NCLEX Renal and GU Review: AKI, CKD, and Dialysis

Quick answer: For the NCLEX, renal and GU questions reward a few patterns: sort AKI into prerenal (BUN:creatinine above 20:1, restore perfusion), intrarenal (ATN, muddy brown casts, specific gravity fixed near 1.010), or postrenal (relieve the obstruction); stage CKD by GFR; protect the dialysis access arm; treat cloudy peritoneal dialysis effluent as peritonitis until proven otherwise; and tell nephrotic (massive proteinuria) from nephritic (hematuria with RBC casts) syndrome.

Renal and genitourinary content shows up on every NCLEX because fluid balance, electrolytes, and drug clearance all live in the kidneys. Get this system down and a huge chunk of pharmacology, cardiac, and acid-base questions start answering themselves. This review covers AKI, CKD, dialysis, UTIs, BPH, renal calculi, and the glomerular syndromes the NCLEX loves to test.

Key takeaways

• AKI sorts into three categories: prerenal (perfusion problem, BUN:Cr greater than 20:1, fix the volume), intrarenal (kidney tissue damage like ATN, BUN:Cr near 10:1, muddy brown casts), and postrenal (obstruction, relieve it).
• The oliguric phase of AKI is the most dangerous: watch for fluid overload, hyperkalemia, and metabolic acidosis.
• CKD is staged by GFR; its complications (anemia, CKD-MBD, hyperkalemia, acidosis, fluid overload, uremia) drive the priority questions.
• Hemodialysis access arm rules are finite and testable: no BP, no IV/venipuncture, no constriction or heavy lifting, and assess for thrill and bruit every shift.
• Cloudy peritoneal dialysis effluent is peritonitis until proven otherwise. UTI is usually outpatient; pyelonephritis often needs admission, especially with sepsis signs, vomiting, or pregnancy.
• Nephrotic syndrome equals massive proteinuria; nephritic syndrome equals hematuria with RBC casts.

Acute kidney injury (AKI): the three categories

AKI is a sudden drop in kidney function, usually within hours to days, with rising creatinine and falling urine output. The NCLEX will not ask you to define AKI. It will give you a patient scenario and expect you to identify which of the three categories it is, what the priority intervention is, and what labs to trend.

Prerenal: before the kidney

The kidney is fine. It just is not getting enough blood. Causes: hypovolemia (hemorrhage, GI losses, burns, dehydration), heart failure, sepsis with vasodilation, renal artery stenosis. The tubules are still working, so they conserve sodium and water aggressively.

• BUN:creatinine ratio greater than 20:1 (classic prerenal finding)
• Urine sodium low (less than 20 mEq/L) – the kidney is holding on
• Urine specific gravity high (concentrated urine)
• Treatment: fix the perfusion. Fluids if hypovolemic, inotropes or afterload reduction if cardiac

Clinical pearl: If a prerenal AKI is not corrected quickly, it becomes intrarenal. Prolonged hypoperfusion causes acute tubular necrosis (ATN), which is an intrarenal process. The NCLEX will test that progression.

Intrarenal: damage to the kidney itself

The kidney tissue is injured. Most common cause: ATN from prolonged ischemia or nephrotoxins (aminoglycosides, contrast dye, NSAIDs, vancomycin, amphotericin B). Other causes: acute glomerulonephritis, interstitial nephritis, rhabdomyolysis.

• BUN:creatinine ratio close to 10:1 (both rise together)
• Urine sodium elevated (greater than 40 mEq/L) – the damaged tubules cannot reabsorb sodium
• Urine specific gravity fixed near 1.010 (isosthenuria)
• Muddy brown casts in urine (classic ATN finding)

Postrenal: obstruction after the kidney

Urine is being made but cannot get out. Causes: BPH, kidney stones, tumors, neurogenic bladder, clots. Relieve the obstruction and kidney function usually recovers.

• Bladder scan to assess for retention
• Catheter placement often fixes it immediately
• Imaging (CT, renal ultrasound) to find the obstruction level

The four phases of AKI

1. Initiation: The insult happens. Hours to days. Often asymptomatic except for the rising creatinine.
2. Oliguric phase: Urine output less than 400 mL/day. Lasts 1-3 weeks. This is the most dangerous phase. Patients are at risk for fluid overload, hyperkalemia, metabolic acidosis, and uremia. Daily weights, strict I/O, potassium restriction, and fluid restriction are critical.
3. Diuretic phase: Urine output rises to 1-3 L/day (sometimes higher). Tubules are recovering but cannot concentrate urine yet. Risk shifts to volume depletion, hypokalemia, and hyponatremia. Replace fluid and electrolytes carefully.
4. Recovery phase: Gradual return of GFR over months. Some patients never fully recover and progress to CKD.

Chronic kidney disease (CKD): staging by GFR

CKD is defined as kidney damage or GFR less than 60 mL/min/1.73m² for three or more months. Stages are based on GFR, with damage markers needed to diagnose stages 1 and 2.

• Stage 1: GFR greater than 90 with kidney damage markers (proteinuria, structural abnormality)
• Stage 2: GFR 60-89 with damage markers
• Stage 3a: GFR 45-59
• Stage 3b: GFR 30-44
• Stage 4: GFR 15-29 – prepare for renal replacement therapy (vascular access, transplant evaluation)
• Stage 5 (end-stage renal disease): GFR less than 15 – dialysis or transplant required

What CKD does to the body

You need to know the systemic complications because they drive NCLEX priority questions.

• Anemia: Low erythropoietin. Treat with epoetin alfa (monitor for HTN and thrombosis) and iron supplementation.
• Bone disease (CKD-MBD): Low vitamin D activation means low calcium, which drives up parathyroid hormone (secondary hyperparathyroidism). Phosphate also rises because the kidney cannot excrete it. Treat with phosphate binders (calcium acetate, sevelamer) given with meals, and active vitamin D (calcitriol).
• Hyperkalemia: Dietary restriction (avoid bananas, oranges, potatoes, tomatoes, salt substitutes). Emergency treatment: calcium gluconate first (stabilizes cardiac membrane), then insulin + D50, albuterol, then sodium polystyrene sulfonate or patiromer to actually remove potassium from the body.
• Metabolic acidosis: Low bicarbonate. Treat with oral sodium bicarbonate.
• Fluid overload: Daily weights are the single most important assessment. A 1 kg gain equals 1 L of retained fluid. Fluid restriction, diuretics while still making urine, dialysis when not.
• Uremia: Pruritus, nausea, confusion, pericarditis, neuropathy, platelet dysfunction. Pericardial friction rub in a CKD patient is an emergency – they are at risk of tamponade.

Diet in CKD

• Protein: restricted before dialysis (0.6-0.8 g/kg/day) to reduce urea production. Liberalized once on dialysis (1.0-1.2 g/kg/day) because dialysis removes amino acids.
• Potassium: restricted
• Phosphate: restricted (avoid dairy, nuts, cola, processed foods)
• Sodium: restricted (less than 2 g/day)
• Fluid: individualized, often about 1000 mL/day plus the previous day’s urine output

Because so much of renal nursing comes down to managing sodium, potassium, calcium, phosphate, and volume, it pays to pair this review with our fluid and electrolytes guide.

Dialysis: hemodialysis, peritoneal, and access types

Vascular access for hemodialysis

Three access types, each with distinct nursing implications.

• Arteriovenous fistula (AVF): Surgically created connection between artery and vein, usually radiocephalic. Takes 6-12 weeks to mature. Gold standard – lowest infection rate, longest life. Requires preserved veins, so start protecting the non-dominant arm early in CKD.
• Arteriovenous graft (AVG): Synthetic tube connecting artery and vein. Usable in 2-4 weeks. Higher infection and thrombosis risk than fistula, but faster to use.
• Central venous catheter (tunneled or non-tunneled): Used when urgent dialysis is needed or when fistula/graft have failed. Highest infection risk. Not for long-term use if avoidable.

Access arm teaching (NCLEX favorite)

• No blood pressure on the access arm – ever
• No IV starts or venipuncture on the access arm – ever
• No constrictive clothing, watches, or jewelry on that arm
• No sleeping or leaning on the access arm
• No carrying heavy bags on that arm
• Assess patency every shift: palpate for a thrill (vibrating buzz under your fingers) and auscultate for a bruit (whooshing sound). If either is absent, the access is clotted – notify the provider immediately.
• Teach the patient to check thrill daily at home and report any absence, pain, redness, swelling, or bleeding from the site.

Hemodialysis nursing care

• Hold antihypertensives and water-soluble medications before dialysis (they will be dialyzed out). Verify with the provider – some patients still need their meds.
• Weigh before and after. The difference is fluid removed.
• Monitor for hypotension during dialysis (rapid fluid shift), disequilibrium syndrome (headache, nausea, confusion from rapid urea clearance early in treatment), and bleeding (heparinized during dialysis).
• Post-dialysis: monitor access site for bleeding, take vitals, assess for fatigue.

Peritoneal dialysis (PD)

Uses the peritoneal membrane as the dialysis filter. Dialysate is instilled, dwells, and is drained. Done at home, more flexible, but slower and prone to peritonitis.

• Cloudy effluent is peritonitis until proven otherwise. This is the most tested PD finding. Send a sample for cell count and culture, notify the provider, start empiric intraperitoneal antibiotics. Fever and abdominal pain support the diagnosis.
• Warm the dialysate to body temperature before instilling – cold fluid causes cramping and vasoconstriction of peritoneal vessels, reducing efficacy.
• If outflow is sluggish, reposition the patient (turn side to side), check for kinks, check for constipation (distended bowel can obstruct the catheter).
• Expected outflow is approximately equal to or slightly greater than inflow. If significantly less is coming out, document it and notify the provider.
• Strict aseptic technique for connections. Exit site care daily.

Urinary tract infection vs pyelonephritis

Both are bacterial infections of the urinary tract. The difference is location and severity.

UTI (lower urinary tract: bladder, urethra)

• Dysuria, frequency, urgency, suprapubic pressure, cloudy or foul-smelling urine, sometimes hematuria
• No fever or minimal low-grade fever
• Urinalysis: positive leukocyte esterase, positive nitrites (gram-negative bacteria like E. coli), elevated WBCs
• Treat with oral antibiotics (nitrofurantoin, TMP-SMX, fosfomycin)
• Teach: finish the full antibiotic course, wipe front to back, void after intercourse, increase fluid intake to 2-3 L/day, cotton underwear, avoid bubble baths

Pyelonephritis (upper: kidney)

• All UTI symptoms plus high fever (102°F+), chills, flank pain, costovertebral angle (CVA) tenderness, nausea and vomiting
• Often requires hospital admission for IV antibiotics (ceftriaxone, piperacillin-tazobactam)
• Risk of urosepsis – monitor for hypotension, tachycardia, altered mental status
• Pregnant patients with pyelonephritis always admit due to preterm labor risk

Clinical pearl: Elderly patients may not present with classic UTI symptoms. Look for new-onset confusion, falls, or decreased appetite. Infection is high on the differential for any sudden mental status change in an older adult.

Benign prostatic hyperplasia (BPH)

Enlargement of the prostate compresses the urethra and causes obstructive urinary symptoms: hesitancy, weak stream, dribbling, incomplete emptying, nocturia, urinary retention. Complications include UTI, bladder distention, overflow incontinence, and postrenal AKI.

BPH medications

• Alpha-1 blockers (tamsulosin, doxazosin, terazosin): Relax smooth muscle in bladder neck and prostate, improving urine flow. Quick symptom relief (days to weeks). Main side effect: orthostatic hypotension. Teach patients to rise slowly and take the first dose at bedtime to avoid falls.
• 5-alpha reductase inhibitors (finasteride, dutasteride): Shrink the prostate over time. Takes 3-6 months for effect. Teratogenic – pregnant women should not even handle crushed tablets. Also lowers PSA by approximately 50%, so interpret screening values carefully.

BPH surgical care (TURP)

Transurethral resection of the prostate is the most common surgical treatment. Post-op nursing care centers on the continuous bladder irrigation (CBI).

• CBI runs isotonic saline through a three-way Foley to flush blood clots and prevent catheter obstruction
• Titrate the irrigation rate to keep the output pink, not cherry red
• Bright red bleeding or clots suggest active hemorrhage – notify the provider, increase irrigation, may need traction on the catheter
• Calculate true urine output: subtract the irrigation infused from the total output to get actual urine production
• Watch for bladder spasms – treat with antispasmodics (belladonna and opium suppositories, oxybutynin)
• Avoid straining, heavy lifting, and long car rides for 4-6 weeks post-op
• TURP syndrome (rare with modern saline irrigation): hyponatremia, confusion, seizures from absorbed hypotonic irrigation fluid

Renal calculi (kidney stones)

Severe flank pain (often described as the worst pain of the patient’s life) radiating to the groin or testicle, hematuria, nausea, vomiting, restlessness (patients cannot lie still – this helps distinguish renal colic from peritonitis, where patients lie very still).

Nursing priorities

• Pain management is the first priority. Ketorolac IV is first-line for renal colic. Opioids are added if needed. Do not wait for pain to escalate before medicating.
• Strain all urine. Collect any passed stones for chemical analysis – the stone type dictates prevention strategy.
• Hydration: 2.5-3 L/day to help flush the stone. IV fluids until oral intake is adequate.
• Most stones less than 5 mm pass on their own. Larger stones may require extracorporeal shock wave lithotripsy (ESWL), ureteroscopy, or percutaneous nephrolithotomy.

Stone types and prevention teaching

• Calcium oxalate (most common): Limit oxalate-rich foods (spinach, rhubarb, nuts, chocolate, tea). Do not restrict calcium – adequate dietary calcium actually binds oxalate in the gut and reduces stone formation.
• Uric acid: Seen in gout, high-purine diets, tumor lysis syndrome. Alkalinize the urine (potassium citrate), limit purines (red meat, organ meats, shellfish).
• Struvite: Associated with urease-producing bacteria (Proteus) and recurrent UTIs. Treat the infection.
• Cystine: Genetic disorder. High fluid intake is mainstay.

Glomerular disorders: nephrotic vs nephritic

Both involve the glomerulus, but the patterns are different. The NCLEX tests whether you can tell them apart from the urinalysis and clinical picture.

Nephrotic syndrome

• Massive proteinuria (greater than 3.5 g/day) – the defining feature
• Hypoalbuminemia (protein is lost in urine)
• Generalized edema (low albumin means low oncotic pressure)
• Hyperlipidemia (liver compensates for protein loss)
• Hypercoagulable state (antithrombin III lost in urine) – risk of DVT, PE
• Treatment: ACE inhibitors or ARBs to reduce proteinuria, diuretics for edema, statin for lipids, corticosteroids for minimal change disease, anticoagulation if high clot risk

Nephritic syndrome

• Hematuria with red blood cell casts – the defining feature
• Proteinuria (usually less than 3.5 g/day, milder than nephrotic)
• Hypertension (sodium and fluid retention)
• Oliguria, azotemia (rising BUN/Cr)
• Classic cause: post-streptococcal glomerulonephritis in a child 1-3 weeks after strep throat, or 3-6 weeks after impetigo or another strep skin infection. ASO titer elevated, complement (C3) low. Usually self-limited.
• Treatment: manage BP, fluid, and symptoms. Antibiotics if infection still active. Most cases resolve.

Memory trick: NephrOtic = prOteinuria (massive). NephrITIC = hematurIa with casts (inflammation). Protein leaks through the nephrotic glomerulus; blood cells leak through the inflamed nephritic one.

Put it all together

Renal content rewards pattern recognition. AKI category determines treatment. CKD stage drives urgency. Dialysis access arm rules are finite and testable. UTI is usually outpatient; pyelonephritis often needs admission. Nephrotic vs nephritic is a urinalysis question. Once you have these frames, renal questions become fast.

For the labs that tie everything together – BUN, creatinine, potassium, sodium, phosphate – review our NCLEX lab values guide. For the drugs that hit the kidney (aminoglycosides, vancomycin, NSAIDs, contrast, ACE inhibitors), see the pharmacology review. For case study questions that combine renal findings with priority and delegation, see the NGN question types guide.

Frequently Asked Questions

How do you tell prerenal from intrarenal AKI on the NCLEX?

Use the BUN:creatinine ratio and the urine findings. Prerenal AKI shows a ratio greater than 20:1, low urine sodium (less than 20 mEq/L), and concentrated urine because the tubules are intact and conserving sodium and water. Intrarenal AKI from acute tubular necrosis shows a ratio closer to 10:1, elevated urine sodium (greater than 40 mEq/L), specific gravity fixed near 1.010, and muddy brown casts. Prerenal is a perfusion problem you fix with volume; intrarenal is kidney tissue damage you manage supportively while avoiding further insult.

Which phase of acute kidney injury is the most dangerous?

The oliguric phase. Urine output drops below 400 mL/day and can last one to three weeks. During this time patients are at high risk for fluid overload, hyperkalemia, metabolic acidosis, and uremia. Priorities are daily weights, strict intake and output, potassium restriction, and fluid restriction. As the patient moves into the diuretic phase the danger shifts to volume depletion, hypokalemia, and hyponatremia.

What are the key teaching points for a hemodialysis access arm?

Protect the arm completely. No blood pressure measurements, no IV starts or venipuncture, no constrictive clothing, watches, or jewelry, no sleeping or leaning on it, and no carrying heavy bags. Assess patency every shift by palpating for a thrill and auscultating for a bruit, and teach the patient to check the thrill daily at home. If the thrill or bruit is absent, the access may be clotted, which is a surgical emergency, so notify the provider immediately.

Why is cloudy peritoneal dialysis effluent important?

Cloudy effluent is peritonitis until proven otherwise, and it is the most tested peritoneal dialysis finding. The nurse should send a sample for cell count and culture, notify the provider, and anticipate empiric intraperitoneal antibiotics. Fever and abdominal pain support the diagnosis. Strict aseptic technique during connections and daily exit site care help prevent it.

What is the difference between nephrotic and nephritic syndrome?

Nephrotic syndrome is defined by massive proteinuria (greater than 3.5 g/day) with hypoalbuminemia, generalized edema, hyperlipidemia, and a hypercoagulable state. Nephritic syndrome is defined by hematuria with red blood cell casts, milder proteinuria, hypertension, and oliguria, classically from post-streptococcal glomerulonephritis. A simple memory trick: nephrOtic equals prOteinuria, while nephrITIc equals hematurIa with casts from inflammation.