD

A

Kidney Damage:

  • Albuminuria ≥30mg/24hr
  • Abnormal urine sediment
  • Electrolyte abnormality
  • Structural abnormality on imaging
  • History of renal transplant
161
Q

What type of casts are seen in CKD

A

Waxy casts

162
Q

What GFR is stage 1 CKD

A

Greater than 90

163
Q

GFR for StageII CKD

164
Q

Stage 3a and B GFR for CKD

165
Q

Stage 4 GFR for CKD

166
Q

A GFR less than 15 is what stage CKD

A

Less than 15

Pt needs dialysis at this point

167
Q

What are the most common causes of CKD

A

DM
HTN
Vasc Dz

168
Q

A pt presents with HTN, urinary abnormalities, edema, excercise intolerance, fatigue, and anorexia

These are all clues to what underlying pathology

169
Q

What is the most common physical exam finding of CKD

A

HTN

+/- fluid overload

170
Q

Persistent protienuria is a sign of…

A

suggestive of CKD, regardless of GFR

171
Q

A pt presents with an elevated BUN/Cr and Decreased GFR over the past 3 months

Think

A

CKD

Also look for

Anemia
CMP
A1C
Metabolic acidosis
Hyperphosphatemia
Hyperkalemia
Hypocalcemia
172
Q

What is the progression of findings for CKD

A 
HTN to increased PTH 
To Anemia
To increased phosphorus 
To Acidosis and HyperK 
And lastly Uremic syndrome
173
Q

How does CKD effect atherosclerosis

A

Accelerates it

Increases vessel stiffness
2/2 increased mineral metabolism

174
Q

What is the most common bone dz in CKD

A

Osteitis fibrosa cystica:
— most common bone disease

  • Bone reabsorption
  • Subperiosteal lesions
  • Bone pain
  • Proximal muscle weakness.
175
Q

What is the 1st step in the Tx of metabolic bone Dz in CKD

A

control of hyperphosphatemia.

176
Q

How does CKD cause Anemia of Chronic Dz

A

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
Q

How does CKD effect Clotting

A 
Mainly due to platelet dysfunction
Presentation:  
-Petechiae
-Purpura
-↑ Bleeding during surgery

-Dialysis → improves bleeding time but doesn’t normalize it

178
Q

When does uremic encephalopathy occur in CKD

A

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
Q

A thiazides effective below a GFR of 30

A

Thiazide diuretics may be less effective at GFR <30

180
Q

What is the most common complication of peritoneal dialysis

A

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
Q

What is the survival rate of kidney transplants

A

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
Q

When do we admit pts with CKD

A

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
Q

Stable creatinine in the face of significant weight loss suggests

A

Progression of Kidney Dz

184
Q

What is the definitive Dx for Glomerular Dz

A

Definitive Diagnosis → visualization of specific histologic patterns on renal biopsy.

185
Q

Are there casts in Nephrotic spectrum

186
Q

Describe Nephritic Specturm

A

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
Q

Describe Nephrotic Spectrum

A

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
Q

What are the two main pathogens of Glomerulonephritis

A

Staph and strep Viridans

189
Q

A pt presents with cola colored urine
With RBC casts and erythrocytes in the urine
With edema and azotemia

Think

A

Nephritic Syndrome

190
Q

What is the tx approach to Nephritic syndrome

A

Admit in most cases
Early consult
Aggressive HTN and Fluid overload reduction

-diuretics ect

REDUCE GLOMERULAR INFLAMMATION

191
Q

What is the cause of post infectious Glomerulonephritis

A

infection with a nephritogenic group A beta-hemolytic streptococcal infection (pharyngitis or impetigo).

192
Q

What titers are high in Post infectious GN

A

(Strep A) anti-streptolysin O (ASO) titers may be high.

193
Q

What is the Tx for post infectious GN

A 
Underlying cause 
And supportive 
-Anti-HTN 
-Salt restriction 
-diuretics
194
Q

What is the most common primary glomerular disease worldwide

A

IgA Nephropathy

195
Q

A pt presents with hematuria after a recent URI

Think

A

IgA Nephropathy

196
Q

What is the difference between IgA Nephropathy and Post Infectious GN

A

It occurs quickly in conjunction with a URI versus post-infectious GN which may take weeks.

197
Q

Describe IgA Vasculitis

A

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
Q

A pt presents with palpable purpura, with arthralgias, nausea, cramps, melena, and bloody diarrhea, with hematuria

Think ?

A

IgA Vasculitis

199
Q

What is the other name of Henoch-Schonlein Purpura

A

IgA Vasculitis

200
Q

What is the Tx for IgA Vasculitis

A

Conservative:
Control HTN
Bed Rest, hydration, analgesics
+/- steroids

201
Q

When should you admit a pt with IgA Vasculitis

A

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
Q

Describe Pauci-Immune GN

A

Pauci-immune necrotizing glomerulonephritis caused by systemic ANCA-associated vasculitides:
-Granulomatosis with polyangiitis
—Formerly —-Wegener’sgranulomatosis.

Eosinophilic granulomatosis with polyangiitis
—Formerly —-
Chugg-Strauss disease
Microscopic polyangitis

Circulating ANCA Ag

203
Q

What is the treatment approach to Pauci-Immune GN

A

Treatment: REDUCE Inflammation!
High dose steroids and cytotoxic agents
Poor prognosis without treatment!

204
Q

Describe Antio-GBM

A

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
Q

Describe Good Pasture Syndrome

A

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
Q

What are the clinical manifestations of Anti-GBM/ Goodpastures

A

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
Q

Kidney Bx shows crescent formation with light microscopy

Think

A

Anti-GBM/Goodpasture Syndrome

208
Q

What are the tx options for Anti-GBM/ Goodpastures

A

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
Q

Describe Cryoglobuliun- Assoc GN

A

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
Q

What is the tx approach to Cryoglobulin- Assoc with GN

A

Treatment consists of aggressively targeting the causative infection.

± Corticosteroids, plasma exchange, rituximab, and cytotoxic agents.

211
Q

Describe Membranoproliferative GN

A

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
Q

You see Tram track on light microscopy

Think

A

Membranoproliferative - GN

213
Q

What are the lab findings in Membranoproliferative GN

A

Hematuria, Nephritic spectrum proteinuria

Light microscopy: “tram track”
I

mmunofluorescence and electron microscopy:
—IgG, IgM and C3 staining.

214
Q

What is the Tx approach to Membranoproliferative GN

A

Find and treat underlying cause.
Mild disease:
—ACE inhibitors and ARBs.
—Steroids and cytotoxic agents.

215
Q

Describe Hepatitis C associ Kidney Dz

A

Often a nephritic condition that progresses to nephrotic

—Membranoproliferative glomerulonephritis

—Cryoglobulinemic glomerulonephritis

—Membranous nephropathy

Typically have hematuria, proteinuria, HTN, & anemia

216
Q

What is the Tx approach to Hepatitis C Kidney Dz

A

Treatment for HCV associated kidney disease:

Viral suppression or eradication is the cornerstone of treatment of HCV–associated kidney disease.

217
Q

What should All pts with Lupus get in the W/u

A

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
Q

What is the tx approach to Lupus renal dz

A

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
Q

Study slide 38 of Glomerulus Dz slides

220
Q

Describe Nephrotic Syndrome

A

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
Q

What is the most common cause for nephrotic syndrome in the US

222
Q

A child pt presents with facial edema, pulm edema, with serum albumin is <3g/dl with positive protienuria

Think what syndrome

A

Nephrotic Syndrome

223
Q

If a kid comes in with an unexaplined DVT think

A

Nephrotic Syndrome cause

224
Q

What is the Tx approach to Nephrotic Syndrome

A

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
Q

When should we admit a kid with nephrotic syndrome

A

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
Q

What is the tx approach to Nephrotic Syndrome

A

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
Q

What is the most common cause of primary nephrotic syndrome in children

A

Minimal Change Dz

228
Q

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

A

Minimal Change Dz

229
Q

You see effacement of podocyte foot processes

Think

A

Minimal Change Dz

230
Q

What is the tx approach to Minimal change Dz

A

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
Q

describe focal segmental glomerulosclerosis

A

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
Q

What is the Tx approach to Focal Segmental Glomerulosclerosis

A

Dieuretics for edema
ACE/ ARB
Statins as needed

Oral prednisone (only if primary)

233
Q

What is the most common causes of primary nephrotic syndrome in adults

A

Membranous Nephropathy

Circulating antibodies combine with antigens to form immune complexes on the epithelial side of the basement membrane leading to proteinuria.

234
Q

An older pt presents with frothy urine and S/s of DVT

Think

A

Membranous Nephropathy

235
Q

If you find PLA2R abs think

A

Membranous Nephropathy

236
Q

Kidney biopsy indicated for all glomerular diseases except for classical presentations of….

A

diabetic nephropathy and minimal change disease.

237
Q

You see a spike and dome pattern on biopsy think

A

Membranous Nephropathy

238
Q

What is the Tx approach to membranous Nephropathy

A

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
Q

What is the most common cause of ESRD in the US

A

DM Nephropathy

240
Q

What is the most common lesion in DM nephropathy

A

Nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) is pathognomonic.

241
Q

If there is a sudden onset of proteinuria, or greater than 10g/day
Or urinary celllurla casts

What should you do

242
Q

Look at the stages of Tx for DM nephropathy on slide 64 of glomeluar dz

243
Q

What is the clinical manifestation of Fibromuscular dysplasia

A

No cardiovascular risk factors
New onset hypertension
Young women
Headache and pulsatile tinnitus

244
Q

What is the gold standard for renal artery stenosis

A

Renal Artireograph

245
Q

What is the C/I for Renal Arteriogrpahy

A

eGFR <30 mL/min → NO gadolinium contrast → gadolinium-associated nephrogenic systemic fibrosis

246
Q

What are the go to imaging for Renal Artery Stenosis

A

CTA or MRA

247
Q

What is the tx approach to renal Art Stenosis

A

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
Q

What is the most common cause of renal infarction

249
Q

A pt presents with acute onset of flank pain, Nausea and fever with HTN

Think

A

Renal Infarction

250
Q

What is the definitive DX for renal infarct

A

CT w and W/o con

251
Q

What is the tx approach to Renal Infarction

A

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
Q

You see enlarged kidney, stretching of the calyces and notching of the uterus

Think

A

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
Q

What is the common cause of acute tubuklointerstitial Dz

A

Acute disease is most commonly associated with medications, infectious agents, and systemic rheumatologic disorders.

254
Q

What is the common cause of chronic tubulointerstitial dz

A

Chronic disease may result from acute factor or progressive “trauma” without any obvious acute cause.

255
Q

What is the most common cause of chronic tubuklointerstitial dz

A

Obstructive Uropathy

Prostate Dz
Stones

256
Q

Describe Vesicourectal reflux

A

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
Q

What effect does NSAIDs have on glutathione

A

Decrease production which means less glutathione detoxifiacation

258
Q

How does tubularinterstial dz manifest

A

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
Q

What is the general manifestation of obstructive uropathy

A

Azotemia and HTN

Poly or oliguria

+Hematuria, Pyruvate, and bacteriuira

260
Q

How can vesicoureteral reflux be detected in utero

A

Can be detected before birth via screening fetal ultrasonography or after birth via voiding cystourethrography.

261
Q

What is the tx of Mesoamérican nephropathy

A

Stay hydrated
Minimize heat exposure
Avoid NSAIDs

262
Q

What stage of CKD needs referal

A

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
Q

What effect do bence-jones proteins have on the kidney

A

Bence Jones protein in the urine cause renal toxicity and tubular obstruction by precipitating in the distal tubules.

Found in Myeloma Kidnay (CA)

264
Q

What is the treatment to plasma cell myeloma (Bence Jones Proteins)

A

Correction of hypercalcemia, volume repletion, and chemotherapy for the underlying malignancy.

265
Q

What med should be used early in sickle cell

266
Q

What is the classic renal manifestation of TB kidney

A

Steroids pyuria

Microscopic hematuria

267
Q

What is the gold standard for TB kidney

A

Urine cultures are the gold standard for diagnosis.

268
Q

What is the tx for gout kidney

A

Avoid hyperuricemic foods
Allopurinol/febuxstat
Increase fluid intake

269
Q

What is the most common renal fusion anomaly

A

Horse shoe kidney

270
Q

Where are Wilms tumors found?

A

In horseshoe kidney

271
Q

If you are specifically looking for uro bleeding what study/>

A

CY urogram

Senoir 21-2 (77 decks)

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