CKD / ESRD

Question 1

CKD is a risk factor for cardiovascular disease. Do most patients die from CV causes or ESRD?

Answer 1

CV causes before ESRD even develops

Question 2

What is a normal GFR vs. a GFR that indicates kidney failure?

Answer 2

• Normal: greater than 90 mL/min

- Kidney failure: less than 15 mL/min

Question 3

Current staging of CKD is based on:

Answer 3

MDRD (Modified Diet in Renal Disease) classification

Question 4

What factors does MDRD take into consideration?

Answer 4

serum creatinine, age, gender, race

Question 5

What is a more accurate predictor of eGFR that is now used by Loyola?

Answer 5

CKD EPI equation (correlates even better w/ CKD mortality and overall mortality)

Question 6

Can formulas for calculation of eGFR be used in AKI?

Answer 6

No, because the patient has to be in a steady state.

Question 7

What are the 2 main causes of CKD?

Answer 7

1) Diabetes

2) HTN

Question 8

Aside from diabetic and hypertensive nephropathy, what are some other causes of CKD?

Answer 8

• Renovascular disease
• Atheroembolic disease
• Glomerulonephritis/nephrotic syndrome
• Polycystic kidney disease

Question 9

What is the treatment of diabetic nephropathy?

Answer 9

tight control of diabetes early in the diagnosis and ACEI/ARBs for BP control

Question 10

What are the main differences between diabetic nephropathy in type I vs. type II DM?

Answer 10

• Type I: occurs 15 years after diagnosis; retinopathy precedes nephropathy
• Type II: occurs 5-10 years after diagnosis; retinopathy does NOT always precede nephropathy

Question 11

What is a contributing factor to the fact that African Americans are at an 8-fold increased risk of hypertensive nephropathy?

Answer 11

APOL-1 gene variation

Question 12

Describe the pathogenesis of hypertensive nephropathy.

Answer 12

Hyaline arteriosclerosis (medial thickening) of small arteries/arterioles in kidneys along w/ focal and segmental sclerosis and interstitial fibrosis. Proteinuria is present but usually less than 1 g/day.

Question 13

Why are ACEIs/ARBs a better choice than vasoactive mediators in treating diabetic nephropathy?

Answer 13

Vasoactive mediators act on the afferent arteriole and cause increased pressure (efferent arteriole is still constricted). ACEIs and ARBs act on the efferent arteriole to dilate it (block the effect of Ang II, thereby blocking vasoconstriction at the efferent arteriole), reduce glomerular pressure, and therefore reduce hyperfiltration injury.

Question 14

What are the main causes of renal artery stenosis (as in renovascular disease)?

Answer 14

• Atherosclerotic plaques (proximal 1/3 of renal artery, common in older males and smokers)
• Fibromuscular dysplasia (distal 2/3 of renal artery, young or middle-aged females)

Question 15

Fibromuscular dysplasia is a cause of renal artery stenosis (and therefore secondary HTN) in predominantly which patient population?

Answer 15

young or middle-aged females

Question 16

How does fibromuscular dysplasia present?

Answer 16

refractory HTN with negative FH and abdominal bruit on exam

Question 17

Describe the pathogenesis of fibromuscular dysplasia.

Answer 17

Chronic ischemia (due to renal artery stenosis of the distal 2/3) leads to cortical thinning and small kidneys. Decreased renal perfusion leads to a high-renin state, contributing to HTN.

Question 18

What is the best/easiest way to diagnose polycystic kidney disease?

Answer 18

ultrasound

Question 19

What is the clinical presentation of a person with polycystic kidney disease?

Answer 19

hematuria, flank pain, kidney stones; there also may be concomitant liver cysts, diverticulosis, MV prolapse, and intracranial aneurysms

Question 20

What is the etiology of cholesterol atheroembolic disease?

Answer 20

severe atherosclerotic disease; generally occurs after an intervention (angiogram, vascular surgery), but may also occur spontaneously due to hemodynamic stress

Question 21

Describe the pathogenesis of cholesterol atheroembolic disease.

Answer 21

cholesterol released from atheromatous plaque in bloodstream –> small particles lodge in small blood vessels of the kidney

Question 22

What are the clinical manifestations of cholesterol atheroembolic disease?

Answer 22

fever, malaise, digital gangrene, livedo reticularis rash, renal failure

Question 23

In individuals with ADPKD, when does renal failure typically occur?

Answer 23

in 50s-60s

Question 24

How is CKD managed with “conservative renoprotection” in stage II/III?

Answer 24

• Healthy living (smoking cessation, exercise to decrease body weight)
• BP and lipid control
• Glycemic control (diabetics)
• Managing co-existing liver and/or cardiac disease
• ACEI/ARB therapy
• Med dose adjustment per eGFR
• Avoid nephrotoxic agents (NSAIDs)

Question 25

What is a key step in managing CKD stage III-IV?

Answer 25

Proteinuria reduction! The goal is <3 g/day, as control of proteinuria slows CKD progression. This is usually done through ACEI/ARB therapy, although reducing dietary intake also helps.

Question 26

What is a key step in managing CKD stage III-V?

Answer 26

Hypertension control! With CKD, there is sodium and water retention due to decreased GFR and a high renin state. Reducing sodium to <2000 mg/day along with weight loss and smoking cessation are great lifestyle changes that can help manage HTN.

Question 27

Patients with CKD should avoid foods high in _________. Examples include:

Answer 27

phosphorus; dairy products, dried beans, processed meat, chocolate, colas, biscuit and pancake mix, liver/organ meats, nuts, seeds

Question 28

What are the contributing factors to anemia in CKD?

Answer 28

• Decreased EPO synthesis
• Iron deficiency and transport dysregulation
• Decreased erythrocyte HL
• Blood loss in dialysis patients

Question 29

What are the long-term effects of metabolic acidosis in CKD?

Answer 29

• progression of CKD by accelerating interstitial fibrosis

- bone resorption and osteopenia (osteodystrophy)