Chapter 28: Acute Kidney Injury and Chronic Kidney Disease Flashcards Preview

Patho Final Exam > Chapter 28: Acute Kidney Injury and Chronic Kidney Disease > Flashcards

Flashcards in Chapter 28: Acute Kidney Injury and Chronic Kidney Disease Deck (31):

Acute Kidney Injury

- formerly called acute kidney failure

- known as AKI

- Broad spectrum of kidney disease ranging form minor changes in renal function to complete renal failure requiring renal replacement therapy


Sudden reduction of kidney function causes

- disruptions in fluid, electrolyte, and acid-base balances

- retention of nitrogenous waste products (comes from breakdown of protein which leads to eleveted BUN)

- increased serum creatine

- decreased glomerular filtration rate (GFR)


Acute Kidney Injury additional info

- results in characteristic alterations in laboratory tests of blood and urine

- Renal function monitored by serum creatine and calculated GFR (serum creatine is most reliable lab testing to identify renal failure)

- Retention of metabolic wastes (azotemia/uremia); monitored by the BUN, produces widespread systemic effects (uremic syndrome)


Etiology and Pathophysiology of Acute Kidney Injury

- abrupt reduction in renal function producing an accumulation of waste materials in the blood

- May be due to aging, associated with comorbidities, or due to insults to the kidney

- 3 sites of disruption (1. renal perfusion 2. urine flow distal to the kidney 3. circumstances within the kidney blood vessels, tubules, glomeruli, or interstitium)

- Distinction between the sites of disruption helps determine appropriate therapy


Prerenal Kidney Injury

- Due to conditions that diminish perfusion of the kidney (hypovelemia, hypotension, heart failure, renal artery obstruction, fever, vomiting, diarrhea, burns, overuse of diuretics, edema, ascites, and drugs including ACE inhibitors, angiotensin II blockers, and NSAIDs)

- Characterized by low GFR, oliguria (less than 30 ccs urine/hr), high urine specific gravity and osmolality, and low urine sodium

- prolonged prerenal ARF leads to acute tubular necrosis


Postrenal Kidney Injury

- due to obstruction within the urinary collecting system distal to the kidney (stones); elevated pressure in the bowman capsule; impedes glomerular filtration

- clinical findings based on duration of the obstruction

- Prolonged postrenal ARF leads to acute tubular necrosis (intrinsic) and if continues leads to irreversible kidney damage


Intrinsic/Intrarenal Kidney Injury

- due to primary dysfunction of the nephrons and the kidney itself

- most common problem withing the renal tubules resulting in ACUTE TUBULAR NECROSIS (ATN); may also occur with glomerular, vascular, or interstitial etiologies

- ATN causes include nephrotoxic insult and ischemic insults

- Vascular Pathophysiological processes include decreased renal blood flow, hypoxia, and vasoconstriction

- tubular pathophysiological processes include inflammation and reperfusion injury, causes casts, obstructs urine flow, tubular backleak

- can repair itself or if injury is sustained leads to end-stage renal disease


Clinical Presentation of Acute Tubular Necrosis

- Divided into three phases (prodromal, oliguric, and post-oliguric)

- clinical presentation varies with the phase

- laboratory findings can help differentiate prerenal from intrinsic/intrarenal kidney injury


Prodromal Phase

- normal or declining urine output

- serum BUN and creatine begin to rise

- Insult to the kidney has occurred and the duration of this phase will vary depending on cause of injury, amount of the toxin ingested, and duration and severity of the hypotension


Oliguric Phase

- may last up to 8 weeks with usual urine output 50-400 mL/day

- characterized by oliguria and progressive uremia; decreased GFR; Hypervolemia (have signs and symptoms of fluid excess, hyperkalemia, and uremic syndrome)

- typically may last 1 to 2 weeks

- dialysis may be required


Post-Oliguric Phase

- termination of oliguric phase represents renal recovery

- sadly, not all recover from it

- urine volume increases (diuresis); tubular function impaired and azotemia continues

- fluid volume deficit until kidneys recover

- may last 2 to 10 days, full recovery takes around 1 year
(full recovery shows normal levels of BUN and creatine. Usually a degree of renal insufficiency persisits)


Chronic Kidney Disease

- Outcome of progressive an irrevocable loss of functional nephrons

- Progressive processes (Chronic Kidney Disease - chronic renal failure - end stage renal disease) (ESRD requires dialysis) (#1 REASON FOR ESRD IS HAPETIC NEUROPATHY)

- a global health problem often linked with other comorbidities, primarly hypertension and diabetes mellitus (highest risk for developing CKD)

- Defined as decreased kidney function or kidney damage of 3 months duration based on blood tests, urinalysis, and imaging studies

- also defined as GFR


Risk Factors of Chronic Kidney Disease

- diabetes

- hypertension

- recurrent pyelonephritis

- glomerulonephritis

- family history of CKD

- History of exposure to toxins

- age over 65

- ethnicity


Pathophysiology of Chronic Kidney Disease


- GFR reduction occurs with nephron loss (kidneys compensate until 75% to 80% of nephrons are damaged/nonfunctional)

- Progression is monitored by a staging system

- 5 stages of progression and with each higher stage the GFR and kidney function declines


Stages of Chronic Kidney Disease

- Stage 1 and stage 2 focuses on minimizing risk factors

- stage 3 symptoms may be starting to appear and treatment may be needed

- in stage 4 planning for dialysis or transplant should begin

- in stage 5 renal replacement therapy needed or death will ensue


Complications of Chronic Kidney Disease

- Hypertension and cardiovascular disease (hypervolemia, escalated atherosclerotic process, heightened RAAS and SNS activity)

- Uremic Syndrome (retention of metabolic wastes; impaired healing, pruritus; dermatitis, uremic frost)

- Metabolic Acidosis (retention of acidic waste products, hyperkalemia; kidneys lose ability to secrete H+ ions and bicarbonate)

- Electrolyte imbalances (retained potassium, phosphorus, and magnesium)

- Bone and Mineral disorders (elevated phosphorus and Parathyroid Hormone (PTH) causes altered bone/mineral metabolism; kidenys unable to reabsorb calcium)

- Malnutrition (decreased intake from uremic syndrome, depression, dietary limitations, changes in taste, protein energy wasting; negative nitrogen balance

- Anemia (lack of erythopoietien; uremia shortens RBCs life; combination of worsening CKD, anemia, and heart failure (cardiorenal anemia syndrome))

- Pain (many reasons; disease itself, treatment, and comorbidities)

- Depression (co-morbid conditions; disease itself; disruption of social interactions and relationships)


Prevention of Acute Kidney Injury

- early identification of risk

- maintenance of fluid volume status and cardiac output

- avoid and monitor nephrotoxic chemicals

- avoid and aggresively treat infections

- remove indwelling catheters ASAP

- dopamine should not be used for treatment

- Avoid contrast media complications (initiate IV saline both before and after contrast administration, Administer antioxidant N-acetylcysteine (mucomyst) to patients at risk (controversial), measure serum creatine if suspect renal dysfunction, use either low-osmolar or iso-osmolar contrast media, and ensure hydration)


Clinical Management of Chronic Kidney Disease

- complex

- requires multidisciplinary

- Slowing the progression of CKD is the focus of intervention until stage 4 or 5

- do this by giving ACE inhibitors if diabetics (or ARBS) (can cause hyperkalemia so monitor K+)


Primary Foci of Chronic Kidney Disease

- appropriate management of ATN

- blood glucose control in diabetes

- ACE inhibitors or angiotensis II blockers to reduce proteinuria (ARBS)

- Agressive Management of hypertension


Chronic Kidney Disease (Hypertension and Cardiovascular disease)

- cardiovascular disease is both a risk factor for CKD and accelerates progression

- BP goal , 130/80 mmHg

- Angiotensin-converting enzyme inhibitor (ACEI)

- Angiotensin II receptor blocker (treatment of choice)

- statins to decrease dyslipidemia (controversial) (thought to minimize all risk factors)


Chronic Kidney Disease (Metabolic Acidosis)

- mild acidosis (pH of 7.30 to 7.35) requires no therapy

- Chronic metabolic acidosis (


Chronic Kidney Disease (Fluid Electrolyte Imbalances)

- fluid restrictions: if sodium , 135 mmol/L

- if edema/heart failure/hypertension : may need 2 g/day sodium restriction

- Mild hyperkalemia ( 6 mmol/L: IV calcium gluconate, D5W, and Insulin; oral/rectal sodium polystyrene sulfonate


Chronic Kidney Disease (Bone and mineral disorders)

- PTH, calcium, and phosphorus should be monitored if GFR less than 60 mL/min/1,73m2

- Hypocalcemia: calcium bicarbonate, calcium acetate, lanthanum carbonate

- Vitamin D: for deficiency and suppress PTH

- Calcimimetics: Suppress PTH


Chronic Kidney Disease (Malnutrition)

- calories, vitamins, calcium increased

- sufficient carbohydrate and fat to meet energy requirements

- Limit dietary phosphorus, protein, sodium, potassium, and water/fluids depending on lab values and other clinical manifestations

- Limit dietary factors that could increase cardiovascular risk

- involving a dietitian is crucial


Chronic Kidney Disease (Anemia)

- recommended Hgb levels 11 and 12 g/dl

- Erythropoiesis-stimulating agents (ESA), such as epoetin alfa and darbepoetin alfa (will dramatically improve quality of life, does not improve cardiovascular mortaility of CKD)

- Balance rest and activity


Chronic Kidney Disease (DIalysis)

- used for ATN and CKD in stage 5 (GFR


Chronic Kidney Disease (Hemodialysis)

- artificial kidney serves as the dialyzing semi-permeable membrane

- access: arteriovenous (AV) fistula (cant take BP with it in and no IVs)

- 3x/week; each session is 4 hours long


Chronic Kidney Disease (Contiunous Renal Replacement Therapy Dialysis)

- limited to in-hospital AKI patients; continuous hemofiltration and hemodialysis procedures filter and dialyze the blood without interruption


Chronic Kidney Disease (Peritoneal Dialysis)

- peritoneum serves as the dialyzing membrane

- access: dialysis catheter surgically placed in abdomen

- Types: Continuous Ambulatory Peritoneal Dialysis (CAPD) and Continuous Cycling Peritoneal Dialysis (CCPD)

- CAPD: exchanges performed by patients in their homes and without machines; instills in abdomen

- CCPD: can also be done at home; uses a special machine (cycler); exchanges occur while sleeping


Chronic Kidnety Disease (Transplantation)

- potential option for patients with ESRD

- Associated with a high degree of success

- allows for increased independence

- return to normal activities of daily living

- normal renal function

- antirejection drub therapy required; immunosuppressants


Chronic Kidney Disease in Older Adults

- Majority of patients diagnosed with CKD are older adults

- Rates of treated ESRD among the elderly (>80 years) have risen by more than 50% in the last decade

- Dialysis for elderly is becoming worldwide

- co-morbid conditions of this population require complex care