Week 9 — Renal & Urinary Guided Notes

Fill in the Blanks

Kidneys regulate…

• Fluid volume / water balance — they decide how much water leaves the body, so they set blood volume
• Electrolytes — sodium, potassium, calcium, phosphate, magnesium
• Acid–base balance — excrete H⁺, reabsorb bicarbonate. Fail → metabolic acidosis.
• Blood pressure — renin → angiotensin II → aldosterone (RAAS) plus direct control of fluid volume
• RBC production (erythropoietin) — failing kidneys make less → anemia of kidney disease
• Activate vitamin D (calcitriol, the active form — 1,25-dihydroxyvitamin D) — no calcitriol → calcium is not absorbed from the gut → hypocalcemia, high phosphorus, and bone disease

The pattern to carry all week: every renal disease is one of these six jobs failing. Ask which one broke and the signs write themselves.

• Normal GFR: 90–120 mL/min/1.73 m² (often written simply as 90–120 mL/min). Below 60 for 3 months or more = chronic kidney disease; below 15 = end-stage, dialysis territory.
• BUN: 10–20 mg/dL (some texts 7–20 mg/dL)
• Creatinine: 0.6–1.2 mg/dL (women run lower, roughly 0.5–1.1; men 0.6–1.2 — because it comes from muscle mass)

Why is creatinine a better indicator of kidney function than BUN?

Because creatinine is made at a steady rate by muscle, is freely filtered by the glomerulus, and is barely reabsorbed — so its blood level tracks GFR almost purely. BUN is a moving target: it rises from dehydration, a high-protein diet, GI bleeding, steroids, and severe catabolism, and it falls in liver failure and overhydration — none of which are kidney problems. A rising creatinine means the filter itself is failing.

Numbers that matter: BUN:creatinine ratio >20:1 points to a prerenal (perfusion) problem — BUN climbs faster than creatinine because a dry kidney reabsorbs urea. A ratio near 10–15:1 with both climbing points to intrarenal damage.

Small creatinine changes are big news: creatinine doubling means GFR has roughly halved. A jump from 1.0 to 2.0 mg/dL is not a small jump.

Other renal labs to recognize

• Potassium: 3.5–5.0 mEq/L — the one that kills first
• Phosphorus: 3.0–4.5 mg/dL — rises in kidney failure
• Calcium: 9.0–10.5 mg/dL — falls as phosphorus rises (they see-saw)
• Urine specific gravity: 1.005–1.030. A fixed 1.010 (same as plasma) means the tubules have lost the ability to concentrate = intrarenal damage.
• Serum albumin: 3.5–5.0 g/dL — drops hard in nephrotic syndrome

🤖 Ask Claire: "Teach me renal labs as if I am preparing for tomorrow's exam. Help me recognize patterns instead of memorizing numbers."

Complete the chart

• Stress = Leaking small amounts with anything that raises abdominal pressure — cough, sneeze, laugh, lift, exercise. The pelvic floor and urethral sphincter are weak (childbirth, menopause/low estrogen, obesity, after prostate surgery). Treat with Kegel/pelvic floor exercises, weight loss, pessary.
• Urge = A sudden, strong need to go followed by a large involuntary loss — "I can't make it to the bathroom." The detrusor muscle contracts on its own (overactive bladder). Causes: UTI, bladder irritants (caffeine, alcohol, artificial sweeteners), stroke, MS. Treat with bladder retraining and timed voiding, then anticholinergics (oxybutynin, tolterodine) or mirabegron.
• Overflow = The bladder over-fills and dribbles constantly in small amounts, never emptying — with a high post-void residual and a distended, palpable bladder. Either an outlet obstruction (BPH, stricture) or a detrusor that won't contract (diabetic neuropathy, spinal injury, anticholinergic drugs). Treat the obstruction; bladder scan and catheterize.
• Functional = The urinary tract works fine, but the person cannot get to the toilet in time — immobility, arthritis, dementia, sedation, restraints, a call light out of reach, side rails, poor lighting. Treat the environment: scheduled toileting, bedside commode, clothing that comes off easily, clear path, night light.
• Reflex / Neurogenic = The bladder empties involuntarily at a predictable volume with no sensation and no urge, because the message between bladder and brain is cut. Spinal cord injury above the sacral level, MS, spina bifida. Managed with scheduled intermittent catheterization and bladder scanning.

Which type is most associated with enlarged prostate?

Overflow incontinence. The enlarged prostate squeezes the urethra, so the bladder never fully empties; it stretches past capacity and urine dribbles out over the top. Classic picture: weak stream, hesitancy, constant dribbling, and a post-void residual well over 100–150 mL.

What nursing intervention is priority for neurogenic bladder?

Establish a scheduled bladder program with clean intermittent catheterization, guided by bladder scanning of post-void residuals — because the patient cannot feel fullness, and an over-distended bladder causes urinary reflux, hydronephrosis, kidney damage, and UTI. In a spinal cord injury at or above T6, a full bladder is also the number one trigger of autonomic dysreflexia, so scheduled emptying is a safety intervention, not just a comfort one.

⚠️ Before you blame age: new incontinence in an older adult is a symptom — screen for UTI, constipation/fecal impaction, and new medications (diuretics, sedatives, anticholinergics) before calling it chronic.

🤖 Ask Claire: "Give me difficult SATA questions on urinary disorders and explain every rationale—even the wrong answers."

Most common organism: Escherichia coli (E. coli) — gram-negative bacteria from the patient's own GI/perineal flora that ascend the short female urethra. It causes roughly 80–90% of uncomplicated UTIs.

Differentiate

• Cystitis = A LOWER UTI — infection and inflammation of the bladder. Frequency, urgency, dysuria (burning), suprapubic pressure or pain, cloudy/foul/dark urine, sometimes hematuria. Usually no fever or only a low-grade one, and the patient does not look septic.
• Pyelonephritis = An UPPER UTI — infection of the renal pelvis and kidney tissue itself, usually bacteria that climbed up from the bladder. The patient is systemically ill: fever, chills, flank pain. This is the one that turns into urosepsis.

The dividing line is the fever and the flank. Burning alone = bladder. Burning + fever + CVA tenderness = kidney.

Expected assessment findings of pyelonephritis

• High fever (often 101–104°F / 38.5–40°C) with shaking chills and tachycardia
• Flank pain and costovertebral angle (CVA) tenderness — pain when you percuss over the kidney at the 12th rib
• Nausea, vomiting, and malaise, plus the lower-tract symptoms (dysuria, urgency, frequency), cloudy foul urine, and labs showing leukocytosis and WBC casts in the urine — WBC casts are formed in the tubules, so they prove the infection is in the kidney, not just the bladder

What older-adult symptom may occur instead of dysuria?

New confusion / acute change in mental status — often with falls, new incontinence, decreased appetite, lethargy, or agitation, and frequently without fever, because older adults mount a blunted febrile and inflammatory response. A sudden change in an older adult's baseline behavior is a UTI until you rule it out.

Nursing care & teaching

• Cultures first: obtain the urine culture before the first antibiotic dose — antibiotics sterilize the specimen and you lose the organism
• Fluids: 2–3 L/day unless contraindicated (heart failure, kidney failure) — flushes bacteria out mechanically
• Finish the antibiotic: take the entire course even after symptoms stop — stopping early breeds resistance and relapse
• Phenazopyridine: a urinary analgesic only — it does not treat the infection, and it turns urine orange-red and will stain contact lenses and clothing
• Prevention teaching: wipe front to back, void every 2–4 hours and after intercourse, cotton underwear, avoid bubble baths/douches, and do not hold urine

🤖 Ask Claire: "Give me an unfolding patient with pyelonephritis that progresses to sepsis. Stop after each section and ask what I would assess first."

• 1. Insert a catheter only when there is a true indication, and remove it as early as possible — review the need every single day. Duration of catheterization is the single biggest risk factor; each additional day adds risk.
• 2. Hand hygiene before and after any catheter contact, and strict sterile technique at insertion with sterile gloves, drape, and single-use lubricant.
• 3. Keep the drainage bag below the level of the bladder at all times and off the floor, with tubing free of kinks and dependent loops. Urine must always flow downhill — backflow carries bacteria straight into the bladder.
• 4. Maintain a closed drainage system — never disconnect the tubing from the catheter, and collect specimens from the needleless sampling port after disinfecting it.
• 5. Daily perineal and meatal care with soap and water, and secure the catheter to the thigh or abdomen to stop tugging and urethral trauma. Empty the bag when 2/3 full using a dedicated container per patient, and encourage fluids.

Never irrigate a catheter routinely, never let the drainage spout touch the collection container or floor, and never raise the bag above the bladder — including during transfers.

• Glomerulonephritis: urine looks dark, smoky, tea- or cola-colored (gross hematuria), and scant because the glomerular membrane is inflamed, so it leaks red blood cells and some protein into the filtrate — RBCs packed in the tubules form RBC casts, which are diagnostic. Filtration slows, so the patient makes less urine and holds on to salt and water.
• Nephrotic syndrome: urine looks foamy / frothy and cloudy because massive amounts of protein are being lost — more than 3.5 g in 24 hours — and protein lowers the surface tension of urine, so it foams like soap in the toilet.
• Which disorder causes severe protein loss? Nephrotic syndrome — >3.5 g/day, which drops serum albumin below 3 g/dL and pulls fluid into the tissues.
• Which commonly causes hypertension and fluid overload? Glomerulonephritis — inflammation drops the GFR, so sodium and water are retained and the renin–angiotensin system fires; the result is hypertension, periorbital edema, and oliguria.

Side by side

One-line memory: GN = blood in the urine and a high blood pressure. Nephrotic = protein in the urine and a swollen everything.

• AKI is SUDDEN — an abrupt drop in kidney function over hours to days, marked by a creatinine rise of ≥0.3 mg/dL within 48 hours (or 1.5× baseline within 7 days) or urine output under 0.5 mL/kg/hr for 6 hours and may be reversible.
• CKD is GRADUAL and permanent — kidney damage or a GFR under 60 mL/min lasting 3 months or longer, staged G1 through G5, with G5 (<15 mL/min) being end-stage renal disease requiring dialysis or transplant and progressive.

Three causes of AKI

🩻 The nurse's first move with new anuria: bladder scan and check the Foley for kinks — rule out the reversible plumbing problem before assuming the kidney died.

Why does AKI commonly cause hyperkalemia?

Because the kidney is the body's only real route for getting rid of potassium — roughly 90% of the daily potassium load leaves in urine, through the distal tubule. When GFR falls and urine output drops, potassium simply has nowhere to go and accumulates in the blood. Two things make it worse and faster: (1) the failing kidney also cannot excrete hydrogen ions, so the patient becomes acidotic — and in acidosis H⁺ moves into the cells while K⁺ moves out into the serum; (2) the tissue breakdown and catabolism that come with critical illness, crush injury, or infection dump even more intracellular potassium into the bloodstream. Add any potassium-sparing diuretic, ACE inhibitor, or K⁺-containing IV fluid and it climbs sooner.

Priority nursing assessments — select all that apply

• ✅ Daily weights — the most accurate and earliest measure of fluid status; 1 kg (2.2 lb) = 1 L of fluid. Same scale, same time, same clothing, after voiding.
• ✅ I&O — urine output is the direct readout of whether the kidney is still filtering; under 30 mL/hr (or 0.5 mL/kg/hr) must be reported.
• ✅ ECG — this is the one that saves the life. It shows hyperkalemia (peaked T waves, flat P, wide QRS) before the potassium result comes back from the lab.
• ✅ Lung sounds — new crackles mean the retained fluid has reached the alveoli — pulmonary edema is the other way these patients die.
• ✅ Labs — potassium, BUN, creatinine, bicarbonate/ABG, calcium and phosphate, H&H. Trend them; a single value means little.

All five are correct — this is a "select all" where nothing is a distractor. If forced to name the single priority: the ECG/cardiac monitor, because hyperkalemia kills before fluid overload does.

Nephrotoxin safety — the prevention side

• Before IV contrast: check the creatinine/eGFR, hydrate with IV normal saline before and after, and hold metformin at the time of the study and for 48 hours after
• Aminoglycosides (gentamicin, tobramycin): monitor peak and trough levels, creatinine, and hearing — nephrotoxic and ototoxic
• NSAIDs: avoid in anyone with low perfusion or existing kidney disease — they constrict the afferent arteriole and shut off glomerular blood flow

🤖 Ask Claire: "Quiz me on AKI vs CKD using only NCLEX Next Gen questions. Do not tell me the answer until I explain my reasoning."

The trap on exams: in the oliguric phase you restrict fluid and potassium; in the diuretic phase you replace them. Same patient, opposite orders, one week apart — so always ask which phase the stem is describing.

📊 The other "stages" you may see (KDIGO severity): Stage 1 = creatinine 1.5–1.9× baseline or ↑≥0.3 mg/dL, urine <0.5 mL/kg/hr for 6–12 hr · Stage 2 = 2.0–2.9× baseline, urine <0.5 mL/kg/hr for ≥12 hr · Stage 3 = ≥3× baseline or creatinine ≥4.0 mg/dL, urine <0.3 mL/kg/hr for ≥24 hr or anuria ≥12 hr, or dialysis started.

When is emergent dialysis indicated? — "AEIOU"

• Acidosis that is severe and unresponsive · Electrolytes — refractory hyperkalemia · Intoxication with a dialyzable drug/toxin · Overload of fluid causing pulmonary edema · Uremia — pericarditis, encephalopathy, seizures, bleeding

Normal K⁺ 3.5–5.0 mEq/L. Above 5.0 = hyperkalemia. Above 6.0–6.5 mEq/L, or ANY level with ECG changes, is an emergency — treat before you re-draw.

ECG progression — in order

• Tall, peaked, tented T waves (earliest sign) → flattened or absent P waves → prolonged PR → widened QRS → sine wave → ventricular fibrillation or asystole. Other findings: muscle weakness that starts in the legs, cramping, paresthesias, diarrhea and hyperactive bowel sounds, irritability.

Treatment order — memorize this sequence

Never give IV potassium as a push or bolus, and never give calcium gluconate through the same line as sodium bicarbonate — they precipitate.

Memory: C BIG K — Calcium, Bicarb, Insulin+Glucose, Kayexalate/binders, then dialysis.

Peritoneal dialysis

Peritoneal dialysis works by using the patient's own peritoneal membrane as the semipermeable filter. Warmed dialysate is instilled into the abdomen through a permanent catheter (fill), left to sit (dwell), and then drained out by gravity (drain). Wastes such as urea, creatinine and potassium move from the blood across the peritoneum into the dialysate by diffusion (high concentration to low), and excess water is pulled out by osmosis/ultrafiltration — the dextrose concentration in the dialysate sets how much fluid is removed: the higher the dextrose (1.5% → 2.5% → 4.25%), the more fluid comes off.

• Cloudy outflow = PERITONITIS — until proven otherwise. Cloudy effluent is the earliest and most reliable sign, and it is the most common complication of PD. Look also for abdominal pain, rebound tenderness, fever, nausea. Nursing action: send the effluent for cell count, Gram stain and culture, notify the provider, and expect intraperitoneal antibiotics added to the dialysate. Reinforce sterile technique with every bag change.
• If outflow is less than inflow: check for kinked tubing and a closed clamp, reposition the patient side to side, lower the drainage bag, and assess for constipation — a full bowel is the most common mechanical cause of poor drainage. Fibrin can also occlude the catheter.
• Warming the dialysate: warm to body temperature with a dry heating pad or approved warmer — cold fluid causes cramping and vasoconstriction of the peritoneal vessels, which lowers exchange. Never microwave the dialysate bag.
• Daily monitoring: weigh after the drain, at the same time each day; log every exchange volume in and out; a positive balance that keeps growing means fluid is being retained.

Hemodialysis access

• Thrill = The buzzing / vibrating sensation you FEEL with your fingertips over the fistula — turbulent arterial blood flowing into the vein. Palpate it.
• Bruit = The swishing, whooshing sound you HEAR with the stethoscope over the fistula. Auscultate it.

Thrill and bruit together = the access is patent. If either one disappears, or the site is cool, pale, painful or pulseless, the access has clotted — notify the provider immediately; it is a surgical emergency for that limb's access. Check the access every shift.

Never do these on an AV fistula arm

• Never take a blood pressure on that arm — the cuff pressure collapses the fistula and can clot it. Post a sign over the bed and band the arm.
• Never draw blood, start an IV, or give an injection in that arm — a puncture outside of dialysis risks bleeding, infection, and loss of the access.
• Never let anything constrict it — no tight sleeves, watches, jewelry, or restraints; no sleeping or lying on that arm; no carrying heavy bags or lifting with it.

Other hemodialysis facts worth points

• Fistula maturation: a new AV fistula needs about 6 weeks to 3–4 months before it can be cannulated; an AV graft is usable in about 2–4 weeks. Until then the patient uses a temporary central catheter.
• Before dialysis: weigh the patient, take vital signs, and hold antihypertensives and any dialyzable medication until after the run — giving them first plus the fluid removal causes profound hypotension.
• Most common complication during a run: hypotension from rapid fluid removal — lower the head of the bed, slow the ultrafiltration rate, and give normal saline per protocol.
• Disequilibrium syndrome: headache, nausea, restlessness, confusion, and possibly seizures near the end of an early treatment — urea is cleared from the blood faster than from the brain, so water shifts into brain cells. Prevented by slower, shorter initial treatments.
• After dialysis: weigh again (the difference is the fluid removed), check vitals and the access site, and monitor for bleeding — the patient was heparinized during the run.

🤖 Ask Claire: "Challenge me with five priority questions on dialysis patients. Make me justify every intervention."

• Classic symptom: Sudden, severe, colicky flank pain that radiates around to the groin, labia or testicle — it comes in excruciating waves as the ureter spasms around the stone. The patient is restless and cannot find a comfortable position (this is how you tell it from peritonitis, where they lie perfectly still), with nausea, vomiting, diaphoresis, and hematuria.
• Priority pain medication: An IV opioid — morphine or hydromorphone — for severe acute renal colic, because the pain is genuinely one of the worst in medicine and should be treated fast and adequately. It is very often paired with IV ketorolac (an NSAID), which relieves the ureteral spasm and prostaglandin-driven inflammation that causes the colic. Caution: hold NSAIDs if kidney function is already impaired. Tamsulosin is added as medical expulsive therapy to relax the ureter and help the stone pass — warn about orthostatic hypotension.
• Why strain all urine? To catch the stone so it can be sent for laboratory analysis — the composition determines the entire prevention plan. Calcium oxalate → limit oxalate foods (spinach, rhubarb, nuts, tea, chocolate); uric acid → limit purines (organ meats, red meat, sardines) and alkalinize the urine; struvite → treat the chronic UTI; cystine → genetic, needs high fluid intake and alkalinization. Straining also confirms the stone has passed, which tells you the obstruction is relieved.

ESWL (extracorporeal shock wave lithotripsy) teaching

• Expected: Bruising and soreness on the flank where the shock waves entered, blood-tinged urine for a few days, and colicky pain as the sand-like fragments pass. Expect to strain all urine, drink 3–4 L a day unless restricted, and stay active/walk to move the fragments along. A ureteral stent may be left in place.
• Report: Fever or chills (infection or urosepsis), bright red bleeding or clots, or hematuria lasting beyond a few days, inability to urinate or no urine output (a fragment has obstructed the ureter), pain not relieved by the prescribed medication, and persistent nausea and vomiting.

Prevention teaching for everyone with a stone history

• Fluid is the number one prevention — 3 L a day, enough to keep urine pale and dilute, including a glass at night since urine concentrates while asleep.
• Do not eliminate dietary calcium — low calcium intake actually increases oxalate absorption and makes calcium oxalate stones more likely. Limit sodium instead.
• Stay physically active — immobility mobilizes calcium out of bone and into the urine.

• What assessment finding tells you kidney disease is becoming life-threatening? A change in the cardiac rhythm from hyperkalemia — peaked T waves, a lost P wave, or a widening QRS — especially together with urine output falling below 30 mL/hr. That combination means potassium is climbing with no way out, and the next step is ventricular fibrillation. The close second is new crackles with dyspnea and a sudden weight gain (fluid overload becoming pulmonary edema). Late uremic red flags: decreasing level of consciousness or seizures, a pericardial friction rub, and Kussmaul respirations from acidosis.
• Which electrolyte causes the greatest immediate cardiac risk? POTASSIUM (normal 3.5–5.0 mEq/L). Both directions are dangerous, but in renal failure it is hyperkalemia — it stops the heart, and it can do it within minutes with no warning symptoms other than the ECG.
• What assessment always comes before giving a diuretic? Blood pressure (with heart rate and volume status) — hold and call if the patient is hypotensive, because a diuretic removes volume from someone who has none left and will drop perfusion to the kidney, turning fluid overload into a prerenal AKI. Right behind it: the potassium level — a loop or thiazide diuretic in a hypokalemic patient is unsafe, and a potassium-sparing diuretic in a hyperkalemic renal patient is unsafe. Also check daily weight, lung sounds, and urine output so you can tell whether the last dose worked.

The pattern questions to run on every renal patient

🤖 Ask Claire: "Give me patients with edema, hematuria, proteinuria, kidney stones, and AKI. Make me determine the diagnosis using only assessment findings."

Focus less on memorizing diseases and more on recognizing patterns: What happened to filtration? What happened to fluid? What happened to potassium? What is the priority assessment? What will kill the patient first?

• 1. Numbers: GFR 90–120 mL/min/1.73 m² · BUN 10–20 mg/dL · creatinine 0.6–1.2 mg/dL · K⁺ 3.5–5.0 mEq/L. Creatinine beats BUN because it comes only from muscle and tracks GFR; BUN moves with hydration, diet, GI bleeds and steroids.
• 2. POTASSIUM KILLS FIRST. In any renal patient, the ECG is the priority assessment — peaked T → flat P → wide QRS → sine wave → VF. Order: calcium gluconate (protect) → insulin+D50 / albuterol / bicarb (shift) → loop diuretic + binder (remove) → dialysis.
• 3. Prerenal = not enough blood IN (BUN:Cr >20:1, concentrated urine). Intrarenal = the nephron is damaged (muddy brown casts, specific gravity fixed at 1.010). Postrenal = urine can't get OUT (bladder scan it — the reversible one). Always rule out the blocked Foley first.
• 4. AKI phases flip the orders: oliguric = restrict fluid, K⁺ and protein, watch for pulmonary edema and hyperkalemia. Diuretic = replace fluid and electrolytes, watch for dehydration and hypokalemia. Recovery takes up to a year.
• 5. GN = blood + high BP. Dark tea-colored urine, RBC casts, periorbital edema, hypertension, after strep. Nephrotic = protein + swelling everywhere. Frothy urine >3.5 g/day, albumin <3, hyperlipidemia, clots.
• 6. Cystitis = burning, no fever. Pyelonephritis = fever, chills, CVA tenderness → watch for urosepsis. E. coli causes most of them. In an older adult, new confusion is the UTI symptom.
• 7. Cloudy PD outflow = peritonitis until proven otherwise → culture the effluent and notify. Feel the thrill, hear the bruit — both present = patent access; either missing = clotted, call now.
• 8. Never take a BP, draw blood, start an IV, or put anything constricting on the AV fistula arm. Sign over the bed, band the arm, tell every person who enters the room.
• 9. Stones: colicky flank pain radiating to the groin in a patient who cannot hold still → opioid (± ketorolac) + strain every drop of urine so the stone can be analyzed. After ESWL, bruising and blood-tinged urine are expected; fever or no urine output is not.
• 10. Before any diuretic: check the blood pressure and the potassium. Then daily weight, lung sounds, and I&O — 1 kg of weight = 1 L of fluid, and weight is the earliest sign that fluid is winning.

🤖 Final Claire challenge: "Act as my nursing instructor. Give me ten unfolding renal cases — AKI, CKD, pyelonephritis, nephrotic syndrome, stones, and a dialysis patient — and make me name the biggest red flag and the nurse's first action before you reveal anything."