Chapter 51: Acute Kidney Injury & Chronic Kidney Disease

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Welcome back to the Deep Dive.

We're here to unpack complex medical topics, really give you those important nuggets of knowledge.

That's the goal.

And today we're tackling a really big one from your Lewis textbook,

kidney failure.

It's huge.

And it's not just, you know, one organ we're talking about.

This condition, it can hit every single body system.

It's a massive challenge for patients, physically, yeah, but emotionally too.

Absolutely.

And when we say kidney failure, it's actually more of a spectrum.

You've got acute kidney injury, AKI on one side that comes on fast, but crucially, it can potentially be reversed.

Okay.

Then on the other end, there's chronic kidney disease, CKD.

That's the slow gradual decline, often irreversible, understanding both, well, it's fundamental for your nursing practice.

So our mission today is really to walk you through AKI and CKD.

We'll cover the causes, how patients present, diagnosis, and importantly, the nursing management, what you do.

Yeah.

Think of it as your roadmap for these conditions, all the key terms, the clinical scenarios you'll encounter.

Exactly.

Let's unpack this.

Okay.

Let's start with acute kidney injury, AKI.

This is that sudden, rapid loss of kidney function.

We're talking hours or days.

Right.

And while it can be reversible, and that's key, it's serious stuff.

It carries a high mortality rate, especially for patients who are already critically ill.

And clinically, you're seeing that rapid rise in markers like BUN, creatinine, potassium,

things you'll be watching like a hawk.

Exactly.

What's really helpful, I think, is how we categorize the causes.

It points you towards the underlying problem.

We break it down into three main areas.

First up, pre -renal causes.

So this is about factors that reduce blood flow to the kidneys.

Before the kidney itself.

Precisely.

Right.

Think severe dehydration, maybe heart failure, even major burns.

The kidney tissue itself isn't damaged yet.

It's a perfusion issue.

So if you fix a blood flow problem.

Often, yeah.

If you restore that perfusion quickly with fluids, kidney function can bounce back.

It's like a plumbing problem before the filter.

Got it.

What of the issue is the filter?

Right.

So that takes us to inter -renal causes.

Here, the damage is actually inside the kidney tissue hitting the nephrons.

The most common cause you'll see in hospitalized patients.

Acute tubular necrosis or ATN.

ATN.

Okay.

And that can happen from prolonged ischemia, basically.

Not enough blood flow for too long or from nephrotoxins.

Like certain drugs.

Contrast die.

Exactly.

Some antibiotics, contrast media used for CT scans, things like that.

Even severe crush injuries can do it.

Releasing toxins.

Wow.

Okay.

So pre -renal, intra -renal.

What's the third?

Post -renal causes.

So now we're after the kidneys.

It's a mechanical obstruction blocking urine from getting out.

Like a blockage.

Yeah.

Common things are an enlarged prostate BPH or prostate cancer, kidney stones.

The good news here is if you relieve that obstruction quickly, ideally within about 48 hours, kidney function often fully recovers.

That framework, pre -renal, intra -renal, post -renal seems really useful for assessment.

How does AKI actually look as it develops in a patient?

What are the phases?

That's a great question because understanding the phases really guides your nursing care.

The first phase and the most common one you'll see initially is the oligaric phase.

Oligaric meaning low urine output.

Exactly.

Less than 400 millililes per day, typically.

This phase can last 10 to 14 days, maybe longer.

And as a nurse, you're immediately thinking fluid retention.

Right.

Distended neck veins.

Bounding, pulse, edema, hypertension, all those signs.

Patients also often develop metabolic acidosis because the kidneys can't excrete hydrogen ions.

And potassium.

Ah, yes.

Hyperkalemia.

That's a critical concern.

The kidneys can't get rid of potassium and high levels can cause fatal heart rhythms.

You'll definitely be watching the ECG for those peaked T waves.

Okay, so after the oligaric phase.

Hopefully the patient moves into the diuretic phase.

Now, urine output increases dramatically, sometimes up to five liters a day and maybe even more.

Wow, that's a big swing.

It is.

And while it shows the kidneys are starting to excrete waste again, they can't concentrate urine properly yet, so you're losing massive amounts of fluid and electrolytes.

So your focus shifts completely.

Completely.

Now you're monitoring closely for hypovolemia, low volume hypotension, low sodium, low potassium, big fluid losses.

And then hopefully recovery.

The recovery phase.

That's when the GFR, the gramerular filtration rate, starts to increase and BUN and creatinine levels begin to normalize.

But this phase can take a long time, up to 12 months.

And not everyone recovers fully.

That's right.

Some patients might progress to chronic kidney disease.

And that rifly classification you mentioned earlier that helps track the severity through these phases.

Exactly.

Ripley risk, injury, failure, loss, end stage renal disease.

It standardizes things, gives the whole team a common language based on creatinine changes, GFR, urine output.

Like a roadmap for progression.

Precisely.

Risk might be a 1 .5 times increase in creatinine while failure is much more severe, like a three times increase or needing RRT.

It helps everyone understand how sick the patient is.

So when you're diagnosing AKI, beyond watching these phases and symptoms, what are the key diagnostic tests?

Well, the patient history is vital trying to pinpoint that cause pre renal, intra renal, post renal.

But labs are key.

Serum creatinine and BUN, obviously.

Standard kidney function tests.

Right.

And a urinalysis is crucial.

It can show things like casts, red blood cells, or protein, which often point towards those intra renal problems.

What about imaging?

A kidney ultrasound is usually the first choice.

It's non -invasive.

It avoids contrast dye, which can be nephrotoxic.

Right.

You don't want to make things worse.

Exactly.

And it's great for ruling out obstructions, those post renal causes.

Okay.

So AKI is confirmed.

What's the game plan?

What are the nursing and interprofessional priorities?

The main goals are always number one, eliminate the cause if possible.

Number two, prevent complications while the kidneys heal.

And nurses are central to managing fluids and electrolytes.

That fluid restriction in the oliguric phase, how does that work?

Yeah, it's often necessary.

The general rule of thumb you'll use is calculate the patient's total output over the previous 24 hours, and then add 600 millimail to that.

The 600 millimail is for Insensible losses, you know, fluid loss through breathing, sweating, stuff you can't easily measure.

This calculation helps you give just enough fluid to avoid overload, but also prevent dehydration.

It's a fine balance.

And managing that dangerous hyperkalemia.

Oh, absolutely critical.

It can be life threatening because of the heart.

So immediate actions might include IV insulin and glucose.

Now that doesn't remove potassium.

It just shifts it.

Right, shifts it into the cells temporarily, buys you time.

Calcium gluconate is different.

It helps stabilize the heart muscle itself against the potassium effects.

And for actually removing potassium.

Longer term, you might use sodium polystyrene sulfonate, kiaxolate.

It works in the osmotic diarrhea, so you'll manage that too.

But in really urgent situations, hemodialysis is the most effective way to pull that potassium off quickly.

And of course, nutrition therapy is key enough calories, but limiting protein, potassium and sodium.

And just the day to day nursing management, what are those absolute must do's at the bedside?

You know, the basics become so important.

Daily weights, same time, same scale, same If possible, strict intake and output,

vital signs, frequently constant monitoring, constant assessment.

You're looking for subtle signs of fluid overload or depletion,

checking urine color, specific gravity, watching mental status.

Uremia can cause confusion and infection prevention is huge.

Why is infection such a big risk?

It's actually the leading cause of death in AKI patients.

Their immune system can be

So meticulous aseptic technique with lines and catheters is non -negotiable, and you need to be vigilant for infection signs, which might even be blunted like maybe no fever.

And teaching the patient too, I imagine.

Absolutely, especially about preventing it from happening again, if possible.

Okay, that's a really good overview of AKI.

Let's shift gears now to chronic kidney disease, CKD.

Right, the long game.

Yeah.

And what always gets me about CKD is how sneaky it can be.

Like you said, it's gradual, often silent until a lot of damage is already done.

It really is.

And it's much more common than AKI affects about one in nine adults in the US.

The biggest culprits, diabetes, causing about half the cases.

50%.

Wow.

Yeah.

And hypertension is next, around 25%.

The definition, according to Katie J.

Goh guidelines, is kidney damage or a GFR less than 60 for more than three months.

And it progresses in stages.

Five stages based on GFR.

Stage five is end -stage renal disease, ESRD, where GFR is typically less than 15.

And patients usually need one -hole replacement therapy, dialysis, or transplant.

So as that GFR slowly drops, what's happening systemically?

You mentioned it affects every body system.

Yeah.

How does that play out?

It's a cascade, like you said.

As function declines, waste products build up.

This leads to a syndrome called uremia, which becomes really evident usually when GFR hits 15 or lower.

And uremia impacts everything.

Okay.

Break that down for us.

What are some key system impacts?

All right.

So metabolically, BUN and creatinine climb, causing nausea, vomiting, fatigue, trouble concentrating.

An interesting point for diabetic patients.

Yeah.

They might actually need less insulin.

Less.

Why?

Because healthy kidneys help break down insulin.

As they fail, insulin hangs around longer, so their requirements can drop.

Also, dyslipidemia abnormal cholesterol is common, raising cardiovascular risk.

Okay.

What about electrolytes?

Still worried about potassium?

Definitely.

Hyperkalemia is a major concern in CKD too.

Sodium retention is also common, leading to edema, hypertension,

and eventually heart failure.

Plus, metabolic acidosis persists because the kidneys can't excrete acid or regenerate by carbonate.

And blood counts.

Big impact on the hematologic system.

Anemia is almost universal.

The kidneys aren't making enough erythrocoietin, the hormone that signals bone marrow to make red blood cells.

They'll need EPO injections, maybe iron.

Often, yes.

And a key nursing tip.

Oral iron supplements shouldn't be taken at the same time as phosphate binders because the binders reduce iron absorption.

Also, platelets don't work as well, so there's a bleeding risk.

And infection risk is higher too.

You mentioned cardiovascular risk earlier.

It's huge.

Cardiovascular disease, CVD, is the leading cause of death for CKD patients.

Hypertension is a major driver, both a cause and a result of CKD.

Managing blood pressure is absolutely critical.

Vascular calcification also happens, calcium depositing in blood vessels.

Is it even stiff?

Exactly.

It increases risk of heart attack and stroke.

What are the GI tract?

GI system issues are common.

Stomatitis, inflammation in the mouth, a metallic taste.

Something called uremic fedor, which is like a urinous odor on the breath.

Anorexia, nausea, vomiting are frequent.

Constipation too, sometimes from iron pills or phosphate binders.

Neurologically.

The neurologic system is affected by those accumulating waste products.

You see CNS depression fatigue, difficulty concentrating.

In severe uremia, seizures or even coma can occur.

Peripheral neuropathy is also common tingling.

Burning in the feet and legs, restless legs syndrome.

Okay, that's a lot already.

What about bones?

Ah, the musculoskeletal system.

This is where we see CKD mineral and bone disorder or CKD -MBAD.

It's complex.

Break it down.

Okay, so failing kidneys can't activate vitamin D.

Without active vitamin D, you can't absorb calcium well from your gut, leading to low blood calcium, hypocalcemia.

And the body tries to compensate.

Right.

The parathyroid gland senses the low calcium and pumps out parathyroid hormone, PTH.

PTH tells the bones to release calcium into the blood.

Which weakens the bones.

Exactly.

It leads to bone demuralization, increased fracture risk.

You get conditions like osteomalacia and osteotis fibrosa.

Plus, the high phosphate levels that also occur in CKD contribute to those vascular calcifications we talked about.

Wow, and the skin.

Skin issues are common too.

Fertilitis, severe, persistent itching is really distressing for patients.

In very advanced cases, you might see uremic frost, where urea crystallizes on the skin as sweat evaporates.

And psychologically.

Huge impact.

Anxiety, depression, body image changes, coping with a chronic illness and its treatments.

It's a massive adjustment.

That really illustrates how CKD affects the whole person.

So given all that, how do we diagnose and manage CKD?

Diagnosis often starts with finding persistent protein area protein in the urine.

That's often the earliest sign.

So routine your analysis or specific albumin checks are key.

Especially for high -risk folks like diabetics.

And confirming function.

The GFR is the gold standard for determining kidney function and staging the disease.

It's usually estimated using formulas based on serum creatinine, age, gender, race.

And management.

Interprofessional care is crucial.

Early referral to an nephrologist helps.

The goals are to preserve remaining kidney function, aggressively manage cardiovascular risk factors, prevent complications, and prepare for eventual renal replacement therapy if needed.

What about medications?

Drug therapy targets those specific problems we discussed.

Managing hyperkalemia with potassium binders like kyexalate or newer ones like poteramer.

Controlling hypertension is vital.

ACE inhibitors or ARBs are often used, especially in diabetics.

But you have to watch potassium levels closely with those.

Then treating CKD, MBD with phosphate binders crucially.

These must be taken with meals to work properly.

They bind dietary phosphate.

Plus activated vitamin D supplements.

And managing anemia with EPO therapy and iron.

And nutrition therapy seems absolutely central.

Oh, it is.

And nurses play a huge role in teaching and reinforcing this.

So, pay close attention here.

Okay.

Protein restriction is usually needed in earlier stages, stages one to four, to reduce the load on the kidneys.

But interestingly, once a patient is on dialysis, they actually need more protein because some is lost during the treatment.

It's individualized.

Pulled restriction.

Not usually needed in early CKD unless there's edema.

But for hemodialysis patients, yes.

It's typically based on their urine output from the day before.

Plus about 600 millivals for insensible losses.

You'll teach them to count things like soup, jello, ice cream as fluid intake.

Sodium and potassium.

Definitely restricted.

Usually around two to four grams a day for sodium, two to three grams for potassium.

But it depends on their lab results.

Patients on peritoneal dialysis often have fewer potassium restrictions.

And phosphate.

Big one.

Phosphate restriction, usually to about one gram a day for ESRD patients, is vital because the kidneys just can't clear it.

That means limiting high phosphate foods like meat and dairy.

And again, those phosphate binders taken with every meal.

It really is a full -body, highly detailed approach to nursing care.

It is.

And a huge part of it is health promotion, identifying people at risk.

Diabetes, hypertension, family history, making sure they get regular checkups, including urinalysis and GFR checks.

And then continuous patient education.

Teaching them about diet, meds, side effects.

Exactly.

Recognizing signs of fluid overload like weight gain or shortness of breath or signs of electrolyte problems.

It's all about empowering them to manage this chronic condition.

Okay, so when that conservative management, the diet, the meds isn't enough, we move to renal replacement therapy, RRT dialysis.

Right.

Dialysis becomes necessary when the kidneys can no longer maintain fluid, electrolyte, and waist balance.

It basically takes over some of the kidneys' filtering job.

How does it work?

What are the principles?

It relies on moving fluid and solutes across a semi -permeable membrane.

Three main principles are at play.

Diffusion, where waste products like urea move from the blood, high concentration, to the dialysate fluid, low concentration.

Okay.

Then osmosis, where water moves from an area of lower solute concentration, usually the blood, to higher solute concentration, the dialysate if glucose is added.

And ultrafiltration, which is fluid removal using pressure gradients, essentially pulling excess fluid off.

Let's talk about the TICE.

Peritoneal dialysis, PD.

How does that one work?

So in PD, the patient's own peritoneal membrane, the lining of their abdomen acts as that semi -permeable membrane.

A catheter is surgically placed into the abdomen.

Okay.

The process involves cycles or exchanges.

First is inflow.

Sterile dialysate solution is infused into the peritoneal cavity, usually one to three liters, then dwell.

The solution sits there for a prescribed time, usually four to six hours, allowing diffusion and osmosis to happen.

Finally, drain.

The fluid, now containing waste products and excess fluid, called effluent, is drained out.

And patients can do this at home?

Many do.

There are two main types.

Automated peritoneal dialysis, APD, uses a machine called a cycler to do the exchanges automatically overnight while the patient sleeps.

Continuous ambulatory peritoneal dialysis, CAPD, involves manual exchanges done by the patient or caregiver several times throughout the day.

What are the big nursing considerations for PD?

The absolute top priority is preventing peritonitis infection of the peritoneal cavity.

It's the most serious complication.

Meticulous aseptic technique during connections and disconnections is crucial.

How would you recognize peritonitis?

Key signs are abdominal pain, rebound tenderness, and especially cloudy peritoneal effluent.

If the drain fluid looks cloudy, like you can't read print through the bag, that's a major red flag for infection.

You'd also look for fever.

Other potential issues are exit site infections, hernias, lower back pain, and some protein loss into the dialysis.

Okay, so that's PD.

What about hemodialysis, HD, the one most people picture?

Right.

HD uses an artificial membrane called a dialyzer or artificial kidney in a machine outside the body.

Because it needs to process a lot of blood quickly, getting good vascular access is essential.

A fistula.

That's the preferred long -term access, yes.

And arteriovenous fistula, AVF.

It's created surgically by connecting an artery and a vein, usually in the forearm.

This makes the vein larger and stronger, able to handle the large needles and high flow rates.

And how do you know it's working?

You need to assess it every shift.

You feel for a thrill, like a buzzing or vibration, and listen with a stethoscope for a brute, a rushing sound.

Thrill and brute mean it's patent, blood is flowing through.

What if they can't get a fistula?

Then an arteriovenous graft, AVG might be placed.

It's a synthetic tube connecting an artery and vein.

These tend to have more complications like clotting or infection than fistulas.

For temporary access, a catheter can be placed in a large vein, like the internal jugular or femoral vein.

You mentioned a safety alert earlier.

Yes.

Crucial for nurses.

Never, ever perform blood pressure measurements, insert 5E lines, or draw blood from the arm that has the AV fistula or graft.

Why not?

It can cause clotting or damage the access, which is literally the patient's lifeline for dialysis.

That arm should be clearly marked, maybe with a wristband, and protected.

Okay, so during the HD treatment itself.

Two large bore needles, usually 14 or 16 gauge, are inserted into the fistula or graft.

One pulls blood out to the dialyzer, the machine filters it, and the other returns the clean blood to the patient.

Heparin is usually given to prevent clotting in the circuit.

And nursing care during treatment.

You're monitoring vital signs very closely, often every 30 to 60 minutes, because large amounts of fluid can be removed quickly, potentially causing hypotension.

You're also watching for muscle cramps, blood loss, and assessing the access site.

Okay, and briefly, what's CRT, continuous renal replacement therapy?

Yes, CRT is usually done in the ICU setting, primarily for patients with AKI who are too hemodynamically unstable for regular HD.

Why is it better for unstable patients?

Because it removes toxins and fluids much more slowly and continuously over 24 hours, kind of like real kidneys.

This gradual process avoids the rapid fluid shifts that can cause hypotension in standard HD.

Nurses managing CRT monitor fluids, electrolytes, vitals, and the circuit itself very closely, often hourly.

Okay, that covers dialysis well.

Now, the final option for ESRD, kidney transplantation.

Right, the gold standard, really.

A transplant offers the best chance at reversing many of the problems of kidney failure, getting patients off dialysis, and improving quality of life significantly, but— There's a shortage of organs.

A huge disparity between supply and demand.

Thousands are waiting.

How are recipients selected?

It involves a very thorough medical and psychosocial evaluation.

Some things might rule a patient out, like active cancer, severe heart disease that can't be treated, or major psychosocial issues like nonadherence.

Interestingly, some patients, especially those with a living donor lined up, can get a preemptive transplant before even needing to start dialysis.

And donors?

Can be living blood relatives, spouses, friends, even altruistic strangers or deceased.

Usually individuals declared brain dead whose families consent to donation.

Living donor transplants generally have better outcomes.

Why is that?

Several reasons.

The kidney is usually healthier, the surgery can be scheduled electively, and critically, the cold time.

The time the kidney is without blood supply between removal and transplantation is much shorter.

So the surgery itself, for the recipient, where does the new kidney go?

It's usually placed extraperitoneally, meaning outside the abdominal cavity proper, down in the iliac fossa, the lower part of the abdomen, near the hip bone.

The surgeon connects the new kidney's artery and vein to the recipient's iliac vessels, and the new ureter is connected to the bladder.

Rapid revascularization is key.

And immediately post -op, what are the nursing priorities?

Fluid and electrolyte balance is huge right after surgery.

The new kidney might kick in right away and start making large amounts of urine, sometimes a liter an hour.

Well, so you replace that.

Yes, typically you replace that output milliliter for milliliter, usually with IV fluids, for the first 12 to 24 hours to prevent dehydration.

You're also monitoring electrolytes closely, especially for low sodium and potassium due to the high urine output.

But sometimes it doesn't work right away.

Right.

Sometimes the transplanted kidney experiences, acute tubular necrosis, ATN, maybe from that cold time or other factors.

So the patient might still need dialysis for days or even weeks after the transplant, which can be really discouraging for them.

You'd watch urine output closely.

Absolutely.

A sudden decrease in urine output is always a concern.

It could mean dehydration, rejection, maybe a leak where the ureter is connected, or even a clot in the bladder catheter needs prompt investigation.

So assuming the initial phase goes OK, what are the big long -term challenges after a transplant?

Lifelong management is needed.

The major complications are rejection, the body's immune system recognizing the kidney as foreign.

It can be hyperacute right away, acute days to months later, or chronic over years.

Which requires immunosuppressants.

Exactly.

Lifelong immunosuppression is necessary to prevent rejection, but that leads to the next major challenge.

Infection.

Because the immune system is suppressed.

Right.

Infection is a leading cause of death after transplant.

Patients are vulnerable to bacterial, fungal, like Candida, and viral, like CMV, infections.

Nurses need to be super vigilant for subtle signs.

Prophylactic meds are common.

What else?

Cardiovascular disease is still the leading cause of death, even after a successful transplant.

Pre -existing risks plus side effects of immunosuppressants contribute.

Cancers, especially skin cancers, and a type called post -transplant lympho -proliferative disorder, PTLD, are more common due to the immunosuppression.

And finally, corticosteroid -related complications from long -term steroid use.

Things like bone necrosis, ulcers, diabetes, cataracts.

This is definitely not a cure, but a different set of challenges to manage.

Exactly.

A new lease on life, but requires intense lifelong medical management and vigilance.

Wow.

Okay, we have really covered a tremendous amount of ground today.

From that rapid hit of AKI, through the slow burn of CKD, and into the complexities of dialysis and transplantation.

It's so clear how kidney failure impacts everything and how vital the nurse's role is.

Absolutely.

I think the key clinical takeaways for you are really about early recognition and that meticulous nursing management, fluids, electrolytes, waste products, it's critical in both AKI and CKD.

And understanding the specific interventions for each situation.

Knowing how to assess that AV fistula, feeling the thrill, hearing the brute,

recognizing cloudy effluent and PD as a sign of peritonitis.

Knowing why phosphate binders go with meals, it all empowers you to give really targeted, effective care.

You definitely have a solid foundation now, pulling all that information from Lewis's right into how you'll think clinically.

We really hope this deep dive makes you feel more prepared when you encounter patients with kidney disease.

And maybe even inspire some of you to look into nephrology nursing.

Could be.

And remember, your role in educating and supporting patients and families through these really tough journeys, well, it's just invaluable.

Helping them navigate it all for the best possible quality of life.

Well said.

Thank you for joining us on the deep dive.

Maybe take a moment to think about the ethical side too, especially with transplantation, resource allocation, donor issues.

And remember the huge responsibility you have in empowering patients living with these chronic conditions.

Keep learning, keep questioning, and keep making that difference.