Renal Disorders

Nephron

• The functional unit of the kidney

• Glomerular filtration → tubular reabsorption → tubular secretion

1000-2000 ml/day (approx. 1ml/kg/hr)

Normal output threshold in normal adults

<0.5 ml/kg/hr or <400 ml/24 hr

• Critical alarm output threshold (oliguria)

• Requires immediate provider notification

Serum creatinine

[SERUM VALUES]

• Most sensitive indicator of renal parenchymal function

0.6-1.2 mg/dl

[SERUM VALUES]

• Normal serum creatinine

Blood urea nitrogen

[SERUM VALUES]

• Influenced by protein intake, hydration, and GI bleeding

7-20 mg/dl

[SERUM VALUES]

• Normal BUN

BUN-to-Creatinine ratio

[SERUM VALUES]

• A ratio of greater than 20:1 suggests pre-renal causes/dehydration

20:1

[SERUM VALUES]

• Normal BUN-to-Creatinine ratio

Glomerular filtration rate (GFR)

[SERUM VALUES]

• Normal is more than 90 ml/min/1.73m²

Cystitis

Inflammation and infection of the bladder mucosa

Urethritis

Inflammation and infection of the urethra

Cystitis and urethritis

The two most common lower urinary tract infections:

• Primary pathogen: Escherichia coli

• Risk factors: Female anatomy (short urethra), urinary stasis, indwelling catheters (CAUTI), sexual intercourse, diabetes mellitus, and postmenopausal estrogen loss

Etiology and risk factors of lower UTI:

Pathogens ascend from the perineum through the urethra into the sterile bladder → bacterial colonization → mucosal adherence and inflammatory response → localized edema and irritation

Pathophysiology of lower UTI

• Classic triad: dysuria, urgency, frequency (> 8 times/day)

• Suprapubic pain/discomfort, hematuria, cloudy or foul-smelling urine

• Geriatric specifics: Often lack typical dysuria, presents with acute delirium/confusion, lethargy, anorexia, and sudden incontinence

Signs and symptoms of lower UTI:

• Urinalysis: Positive leukocyte esterase (indicates WBCs) and positive nitrates (indicates Gram-negative bacteria)

• Clean-catch midstream urine culture: colony count of more than or equal to 10^5 CFU/ml

Diagnostics of lower UTI:

• First-line antibiotics: Nitrofurantoin, trimethoprim-suflamethoxazole, or fosfomycin

• Urinary analgesic: Phenazopyridine (relieves burning/spasms)

Medical management of lower UTI:

• Critical patient teaching: Warn patients that phenazopyridine turns urine into a bright orange/red color and stains soft contact lenses

• Hydration: Encourage 2-3 L/day of fluids to mechanically flush out bacteria

• Avoid bladder irritants: Restrict caffeine, alcohol, citrus juices, and artificial sweeteners

• Hygiene education: Wipe front-to-back; void immediately after sexual intercourse, and avoid bubble baths and douching

Nursing assessment and interventions for lower UTI:

Upper UTI (Acute pyelonephritis)

Bacterial infection involving the renal pelvis, tubules, and interstitial tissue of one or both kidneys

Ascending infection from a lower UTI (vesicoureteral reflux) or hematogenous spread

Etiology of upper UTI or acute pyelonephritis

Bacteria invade the renal parenchyma → intense acute inflammatory response → tubular necrosis and micro-abscess formation → potential permanent renal scarring if untreated

Pathophysiology of upper UTI

• Flank pain or costovertebral angle (CVA) tenderness upon percussion

• Systemic signs: High fever, shaking, chills, nausea, vomiting, malaise, leukocytosis

Clinical manifestations of upper UTI:

• 14-day course of broad-spectrum IV/oral antibiotics (Fluoroquinolones, Cephalosporins)

• Monitor for urosepsis (hypotension, tachycardia, tachypnea, fever/hypothermia)

• Ensure full completion of the antibiotic regimen; schedule follow-up repeat urine cultures

Medical and nursing management of upper UTI

Urolithiasis and nephrolithiasis (urinary calculi)

Formation of calcified stones (calculi) within the urinary tract or kidney parenchyma

• Calcium oxalate/phosphate (75-80%), uric acid, struvite (infection-associated), cystine

Etiology of urinary calculi and stone types:

Dehydration, immobility, hyperparathyroidism, gout, warm climates

Risks that may lead urinary calculi

• High urinary supersaturation of stone-forming salts + deficiency of stone inhibitors → crystallization → stone aggregation → lodgment in renal pelvis or ureter → obstruction → urinary back pressure and painful ureteral spasm (colic)

• Stone obstruction in ureter → ureteral smooth muscle spasm (severe renal colic) → hydronephrosis (urine backup into renal pelvis) → increased intrarenal pressure → risk of acute kidney injury

Pathophysiology of urinary calculi

• Renal colic: Sudden, excruciating, radiating flank pain (moves down toward the groin, scrotum, or labia)

• Hematuria (macro- or microscopic), nausea, vomiting, diaphoresis, dysuria

Signs and symptoms of urinary calculi:

Non-contrast spiral CT scan (gold standard), KUB (Kidney, ureter, bladder) X-ray, ultrasound

Diagnostic test for urinary calculi

• Pain control: IV NSAIDs (Ketorolac) and opioids

• Alpha-blockers (Tamsulosin) to relax ureteral smooth muscle and facilitate passage

• For stones > 10 mm or non-passing; Extracorporeal shock wave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy

Medical and surgical management of urinary calculi:

• Strain all urine: Collect passed stone using a urine strainer/filter and send to the laboratory for chemical analysis

• Push fluids (>3L/day) to promote hydrostatic propulsion of the stone

• Post-ESWL care: Educate the patient that mild flank soreness, slight hematuria, and bruising over the flank are expected findings; report gross clots or intractable pain immediately

Essential nursing interventions for urinary calculi:

Neurogenic bladder and urinary retention

Bladder dysfunction resulting from central or peripheral nervous system lesions, leading to retention or incontinence

Spastic (Hyperreflexic/upper motor neuron)

[CLASSIFICATION OF NEUROGENIC BLADDER]

• Spinal cord injury above T12, stroke, MS. Loss of voluntary control; reflex bladder contractions cause uninhibited, frequent emptying/spasms

Flaccid (Atonic/lower motor neuron)

[CLASSIFICATION OF NEUROGENIC BLADDER]

• Spinal cord injury below T12, diabetic neuropathy. Loss of sensory/motor reflex arc; bladder overfills and becomes distended, causing overflow incontinence

Chronic urinary stasis, severe vesicoureteral reflux, hydronephrosis, and renal failure

Complications of neurogenic bladder:

Post-vid residual via bladder scanner

• Normal PVR: <50 ml in young adults, <100 ml in older adults

• PVR > 100-200 ml indicates pathological urinary retention

Diagnostic assessment of neurogenic bladder and urinary retention

• Intermittent self-catheterization: Gold standard for flaccid bladder; perform every 4-6 hours (clean technique at home, sterile technique in acute care)

• Bladder training schedule: Scheduled voiding every 2 hours; teach the Crede Maneuver (gentle manual suprapubic pressure during voiding for flaccid bladder - contraindicated if reflux is present)

• Medications:

  • Anticholinergics/antimuscarinics (Oxybutynin) to calm spastic contractions

  • Cholinergic agonist (Bethanechol) to stimulate detrusor tone in flaccid bladdders

Interventions and nursing considerations for neurogenic bladder and urinary retention

Check and drain the bladder

Autonomic dysreflexia: In patients with spinal cord injury at or above T6, bladder distention can trigger severe hypertension, bradycardia, diaphoresis, and pounding headache. What is the immediate action?

Acute nephritic syndrome (Glomerulonephritis)

Acute inflammation of the glomerular capillaries, most classically post-streptococcal glomerulonephritis

Occurs 10-14 days following a Group A beta-hemolytic streptococcal pharyngitis or skin infection (impetigo)

Etiology of acute nephritic syndrome

Antigen-antibody immune complexes deposit in glomerular basement membranes → complement activation → cellular proliferation and capillary damage → marked decrease in GFR + leakage of red blood cells and protein

Pathophysiology of acute nephritic syndrome

• Hematuria (Cola/tea-colored or smokey urine)

• Periorbital edema (prominent in the morning) and peripheral edema

• Hypertension and oliguria

• Mild-to-moderate proteinuria

Signs and symptoms of acute nephritic syndrome:

Elevated antistreptolysin O titer, decreased serum complement levels, RBC casts on urinalysis

Diagnostics of acute nephritic syndrome

• Sodium and fluid restriction

• Daily weights

• Close blood pressure monitoring

Nursing priorities in acute nephritic syndrome:

Nephrotic syndrome

A constellation of clinical findings resulting from marked increased glomerular permeability

Massive proteinuria (> 3.5 g/24 hr)

Diagnostic hallmark of nephrotic syndrome:

Increased glomerular permeability → massive proteinuria (albumin loss) → hypoalbuminemia → decreased oncotic (colloid osmotic) pressure → fluid shift into interstitium → severe anasarca and ascites → compensatory hepatic lipid synthesis → hyperlipidemia

Pathophysiology of nephrotic syndrome:

• Severe generalized pitting edema (Anasarca)

• Soft/foamy urine

• Hyperlipidemia

• Thromboembolic events (loss of Antithrombin III in urine)

Clinical findings on nephrotic syndrome:

• Corticosteroids (Prednisone)

• Loop diuretics

• ACE inhibitors (reduce proteinuria)

• Statins and anticoagulants if thrombus forms

Medical management in nephrotic syndrome:

• Monitor abdominal girth and daily weights

• Meticulous skin care to prevent breakdown over edematous area

• Low-sodium, moderate-protein diet

Nursing care for nephrotic syndrome:

Acute kidney injury

Rapid, sudden decline in renal function over hours to days with retention of nitrogenous wastes (azotemia) and loss of fluid/electrolyte regulation

Pre-renal (Hypoperfusion)

[FUNCTIONAL CATEGORY OF AKI]

• Issue before the kidney

• Causes: Hypovolemia, hemorrhage, severe dehydration, heart failure, shock, sepsis

Intra-renal (Parenchymal damage)

[FUNCTIONAL CATEGORY OF AKI]

• Structural damage inside the kidney tissue

• Causes: Acute tubular necrosis, IV iodinated contrast dyes, aminoglycosides (Gentamycin), NSAIDs, myoglobinuria (rhabdomyolysis)

Post-renal (Obstruction)

[FUNCTIONAL CATEGORY OF AKI]

• Urine flow obstruction after the kidney

• Causes: BPH, nephrolithiasis, urethral stricture, pelvic tumors

Initiation/onset

[PHASES OF AKI]

• Initial insult occurs

• Asymptomatic

Oliguric phase

[PHASES OF AKI]

• Urine output < 400 ml/day

• Hyperkalemia, metabolic acidosis, fluid volume excess, elevated BUN/creatinine

Diuretic phase

[PHASES OF AKI]

• Urine output surges (1-5 L/day) as nephrons recover filtration but lack concentrating ability

• Major risks: Severe hypovolemia, hypokalemia, and hyponatremia

Recovery phase

[PHASES OF AKI]

• GFR stabilizes toward baseline (takes 3-12 months)

IV calcium gluconate

[ACUTE POTASSIUM-LOWERING REGIMEN]

• Stabilizes the myocardial membrane (prevents arrhythmias; does not lower potassium)

IV regular insulin + D50W

[ACUTE POTASSIUM-LOWERING REGIMEN]

• Shifts potassium intracellularly

Inhaled albuterol

[ACUTE POTASSIUM-LOWERING REGIMEN]

• Drives potassium into cells

Sodium polystyrene sulfonate (Kayexalate) or Patiromer

[ACUTE POTASSIUM-LOWERING REGIMEN]

• Eliminates potassium via the GI tract

Emergency hemodialysis

[ACUTE POTASSIUM-LOWERING REGIMEN]

• Definite and fastest removal of potassium

Chronic Kidney Disease & End-Stage Kidney Disease

Progressive, irreversible loss of nephron function lasting > 3 months

Diabetes mellitus and hypertension

Top two causes of CKD and ESKD

Stage 1

[STAGES OF CKD]

• Kidney damage with normal/high GFR (more than/equal to 90)

Stage 2

[STAGES OF CKD]

• Mild drop in GFR (60-89)

Stage 3a/3b

[STAGES OF CKD]

• Moderate drop in GFR (30-59)

Stage 4

[STAGES OF CKD]

• Severe drop in GFR (15-29)

• Preparation for renal replacement therapy

Stage 5

[STAGES OF CKD]

• Kidney failure (GFR < 15)

• Dialysis or kidney transplantation required for survival

• Cardio: Fluid overload, hypertension, pericarditis (due to uremic toxins), heart failure

• Hematologic: Normocytic anemia due to decreased synthesis of erythropoietin by failing renal peritubular cells

  • Management: Administer epoetin alfa/darbepoetin subcutaneously + Iron supplementation

• Mineral and bone disorder:

  • Loss of vitamin D activation → Hypocalcemia → Secondary hyperparathyroidism → Calcium leached from bone

  • Concurrently, hyperphosphatemia occurs

  • Management: Phosphate binders (Calcium acetate, Sevelamer) given strictly with meals to bind dietary phosphorus in the gut

• Neurologic: Uremic encephalopathy, peripheral neuropathy, severe pruritus (uremic frost)

• Hemodialysis AV fistula care:

  • Auscultate for a whooshing bruit; palpate for a vibrating thrill; absence indicates thrombosis

  • No blood pressures and venipunctures

  • No tight clothing/straps on the arm with the vascular access

Systemic manifestations of CKD/ESKD

• Peaked T waves (first identifiable sign)

• Omit potassium-sparing diuretics and ACE inhibitors

• Toxic to myocardium (leads to lethal dysrhythmias)

• Albuterol nebulizers drive potassium into cells

• Sodium bicarbonate (corrects underlying acidosis)

• Shift potassium with IV regular insulin +D50W

• Intravenous calcium gluconate (protects cardiac cells)

• Urgent hemodialysis needed if refractory

• Manage with GI binders (sodium polystyrene sulfonate)

ECG signs and risks of hyperkalemia in renal failure:

• Water balance

• Electrolyte balance

• Toxin excretion

• Waste clearance

• Acid-base balance

• Secretion of erythropoietin

• Transformation of vitamin D

• Endocrine control of blood pressure

• Drug metabolism

Six core functions lost in renal failure