NURS 370 Renal & Electrolytes Updated Final Exam Study Guide

Pre-renal Acute Kidney Injury (AKI) Causes/Mechanisms

Most common; results from decreased perfusion.

Hypovolemia ECV depletion (hemorrhage, dehydration, burns)

Hypotension/shock States

Sepsis

CV Pump Failure: Heart failure, MI, Tamponade, dysrhythmia.

Renal artery stenosis (narrowing), ​

Obstructed Blood Flow: vena cava obstruction, renal artery stenosis, thrombosis.

Pre-renal Acute Kidney Injury (AKI) Presentations

oliguria, concentrated urine, high BUN/Cr ratio, hypotension, tachycardia, dry mucosa, poor skin turgor, weight loss or acute gain if third‑spacing.​

Intra-renal Acute Kidney Injury (AKI) Causes/Mechanisms

Direct injury to the nephron

Acute tubular necrosis (ischemia/toxins)

Nephrotoxic drugs (NSAIDs, aminoglycosides, IV contrast, ABX)

Glomerulonephritis: including allergic reactions or infections.

Vasculitis: caused by infections or autoimmune diseases.

Interstitial Nephritis: inflammation of the kidney interstitium, often due to medications or infections. (HIV, Nephropathy, DM, transfusion reactions, SLE, DIC)

Trauma

Intra-renal Acute Kidney Injury (AKI) Presentations

Oliguria or non‑oliguric AKI

Muddy brown casts

Rising creatinine and BUN

Variable BP and edema

Often hematuria/proteinuria in GN.

Post-renal Acute Kidney Injury (AKI) Causes/Mechanisms

Obstruction to urine outflow

Stones (Calculi)

Tumors

Clots

BPH

Strictures

Neurogenic bladder.

All leading to Ureteral, Bladder, and Urethral Obstructions.

Post-renal Acute Kidney Injury (AKI) Presentations

Initial frequency/hesitancy

Flank/suprapubic pain

Distended bladder, then oliguria/anuria; hydronephrosis on imaging

Acute Kidney Injury (AKI) Presentations: Oliguric/Anuric Phase

• Output <400 mL/day, often near zero

• Fluid overload: progressive weight gain, edema, JVD, crackles, pulmonary congestion, hypertension

• Uremic symptoms: nausea, vomiting, pruritus, confusion, seizures, metallic taste​

• Electrolyte imbalance: rapid rises in K (hyperkalemia), metabolic acidosis (low bicarbonate), dilutional hyponatremia/hypervolemia

• Labs: BUN/Cr climb rapidly, Ca↓, PO₄↑, anemia develops (↓EPO)​

Acute Kidney Injury (AKI) Presentations: Diuretic Phase

• Massive urine loss (1–5+ L/day) but poor concentration: risk of dehydration, hypotension, loss of Na/K​

• K, Na fall—careful replacement required

• BUN/Cr begin to drop but remain high, output gradually normalizes​

Acute Kidney Injury (AKI) Presentations: Recovery Phase

Gradual restoration of output and normalization of acid/base/electrolyte balance over weeks to months; some may never fully recover​

Major CKD Complications

• Fluid overload → hypertension, edema, pulmonary edema, HF.

• Hyperkalemia → life‑threatening dysrhythmias.

• Metabolic acidosis → fatigue, Kussmaul respirations, confusion.

• Mineral–bone disorder: hyperphosphatemia, hypocalcemia, low vitamin D → renal osteodystrophy, fractures, bone pain.

• Anemia and platelet dysfunction → fatigue, pallor, bleeding risk.

• Uremic symptoms: N/V, pruritus, uremic frost late, pericarditis, encephalopathy.

• End‑organ effects: cardiomyopathy, accelerated atherosclerosis, immune suppression, poor wound healing.

BUN

• Blood Urea Nitrogen

• A byproduct of protein -> protein breakdown

• Highly affected by hemodynamics (concentrated vs. diluted) = remember your Hematocrit, Sodium, BUN (“He’s So Bloody)

• Kidney should be clearing the urea from the blood 

• Elevated w/ hepatic or renal impairment, dehydration, high protein diet, infection, steroid use, GIB (GI bleed) 

• Decreased w/ malnutrition, fluid volume excess, severe hepatic damage

BUN Normal Rate

8-25mg/dL (HESI 10-20)

Creatinine

• A byproduct of muscle breakdown

• INC Cr is an indication of a confirmed renal dysfunction 

• Kidney should be clearing the creatinine from the blood 

• Elevated only w/ renal impairment 

• Decreased w/ reduced muscle mass (ie: muscle breakdown) 

• Measured in the blood - the build of creatinine (a byproduct of muscle breakdown)

• INCREASED Creatinine in the blood = kidney dysfunction

Creatinine Normal Range

0.6-1.5 mg/dL (HESI: 0.6-1.2)

Creatinine Clearance

• Measured in the urine - Cr that was cleared = excreted

• DECREASED Creatinine in the urine = kidney dysfunction

BUN/Cr Ratio

• Rise in both means renal impairment

• Increased ratio = fluid volume deficit or hypoperfusion of kidneys

• Decreased ratio = fluid volume excess or malnutrition

• A pt w/ chronic renal failure may have a different baseline -> consult their healthcare team about what their normals are

BUN/Cr Ratio Normal Range

BUN/Cr ratio (10:1 - 20:1)

Glomerular Filtration Rate (GFR)

This shows how well your kidneys are filtering to filter out wastes and remove excess water (making urine).

Glomerular Filtration Rate (GFR) Normal Range

• A GFR of 60 or higher is the normal range.

• A GFR below 60 may mean kidney disease.

• A GFR of 15 or lower may mean kidney failure.

Urinalysis

• Bacteria & Leukocytes

• Color – dark yellow, straw yellow

• Clarity – cloudy (inc # protein or UTI), or clear

• Specific Gravity – 1.010 to 1.030 

• pH (4-8) – ability for acid base balancing 

• Protein – muscle breakdown or break too much protein 

• Ketones – byproduct of fat breakdown (DKA) 

• Glucose

• Nitrites – cue us into a UTI

• Bilirubin/urobilinogen - byproduct of accessory GI system (liver fn and gallbladder)

Peritoneal Dialysis (PD): Disadvantages and Complications

Peritonitis: Watch for cloudy effluent, abdominal pain, fever. Nursing Action: Send sample/culture, start antibiotics per order.

2. Catheter Site/Tunnel Infection: Risk of exit site infection.

3. Protein Loss: Can lead to malnutrition.

4. Poor Ultrafiltration/Fluid Overload: If membrane is less effective.

5. Abdominal Discomfort: Can include hernias, back pain due to intra-abdominal pressure.

Peritoneal Dialysis (PD) Complications: Peritonitis

Most Important

• Inflammation/infection of the peritoneum/membrane lining the abdominal wall and covering the abdominal organs

• Often caused by the percutaneous catheter.

S/SX: cloudy effluent, abdominal pain or tenderness, rebound, fever, N/V, general malaise.

Sx of Peritonitis

• Rigid board like abdomen with rebound tenderness and distention -> abdomen feels firm like a table or surface

• Increased pulse, blood pressure, dehydration, pain (all d/t infection)

• Decreased bowel sounds (body fighting infection, decreased parasympathetic activity)

• Fever (infection)

• N/V 

• Anorexia (not wanting to eat/absorbing nutrients)

Peritoneal Dialysis (PD) Complications: Exit-site/tunnel Infections

Infections occurring at the site where the dialysis catheter exits the body or along the tunnel where the catheter is placed, potentially leading to peritonitis.

S/SX: Redness, tenderness, drainage around catheter, sometimes fever.

Require local care and systemic antibiotics; prevent with meticulous daily exit-site care and aseptic technique during exchanges.

Peritoneal Dialysis (PD) Complications: Poor inflow/outflow and Mechanical Problems

Issues with dialysis fluid entering or exiting the peritoneal cavity due to catheter kinking, migration, or blockage. These complications can lead to inadequate dialysis and require evaluation and intervention.

S/SX: Constipation, kinked tubing, catheter malposition, fibrin clots.

Nursing: check tubing for kinks, reposition patient (side‑to‑side, sitting upright), encourage bowel regimen for constipation, use heparin in dialysate if fibrin present (if ordered).

Assessing the Dialysate

• Blood in dialysate: trauma during insertion

• Yellow in dialysate: protein in fluid (expected)

• Cloudy dialysate: presence of bacteria in peritoneum dt insertion/contamination of PD cath

• Brown or green dialysate: suspect bowel perforation

  • STOP PD, clamp tubing

  • THEN call the physician STAT (bowel perforation is a surgical emergency!)  

Indications for Emergent Hemodialysis

• A – Acidosis: severe metabolic acidosis (pH ≲7.1–7.2) unresponsive to medical therapy.

• E – Electrolytes: especially refractory hyperkalemia (K typically ≥6.0 with ECG changes) despite meds.

• I – Intoxications: certain dialyzable toxins if listed in protocol.

• O – Overload: fluid overload/pulmonary edema not responsive to diuretics causing hypoxia or hemodynamic compromise.

• U – Uremia: uremic pericarditis, encephalopathy, seizures, severe nausea/vomiting or bleeding from platelet dysfunction.​

Practical triggers: rising K with arrhythmias, severe dyspnea from pulmonary edema, uremic pericardial friction rub, rapidly increasing creatinine with anuria, or severe symptoms not improving with conservative care.

Indications for Dialysis: “HAVE PEE”

• Hyperkalemia

  • Due to inability to excrete K+

• Acidosis

  • Cannot excrete H+ ions and cannot make HCO3

  • Loss of nephrons leads to loss of compensation for acid load causing HCO3 deficit leading to metabolic acidosis

• Volume overload

  • Cannot excrete the fluid -> retention

• Elevated BUN

  • The amount of urea/nitrogen in blood (byproducts of protein metabolism/catabolism) -> elevated bc kidneys cannot excrete 

• Pericarditis

  • Inflammation of the visceral and parietal layers of the pericardium by metabolic toxins that accumulate in the body

• Encephalopathy

  • Uremic encephalopathy is a cerebral dysfunction caused by the accumulation of toxins as a result of acute or chronic renal failure

Edema (Pulmonary)

Volume overload stretching the vessels causing leakage into lungs

High-Risk Electrolyte Disturbances in Renal Failure: Hyperkalemia (K>5.5)

Most life-threatening! Results from inability to excrete K; seen in oliguria, ESRD, missed dialysis, ACE-Is/ARBS, K-sparing diuretics, tissue breakdown, metabolic acidosis

Hyperkalemia (K>5.5) Symptoms

Muscle Weakness

Flaccidity

Paresthesia’s; can progress to paralysis.

Hyperkalemia (K>5.5) EKG Changes

Peaked T Waves

Widened QRS

Prolonged PR

Risk of heart block or arrest.

VF

Hyperkalemia (K>5.5) Medication Considerations & Treatment

Restrict K intake, avoid excess K in IV fluids and diet; hold ACE‑Is/ARBs/K‑sparing diuretics if hyperkalemic

Urgent medical management includes insulin/glucose, sodium bicarbonate (if acidotic) calcium gluconate (Stabilizes Myocardium), Beta-agonists, kayexalate, or dialysis.​

High-Risk Electrolyte Disturbances in Renal Failure: Hyperphosphatemia/Hypocalcemia

CKD leads to phosphate retention, binding/free calcium reduction, and decreased vitamin D activation.

Due to phosphate retention and impaired vitamin D activation.

Hyperphosphatemia/Hypocalcemia Symptoms

Bone Pain

Fractures (renal Osteodystrophy

Pruritus

Calcifications in Soft Tissues

Muscle Cramps

Tetany

Chvostek’s/Trousseau Signs

Hypocalcemia EKG Changes

Prolonged QT Interval

Possible ST segment changes.

Hyperphosphatemia/Hypocalcemia Management & Treatment

Phosphate binders

Dietary avoidance

Ca supplements

Activated vitamin D

High-Risk Electrolyte Disturbances in Renal Failure: Metabolic Acidosis

• HCO₃ is depleted; kidneys can’t excrete acid load or reabsorb bicarbonate

• Symptoms: confusion, Kussmaul respirations, fatigue, vomiting, arrhythmias

• Management: sodium bicarbonate if pH <7.2, treat underlying AKI/CKD​

High-Risk Electrolyte Disturbances in Renal Failure: Hyper/Hyponatremia

• Can be low (dilutional, SIADH, fluid excess) → seizures, coma

• Can be high (profound water loss, DI) → neurologic instability​

• Management: depends strictly on underlying pathology and fluid status, slow correction needed to avoid Osmotic Demyelination

Hyponatremia S/SX

Headache

Confusion

Seizures

High‑risk electrolyte disturbances in renal failure

• Hyperkalemia: most immediately life‑threatening; tight monitoring of K, continuous ECG if high or rising, and readiness for rapid treatment or dialysis.

• Hyperphosphatemia/hypocalcemia: drive bone disease and soft‑tissue calcification; require chronic binding and vitamin D therapy.

• Metabolic acidosis: contributes to bone loss, muscle wasting, fatigue, and arrhythmias; may be treated with oral or IV bicarbonate and dialysis depending on severity.

• Volume overload/hyponatremia: can precipitate pulmonary edema and HF; requires strict fluid and sodium control and often dialysis.​

Pharmacological Considerations For Complications of Renal Failure

• For HTN: give prescribed anti-hypertensive meds

• For Volume overload: diuretics  + Potassium-wasting diuretics

• For Anemia: Folic Acid & Ferrous Sulfate (iron) 

• For Hypocalcemia: Phosphate binders – when phosphate binder is administered, you LOWER it ⇒ increases calcium; CA+ + supplements

• Stool softeners & laxatives (iron causes constipation)

SIADH (Syndrome of Inappropriate ADH)

Endocrine-Related Fluid/Electrolyte Disorders that leads to excessive release of antidiuretic hormone (ADH), causing water retention, dilutional hyponatremia, and potential neurological symptoms.

• Patho: Excess ADH → water retention, dilutional hyponatremia, low serum osmolality, high urine osmolality

SIADH (Syndrome of Inappropriate ADH) LABS

Na <135

Low serum osmolality < 280 mOsm/kg (NR: 280-300mOsm/kg)

Urine osmolality > 100 mOsm/kg.

High urine specific gravity >1.03 (NR: 1.010-1.030)

Serum Osmolality

• What it measures: The number of dissolved particles, such as sodium, chloride, glucose, and urea, in the liquid portion of blood.

• Purpose: Helps determine if there is a good balance of fluid and dissolved substances in the blood. 

Low Specific Gravity

(below 1.010): Indicates dilute urine, often due to drinking too many fluids or impaired kidney function.

High Specific Gravity

(above 1.030): Indicates concentrated urine, often due to dehydration.

SIADH (Syndrome of Inappropriate ADH) Presentation

Confusion

Seizures

Muscle cramps

Headache

Weight gain

Decreased urine output.​

SIADH (Syndrome of Inappropriate ADH) Management

Fluid restriction

Salt tabs

Correct cause

Slow Na correction to prevent central pontine myelinolysis.​

Nursing priorities:

• Fluid restriction (often 800–1000 mL/day or as ordered), frequent neuro checks, seizure precautions.

• Monitor Na closely, strict I/O and daily weights.

• Treat underlying cause; hypertonic saline and vasopressin receptor antagonists per provider for severe cases

DI (Diabetes Insipidus, Central or Nephrogenic)

Endocrine-Related Fluid/Electrolyte Disorders

• Patho: ADH deficit (central) or renal resistance (nephrogenic) → massive polyuria, hypernatremia, dehydration

DI (Diabetes Insipidus, Central or Nephrogenic) Labs

Na >145

Polyuria (4–18+ L/day)

Dilute urine (SG <1.005)

High serum osmolality

Low urine osmolality

DI (Diabetes Insipidus, Central or Nephrogenic) S/SX

Polydipsia (Thirst)

Dry mucosa

Hypotension

Tachycardia

Confusion

Fatigue

DI (Diabetes Insipidus, Central or Nephrogenic) Management & Treatment

Vasopressin/desmopressin for central DI

Thiazide diuretics for nephrogenic

Careful fluid replacement.

Nursing priorities:

• Replace water losses carefully (oral/IV), monitor Na and osmolality, daily weights, strict I/O.

• For central DI, administer desmopressin/vasopressin as ordered and monitor for water intoxication; for nephrogenic, thiazides and salt restriction may be used.

Common Risk Factors for Progression to Advanced Kidney Disease

Most significant factors (with mechanisms):

• Diabetes Mellitus: Persistent hyperglycemia causes glomerulosclerosis and vascular injury, leading to proteinuria and nephron death.​

• Hypertension: High pressure damages glomeruli and microvasculature; RAAS activation worsens retention and fibrosis.​

• Autoimmune/Glomerular disease: Lupus, IgA nephropathy, vasculitis trigger chronic inflammation and scarring.​

• Chronic obstruction: Stones, BPH, tumors cause pressure damage and repeated infection risk.​

• Nephrotoxins: NSAIDs, aminoglycosides, IV iodine contrast—direct tubular toxicity and necrosis.​

• Infections: Untreated pyelonephritis or urosepsis can destroy nephrons.​

• Genetic diseases: PKD—large cysts crowd functional tissue, leading to ischemia and failure.​

• Older age, family history, smoking, CVD: Accelerate decline by compounding vascular/nephron injury.​

• Non-adherence: Missing BP/glucose control, dialysis, or nephroprotective diet accelerates GFR loss.​