Renal Disorders: AKI, CKD, Dialysis, Transplantation, and ADPKD

Comprehensive vocabulary flashcards reviewing the key concepts, mechanisms, complications, pharmacology, and clinical interventions for renal disorders based on the NURS 433 curriculum.

Acute Kidney Injury (AKI)

An abrupt decline in kidney function occurring over hours to days; filtration decline can precede rises in serum creatinine, and the condition can present as nonoliguric.

Prerenal AKI

A category of acute kidney injury caused by inadequate renal perfusion (such as from volume loss, hypotension, or low cardiac output); potentially reversible if renal perfusion is promptly restored. This type of AKI is characterized by low blood flow to the kidneys, leading to decreased glomerular filtration rate (GFR) and is often secondary to systemic issues.

Treatment:

• treat hypovolemia

• control hemorrhage

• treat shock/sepsis

• optimize cardiac function

Intrarenal AKI

A category of acute kidney injury resulting from direct damage to kidney tissue, including acute tubular injury/necrosis secondary to prolonged ischemia, nephrotoxin exposure, or glomerular, interstitial, and vascular lesions. Common causes include nephrotoxic medications, radiographic contrast in susceptible patients, toxic exposures, pigment injury like severe rhabdo, major surgery, shock, sepsis, and acute glomerulonephritis.

Treatment:

• treat underlying renal disease

• maintain appropriate perfusion

• support the patient while kidneys recover

Postrenal AKI

A category of acute kidney injury resulting from obstructed urine outflow (due to conditions such as BPH, calculi, tumors, or retention); managed by assessing bladder/catheter patency and relieving the obstruction.

Intravenous Calcium (in Hyperkalemia)

A critical emergency medication that stabilizes the cardiac membrane and protects the myocardium against potentially lethal dysrhythmias; it does not lower serum potassium levels.

Insulin and Dextrose (in Hyperkalemia)

A medical intervention that temporarily lowers extracellular serum potassium by shifting potassium intracellularly.

AEIOU Mnemonic

A clinical memory aid outlining the classic indications for urgent dialysis:

Acidosis: severe/refractory metabolic acidoisis

Electrolytes (e.g., hyperkalemia): especially dangerous/refractory hyperkalemia

Intoxications: certain dialyzable toxins

Overload (fluid): severe fluid overload/pulmonary edema not responding adequately to medical therapy

Uremia: serious uremic complications, encephalopathy, pericarditis, and significant symptomatic uremia

Chronic Kidney Disease (CKD)

Structural or functional abnormalities of the kidney persisting for $\ge 3\text{ months}$, most commonly caused by diabetes mellitus and hypertension. Other causes include glomerular disease, polycystic kidney disease, chronic obstruction, recurrent kidney injury, or autoimmune disease.

Albuminuria

The excretion of albumin into the urine indicating glomerular barrier breakdown, which provides significant prognostic risk stratification beyond eGFR alone. provides additional information about kidney damage and risk of progression and greater cardiovascular risk.

Normocytic/Normochromic Anemia of CKD

Anemia resulting from reduced renal production of erythropoietin (EPO), leading to decreased bone marrow stimulation and insufficient red blood cell production.

Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)

A systemic mineral and bone disorder initiated by phosphate retention and reduced calcitriol (active vitamin D) synthesis, resulting in altered calcium balance, secondary hyperparathyroidism, and abnormal bone remodeling.

• Clinical Manifestations:

  • Bone pain, osteomalacia/osteitis fibrosa, and increased fracture risk

  • Vascular and extraosseous soft tissue calcifications

  • Uremic pruritus

• Management Strategies:

  • Phosphate Binders: Administered directly with meals to bind dietary phosphorus in the gastrointestinal tract and prevent systemic absorption (eg. sevelamer, calcium acetate)

  • Calcitriol: Supplemented in selected cases to manage secondary hyperparathyroidism and suppress parathyroid hormone (PTH) excess

  • Individualized Dietary Adjustments: Restricting dietary phosphorus as tailored to the patient

  • Biochemical Monitoring: Routine surveillance of serum calcium, phosphate, and PTH levels

Phosphate Binders

Medications that bind dietary phosphorus within the gastrointestinal tract to prevent absorption; must be administered directly with meals.

ACE Inhibitors / Angiotensin Receptor Blockers (ACEI/ARB)

Renoprotective antihypertensives that cause efferent arteriolar vasodilation ( widens outflow)to reduce intraglomerular pressure and albuminuria in proteinuric CKD; require routine monitoring of serum potassium and creatinine (particularly after initiation).

Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors

Agents that reduce intraglomerular pressure by reducing sodium and glucose reabsorption in the proximal tubule to slow CKD progression in appropriate patients, and offer cardiovascular and heart failure risk reduction benefits.

Examples: Empagliflozin, dapagliflozin

Dry Weight

An estimate approximating a dialysis patient's euvolemic body weight without excess fluid; evaluated using pre- and post-dialysis weights based on the standard $1\,\text{kg} \approx 1\,\text{L}$ of water volume.

Arteriovenous (AV) Fistula

A surgically created direct connection between an artery and a vein that causes the vein to enlarge and its wall strengthens to tolerate repeated large-bore needle access for high blood flow for dialysis;

Advantages

• its durability

• lowest infection risk

• lower thrombosis rate compared to grafts,

Disadvantages:

• requires time to mature.

Arteriovenous (AV) Graft

A synthetic conduit surgically connecting an artery and a vein for dialysis access; usable sooner than a fistula but associated with higher infection rates, higher thrombosis rates, and shorter patency lifespan.

Dialysis Catheter

A central venous vascular device offering immediate access for hemodialysis, with bloodstream infection representing its primary disadvantage. Can only be used for a week.

Thrill and Bruit

A continuous palpable vibration (thrill) and audible vascular murmur (bruit) that signify patent blood flow through a functioning AV fistula or graft; their disappearance warrants immediate evaluation.

Dialysis Disequilibrium Syndrome

A central nervous system complication caused by cerebral edema that typically occurs during initial hemodialysis sessions or with severe pre-treatment azotemia; manifests as headache, confusion, and seizures. It is characterized by an electrolyte imbalance resulting from rapid changes in blood chemistry. Most frequently associated with first dialysis treatments.

Intradialytic Hypotension

An acute drop in blood pressure during hemodialysis causes dizziness, nausea, muscle cramping, or syncope; it is managed by stopping or reducing ultrafiltration, patient repositioning, administering IV normal saline as prescribed, and reassessing BP and symptoms. This is often due to rapid fluid removal during treatment. .

Peritoneal Dialysis (PD)

A renal replacement modality utilizing the patient's peritoneum as a semipermeable membrane across an inflow, dwell, and drain cycle; uses a glucose-containing dialysate to remove excess water via an osmotic gradient.

PD Peritonitis

A severe infection of the peritoneal cavity in peritoneal dialysis patients, classically signaled by cloudy dialysate drainage effluent accompanied by abdominal pain and tenderness. Other symptoms include fever, N/V, and malaise.

Nursing responsibilities:

• notify dialysis/nephrology team promptly

• obtain effluent speimen/cultures as ordered

• assess vital signs and patient condition

• administer prescribed antimicrobial therapy

• maintain meticulous aseptic technique

Hyperacute Rejection

An antibody-mediated graft rejection occurring within minutes to hours after kidney transplantation, caused by pre-existing anti-donor antibodies that lead to rapid graft failure.

Rare due to compatibility screening and effective cross-matching prior to transplantation. Symptoms may include fever, malaise, and decreased urine output.

Acute Rejection

An immune-mediated attack on a transplanted graft developing within days to months post-transplant (though possible later); frequently reversible if detected and managed promptly.

Major clinical concern! It typically involves a T-cell response against donor antigens, leading to inflammation and potential graft damage. Symptoms may include tenderness over the graft site, increased serum creatinine, and possible fever.

Chronic Rejection

An insidious, progressive immune and non-immune graft injury occurring over months to years that leads to irreversible, gradual loss of allograft function. It is characterized by chronic inflammation and fibrosis of the graft, generally resulting in a slow decline in kidney function. Symptoms can include slow worsening of renal function and eventual need for dialysis or retransplantation.

Tacrolimus (prograf)

A calcineurin inhibitor immunosuppressive agent characterized by toxicities including nephrotoxicity, neurotoxicity, hypertension, hyperglycemia, and hyperkalemia; necessitates frequent drug level, creatinine, blood glucose, BP, and electrolyte (K+) monitoring.

Increased creatinine may be from medication and not rejection.

Mycophenolate (CellCept)

An antiproliferative immunosuppressive drug whose adverse effects include bone marrow suppression, gastrointestinal distress, and heightened risk of infection; requires regular complete blood count (CBC) monitoring and signs of infection.

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A genetic renal disorder characterized by progressive fluid-filled cyst enlargement that compresses parenchyma, induces ischemia, activates the RAAS, and leads to nephron destruction; carries a $50\%$ inheritance risk per child.

Intracranial Aneurysm (in ADPKD)

A critical extrarenal vascular complication of ADPKD; the onset of a sudden, severe 'thunderclap' or 'worst headache of life' suggests possible rupture and subarachnoid hemorrhage, necessitating emergent evaluation.

Recognition and Diagnostic Pitfalls of AKI

Characterized by an abrupt decline in kidney function over hours to days; key clinical traps include relying solely on serum creatinine (which lags behind the true drop in filtration) and assuming preserved urine volume excludes injury, as the condition frequently presents as nonoliguric.

Serum Creatinine vs. Blood Urea Nitrogen (BUN)

Key diagnostic differences in evaluating renal clearance: creatinine is a more specific marker of glomerular filtration rate (GFR) derived from steady muscle metabolism (though its serum elevation lags behind acute filtration decline), whereas BUN measures urea produced from protein catabolism and is disproportionately influenced by volume status, catabolic state, and dietary protein intake. Both accumulate systemically as functional nephron mass declines.

Hyperkalemia in AKI

A high-priority complication resulting from impaired renal potassium excretion that carries a significant risk for lethal cardiac dysrhythmias. Immediate management centers on stabilizing the myocardium with intravenous calcium (which does not lower serum potassium levels), temporarily shifting potassium intracellularly using regular insulin and dextrose, and achieving definitive removal via diuretics, potassium binders, or emergent dialysis.

ECG Manifestations of Hyperkalemia

Progressive cardiac conduction abnormalities that typically begin with tall, peaked T waves, followed by prolonged PR intervals and flattened or absent P waves, widening of the QRS complex, and eventual deterioration into a sine wave pattern, ventricular dysrhythmias, or asystole.

Metabolic Acidosis in AKI

A common complication characterized by the accumulation of organic acids and the inability of the kidneys to excrete hydrogen ions, leading to a decrease in blood pH. It often results from renal failure due to a reduction in the excretion of acid waste products.

Uremia in AKI

A clinical syndrome resulting from the systemic retention of nitrogenous waste products and toxins due to severe filtration impairment; manifests across multiple organ systems through neurologic changes (fatigue, difficulty concentrating, confusion, encephalopathy, seizures in severe cases), gastrointestinal distress (Norexia, nausea, vomiting, altered taste), platelet dysfunction predisposing to bleeding, and pericarditis.

AKI Nursing Management

Monitor renal function

• creatinine, BUN, urine output

Monitor volume status

• strict I/O

• daily weights

• edema

• lung sounds

• blood pressure

• oxygenation

Monitor electrolytes/acid-base

• potassium, bicarbonate, sodium, phosphate

Medication Safety:

• Kidney dysfunction changes drug clearance so consider

  • renal dose adjustments

  • avoiding/minimizing nephrotoxins when possible

  • Monitoring medication level when indicated and assessing patient symptoms for complications.

CKD Progression

The progressive loss of functioning nephrons over time, resulting in multi-system pathophysiologic consequences and requiring targeted renoprotective strategies:

• Consequences of Progressive Nephron Loss:

  • Decreased waste clearance: Elevation of BUN and serum creatinine, eventually producing uremic manifestations

  • Fluid and electrolyte retention: Inability to excrete sodium and water (leading to hypertension and edema), reduced potassium excretion (hyperkalemia), and impaired acid excretion (metabolic acidosis)

  • Endocrine and mineral disturbances: Reduced erythropoietin (EPO) synthesis causing normocytic/normochromic anemia; phosphate retention and decreased calcitriol causing secondary hyperparathyroidism and CKD-MBD

  • Decreased drug clearance: Slower excretion predisposing to drug accumulation and toxicity

• Nephroprotective Strategies:

  • Controlling systemic blood pressure and blood glucose

  • Reducing intraglomerular pressure and albuminuria using ACE inhibitors, ARBs, or SGLT2 inhibitors

  • Avoiding nephrotoxins, preventing recurrent AKI, and adjusting medication dosing for reduced renal clearance

Anemia in CKD

A normocytic, normochromic hematologic complication primarily caused by reduced renal production of erythropoietin (EPO), leading to decreased bone marrow stimulation and insufficient red blood cell production.

Key Management Principles:

• Treated with iron supplementation and erythropoiesis-stimulating agents (ESAs); adequate iron stores are required for ESAs to be effective.

• Target hemoglobin levels should not be completely normalized with ESAs because higher hemoglobin targets increase cardiovascular and thrombotic risks.

CKD Nutrition

The dietary management that focuses on restricting protein, potassium, phosphorus, and sodium intake while ensuring adequate caloric intake to maintain nutritional status and minimize uremic symptoms. Recommendations depend on the CKD stage, lab values, medications, comorbidities, dialysis status, and nutritional status.

Hemodialysis (HD)

A renal replacement modality where blood is circulated through an extracorporeal artificial dialyzer to achieve solute clearance via diffusion and fluid removal via pressure-driven ultrafiltration.

• Function: Partially replaces waste clearance, fluid balance, and electrolyte/acid-base regulation; does not restore endocrine functions like erythropoietin production or vitamin D activation.

• Fluid Shifts: Produces rapid fluid removal; patients can experience intravascular volume depletion while still having total-body fluid overload.

• Vascular Access: Utilizes an AV fistula (preferred long-term, lowest infection/thrombosis risk), AV graft (synthetic conduit, usable sooner), or central venous catheter (immediate access, highest bacteremia risk).

Peritoneal Dialysis Exchange and Complications

A renal replacement modality utilizing the peritoneum as a semipermeable membrane across an inflow, dwell, and drain sequence, using glucose-containing dialysate to draw fluid across an osmotic gradient.

• PD Peritonitis: A major infectious complication signaled by cloudy effluent drainage with abdominal pain and tenderness.

• Inadequate Outflow: Managed by checking lines for kinks or closed clamps, repositioning the patient, and managing constipation; catheter drainage must never be forced.

• Metabolic and Mechanical Effects: Dialysate protein loss, hyperglycemia and weight gain from glucose absorption, increased intra-abdominal pressure causing hernias, and diaphragmatic elevation causing respiratory compromise.

Comparison of Hemodialysis (HD) vs. Peritoneal Dialysis (PD)

Key differences between HD and PD across clinical parameters:

• Membrane: HD uses an extracorporeal artificial dialyzer; PD uses the living peritoneal membrane.

• Fluid Removal: HD utilizes pressure-driven ultrafiltration; PD relies on an osmotic gradient generated by dextrose.

• Fluid Shift Rate: HD produces rapid volume shifts; PD achieves gradual fluid removal.

• Infection Risk: HD carries vascular access and bloodstream infection risks; PD carries peritonitis risk.

• Assessment Clues: Patent HD access presents with a palpable thrill and audible bruit; normal PD effluent is clear.

• Common Acute Issues: HD is prone to intradialytic hypotension and disequilibrium syndrome; PD is prone to catheter drainage problems and peritonitis.

Diffusion vs. Ultrafiltration in Dialysis

The two primary transport principles responsible for clearance and volume management during renal replacement therapy:

• Diffusion: The passive movement of dissolved solutes (such as urea, creatinine, and electrolytes) across a semipermeable membrane down a concentration gradient.

• Ultrafiltration: The bulk removal of excess water across a membrane, driven by hydrostatic pressure gradients in hemodialysis (HD) or an osmotic gradient established by glucose dialysate in peritoneal dialysis (PD).

Hemodialysis Fistula/Graft Protection

Techniques used to maintain the integrity of vascular access for hemodialysis, including methods to prevent thrombosis and infection while ensuring adequate blood flow. Regular monitoring and care of the access site are crucial.

Precautions include no blood pressure, no IVs, and no venipuncture on the access arm. Avoid constrictive clothing, prolonged compression, and sleeping with significant pressure on access arm.

Peritoneal Dialysis Complications

Key adverse events and clinical challenges associated with peritoneal dialysis (PD):

• Infectious Complications (Peritonitis):

  • Hallmark signs: cloudy dialysate effluent drainage along with abdominal pain, tenderness, fever, and nausea/vomiting.

  • Priority actions: promptly notify the nephrology team, obtain effluent specimens for culture, administer prescribed antibiotics, and enforce strict aseptic technique.

• Mechanical / Outflow Problems:

  • Poor catheter drainage often caused by kinked tubing, closed clamps, catheter migration, or constipation.

  • Management: check lines, reposition the patient, and treat constipation; never force catheter drainage.

• Metabolic Effects:

  • Hyperglycemia and weight gain secondary to peritoneal glucose absorption.

  • Significant protein loss across the peritoneal membrane into dialysate.

• Intra-abdominal Pressure Effects:

  • Hernia formation resulting from elevated intra-abdominal pressure.

  • Upward diaphragmatic displacement leading to respiratory compromise and dyspnea.

Kidney Transplant Graft Placement

The standard anatomical location and surgical arrangement for a renal allograft:

• Anatomical Site: Typically placed in the iliac fossa / lower abdomen.

• Native Kidneys: Usually left in place rather than being removed.

• From the donor:

  • renal artery —>connected to recipient iliac artery

  • renal vein —> connected to recipient iliac vein

  • ureter —> connected to the bladder

Post-Transplant Nursing Priorities

Key clinical priorities and surveillance areas for managing a kidney transplant recipient:

• Graft Function Surveillance: Monitor serum creatinine, BUN, and urine output; recognize that a rising creatinine signals graft dysfunction but requires differentiating between rejection, calcineurin inhibitor toxicity (e.g., tacrolimus), infection, and hypoperfusion.

• Fluid, Electrolyte, and Hemodynamic Balance: Closely monitor blood pressure, fluid volume status, strict intake and output, and electrolyte changes.

• Infection and Rejection Assessment: Maintain high vigilance for subtle signs of systemic infection (due to lifelong immunosuppressive therapy) as well as acute rejection signs (fever, graft tenderness, oliguria, fluid retention).

• Medication Monitoring and Adherence: Routinely measure immunosuppressive drug levels, screen for adverse drug effects/interactions, and reinforce strict, lifelong medication adherence.

Kidney Transplant Patient Teaching

Essential educational topics for kidney transplant recipients to protect graft survival and minimize complications:

• Lifelong Immunosuppressive Adherence: Reinforce that immunosuppressive therapy is lifelong and must be taken exactly as prescribed; missing doses significantly increases the risk of graft rejection, and dosages must never be adjusted without provider guidance.

• Infection Vigilance and Prevention: Explain that immunosuppressive medications heighten susceptibility to infections and malignancies; signs of infection may be subtle (such as a low-grade fever or mild malaise) and warrant immediate evaluation.

• Recognizing Graft Rejection: Educate the patient on warning signs such as tenderness over the graft site, decreased urine output, fluid retention/edema, sudden weight gain, fever, or elevated blood pressure, while highlighting that rejection may also occur silently with only an elevated serum creatinine.

• Routine Surveillance and Lab Monitoring: Stress the critical importance of attending scheduled clinic visits for routine lab draws (immunosuppressive drug levels, serum creatinine, BUN, electrolytes, and CBC), home blood pressure/glucose tracking, and avoiding nephrotoxic agents.

Impact of Cyst Enlargement on Renal Function in ADPKD

The pathophysiologic sequence by which cyst growth leads to progressive kidney dysfunction:

• Compression and Ischemia: Expanding fluid-filled cysts compress surrounding parenchyma and renal vasculature, producing local tissue ischemia.

• Nephron Loss: Mechanical compression and reduced perfusion lead to progressive nephron destruction.

• Compensatory Hyperfiltration: Surviving nephrons undergo compensatory hyperfiltration, which contributes to long-term glomerular damage.

• RAAS Activation and Hypertension: Renal ischemia stimulates the renin-angiotensin-aldosterone system, triggering hypertension that accelerates further kidney injury and progression toward chronic kidney failure.

ADPKD Management

Key clinical priorities and therapeutic strategies for managing autosomal dominant polycystic kidney disease (ADPKD):

• Blood Pressure Control: Aggressively manage hypertension (often driven by RAAS activation from local tissue ischemia) to slow renal decline and decrease cardiovascular risk with ACE inhibitors or ARBS.

• Complication Treatment: Promptly manage recurrent urinary tract and cyst infections, nephrolithiasis (kidney stones), hematuria, and chronic flank/abdominal pain.

• Intracranial Aneurysm Vigilance: Ensure emergent evaluation for sudden 'thunderclap' or 'worst headache of life' to assess for subarachnoid hemorrhage.

• Renoprotection and Surveillance: Avoid nephrotoxins to prevent superimposed kidney injury, manage cardiovascular risk factors, and routinely monitor CKD progression.