Kidney and Urologic Disorders - PathoPharm Exam 4

Nephrolithiasis

Definition: Stones in urinary tract (kidney → ureter → bladder → urethra)

•Risk Factors:

•Dehydration, genetics, ↑ Ca intake, hypercalcemia, hyperparathyroidism, gout,

hyperuricemia, UTI (Proteus), immobility

•Types of Stones:

•Calcium (75%) → calcium oxalate most common

•Struvite → Proteus UTI, ↑ urine pH, staghorn calculi

•Uric Acid → gout, acidic urine, ↑ in diabetes

•Cystine → rare, genetic disorder

Nephrolithiasis signs and symptoms

•Severe flank pain (renal colic) → waves, ureteral spasm

•Pain ↓ to groin/testicle/labia

•Hematuria → mucosal irritation

•N/V → visceral response

•Urinary urgency/frequency/dysuria (distal stone)

•Restlessness → cannot get comfortable

•Fever/chills → infection + obstruction

Nephrolithiasis diagnostics

Urinalysis → hematuria, crystals

•CT / Ultrasound → stone, hydronephrosis

Nephrolithiasis complications

Obstruction → ↑ pressure → hydronephrosis → ischemia → nephron damage

•Stasis → ↑ bacteria → UTI → pyelonephritis → sepsis

•Recurrent stones → inflammation/fibrosis → ↓ GFR → CKD

Nephrolithiasis treatment and management

. Determine stone composition

▪ Collect and strain urine for stone analysis

2. Pain management: ketorolac, opiates (oral/IV)

3. Flushing out stones:

▪ Increase fluids (>3 liters/day)

▪ Administer Tamsulosin and/or diuretics

▪ Stones >6mm: Lithotripsy or surgery

4. For hydronephrosis:

▪ Ureteral stents, nephrostomy if needed

5. Chronic prevention:

▪ Dietary changes

▪ Hydration

Allopurinol

Therapeutic Class: Antigout agent

• Pharmacologic Class: Xanthine oxidase inhibitor

• Mechanism of Action: Inhibits xanthine oxidase, reducing

uric acid production in blood and urine.

• Uses: Chronic gout, hyperuricemia

• ADR: Rash, nausea, diarrhea, hepatotoxicity, renal toxicity,

SJS

• Contraindications: Acute gout flare (use only in

prophylactic doses), Severe renal or hepatic impairment

▪ Drug Interactions: warfarin, diuretics, others

• Nursing Considerations:

• Monitor BUN, creatinine, liver function tests, uric acid

levels

• Encourage adequate fluid intake

• Administer with food to reduce GI upset

• Patient Education:

• Take daily, even if asymptomatic

• Notify provider if rash occurs

• Avoid alcohol, high-purine foods (e.g., red meat,

shellfish)

Ketorolac

▪ Therapeutic Class: NSAID

▪ Pharmacologic Class: Acetic acid derivative

▪ MOA: Inhibits COX-1 & COX-2, reducing pain and

inflammation.

▪ Uses: Short-term pain management, inflammatory

conditions.

▪ Adverse Effects: Nausea, headache, GI bleeding, renal

impairment, anaphylaxis, liver toxicity

▪ Drug Interactions: Monitor with anticoagulants, NSAIDs,

diuretics

▪ Contraindications: Active GI bleeding, severe renal

impairment, pregnancy (3rd trimester)

▪ Nursing Considerations:

▪ Monitor renal/liver function, bleeding

▪ Administer with food; ensure hydration

▪ Patient Education: Take with food, report bleeding

signs, avoid alcohol/smoking

Causes of kidney injury

Prerenal (↓ perfusion → ischemia):

•Shock (hypovolemic, cardiogenic, septic)

•Renal artery occlusion/trauma

•Intrarenal (direct kidney damage):

•Nephrotoxic drugs (e.g., vancomycin)

•Hemolysis (↑ Hgb), rhabdomyolysis (↑ myoglobin)

•Tumor lysis (↑ purines)

•Pyelonephritis, glomerulonephritis

•Postrenal (obstruction → backflow):

•Nephrolithiasis, BPH

•Ureteral stricture, bladder tumor

•Hydronephrosis

Renal dysfunction pathophysiology

Ischemia/toxins → tubular cell injury → Acute Tubular Necrosis (ATN)

Sloughed cells → tubular obstruction → ↓ urine flow

• ↓ GFR → ↓ filtration → azotemia (↑ BUN, ↑ Cr)

• Fluid retention → edema, pulmonary congestion, HTN (RAAS ↑)

• ↓ excretion:

↑ K⁺ → hyperkalemia

↑ H⁺ → metabolic acidosis

↑ phosphorus, ↓ calcium

• ↓ kidney function:

↓ erythropoietin → anemia

↓ vitamin D activation → hypocalcemia

Key Flow:

Ischemia/toxin → ATN → ↓ GFR → ↑ waste + ↓ urine → fluid overload +

electrolyte imbalance

Dignostic findings of renal dysfunction

1. Serum Creatinine (Cr): 0.5–1.2 mg/dL

1. ↑ Cr → ↓ GFR (most specific indicator of renal function)

2. Blood Urea Nitrogen (BUN): 7–20 mg/dL

1. ↑ BUN → ↑ nitrogenous waste (less specific; affected by hydration, protein)

3. Glomerular Filtration Rate (GFR): 90–120 mL/min

1. ↓ GFR → impaired filtration

2. < 60 → kidney disease; < 15 → kidney failure

4. Urine Output:

1. Normal: > 0.5–1.5 mL/kg/hr

2. Oliguria: < 0.5 mL/kg/hr or < 400 mL/day

3. Anuria: < 100 mL/day

4. Polyuria: > 2 L/day

5. Urine Findings:

1. Proteinuria → glomerular damage

2. Hematuria → inflammation/injury

3. Casts → tubular damage

4. ↓ Specific gravity → poor concentrating ability

Key Pattern: ↓ GFR → ↑ Cr/BUN → ↓ urine output → electrolyte + acid-base imbalance

AKI

Definition: Sudden ↓ renal function → impaired filtration

•Clinical Findings:

•Azotemia → ↑ BUN, ↑ Cr

•↓ Urine output (oliguria)

•Fluid retention → edema, pulmonary congestion

•Electrolyte imbalance → ↑ K⁺, metabolic acidosis

•Diagnostic Criteria:

•↑ Cr ≥ 0.3 mg/dL (48 hr)

•↑ Cr ≥ 1.5× baseline (7 days)

•Urine output < 0.5 mL/kg/hr × 6 hr

AKI causes and pathophysiology

Prerenal: ↓ perfusion → ↓ GFR → azotemia

•(initially no structural damage → reversible)

•Intrarenal: ischemia/toxins → tubular injury (ATN)

•Sloughed cells → tubular obstruction → ↓ urine flow

•Postrenal: obstruction → ↑ pressure → ↓ GFR

•Common Outcomes:

•↓ GFR → ↑ BUN, ↑ Cr

•Fluid retention → edema, pulmonary congestion

•↓ Excretion:

•↑ H⁺ → metabolic acidosis

•↑ K⁺ → hyperkalemia

Key Flow:

↓ perfusion → ↓ GFR → ↑ waste + ↓ urine → fluid overload + electrolyte imbalance

AKI phases

1. Initiation: Initial insult → ↓ perfusion/injury

2. Oliguric: ↓ GFR, ↓ urine → fluid overload, electrolyte imbalance

3. Diuretic: ↑ dilute urine → risk dehydration, electrolyte loss

4. Recovery: Nephrons recover → GFR improves

AKI management

•Dialysis → fluid overload, uremia

•Strict I&O → fluids ~ output or ~1 L/day

•↑ K⁺ → insulin + glucose, Kayexalate

•↑ Phos → Ca carbonate / Ca acetate

•Diuretics → ↓ fluid overload

•Antihypertensives / vasopressors as needed

•Renal doses ↓ (e.g., aminoglycosides, digoxin, ACEi)

•Diet → ↑ carbs, ↓ protein, ↓ K⁺/Na⁺/Phos

Sodium polystyrene sulfonate (kayexalate)

Therapeutic Class: Electrolyte modifier

• Pharmacologic Class: Cation exchange resin

▪ Mechanism of Action (MOA): Binds with potassium ions

in the gastrointestinal tract, exchanging sodium ions to

increase fecal potassium excretion.

▪ Uses: Treatment of hyperkalemia (high potassium levels).

▪ Adverse Drug Reactions (ADR): Gastrointestinal upset

(nausea, vomiting, constipation), Hypokalemia (low

potassium levels), Sodium retention

▪ Contraindications: Bowel obstruction, Severe

constipation

▪ Nursing Considerations:

▪ Monitor electrolyte levels (potassium, sodium) regularly.

▪ Assess for gastrointestinal symptoms.

▪ Administer with sorbitol to enhance efficacy and reduce risk

of constipation.

▪ Educate patient on dietary potassium restrictions.

CKD

▪ Definition: Progressive, irreversible ↓ renal function (months–years)

•Causes:

•Diabetes → glomerular damage

•HTN → vascular damage, glomerulosclerosis

•Glomerulonephritis, PKD, nephrotic syndrome

•Pathophysiology:

•Nephron loss → ↓ GFR → compensatory hyperfiltration → further damage

•Key Effects:

•↑ waste (uremia), fluid retention

•↑ K⁺, ↑ H⁺ → metabolic acidosis

•↑ phosphorus, ↓ calcium

•↓ erythropoietin → anemia

CKD progression

•Stage 1: ≥ 90 (damage with normal GFR)

•Stage 2: 60–89 (mild ↓)

•Stage 3: 30–59 (moderate ↓)

•3A: 45–59

•3B: 30–44

•Stage 4: 15–29 (severe ↓)

•Stage 5: < 15 → ESRD

AKI vs CKD Management

Slow Progression:

•Control glucose, HTN, lipids

•Avoid nephrotoxins (NSAIDs, contrast, certain antibiotics)

•Renal dose adjustments

•Correct Complications:

•Anemia → iron, epoetin

•↑ Phos / ↓ Ca → phosphate binders, vitamin D

•Acidosis → oral bicarbonate

•Monitor:

•I&O, daily weights, electrolytes

Advanced CKD Management and LIfestyle

Diet:

•↓ protein, ↓ Na⁺, ↓ K⁺, ↓ phosphorus

•Maintain glucose control

•Medications:

•Diuretics (fluid, BP control)

•Supplements → Ca, vitamin D, iron, folate

•Dialysis:

•Initiate when unable to maintain homeostasis

ESRN pathophysiology and manifestations

•Severe ↓ GFR → failure of filtration

•Effects:

•↑ uremia → encephalopathy

•Fluid overload → edema, pulmonary edema, HF

•↑ K⁺ → arrhythmia risk

•↑ H⁺ → metabolic acidosis

•↓ erythropoietin → anemia

•↓ vitamin D → hypocalcemia

•↑ phosphorus → secondary hyperparathyroidism

•Other:

•Proteinuria, hypoalbuminemia → edema

Uremic frost, fetor

Hemodialysis

Blood filtered via dialyzer 2-4x/week, 3-5 hr/session. Rapid fluid/electrolyte shifts. Requires vascular access. Risk: hypotension, cramps

Peritoneal Dialysis

Peritoneum acts as filter. Daily (CAPD or APD). SLower, continuous removal. Uses peritoneal catheter. Risk: peritonitis

Dialysis access and complications

•AV Fistula:

•Preferred → ↓ infection, ↑ longevity

•AV Graft:

•Alternative → ↑ clotting/infection risk

•Dialysis Catheter:

•Temporary → ↑ infection risk

•Dialysis Complications:

•Infection

•Hypotension

•Fluid imbalance

•Bleeding

ESRD diet and management

•Diet & Meds: Same principles as CKD (more strict)

•Fluid: ~1200 mL/day or output + 500 mL

•Na⁺: ↓ (≤ 2 g/day)

•K⁺: ↓ (≤ 2 g/day)

•Phosphorus: ↓ (1000–1200 mg/day)

•Avoid: processed foods, ↑ K⁺, ↑ phosphorus foods

•Management:

•Dialysis or transplant

•Medication + electrolyte control

Kisney Transplant

•Definitive treatment for ESRD

•Limited by donor availability, eligibility

•Sources:

•Living donor, brain-dead donor,

cardiac death

•Post-Transplant:

•Immunosuppressants +

corticosteroids

•Rejection (early risk):

•Fever, ↑ creatinine, weight gain, graft

tenderness

Urinary incontinence

•Definition: Involuntary urine leakage

•Types & Patho:

•Stress: ↑ intra-abdominal pressure → weak

pelvic floor

•Urge (overactive bladder): ↑ detrusor activity

(ACh mediated)

•Overflow: bladder overdistention →

incomplete emptying

•Functional: impaired mobility/cognition

•Key Concept:

•↓ sphincter support or ↑ detrusor activity → leakage

Urinary retention

Definition: Inability to fully empty

bladder

•Causes (Patho):

•Obstruction: BPH (most common),

stones, tumors

•Neurogenic: ↓ detrusor contraction

(nerve dysfunction)

•Medications: anticholinergics, opioids

•Clinical Findings:

•↓ urine output, bladder distention

•Overflow incontinence, ↑ infection risk

•Key Concept:

•↓ detrusor contraction or obstruction →

urine retention

Urge incontinence drug

▪ Prototype: Oxybutynin (anticholinergic)

▪ MOA: Blocks muscarinic receptors → ↓ detrusor contraction

▪ ADR: dry mouth, constipation, urinary retention, confusion

▪ Key risk: worsens retention

Urinary retention (BPH) drug

▪ Prototype: Tamsulosin (α₁-blocker)

▪ MOA: Relaxes smooth muscle in prostate/bladder neck → ↑ urine flow

▪ ADR: orthostatic hypotension, dizziness

▪ Teaching: take at bedtime, fall risk

Urinary retention (non-BPH) drug

▪ Prototype: Bethanechol (cholinergic)

▪ MOA: stimulates muscarinic receptors → ↑ detrusor contraction

▪ ADR: bradycardia, diarrhea, bronchospasm

▪ Teaching: use only for non-obstructive retention; avoid if obstruction

present