Renal - Pathology (Renal Failure, Osteodystrophy, and Cysts)

Question 1

In a normal nephron, is BUN reabsorbed? Is creatinine reabsorbed?

Answer 1

In normal nephron, BUN is reabsorbed (for countercurrent multiplication), but creatinine is not.

Question 2

What is the definition of acute renal failure?

Answer 2

Acute renal failure is defined as abrupt decline in renal function with increased creatinine and increased BUN over a period of several days

Question 3

What causes prerenal azotemia?

Answer 3

As a result of decrease RBF (e.g., hypotenstion) –> decreased GFR

Question 4

In response to pre-renal azotemia, what does the kidney do, and why? What clinical significance does this have?

Answer 4

Na+/H2O and urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ratio increased.

Question 5

What is generally the cause of intrinsic renal failure? What is a less common cause of intrinsic renal failure?

Answer 5

Generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis (e.g., RPGN).

Question 6

What effect does intrinsic renal failure have on GFR, and how?

Answer 6

Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule –> decreased GFR.

Question 7

What is seen in the urine of intrinsic renal failure patients?

Answer 7

Urine has epithelial/granular casts

Question 8

What happens to the BUN/creatinine ratio is intrinsic renal failure, and why?

Answer 8

BUN reabsorption is impaired –> decreased BUN/creatinine ratio

Question 9

In general, what causes postrenal azotemia? Give 4 reasons this cause might happen. What is required for development of postrenal azotemia?

Answer 9

Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies); Develops only with bilateral obstruction

Question 10

What is the expected urine osmolality (mOsm/kg) in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal?

Answer 10

(1) > 500 (2) < 350 (3) < 350

Question 11

What is the expected urine Na (mEq/L) in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal?

Answer 11

(1) < 20 (2) > 40 (3) > 40

Question 12

What is the expected FE Na in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal (mild versus severe)?

Answer 12

(1) < 1% (2) > 2 % (3) > 1% (mild), > 2 % (severe)

Question 13

What is the expected serum BUN/Cr in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal?

Answer 13

(1) > 20 (2) < 15 (3) > 15

Question 14

What are the 2 forms of renal failure? Give at least one example of each.

Answer 14

2 forms of renal failure - acute (e.g., ATN) and chronic (e.g., hypertension, diabetes, congenital anomalies)

Question 15

What 2 main things are the kidneys of a patient in renal failure unable to do?

Answer 15

Inability to (1) make urine and (2) excrete nitrogenous wastes.

Question 16

What are 8 consequences of renal failure?

Answer 16

Consequences: (1) Metabolic Acidosis (2) Dyslipidemia (especially increased triglycerides) (3) Hyperkalemia (4) Uremia (clinical syndrome marked by high BUN and high creatinine) (5) Na+/H2O retention (CHF, pulmonary edema, hypertension) (6) Growth retardation and developmental delay (in children) (7) Renal osteodystrophy; Think: “MAD HUNGER”

Question 17

What are 3 conditions that may result from Na+/H2O retention due to renal failure?

Answer 17

(1) CHF (2) Pulmonary edema (3) Hypertension

Question 18

What defines uremia? What are 5 of its signs/symptoms?

Answer 18

Clinical syndrome marked by increased BUN and increased creatinine; (1) Nausea and anorexia (2) Pericarditis (3) Asterixis (4) Encepalopathy (5) Platelet dysfunction

Question 19

What causes anemia in renal failure patients?

Answer 19

Failure of erythropoietin production

Question 20

As a consequence of renal failure, dyslipidemia especially pertains to what change?

Answer 20

Dyslipidemia (especially increased triglycerides)

Question 21

What consequence can renal failure have especially on children?

Answer 21

Growth retardation and developmental delay (in children)

Question 22

What is the definition of renal osteodystrophy? In other words, what factors cause it & what results?

Answer 22

Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia –> secondary hyperparathyroidism

Question 23

Besides leading to secondary hyperparathyroidism, like all factors involved in renal osteodystrophy, what additional independent effect does hyperphosphatemia have?

Answer 23

Hyperphosphatemia also independently decreases serum Ca2+ by causing tissue calcifications, whereas decreased 1,25-(OH)2 vitamin D –> decreased intestinal Ca2+ absorption

Question 24

What symptom/sign does renal osteodystrophy cause?

Answer 24

Causes subperiosteal thinning of bones

Question 25

What are 3 different diseases involving renal cysts?

Answer 25

(1) ADPKD (Autosomal-Dominant Polycystic Kidney Disease) (2) ARPKD (Autosomal-Recessive Polycystic Kidney Disease) (3) Medullary cystic disease

Question 26

What does ADPKD stand for? What was it formerly known as?

Answer 26

Autosomal-Dominant Polycystic Kidney Disease; Formerly adult polycystic kidney disease.

Question 27

What gross features are found in ADPK, and what effect do they have?

Answer 27

Innumberable cysts causing bilateral enlarged kidneys that ultimately destroy the kidney parenchyma

Question 28

How does ADPK present?

Answer 28

Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure

Question 29

What are the 2 mutations associated with ADPK? What percentage of cases does each cause, and on what chromosome is each found?

Answer 29

Autosomal-Dominant mutation in PKD1 (85% of cases, chromosome 16) or PKD2 (15% of cases, chromosome 4)

Question 30

What causes death in ADPK patients?

Answer 30

Death from complications of chronic kidney disease or hypertension (caused by increased renin production).

Question 31

What are 3 conditions with which ADPK is associated?

Answer 31

Associated with (1) berry aneurysms, (2) mitral valve prolapse, (3) benign hepatic cysts

Question 32

What does ARPKD stand for? What was it formerly known as?

Answer 32

Autosomal Recessive Polycystic Kidney Disease; Formerly infantile polycystic kidney disease

Question 33

Describe the presentation of ARPKD.

Answer 33

Infantile presentation in parenchyma.

Question 34

With what disorder is ARPKD associated? What can ARPKD lead to if there is significant real failure in utero?

Answer 34

Associated with congenital hepatic fibrosis; Signifiant renal failure in utero can lead to Potter’s syndrome

Question 35

What are 3 ARPKD concerns beyond the neonatal period?

Answer 35

Concerns beyond neonatal period include hypertension, portal hypertension, and progressive renal insufficiency

Question 36

What is Medullary cystic disease? In other words, what causes it & what does it cause?

Answer 36

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine.

Question 37

What defines Medullary cystic disease on imaging? What is not visualized?

Answer 37

Shrunken kidneys on ultrasound; Medullary cysts usually not visualized

Question 38

What is the prognosis like for Medullary cystic disease?

Answer 38

Poor prognosis

Question 39

Where are simple renal cysts usually found, and with what are they filled?

Answer 39

Simple cysts usually found in outer cortex, filled with ultrafiltrate

Question 40

In general, how common are simple renal cysts?

Answer 40

Very common, and account for majority of all renal masses

Question 41

How are simple renal cysts found, and how do they typically present?

Answer 41

Found incidentally and typically asymptomatic.

Question 42

What kind of cysts are included in the term complex renal cyst? How are they managed, and why?

Answer 42

Complex cysts, including those that are septated, enhanced, or have solid components as seen on CT, require follow-up or removal due to risk of renal cell carcinoma