Critical Care & Adv Nephrology Final - Lecture 4 Chronic Kidney Disease (CKD)

Dr. Schonder: Slide Sledge Hammer Approach

What is the Cockcroft-Gault equation for estimating creatinine clearance?

CrCl = [(140 − age) × IBW] / (SCr × 72), × 0.85 if female

What is the equation for ideal body weight (IBW) in males?

IBW = 50 kg + (2.3 × inches > 60)

What is the equation for ideal body weight (IBW) in females?

IBW = 45.5 kg + (2.3 × inches > 60)

What is a major limitation of the Cockcroft-Gault equation in patients with CKD?

It overestimates GFR in patients with CKD

JD is a 68-year-old female, 5'5" tall. What is her ideal body weight?

57 kg

JD is a 68-year-old female, 5'5", weighs 150 lbs, SCr 1.4 mg/dL. Using Cockcroft-Gault, her estimated CrCl is closest to:

~35 mL/min

Per KDIGO, the definition of CKD is:

GFR < 60 mL/min/1.73 m² for > 3 months and/or markers of kidney damage

Which of the following is a marker of kidney damage used in the CKD definition?

Albuminuria

A patient has a GFR of 50 mL/min/1.73 m². What CKD stage?

G3a

A GFR of 28 mL/min/1.73 m² corresponds to which CKD stage?

G4

What GFR range defines CKD stage G5 (kidney failure)?

< 15 mL/min/1.73 m² (or on dialysis)

A patient has an albumin excretion rate of 200 mg/24 hr. This corresponds to:

A2 (Moderately increased)

Albuminuria category A3 (severely increased) is defined as:

300 mg/g

In stages 1 & 2 CKD, GFR can decrease by approximately how much before SCr rises above the normal range?

Up to 50%

Which signs/symptoms are most characteristic of Stage 5 CKD?

Pruritus, intractable N/V, asterixis, myoclonus, uremia

What are the two major mechanisms causing proteinuria in CKD?

Increased glomerular pressure (hyperfiltration) and glomerular/tubular endothelial injury

Which adaptive change in the remaining nephrons leads to glomerulosclerosis and progression of CKD?

Hyperfiltration with increased glomerular capillary pressure

What dietary protein intake does KDIGO recommend for patients with CKD stages 3–5?

0.8 g/kg/day; avoid > 1.3 g/kg/day

In a metabolically stable patient with CKD, what very-low-protein diet may be considered (with supplementation)?

0.3–0.4 g/kg/day with essential amino acids or ketoacid analogs

What is first-line pharmacologic therapy for albuminuria category A2 (uACR > 30 mg/g) in CKD?

ACEi or ARB (RAS inhibitor)

RAS inhibitors used for proteinuria in CKD should be:

Titrated to the maximum tolerated dose

RAS inhibitors for proteinuria in CKD are recommended:

Regardless of GFR category

If hyperkalemia develops in a patient on a RAS inhibitor for CKD, what is the preferred initial step?

Treat the hyperkalemia (diet, K⁺ binders) and continue RAS inhibitor at maximally tolerated dose

A patient on a RAS inhibitor for proteinuria has persistent hyperkalemia despite dietary changes and a K⁺ binder. The next step is:

Consider stopping the RAS inhibitor if hyperkalemia cannot be controlled

SGLT2 inhibitors are first-line for proteinuria in patients with type 2 DM and CKD when eGFR is:

20 mL/min/1.73 m²

Dapagliflozin is FDA-approved for use in CKD when eGFR is:

25 mL/min/1.73 m²

Empagliflozin is approved for CKD when eGFR is:

30 mL/min/1.73 m²

If eGFR falls below 20 mL/min/1.73 m² in a patient already on an SGLT2 inhibitor for CKD, the recommendation is to:

Continue the SGLT2 inhibitor until dialysis or transplant (do not initiate new therapy below this threshold)

Mineralocorticoid receptor antagonists (e.g., finerenone) are indicated for proteinuria in CKD with all of the following criteria:

Type 2 DM, eGFR > 25 mL/min/1.73 m², normal K⁺, albuminuria > 30 mg/g despite max RASi

A renal effect of MRAs in CKD that supports their use is:

Decreased albumin excretion

What are the main mechanisms underlying hypertension in CKD?

Increased sodium retention, RAS hyperactivity, and adaptive responses

Per the KDIGO 2021 BP guideline, the goal blood pressure for adults with CKD is:

SBP < 120 mmHg (when tolerated, using standardized office BP)

First-line antihypertensive class in CKD with albuminuria:

ACEi or ARB

Which adaptive responses occur in CKD to attempt to maintain Na/water homeostasis?

↑ ANP, ↑ fractional excretion of Na in remaining nephrons, osmotic diuresis

As CKD progresses, what is the net effect of impaired Na and water handling?

Volume overload (and HTN)

As CKD progresses, sodium handling shifts in which way?

↓ Na glomerular filtration and ↑ Na tubular excretion (per nephron compensation)

Nocturia in CKD typically begins to present at which stage?

Stage 3

Which of the following best describes water handling adaptation in early-to-mid CKD?

Osmotic diuresis develops in remaining nephrons, leading to inability to concentrate urine and nocturia

For a CKD patient with NO hypertension or edema, dietary sodium restriction:

Is not recommended; the kidney cannot adequately decrease urinary Na content, and restriction may cause negative Na balance

For a CKD patient WITH hypertension or edema, sodium restriction:

Is recommended (reduces intravascular volume)

In CKD, fluid restriction is generally:

Not necessary until ESRD

In ESRD, what is the necessary intervention for refractory volume overload?

Renal replacement therapy (dialysis)

First-line diuretic class for fluid management in advanced CKD:

Loop diuretics (e.g., furosemide)

Why do thiazide diuretics lose effectiveness as CKD progresses?

Decreased tubular secretion in CKD limits delivery to the site of action

As CKD progresses, achieving adequate diuresis with loop diuretics generally requires:

Higher doses to overcome decreased tubular secretion

Recommended management of diuretic tolerance that develops with prolonged loop diuretic use in CKD:

Add a second diuretic from a different class (e.g., thiazide for sequential nephron blockade) and use higher doses to achieve effect

When initiating diuretic therapy in CKD, the recommended approach is:

Start at the lowest dose and titrate up

The primary mechanism leading to hyperkalemia in CKD is:

Decreased renal K⁺ excretion (↓ glomerular filtration AND ↓ distal tubular secretion)

Overt hyperkalemia in CKD typically develops when eGFR falls below:

20 mL/min/1.73 m²

What is the goal pre-hemodialysis serum potassium level?

4.5–5.5 mEq/L

What dietary potassium restriction is recommended for CKD with hyperkalemia?

50–80 mEq/day

Which non-pharmacologic measure also helps control hyperkalemia in CKD?

Maintaining a good bowel regimen (avoid constipation)

For severe hyperkalemia in ESRD, the treatment of choice is:

Dialysis (with adjustment of dialysate K⁺ concentration)

Which class of antihypertensive can inhibit the Na⁺/K⁺ ATPase pump and worsen hyperkalemia?

Beta-blockers

Which class of diuretics can be used to increase K⁺ excretion in CKD with hyperkalemia?

Loop diuretics

What is the mechanism of action of patiromer?

Non-absorbed cation exchanger that exchanges Ca²⁺ for K⁺ in the distal colon

What is the onset of action of patiromer?

~7 hours (max effect in 48 hours)

What is the standard initial dose of patiromer (Veltassa)?

8.4 g daily (max 25.2 g/day)

Patiromer should be separated from other oral medications by:

3 hours before/after

Which adverse effect is associated with patiromer?

↓ Mg levels (along with diarrhea/constipation)

What is the mechanism of action of sodium zirconium cyclosilicate (Lokelma)?

Inorganic cation-exchange crystal that exchanges Na⁺ for K⁺ throughout the GI tract

What is the onset of action of sodium zirconium cyclosilicate?

~1 hour (max effect in 48 hours)

What is the typical initial/maintenance dosing of sodium zirconium cyclosilicate?

10 g TID initial; 10 g daily maintenance

Sodium zirconium cyclosilicate should be separated from other oral drugs by:

2 hours before/after

Which adverse effect is most associated with sodium zirconium cyclosilicate?

Edema (due to Na⁺ load)

Sodium polystyrene sulfonate (SPS) acts as a:

Non-absorbed cation exchanger that exchanges Na⁺ for K⁺ in the distal colon

What is the onset of action of sodium polystyrene sulfonate?

~6 hours (max effect in 72 hours)

The dose range for sodium polystyrene sulfonate is:

15–60 g PO or PR

A serious (rare) adverse effect associated with sodium polystyrene sulfonate is:

Serious GI adverse events (e.g., intestinal necrosis)

What is the mechanism of action of fludrocortisone in treating hyperkalemia?

Mineralocorticoid that stimulates aldosterone activity to increase renal K⁺ excretion

What is the standard dose of fludrocortisone for hyperkalemia?

0.1 mg daily (max 0.3 mg/day)

What is the onset of action of fludrocortisone for K⁺-lowering?

Several days

A key adverse effect that limits fludrocortisone use in CKD is:

Hypertension and edema (due to mineralocorticoid Na⁺ retention)

Which K⁺ binder has the FASTEST onset of action?

Sodium zirconium cyclosilicate (~1 hr)

Which K⁺ binder exchanges calcium (rather than sodium) for potassium?

Patiromer

Which K⁺ binder is most likely to cause edema due to its sodium load?

Sodium zirconium cyclosilicate

Which K⁺ binder is most associated with hypomagnesemia?

Patiromer

As functional nephron mass decreases in CKD, which adaptive response in remaining nephrons drives ongoing nephron damage?

Hyperfiltration with ↑ glomerular capillary pressure → glomerulosclerosis and proteinuria

Which is an adaptive response that helps maintain potassium homeostasis until late CKD?

Increased K⁺ secretion in remaining functioning nephrons and increased GI K⁺ excretion

A patient with eGFR 60–89 (G2) has severely increased albuminuria (A3). The recommended action per KDIGO is:

Refer to nephrology