The FNP Review

The 4 Nephrology Concepts Every FNP Student Must Master Before Board Day

Nephrology · 4 min read · September 18, 2026

Decoding Acute Kidney Injury: Prerenal Versus Intrinsic

Nephrology questions on the AANP and ANCC exams love to test your ability to differentiate the causes of Acute Kidney Injury (AKI). When a patient presents with a sudden rise in serum creatinine and BUN, your very first step is to determine if the insult is prerenal, intrinsic, or postrenal. Prerenal azotemia is all about perfusion. Think of it as a plumbing problem upstream: decreased blood flow to the kidneys due to dehydration, heart failure, or sepsis. Because the kidney parenchyma is initially intact, the tubules desperately try to hold onto sodium and water.

To ace these questions on exam day, you must memorize the hallmark lab findings. In prerenal AKI, the BUN-to-creatinine ratio is typically greater than 20:1, the fractional excretion of sodium (FENa) is less than 1%, and urine sodium is low (under 20 mEq/L) because the tubules are reabsorbing everything they can. Conversely, intrinsic AKI—most commonly Acute Tubular Necrosis (ATN) from ischemia or nephrotoxins like contrast dye or NSAIDs—features a BUN-to-creatinine ratio around 10:1 to 15:1, a FENa greater than 2%, and the presence of muddy brown casts on microscopic urinalysis.

Clinical Pearl: Always check the medication list for recent NSAID or ACE inhibitor use when evaluating an unexplained bump in creatinine. ACE inhibitors dilate the efferent arteriole, dropping glomerular filtration pressure—a major trigger for prerenal azotemia in vulnerable patients.

Chronic Kidney Disease Staging and Complications

Chronic Kidney Disease (CKD) is staged from 1 to 5 based on the Glomerular Filtration Rate (GFR), regardless of the underlying etiology. Stage 1 indicates normal or high GFR (greater than 90 mL/min/1.73m²) with structural kidney damage, while Stage 5 represents Kidney Failure (GFR less than 15 mL/min/1.73m²). Board questions frequently test your management of CKD complications rather than just the staging itself. As kidney function declines, the failing nephrons can no longer hydroxylate Vitamin D into its active form, leading to decreased calcium absorption and secondary hyperparathyroidism.

Furthermore, the failing kidneys lose their ability to excrete phosphorus and clear erythropoietin. This results in hyperphosphatemia, hypocalcemia, and normocytic anemia of chronic disease. You must also remember to screen for proteinuria using the urine albumin-to-creatinine ratio (uACR). If a patient with diabetes or hypertension develops persistent microalbuminuria, initiating an ACE inhibitor or ARB is gold-standard practice to reduce intraglomerular pressure and slow disease progression.

Board Tip: Do not panic if a patient's serum creatinine bumps by up to 30% after starting an ACE inhibitor or ARB. This is a normal hemodynamic response to efferent arteriole dilation, provided hyperkalemia does not develop. Do not immediately stop the medication!

Urinalysis Interpretation: Spotting the Clues

Microscopic urinalysis is a staple of primary care and a frequent testing point on certification boards. When looking at sediment analysis, certain findings point directly to specific glomerular or tubular pathologies:

  • Red blood cell (RBC) casts: Pathognomonic for glomerulonephritis (such as post-streptococcal glomerulonephritis or IgA nephropathy).
  • White blood cell (WBC) casts: Highly indicative of acute pyelonephritis or tubulointerstitial nephritis.
  • Hyaline casts: Often normal, seen after strenuous exercise or mild dehydration.
  • Broad and waxy casts: Signify chronic, severe renal failure due to dilated, fibrotic tubules.

When evaluating a patient with painless hematuria, always consider the patient's age and smoking history. In older adults, gross or microscopic hematuria must be evaluated with a urology referral and cystoscopy to rule out bladder or renal cell carcinoma, even if a urinary tract infection is treated.

Electrolyte Imbalances Secondary to Renal Dysfunction

Because the kidneys are the master regulators of fluid and electrolyte balance, renal failure inevitably triggers cascading electrolyte shifts. Hyperkalemia is the most feared complication because of its potential to cause fatal cardiac arrhythmias. On an ECG, mild-to-moderate hyperkalemia presents with tall, peaked T-waves. As potassium climbs higher, you will see prolonged PR intervals, widened QRS complexes, and eventually a sine wave pattern.

Management of severe hyperkalemia follows a logical acute sequence: first, protect the myocardium with intravenous calcium gluconate or calcium chloride. Next, shift potassium intracellularly using a combination of regular insulin with dextrose, inhaled albuterol, or sodium bicarbonate. Finally, remove potassium from the body using diuretics, gastrointestinal binders (like sodium zirconium cyclosilicate), or emergency hemodialysis.

Clinical Pearl: Never administer potassium supplements to a patient with Stage 4 or Stage 5 CKD without careful monitoring, and always review their medication profile for potassium-sparing diuretics, spironolactone, and ACE inhibitors that can synergistically push them into dangerous hyperkalemia.

You have got this! Nephrology can feel intimidating with all its numbers and pathways, but breaking it down into core physiological principles makes it entirely manageable. Keep pushing forward, trust your clinical reasoning, and remember that every practice question brings you one step closer to earning those coveted FNP letters.