FNP Chronic Kidney Disease Practice Questions

Mild hyperkalemia up to 5.5 mEq/L is common when treating diabetic nephropathy with an ACE inhibitor. Because the renal protective benefits of the drug are crucial and the creatinine is stable, the best initial approach is to implement a low-potassium diet rather than stopping the medication. Option A is incorrect because stopping the drug deprives the patient of essential proteinuria reduction, and 5.2 mEq/L is not acutely life-threatening. Option C is incorrect because while a thiazide might lower potassium, it lacks the specific renoprotective effects needed for diabetic nephropathy. Option D is a massive overreaction, as mild asymptomatic hyperkalemia in the outpatient setting does not require inpatient cardiac monitoring.

For African American patients with hypertension and diabetes, but without chronic kidney disease or proteinuria, initial therapy should be a calcium channel blocker or a thiazide diuretic. Amlodipine is the best choice here. Lisinopril and losartan are indicated if the patient had an elevated urine microalbumin-to-creatinine ratio, but his is normal. Metoprolol is a beta-blocker and is not recommended as first-line therapy for essential hypertension without a specific compelling indication like heart failure or post-myocardial infarction.

When initiating an ACE inhibitor, it is standard practice to evaluate the serum creatinine and potassium levels within one to four weeks to ensure the patient is not developing hyperkalemia or an unacceptable decline in renal function. Option B is incorrect because waiting six months delays the detection of potential early adverse pharmacotherapeutic outcomes. Option C is incorrect because drawing labs the very next day does not allow enough time for the medication to reach steady state and exert its hemodynamic effects on the kidneys. Option D is unnecessary because a normal baseline metabolic panel does not warrant a 24-hour urine collection for uncomplicated essential hypertension.

KDIGO guidelines strongly recommend adding an SGLT2 inhibitor for patients with type 2 diabetes and CKD who have an eGFR of at least 20 mL/min/1.73 m2, due to significant cardiovascular and renal benefits. Adding a sulfonylurea (A) or switching to a DPP-4 inhibitor (B) might improve glycemic control but neither provides the targeted renoprotective effects that slow CKD progression. Referring for renal replacement therapy (D) is incorrect because an eGFR of 35 indicates stage 3b CKD, which is managed medically and does not yet require dialysis or transplantation.

A UACR between 30 and 300 mg/g indicates moderately increased albuminuria. Adding an ACE inhibitor or ARB is the standard of care to reduce proteinuria and slow the progression of chronic kidney disease. Option A is incorrect because amlodipine, a calcium channel blocker, does not offer targeted renal protection against albuminuria. Option C is incorrect because beta blockers do not reduce proteinuria and are not first-line for uncomplicated hypertension. Option D is premature; nephrology referral is typically reserved for Stage 4 CKD (eGFR < 30) or rapidly progressing disease.

The diagnosis of Stage 5 chronic kidney disease, also known as kidney failure, is established when the estimated glomerular filtration rate falls below 15 mL/min/1.73 m². This patient's eGFR of 12, which has been persistently low for six months, confirms Stage 5 disease. Additionally, his UACR of 450 is well above the 300 mg/g threshold, placing him in the A3 category for severely increased albuminuria. Option A is incorrect because Stage 4 indicates an eGFR of 15 to 29, and moderately increased albuminuria is 30 to 300 mg/g. Option C is incorrect because it misidentifies the eGFR stage as Stage 4. Option D is incorrect because it underestimates the severity of the albuminuria, categorizing it as moderate rather than severe.

An increase in serum creatinine of up to 30 percent is an expected hemodynamic response when initiating an ACE inhibitor due to efferent arteriole dilation. The patient's creatinine went from 1.0 to 1.25, which is a 25 percent increase and well within the acceptable range. Option B is incorrect because a dose reduction is unnecessary for an expected physiologic response. Option C is incorrect because discontinuing the drug deprives this diabetic patient of vital renal protection. Option D is incorrect because evaluating for bilateral renal artery stenosis is only indicated if the creatinine increases by more than 30 percent. Continuing the medication and monitoring routinely is the safest and most appropriate management plan for this patient.

This patient's presentation of severe volume loss from gastroenteritis combined with a BUN to creatinine ratio of 30:1 strongly indicates prerenal acute kidney injury. In prerenal states, decreased renal perfusion prompts increased urea reabsorption relative to creatinine, typically elevating the ratio above 20:1. Intrinsic acute tubular necrosis usually presents with a ratio of less than 15:1 because the damaged tubules cannot effectively reabsorb urea. Advanced chronic kidney disease would show long-standing structural changes and a relatively normal ratio rather than this acute, disproportionate BUN elevation. Postrenal obstructive nephropathy typically requires a history of urinary retention, prostatic hypertrophy, or nephrolithiasis, none of which are present here.

For patients who cannot tolerate dopamine agonists, alpha-2-delta ligands are the preferred alternative. However, medications like gabapentin and pregabalin undergo renal clearance and require strict dose reductions in the setting of chronic kidney disease. Initiating a renally adjusted gabapentin dose ensures safe symptom management while preventing medication toxicity and excessive somnolence. Prescribing a standard pregabalin or gabapentin enacarbil dose is unsafe for a patient with an estimated glomerular filtration rate of 28, as it will lead to rapid drug accumulation. Recommending ropinirole is incorrect because the patient has a documented intolerance to dopamine agonist therapy.

For patients with type 2 diabetes, chronic kidney disease, and severe albuminuria, ADA guidelines recommend an SGLT2 inhibitor to slow kidney disease progression and reduce cardiovascular events. This patient's eGFR of 42 and elevated albumin-to-creatinine ratio make this the optimal choice. Adding a thiazolidinedione does not specifically protect renal function and can cause fluid retention. Adding a GLP-1 agonist is an acceptable alternative if SGLT2 inhibitors are contraindicated, but it is not the first-line preference for primary renal protection in the presence of significant albuminuria. Adding a DPP-4 inhibitor offers mild glycemic control without the necessary renal protective benefits required for this patient's advancing nephropathy.