.renal: Acute And Chronic Kidney Disease, Esrd, And Diabetic Nephropathy

Front 1

What is the creatinine criteria for acute renal failure?

Back 1

Increase in creatinine of:
0.5 mg/mL if baseline is 2.5-3.0 or
1.0 mg/dL if baseline is > 3.0.

Front 2

Pre-renal ARF and hepatorenal syndrome present nearly identical. How do you differentiate them?

Back 2

Both have pts that have low EABV, thus reduced profusion to kidneys. Hepatorenal syndrome is UNRESPONSIVE TO PLASMA VOLUME EXPANSION and there is increased blood pressure elevation.

Mech is unkown. Reversible if: hepatic function improves, or liver transplantation occurs.

Remember, the problem here is the diseased liver, not the kidney itself.

Front 3

When thinking of ARF, what three categories do we think of?

Back 3

Pre-renal (problem with renal perfusion) , rena (damage of renal parenchyma), and post-renal (obstruction of urine flow).

Front 4

Name some of the many causes of post-renal ARF.

Back 4

Post-renal ARF think urinary tract obstruction. Remember, to present with symptoms, must be bilateral unless single kidney or one nonfunction kidney is present.

Urethral obstruction, bladder neck obstruction (BPH in men, cancer), obstruction of ureters

Complete obstruction causes ARF with anuria. Otherwise, can be olguric (too little urine), polyuric (too much urine) too.

Front 5

What are some common causes of pre-renal ARF?

Back 5

Common denomi of inadequate renal perfusion. Thus: volume depletion/ hypovolemia (extrarenal fluid loss like vomiting, diarrhea, sweating, burns; obligatory diuresis from excessive diuretic use, osmotic diuresis, post-bostructive diuresis, lithium), impaired cardiac function (CHF, MI), vascular disease (renal artery stenosis, peripheral vasodilation due to sepsis), increase renal vascular resistance (hepatorenal syndrome, NSAIDs).

The kidney itself is normal. The problem is renal hypoperfusion and thus reduced GFR.

Front 6

True or False:
Hepatorenal syndrome is irreversible.

Back 6

TRUE.

Treatment consists of maintaining patient with dialysis in hopes that liver function will improve or patient can recieve a liver transplant.

Hepatorenal syndrome occurs exclusively in patients with severe liver disease and basically is identical to general pre-renal ARF except hepatorenal syndrome is unresponsive to plasma volume expansion.

Front 7

______________occurs exclusively in patients with severe liver disease and basically is identical to general pre-renal ARF except hepatorenal syndrome is unresponsive to plasma volume expansion.

Back 7

Hepatorenal syndrome

Front 8

Prostaglandins regulate renal blood flow and have the action of...

A. vasoconstricting
B. vasodilating

Back 8

B. vasodilating

Thus, prostaglandins are important when renal blood flow is low , as in volume depletion, CHF, and hepatic cirrhosis.

NSAIDs, then, which block PG production, decrease blood flow, and lead to increased sodium retention, decreased potassium excretion and water excretion, which leads to hypertension, edema and ARF. This is especially prominent in pts with CHF, hepatic cirrhosis…they have a kind of constricted state versus normal people. These patients kind of de facto rely on vasodilation that prostaglandins do.

Front 9

In normal people, NSAIDs have little effect on kidney function but in what clinical setting does NSAIDs induce a form of pre-renal ARF?

Back 9

In patients that depend on systemic vasoconstriction to operate normally: volume depletion, CHF, cirrhosis patients.

Front 10

Angiotensin II is a potent

A. vasodilator
B. vasoconstrictor

Back 10

B. vasoconstrictor

Think about it: when EABV decreases, RAAS is stimulated to maintain GFR bloodflow, how better than for AAII to be a potent vasoconstrictor?

That said, thus ACEi (angiotensin converting enzyme inhibitors) reduce AII levels and ARBs (angiotensin receptor blocker) blocks the effect of AII. So, in the setting of bilateral renal artery stenosis, ACEIs and ARBs, ARF can be induced acutely.

Front 11

NSAIDs are potent

A. vasodilators
B. vasoconstrictors

Back 11

A. vasodilators

In pateints with volume depletion, CHF, and cirrhosis, acute ARF can occur.

Front 12

Angiotensin II is a potent

A. vasodilator
B. vasoconstrictor

Back 12

B. vasoconstrictor

Think about it: when EABV decreases, RAAS is stimulated to maintain GFR bloodflow, how better than for AAII to be a potent vasoconstrictor?

That said, thus ACEi (angiotensin converting enzyme inhibitors) reduce AII levels and ARBs (angiotensin receptor blocker) blocks the effect of AII. So, in the setting of bilateral renal artery stenosis, ACEIs and ARBs, ARF can be induced acutely.

Front 13

Angiotensin II is a potent

A. vasodilator
B. vasoconstrictor

Back 13

B. vasoconstrictor

Think about it: when EABV decreases, RAAS is stimulated to maintain GFR bloodflow, how better than for AAII to be a potent vasoconstrictor?

That said, thus ACEi (angiotensin converting enzyme inhibitors) reduce AII levels and ARBs (angiotensin receptor blocker) blocks the effect of AII. So, in the setting of bilateral renal artery stenosis, ACEIs and ARBs, ARF can be induced acutely.

Front 14

ACEi (angiotensin converting enzyme inhibitors) reduce Angiotensin II levels and ARBs (angiotensin receptor blocker) blocks the effect of Angiotensin II. So, in the setting of [ what condition ], ACEIs and ARBs, ARF can be induced acutely.

Back 14

bilateral renal artery stenosis

Front 15

Why /how does ACEIs and ARBs induce ARF acutely in condition of renal artery stenosis?

Back 15

Think about it: Angiotensin 2 is a potent vasoconstrictor. When EABV decreases, RAAS is stimulated to maintain GFR bloodflow, how better than for AAII to be a potent vasoconstrictor?

That said, thus ACEi (angiotensin converting enzyme inhibitors) reduce AII levels and ARBs (angiotensin receptor blocker) blocks the effect of AII. So, in the setting of bilateral renal artery stenosis, ACEIs and ARBs, ARF can be induced acutely.

Front 16

Which of the following is FALSE regarding Acute Tubular Necrosis (ATN)?

A. Usually tubules show minimal or no evidence of necrosis by LM though subtle changes are found on EM
B. urinalysis usually shows coarse granular casts
C. urinalysis usually shows renal tubular epithelial cells/casts
D. urinalysis shows RBC casts
E. urine sodium levels ~ 30-90 mmol/L

Back 16

ATN usually DOES NOT show

D. urinalysis shows RBC casts

Front 17

What type of casts are in pre-renal ARF (1) and renal ARF (2)?

Back 17

pre-renal ARF: hyaline casts

renal ARF: granular casts, renal tubular casts

Front 18

What type of casts are in pre-renal ARF (1) and renal ARF (2)?

Back 18

pre-renal ARF: hyaline casts

renal ARF: granular casts, renal tubular casts

Front 19

Compare pre-renal and renal ARF with regards to:
A. casts seen in UA
B. osmolality ( > or < 500)
C. Na
D. U Cr/ P Cr
E. FE Na

Back 19

Front 20

Which drug can induce acute renal failure in 10-20% of patients on which the drug was used?

A. amioglycoside
B. amphotericin B
C. cyclosporine

Back 20

A. amioglycoside

Delayed onset (7 days) from medication initiation, often non-oliguric.

Front 21

Which drug can induce acute renal failure in 10-20% of patients on which the drug was used?

A. amioglycoside
B. amphotericin B
C. cyclosporine

Back 21

A. amioglycoside

Delayed onset (7 days) from medication initiation, often non-oliguric.

Front 22

What is the definition of chronic kidney disease?

Back 22

structural or functional kidney damage, or substantially decreased GFR of < 60 mL/min

+

persistent for at least 3 months

Front 23

Which are the two most common causes of chronic kidney disease?

A. Diabetic nephropathy
B. Hypertensive glomerulosclerosis
C. Glomerulonephritis
D. Polycistic kidney disease
E. Tubulo-interstitial disease (chronic pyelonephritis, interstitial nephritis, stones, obstruction)

Back 23

A. Diabetic nephropathy
B. Hypertensive glomerulosclerosis

Front 24

Name the two most common causes of chronic kidney disease.

Back 24

Diabetic nephropathy

Hypertensive glomerulosclerosis

Front 25

List the 1-5 stages of chronic kidney disease with description and GFR ranges of each.

Back 25

note stages are based on GFR only, not creatinine or anything else

Front 26

What events lead to Chronic Kidney Disease progression?

Back 26

Front 27

What are the maladaptive functional and structural events that lead to chronic kidney disease progression?

Back 27

Functional: glomerular hypertension and hyperfiltration
Structural: glomerular hypertrophy
BOTH OF THE ABOVE CAUSE
-injury to epithelial and endothelial cells, increase in glomerular permeability, proteinuria
AND THUS
secondary glomerulosclerosis

Other factors contributing to renal damage are:
Glomerular damage: from systemic hypertension, hyperlipidemia with increased mesangial injury
Tubular damage: HYPERparathyroidism with intrarenal Ca Phos precipitation, metabolic acidosis with intrarenal accumulation of ammonia

Front 28

What are treatments directed at slowing renal disease progression?

Back 28

Front 29

________ is as or more important than using ACEI, ARBs when treating to slow renal disease progression.

A. Antihypertensives
B. Calcium channel blockers
C. Lipid lowering agents

Back 29

A. Antihypertensives

Front 30

What are common fluid-electrolyte balances with chronic kidney disease? (3)

Back 30

- By Stage 4, kidney can't handle wide variations in sodium intake
- Urinary concentration and dilution capacity is impaired. Isothenuria refers to fixed urine osmolarity, usually isotonic to plasma (~300 mOsm/L)
- Renal diluting capacity might be compromised, causing hyponatremia

- also watch out for potassium balances as both hyperkalemia and hypokalemia can occur; and acid-base balance disturbances

Front 31

Regarding chronic kidney disease fluid electrolyte disturbances, and potassium balance, which of the following are common causes of hyperkalemia and which are common causes of hypokalemia?

A. dietary indescretion
B. diuretics
C. drugs (ACEI, ARBs, spironolactone, NSAIDs, beta-blockers)
D. hyperaldosteronism
E. hypoaldosteronism
F. metabolic acidosis
G. metabolic alkalosis
H. poor nutrition

Back 31

HYPERkalemia:
A. dietary indescretion
C. drugs (ACEI, ARBs, spironolactone, NSAIDs, beta-blockers)
E. hypoaldosteronism
F. metabolic acidosis


HYPOkalemia:
B. diuretics
D. hyperaldosteronism
G. metabolic alkalosis
H. poor nutrition

Front 32

True or False:

By chronic kidney disease stage 4, patients usually develop metabolic acidosis.

Back 32

True

p. 260

Front 33

True or False:
Anemia is practically universal by CKD stage 3-4.

Back 33

True

It is caused by the lack of EPO production by the kidney. Can give EPO injections, but first make sure any pre-existing iron deficiency is corrected sicne EPO itself induces iron deficiency.

Front 34

Anemia is practically universal by CKD stage 3-4. At what level of EPO is treatment with EPO injection indicated?

Back 34

EPO use if < 11 Hgb

Front 35

Why is there hyperparathyroidism in chronic kidney disease?

Back 35

Early in CKD, the kidney becomes deficient in producing calcitriol. Calcitriol is important for maintaining appropriate calcium and phosphate levels. Lack of calcitriol --> hypocalcemia (early in CKD) and hyperphosphatemia (later in CKD, when kidneys fail to excrete phsohpate) --> PTH overstimulation.

Remember, PTH is stimulated by hypocalcemia and hyperphosphatemia.

Front 36

Hyperparathyroidism is present in chronic kidney disease because, in general, PTH stimulation is triggered by: (2)

A. hypocalcemia
B. hypokalemia
C. hypermagnesia
D. hyperphosphatemia

Back 36

A. hypocalcemia
D. hyperphosphatemia

Early in CKD, the kidney becomes deficient in producing calcitriol. Calcitriol is important for maintaining appropriate calcium and phosphate levels. Lack of calcitriol --> hypocalcemia (early in CKD) and hyperphosphatemia (later in CKD, when kidneys fail to excrete phsohpate) --> PTH overstimulation.

Front 37

Vitamin D production occurs when you go get some sunlight. You skin/diet takes in D3 (cholecalciferol) --> the liver changes that into storage form _______ --> kidney changes that to active form ________

Back 37

D3 --> the liver changes that into storage form 25(OH) D3 calcifediol --> kidney changes that to active form 1,25 (OH)2 D3 calcitriol .

Early in CKD, the kidney becomes deficient in producing calcitriol. Calcitriol is important for maintaining appropriate calcium and phosphate levels. Lack of calcitriol --> hypocalcemia (early in CKD) and hyperphosphatemia (later in CKD, when kidneys fail to excrete phsohpate) --> PTH overstimulation.

Front 38

The main effects of PTH is on on kidney and bones. In early CKD, elevated PTH facilitates Ca reabsorption, calcitriol production, and phos excretion. For some time, the stepwise increases in Ca would lead to normalization of Ca and Phos levels. But in ESRD, when PTH loses its influence on the failing kidney, what happens?

Back 38

Hypocalcemia and hyperphosphatemia get out of hand yet PTH would still be produced moreso. All the PTH will thus work on the bones now since the kidneys are shot. In bones,

Front 39

How do you treat secondary hyperparathyroidism that occurs with CKD?

Back 39

Overall goal should be to suppress parathyroids!

- Phos control with dietary restriction and phosphate binders
- Ca supplementation
- Vitamin D supplementation
- Modification of responsiveness of calcium receptors

Be careful though because overzealous suppression of parathyroids can cause low turnover bone disease.

Front 40

What are some neurologic abnormalities and cardiovascular disease conditions related to chronic kidney disease?

Back 40

Neurologic: Peripheral neuropathies like carpal tunnel syndrome, "stocking glove" distal polyneuropathy, restless leg syndrome

Cardiovascular disease: HTN, accelerated coronary artery disease and peripheral vascular disease due to hyperlipidemia and vascular calcification, pericarditis (part of uremic syndrome)

Front 41

Of the various clinical manifestations of chronic kidney disease, which is the #1 cause of mortality?

A. fluid-electrolyte imbalances
B. anemia
C. uremic osteodystrophy (bone disease)
D. cadiovascular disease
E. neurologic abnormalities
F. GI symptoms

Back 41

D. cadiovascular disease

Front 42

What is the definition of End Stage Renal Disease?

Back 42

the final phase of CRF, when kidneys have failed and life is conditional on renal replacement therapy. Renal replacement therapy applies to dialysis or transplantation- the only available treatments for ESRD.

Front 43

[ Hemodialysis / Hemofiltration ] is a renal replacement therapy, which involves diffusion of blood solute across a semi-permeable membrane; [ hemodialysis / hemofiltration ] is a renal replacement therapy, which involves ultrafiltration (transfer of solute molecules by water flux) of blood solute across a semi-permeable membrane.

Back 43

HEMODYALISIS is a renal replacement therapy, which involves diffusion of blood solute across a semi-permeable membrane; HEMOFILTRATION is a renal replacement therapy, which involves ultrafiltration (transfer of solute molecules by water flux) of blood solute across a semi-permeable membrane.

Front 44

What are the indications for acute dialysis in renal failure? (5)

Back 44

1. Hyperkalemia
2. Volume overload
3. Intractable acidosis
4. Uremic pericarditis
5. Uremic encephalopathy

Front 45

What are the indications for acute dialysis in renal failure? (5)

Back 45

1. Hyperkalemia
2. Volume overload
3. Intractable acidosis
4. Uremic pericarditis
5. Uremic encephalopathy

Front 46

What are the indications for acute dialysis in renal failure? (5)

Back 46

1. Hyperkalemia
2. Volume overload
3. Intractable acidosis
4. Uremic pericarditis
5. Uremic encephalopathy

Front 47

What are the indications for acute dialysis in renal failure? (5)

Back 47

1. Hyperkalemia
2. Volume overload
3. Intractable acidosis
4. Uremic pericarditis
5. Uremic encephalopathy

Front 48

What are the indications for chronic dialysis? (2)

Back 48

Early uremic signs and / or GFR < 15 mL/min

Uremic syndrome is a combo of signs and symptoms of severe prolonged renal dysfunction. Uremic syndrome requires institution of renal replacement therapy. Most prominent features are: uremic encephalopathy, severe fatigue, anorexia, nausea, vomiting, pericarditis.

Front 49

What are the indications for chronic dialysis? (2)

Back 49

Early uremic signs and / or GFR < 15 mL/min

Uremic syndrome is a combo of signs and symptoms of severe prolonged renal dysfunction. Uremic syndrome requires institution of renal replacement therapy. Most prominent features are: uremic encephalopathy, severe fatigue, anorexia, nausea, vomiting, pericarditis.

Front 50

There are several types of solute transport when it comes to renal replacement therapy. Differentiate continuous veno-venous hemofiltration from hemodialysis.

Back 50

CVVH is based on ultrafiltration, where the solute of appropriate size is dragged across the membrane with water. Hemodialysis, on the other hand is based on diffusion, where equilibration of solute across a semi-permeable membrane occurs according to the concentration gradient.

Front 51

What are complications of chronic dialysis? (8)

Back 51

- Hypotension (due to delayed mobilization of interstitial fluid)
- Hypertension (RAS activation due to volume removal)
- Anaphylactoid reactions to dialyzer membrane
- Muscle cramps
- bleeding
- electrolyte disturbances
- air embolism
- dialysis dysequilibirum

Front 52

What is the preferred modality for each circumstance - peritoneal dialysis or hemodialysis?

1. abdominal surgery
2. coagulopathy
3. elderly patient
4. large body habitus
5. severe CHF

Back 52

1. abdominal surgery - HD
2. coagulopathy - PD
3. elderly patient - HD
4. large body habitus - HD
5. severe CHF - PD

Front 53

What are complications of chronic dialysis?

Back 53

CARDIOVASCULAR DISEASE!
- HTN, CHF, Accelerated CAD and PVD

Other:
- Malnutrition
- Secondary PTH
- Arthritis
- dialysis dementia
-

Front 54

Although MHC or HLA antigens are important, except in a 6 antigen match (perfect match), graft survival [ does / does not ] correlate with the degree of match so long as there is ABO compatibility and the cross match is negative.

Back 54

Graft survival DOES NOT correlate with the degree of match so long as there is ABO compatibility and the cross match is negative.

Front 55

Although MHC or HLA antigens are important, except in a 6 antigen match (perfect match), graft survival does not correlate with the degree of match so long as... [ what 2 things ] ?

Back 55

there is ABO compatibility and the cross match is negative

Front 56

True or False:
Living donor even if unrelated has a better 1 year graft survival than deceased donor.

Back 56

True

Front 57

Who can be a kidney donor?

Back 57

Individuals between 18 and 65 years of age can be considered.

The potential donor may not have HTN, diabetes mellitus, proteinuria or potentially transmissible diseases.

Front 58

Do the donor and recipient have to share a certain number or percentage of HLA antigens?

Back 58

No. The donor and receipient may have no HLA antigens in common but they must be ABO compatible and crossmatch negative.

Front 59

Just for fun:

The half-life of a cadaveric kidney is approximately 7-10 years whereas the half-life of a living donor kidney is approximately 15-20 years.

Back 59

The half-life of a cadaveric kidney is approximately 7-10 years whereas the half-life of a living donor kidney is approximately 15-20 years.

Front 60

What are the reasons for allograft non-function?

Back 60

Front 61

What is the primary cause of nonfunction?

A. Hypovolemia
B. Ureteral necrosis.leak
C. Thrombosis of renal artery or vein
D. ATN (acute tubular necrosis)
E. Drug toxicity (calcineurin inhibitors are more common)
F. Rejection

Back 61

D. ATN (acute tubular necrosis)

Front 62

Which transplant rejection is detailed?

Occurs immediately on operating table after clamps released- kidney becomes flaccid and cyanotic.

A. Hyperacute rejection
B. Accelerated acute rejection
C. Acute rejection
D. Chronic rejection

Back 62

A. Hyperacute rejection

Front 63

Which transplant rejection is detailed?

Rare event due to advanced crossmatch techniques.

A. Hyperacute rejection
B. Accelerated acute rejection
C. Acute rejection
D. Chronic rejection

Back 63

A. Hyperacute rejection

Front 64

Which transplant rejection is detailed?

occurs on post-op day 5-7, manifests as oligoanuria and graft dysfunction and may occur in presence of antibody directed against donor vascular endothelial cells.

A. Hyperacute rejection
B. Accelerated acute rejection
C. Acute rejection
D. Chronic rejection

Back 64

B. Accelerated acute rejection

Front 65

Which transplant rejection is detailed?

Generally occurs in first 3-6 months after transplantation. Classic signs of fever, edema and graft tenderness. Elevation of serum creatinine, diminished urine ouput, edema

A. Hyperacute rejection
B. Accelerated acute rejection
C. Acute rejection
D. Chronic rejection

Back 65

C. Acute rejection

Front 66

Which transplant rejection is detailed?

The most common type of allograft rejection.

A. Hyperacute rejection
B. Accelerated acute rejection
C. Acute rejection
D. Chronic rejection

Back 66

C. Acute rejection

Front 67

Which transplant rejection is detailed?

Hallmarks are progressive azotemia, proteinuria, HTN. All components of renal parenchyma involved.

A. Hyperacute rejection
B. Accelerated acute rejection
C. Acute rejection
D. Chronic rejection

Back 67

D. Chronic rejection

Front 68

Cyclosporine and Tacrolimus are calcineurin inhibitors, a class that has revolutionized transplantation. How does this class work?

Back 68

Calcineurin inhibition impairs the expression of several critical cytokines that promote T cell activation (IL-2, IL-4, IFN-gamma, TNF). Thus, decreases the "revving up" of T-cells while not totally abolishing them such that patients are able to maintain a degree of immune responsivenss that is still efficient to maintain host defenses.

Side effects: multiple drug intrxs, HTN, neurotox, GI tox, Hepatic dysfunction, hyperlipidemia, NEPHROTOXICITY (!)

Front 69

It is very difficult to distinguish chronic calcineurin inhibitor toxicity from

A. acute nephrotoxicity
B. chronic nephrotoxicity

Back 69

B. chronic nephrotoxicity

both look the same histologically - all components of the parenchyma are involved. Glomeruli has wrinkled basement membrane, increased mesangial matrix, sclerosis. Tubules atrophy, Fibrosis occurs in interstitium.

Front 70

True or False:
Cardiovascular disease is the leading cause of death in renal allograft recipients.

Back 70

FALSE.

Cardiovascular disease is the leading cause of death in ESRD patients but in those that have recieved renal allografts, INFECTION is the leading cause of death!

Front 71

What are the macrovascular and microvascular complications of diabetes mellitus?

Back 71

Macrovascular complications are associated with accelerated atherosclerosis: coronary artery disease (MI), cerebrovascular disease (strokes), peripheral vascular disease (gangrenous limbs)

Microvascular complications: retinopathy (blindness), neuropathy, demopathy, NEPHROPATHY

Front 72

Diabetic nephropathy is a microvascular complication of diabetes mellitus that is characterized by progressive development of what three things?

Back 72

microalbuminuria (not picked up by urine dipstick), macroalbuminuria (picked up by urine dipstick), renal failure

Front 73

What are some risk factors for developmentn of diabetic nephropathy if you are diabetic?

Back 73

- Being African American, Hispanic, or American Indian
- Family history of kidney disease
- High blood pressure
- Type 1 diabetes before age 20
- smoking
- Retinopathy

Front 74

Diabetic nephropathy is rare before 10 years of diabetic mellitus onset, peaks at _________ years. The patient not affected by ______ is unlikely to get the disease.

Back 74

peaks at 10-15 years, but if unaffected by 20 years then they are unlikely to get the disease

Front 75

______% of diabetics develop renal failure and it has a familial predisposition

Back 75

25-30% of diabetics develop renal failure and it has a familial predisposition

Front 76

What are the clinical stages of Diabetic Nephropathy?

Back 76

Front 77

Match the histopathology to the correct clinical stage of diabetic nephropathy. (clinical latency, microalbuminuria stage, macroalbuminuria stage to renal failure stage)

- mesangial matrix expansion
- glomerular basement membrane (GBM) thickening
- Kimmerstiel-Wilson nodules
- gloemrular hypertrophy
-arteriosclerosis and hyalinosis

Back 77