1
Q
A patient presents with hematuria and oliguria. Kidney biopsy with silver stain is shown below.
- What is the diagnosis?
- The abnormal deposition is made up of what?
A
- Rapidly Progressive Glomerulonephritis
(crescents in bowman space)
- Crescents are filled will fibrin and macrophages
2
Q
A biopsy of a cancerous lung lesion is shown below.
Where did this cancer originate from and why?
A
The Kidneys (renal cell carcinoma)
Due to the empty/clear cytoplams
(clear cell renal carcinoma - most common type)
3
Q
How and does Benign Prostatic Hyperplasia affect the ability to urinate? Why? Major complication?
A
It increases resistance to urine flow due to compressing the urethra (increasing the hydroostatic pressure required to overcome resistance to flow)
This results in incomplete emptying of the bladder.
(as bladder empties urinary pressure will soon fall below the bladders leaving a residual volume of urine)
Most common complication is UTI
4
Q
In poststreptococcal glomerulonephritis (PSGN) what is the most important poor prognostic factor?
A
Increased Age
5
Q
In a patient recovering from acute tubular necrosis, what is the major complication and why?
A
Major complication: Electrolyte Imbalances + Oliguria
(hypokalemia, hypocalcemia, hypophosphatemia)
This occurs due to GFR improving before tubular cell recovery
(tubular cells are stable cells and take some time to reenter cell cycle)
6
Q
How would the following be altered in a hypovolemic patient in comparison to a regular person:
- RPF (renal plasma flow)
- GFR (glomerular filtration rate)
- FF (Filtration Fraction)
A
1. RPF is decreased
(RPF = amount of blood going to kidneys)
2. GFR is decreased
(GFR = amount of filtered blood in kidneys)
3. FF is increased
(FF = GFR/RPF)
(FF is increased during hypovlemia to try to maintain GFR)
7
Q
Which toxic agents can result in Acute Tubular Necrosis?
A
- Aminoglycosides (ex: gentamycin)
- Heavy metals (ex: lead)
- myoglobinuria (ex: from crush injury to muscle)
- ethylene glycol/antifreeze
- radiocontrast dye
- urate (used for chemotherapy, prevented by also giving allopurinol)
8
Q
How can Heart Failure affect the renal system?
A
Cardiorenal Syndrome
- HF results in decreased renal perfusion
- Activation of RAAS + ADH release + sympathetic stimulation
- Na and H2O reabsorption and systemic vasoconstriction
- Exacerbation of HF and further renal hypoperfusion
9
Q
How would hypovolemia affect the following:
- Vasopressin
- Norepinephrine
- Angiotensin II
- Endothelin 1
A
All will be increased
10
Q
In minimal change disease, what are the effects of albumin loss on:
- Plasma Oncotic Pressure
- Lipoprotein production
A
- decreased plasma oncotic pressure
- increased lipoprotein production –> hyperlipedemia
(stimulated by decreased oncotic pressure)
11
Q
In acute tubular necrosis, which structures are most susceptible to ischemic damage?
A
- medulla
- proximal tubule
- thick ascending limb
12
Q
How would uterolithiasis (stone in ureter) present?
A
- hydronephrosis (swelling of kidney due to build up urine)
- Hematuria (RBCs with no RBC casts)
- Stone crystals
13
Q
How/why does Osteodystrophy occur with chronic renal disease/failure?
A
- Impaired renal fcn –> hyperphosphatemia + hypocalcemia
2. Increased PTH (secondary hyperparathyroidism)
3. Increased osteoclast function
4. Osteodystrophy
14
Q
What is the earliest sign of diabetic nephropathy?
A
Albuminuria
15
Q
What are 2 general things that can decrease renal stone formation?
A
- Increased fluid intake
- increased urinary citrate
16
Q
A 65 yo patient comes in complaining of abdominal pain after eating who has a BP of 175/110.
CT scan of the abdomen reveals the following:
What condition is this patient most likely suffering from?
A
Renal artery stenosis
- marked unilateral kidney atrophy
- commonly occurs in elderly with other atherosclerotic diseases (in this case: mesenteric ischemia)
17
Q
How can chronic kidney disease cause spasms?
A
- impaired kidney function results in hyperphosphatemia
2. Phosphate binds calcium
3. hypocalcemia
4. spasms
18
Q
IgA Vasculitis / Henoch-Schonlein Purpura
- What is it?
- Who comonly gets it?
- How does it present?
A
- Small vessel vasculitis due to IgA immune complex deposition
- Most commonly occurs in children
3.
- palpable purpura on buttocks
- GI pain + bleeding
- joint pain
- Hematuria
19
Q
Interstial Nephritis
- What is it?
- What can cause it?
- How does it present?
- What can it progess to?
A
- Drug-induced hypersensitivity that results in acute renal failure (intrarenal azotemia)
- P’s
Diuretics (Pee), NSAIDs (Pain-free), Penicillins, PPIs, RifamPin
- Oliguria, fever, rash (eosinophils may be present in urine)
- Renal Papillary necrosis
20
Q
Renal Papillary Necrosis
- How does it present?
- What causes it?
A
- Flank pain and Hematuria
- “SAAD”
Sickle cell disease/trait
Acute Pyelonephritis (kidney infection)
Analgesic/NSAID abuse
Diabetes
21
Q
How can BPH damage the kidney structure?
A
- BPH blocks prostatic urethra
- Hydronephrosis occurs
- Build-up of urine causes parenchymal pressure atrophy of kidney
22
Q
IgA Nephropathy (Berger’s Disease)
- Clinical presentation?
- Microscopic Presentation?
A
- hematuria that occurs following a mucosal infection
2. IgA deposition in mesangium of glomeruli
23
Q
Hemolytic Uremic Syndrome
- What is the classical ‘triad’ presentation?
- What causes the kidney effects?
A
1. Triad of:
- Thrombocytopenia
- Microangiopathic Hemolytic Anemia
- Acute Kidney Injury
2. Acute kidney injury occurs due to microthrombi in small blood vessels
24
Q
How would the following values in a patient with long-standing Polycysitic Kidney Disease compare to a healthy individual:
- Phosphate
- PTH
- Calcitriol
A
Chronic Kidney Disease (in this case PKD) results in:
- Phosphate is increased (causes hypocalcemia)
- PTH is increased (to try and increase Ca levels
- Calcitriol is decreased
(even though it functions to increase Ca, it is inhibited by phosphate)
25
If a normal patient PTH and calcium are represented by "C" in the circle, what letter would represent a patient with **chronic kidney disease?**
**_A_**
chronic kidney disease results in:
- **hypocalcemia** (due to hyperphosphatemia)
- **secondary hyperparathyroidism (**to try and increase Ca)
26
**_Fibromuscular Dysplasia_**
1. What is it?
2. What does it commonly effect?
1. Abnormal tissue growth within arterial walls resulting in:
- **fibromuscular webs** --\> arterial stenosis
- **aneurysms**
- **loss of internal elastic lamina**
2. Brain --\> **_stroke_** , Kidneys --\> **_renal artery stenosis_**
27
**_Tumor Lysis Syndrome_**
1. What is it? How does it happen?
2. How can it be prevented?
3. Where in the kidney would precipitation most commonly occur?
1. It is a cause of **acute kidney injury/failure** that can occur **after chemotherapy** due to increased lysis of cells that release intracellular substances into the blood, namely **uric acid**
2. Prevented with: **hydration + allopurinol**
**3.** Precipitation into a stone occurs in the **distal tubules or collecting ducts due to their low pH**
28
**_Autosomal Dominant Polycystic Kidney Disease_**
1. How does it present?
2. What is it associated with?
1.
- **bilateral enlarged kidneys with cysts** in renal cortex + medulla
- **Hematuria** and **hypertension**
2. **Berry aneurysm, hepatic cysts, mitral valve prolapse**
"Cysts in kideys, brain, liver and heart"
29
A patient presents with hematuria and hypertension, CT scan of the abdomen is shown below, what is the diagnosis?
**_AD Polycystic Kidney Disease_**
- enlarged kidneys with cysts
- hepatic cysts
30
What would be the most likely diagnosis of a patient with signs and symptoms of **SLE** (lupus) and:
1. **Nephrotic** Syndrome
2. **Nephritic** Syndrome
1. **Membranous Glomerulonephritis**
2. **Diffuse Proliferative Glomerulonephritis**
31
**_Urothelial (Transitional Cell) Carcinoma_**
1. What areas does it affect?
2. Major risk factor?
1. Urothelial lining of **bladder, ureters, urethra and renal pelvis**
**2. Smoking** (the major risk factor)
Occupational exposure to **rubber, plastics and dyes**
32
**_Postreptococcal Glomerulonephritis_**
1. How does it present on histology?
2. How are the following lab values affected:
a. Total complement levels
b. Levels of C3
c. Levels of C4
1. **Enlarged hypercellular glomeruli**
2.
a. **Decreased total** complement
b. **decreased C3**
c. **normal C4**
33
**_Minimal Change Disease_**
1. What causes the **effacement of foot proceses**?
2. What causes the **selective loss of albumin**?
1. **overproduction of glomerular permeabilty factor** that damages podocytes
2. **Loss of anions / negative charge**
34
Which nephropathy is associated with I**gG4 antibodies to the phospholipase A2 receptor**?
Membranous Nephropathy
35
**_Goodpasture Syndrome_**
1. How does it present?
2. What is it caused by?
1.
- **hemoptysis**
- **hematuria** (due to rapidly progressive glomerulonephritis)
2. **Antibody againt type _4 collagen_ in _glomerular_ and _alveolar_ basement membranes**
36
Is it normal for there to be **microscopic or gross hematuria** in a patient with **_BPH_**? Why?
Yes, BPH can result in the formation of **new friable/easily torn blood vessels** that can cause hematuria
37
Why are the cells in **_clear cell renal carcinoma_** clear?
Due to their origination from the **proximal tubule**, they have a **_high glycogen and lipid content_** that dissolves during slide/tissue preperation
38
What are the major risk factors for **Uric Acid Stones? (3)**
**1. Increased Uric Acid Secretion**
(gout, myeloproliferative disorders)
**2. Increased Urine concentration**
(hot, arid climates + dehydration)
3. **_Low Urine pH_** --\> favors insoluble uric acid
(chronic diarrhea due to loss of bicarbonate)
39
Why do some patients with **_Multiple Sclerosis_** develop urinary frequency and incontinence?
Due to **bladder hypertonia**
| (due to an upper motor neuron lesion)
40
In what nepthropathy would you be most likely to see serum **antineutrophil cytoplasmic antibodies (ANCA)?**
**_Pauci- Immune_ (negative IF) Rapidly Progressive Glomerulonephritis (**vasculitides):
- Wegener (c-ANCA)
- Microscopic Polyangitis (p-ANCA)
- Churg-Strauss (p-ANCA)
41
**_Calcium Kindey Stones_**
1. **Serum levels** of calcium
2. **Urine levels** of calcium
1. **Normocalcemia**
2. **Hypercalciuria**
NOTE: Calcium stones are most commonly caused by *idiopathic hypercalciuria*
42
A patient comes in with left flank pain, hematuria and recurrent UTIs. CT of scan of the abdomen is shown below:
1. What is the diagnosis?
2. What causes this?
3. What is the urine pH most likely to be?
1. Ammonium Magnesium Phosphate **_(AMP / Struvite) Stone_**
2. **Urease** producing organisms (**Klebsiella**, **Proteus**)
**_3. Urinary pH \> 8,_** due to hydrolysis of urea forming ammonia which alkalinizes the urine
43
What is most significant risk factor for **UTI's due to catheterization?**
**_Duration_** of catheterization
(i.e. the best way to prevent a UTI is to remove the catheter whenever is it not needed)
44
What type of kidney stone is pictured below:
**_Calcium Stone_**
'envelope shaped'
45
What type of kidney stone is pictured below:
**_AMP Stone_**
'coffin-lid shaped'
46
What type of kidney stone is pictured below:
**_Uric acid Stone_**
'rhomboid shaped'
47
What type of kidney stone is pictured below:
**_Cystine Stone_**
'hexagonal shaped'
48
**Acute tubular necrosis** with **vacuolar degeneration** and **ballooning of the proximal convoluted tubule** is most likely due to what?
**Ethylene Glycol (Antifreeze) ingestion**
49
In most cases patients recover from **acute tubular necrosis.**
In this **recovery phase,** what would be seen on kidney **biopsy?**
**Tubular re-epithelialization**
50
Renal Infarction
1. How does kidney appear on gross pathology?
2. How is it most commonly caused?
1. **Sharply demarcated, yellow-white, wedge shaped areas with hyperemia**
2.
**Cardioembolic Disease** (usually due to ***Atrial Fribrillaiton***)
51
Where does **renal cell carcinoma** most commonly originate from?
Epithelial cells of **proximal renal tubules**
52
What area of the kidney to ACE inhibitors affect?
**Efferent Arteriole Dilation**
| (due to reduced AT II)
53
In patient with **renal artery stenosis**, which cell type is most likely to undergo hyperplasia and why?
**Modified smooth muscle (Juxtaglomerular) cells of the _afferent_ arteriole**
Due to decreases perfusion thet will secrete renin and activate the RAAS
54
Which nephropathy is **IgG4 antibodies to the phospholipase A2 receptor** recetor associated with?
**Membranous Nephropathy**
55
A 2 year old presents with failure to thrive, polyuria, glucosuria and normal serum glucose.
1. Whats the main issue?
2. Diagnosis?
1.
**_Defect in proximal tubule reabsorption_**
2.
Fanconi Syndrome
(Glucose, bicarbonate, calcium, phosphate, amino acids are lost. They also often present with rickets)
56
What can occur _following_ **acute tubular necrosis**? Why?
(during the recovery phase)
**_Ployuria and Electrolyte Wasting_**
(Decreased K, Ca, Mg, P)
This occurs since **GFR improves before tubular function** is restored
57
A patient presents with hematuria following an upper respiratory infection.
1. If serum **complement is _normal_** whats the diagnosis?
2. If serum **complement is _low_** whats the diagnosis?
1. **IgA Nephropathy**
(normal serum complement)
2. **Poststrep Glomerulonephritis**
(low serum complement)
58
Which organisms can cause a struvite/AMP stone?
Proteus and Klebsiella
59
How to **_NSAIDs_** affect the kidney? (2)
1. They could cause **_Acute Interstitial Nephritis_**
(Nephrotic syndorme with **rash**, fever, eosinophils in urine)
2. They **inhibit prostaglandin production** which is needed to dilate the **_afferent_** arteriole and maintain GFR when a patient is volume depleted which can then lead to **prerenal azotemia**
60
How does **_Poststreptococal Glomerulonephiritis_** appear on:
1. Electron Microscopy
2. Immunofluorecense
1. **Subepithelial humps**
2. Granular staining
61
1. What is the most common type of **nephrotic** syndrome in **children**?
2. What is the most common type of **nephritic** syndrome in **children**?
**Minimal Change Disease**
**Poststrep. Glomerulonephritis**
62
What lab changes would be seen in a patient with **_PSGN_**?
**Elevated ASO**
**Decreased C3** (normal C4)
63
Why do patients with **_multiple sclerosis_** have increased urinary frequency and urinary incontinence?
Spastic Bladder
64
What is the most common type of renal cell carcinoma?
In what part of kidney does it originate?
**_Clear-Cell Carcinoma_**
Originates in the **proximal renal tubule**
65
In a patient with **kidney stones**, what is most likely to been on **urinalysis**? (2)
1. RBCs (hematuria)
2. Crystals consistent with the type of stone
66
What should be given to a patient with **_nephrogenic_ diabetes insipidus**?
**_Thiazide diuretics_** **+ water replacement**
(even though this makes them pee more it allows for better water retention overall)
67
What is the first sign of **diabetic nephropathy**?
increased **_albumin_** in urine
68
In a **_hypovolemic_** patient how would the kidney alter its absorption of the following:
1. Sodium
2. Chloride
3. Water
4. Urea
5. Potassium
1. **Increased sodium** absorption
2. **Increased chloride** absorption
3. **Increased water** absorption
4. **Increased urea** absorption
5. **Decreased potassium** absorption
69
Which letter best represents a patient with **chronic kidney disease? Why?**
**_"A"_**
- CKD results in hyperphosphatemia which binds serum Ca
- CKD results in decreased levels of active vitamin D so theres less Ca absorption and Ca release from bone
These result in increase PTH release
70
What part of the kidney to **_ACE-Inhibitors_** effect?
How does this effect GFR?
They **_dilate the efferent_** arteriole
This **_decreases GFR_**
71
How does **_severe vomitting_** effect the following:
1. Sodium
2. Potassium
3. Chloride
4. Bicarbonate
1. decreased sodium
2. decreased potassium
3. decreased chloride
4. increased bicarbonate
Severe vomitting results in a hypokalemic, hypochloremic metabolic alkalosis
72
How do ACE-Inhibitors effect the GFR?
They **_lower GFR_** by preventing constriction of **_efferent_** arterioles
73
What are the 3 **_Thiazide diuretics?_**
Why can they cause **_muscle pain_**?
**1. Hydrochlorothiazide**
**2. Chlorthalidone**
**3. Metolazone**
Muscle pains due to **_hypokalemia_**
74
**_Patiromer_**
1. What is it used for?
2. How does it work?
1. Used to treat **hyperkalemia**
2. Exchanges a calcium for a potassium
75
**_Sevelamer_**
1. What is it used for?
2. How does it work?
1. Treats **hyperphosphatemia**
2.
Binds intestinal phospate to **reduce its absorption**
76
Patients with CKD often develop normocytic anemia due to EPO deficiency so they are given EPO.
## Footnote
**What is the major risk of taking EPO for a prolonged amount of time?**
**Thromboembolism & Hypertension**
77
How would **_ACE-Inhibitors_** effect the following levels:
1. Renin
2. AT I
3. AT II
4. Aldosterone
5. Bradykinin
1. Increased renin
2. Increased AT I
**3. Decreased AT II**
**4. Decreased Aldosterone**
5. Increased Bradykinin
78
How would a **_Vasopressin-V2-Antagonist (Vaptan)_** affect the following:
1. Urine Output
2. Serum Osmolality
3. Urinary Sodium excretion
4. Urinary Potasisum Excretion
1. Increased urine output
2. Increased serum osmolality
**3. No change in sodium excretion**
**4. No change in potassium excretion**
79
What is first-line therapy for rapid-relief of **_symptoms_** in patients with HF?
**Loop diuretics**
80
How would a **Beta-Blocker** affect the following:
1. Renin
2. AT I
3. AT II
4. Aldosterone
Beta-blockers **inhibit renin release** so they will all be **decreased**
81
How would **_Furosemide_** affect the following
1. _Serum_ **Bicarbonate**
2. _Serum_ **Chloride**
3. _Urine_ **Sodium**
4. _Urine_ **Potassium**
1. **Increased serum bicarb** (can cause contraction alkalosis)
2. **Decreased serum Cl** (due to inhibition of Na/K,2Cl)
3. **Increased urine Sodium** (since not being reabsorbed)
4. **Increased urine Potassium** (since not being reabsorbed)
**_Furosemide causes decreased absorption of Na, K, Cl_**
**(inhibits Na/K/2Cl transporter)**
UWorld - Renal
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